Beruflich Dokumente
Kultur Dokumente
One objective of this book is to make information quickly available. To this end, we have organized the breeds alphabetically. At the end of
the book, there are appendices that contain quick reference to conditions by breed, available genetic tests, and registries.
This book is not an indictment on the health of purebred dogs and pedigreed cats. The majority of genetic disease that is seen in dogs and
cats appears equally in purebred, designer cross-bred, and random-bred individuals. However, the improved genetic health of all dogs and
cats is dependent on breeder selection of genetically healthy parents. Indeed, it is the ethical responsibility of breeders to do so. This book
provides the information necessary to make those breeding decisions.
This first edition constitutes an important, up-to-date medical reference source for the reader. We strived to make it complete yet practical
and easy to use. Our dreams are realized if this text helps you to quickly locate and use the information that is essential to high-quality
veterinary medical care. We would appreciate your input so that we can make future editions even more useful. If you would like to see any
changes in content or format, additions, or deletions, please let us know. Send comments to the following:
Jerold S. Bell
Kathleen Cavanagh
Larry P. Tilley
Jerold S. Bell
I would like to thank my family (Dave, Kevin, and Patrick, and my now deceased father Ray) for their patience, while considerable family
time was dedicated to the research, writing and reviews for this project. My Burmese cat was 24 years old in 2010 as I wrote this, and was
a constant companion to me at the computer while working on the book over the years. Her loving and gentle, warm presence epitomized
the deep human-animal bond that inspires us to help our 4-legged friends live a long, healthy, and fulfilling lifespan, hopefully free of
genetic and other disorders.
Kathleen Cavanagh
To my wife, Jeri, my son, Kyle, my grandson, Tucker, in honor of that secret correspondence within our hearts; to family and animals who
represent the purity of life.
To my wife, May, my son, Ben, and my daughter, Jade, I cherish our time together and your constant love and support. To my father, Frank,
thanks for being my perfect role model.
In addition to thanking veterinarians who have referred patients to us, we would like to express our gratitude to each of the veterinary
students, interns, and residents whom we have had the privilege of teaching. Their curiosity and intellectual stimulation have enabled us to
grow and have prompted us to undertake the task of writing this book.
We would like to thank the cat and dog fancy, breeders and breed clubs, committed veterinarians, genetics researchers, educators, genetic
testing facilities, animal health associations, foundations, and many others worldwide who work together to provide optimal health and
welfare, through research and application of new knowledge towards canine and feline health. Without their dedication, the field would
not be advancing. Our sincere thanks go out to all for their continuing support of this exciting field of endeavor.
Finally, a special thank you goes to Carroll Cann and to all the rest of the staff at Teton New Media and everyone in the production and
editing departments. They are all meticulous workers and kind people who have made the final stages of preparing this book both inspiring
and fun. An important life goal of ours has been fulfilled: to provide expertise in small animal internal medicine and to teach the principles
contained in this textbook to veterinarians, students, breeders, and pet owners everywhere.
Appendix A: Available Genetic Tests for Breed Specific Canine and Feline Genetic Disorders......................... 591
Appendix B: Genetic Testing Centers........................................................................................................................................................................ 599
Appendix C: Quick Reference to Conditions by Breed
Part 1: Breed Specific Conditions in Dogs........................................................................................................................................ 601
Part 2: Breed Specific Conditions in Cats.......................................................................................................................................... 640
Appendix D: Cat Fancy Registries and Kennel Clubs.................................................................................................................................. 645
Appendix E: Other Resources............................................................................................................................................................................................ 647
Appendix F: General References for the Dog and Cat.............................................................................................................................. 648
Appendix G: Glossary of Terms....................................................................................................................................................................................... 649
Index.......................................................................................................................................................................................................................................................... 657
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Section 1 General Information
How to use this Book
Each species section of the book has a foreword that provides orientation to the content of the section. All chapters are consistent in
layout and presentation. Appendices have been provided where there is a need for summary information applicable to all breeds. The
sections on genetic concepts and genetic counselling are designed as a concise review only. Standard genetics texts should be consulted
for in-depth material. The glossary (terms definitions list) is limited primarily to genetic terms and conformation/color terms. A standard
medical dictionary should be consulted for terms not defined. Where conditions have been covered in detail in internal medicine texts,
coverage herein is cursory. Internal medicine texts should be referred to during case management.
This book is not meant to be a breed promotion book, but rather a presentation of scientific facts. This is especially difficult in one section
of the chapters, the Recognized Behavior Issues and Traits. Reported breed characteristics are collated from many sources, including cat
fancy organizations, kennel clubs and lay breed books whose mission is to promote breeds. For this reason, and because temperament and
personality traits of an individual cannot be generalized to a population, this section should be interpreted in a general way only.
As with all published works, because of advances in knowledge, this is a work that represents the state of our understanding as of the year
of publication only. As we continue to update the resource in the next few years, we hope to hear from readers to help us identify gaps
in content, and hear from those carrying out research who are aware of new findings in order to help us maintain a state-of-the-art fact
finder book. As a first edition, this is a first pass through the literature and first proof of concept. If any reader would like to provide input
on format, content or concept, please contact us to help us make our next edition even better. Our goal is to provide regular updates to
maintain contemporary content. Our next edition will include some additional rare breeds, and updates on active areas of research.
We hope that this new textbook provides an effective, concise source of information to help your practice achieve a best practices quality
approach to the care of dog and cat breeds.
The authors
1
Genetic Concepts
Any trait or disorder that has a hereditary component is genetic. Congenital disorders are those present at birth. Some congenital disorders
are hereditary, and others are not. Those occurring spontaneously may be caused by environmental exposures to infections, or compounds
such as drugs or toxins. Genetic disorders will sometimes only be evident much later in life, even though the genetic coding for the
disorder is present at birth. The age of onset of a trait or disorder does not differentiate whether it is genetic or environmental. Some
disorders can be caused by either a genetic or acquired (phenocopy) origin, and need to be differentiated in order to determine if genetic
counseling is warranted. For example, the neurological incoordination disorder cerebellar hypoplasia in cats can be a hereditary disease, but
can also be caused by in-utero infection with feline panleukopenia virus.
As our understanding of genetic mechanisms evolves, we are finding out that a lot more disorders have genetic influences than previously
thought. The inheritance of genes that cause liability or susceptibility to disease can present as breed predispositions. Identifying specific,
testable genes for these disorders will be helpful in their control.
Genes are pieces of deoxyribonucleic acid (DNA). Coding genes produce proteins and enzymes. Regulatory genes act to turn coding
genes on or off. Genes are contained on paired chromosomes that are either autosomes, or sex chromosomes. Females have two X sex
chromosomes, and males have an X and a Y. Dogs have 38 pairs of autosomal chromosomes, and cats have 18 pairs. One gene in each gene
pair comes from the father and the other from the mother. If the two genes in a pair are identical, they are referred to as homozygous, and
if they are different, they are called heterozygous. The location of a gene on the chromosome is called its locus, and each gene in a gene
pair is called an allele.
The interaction of the two alleles determines the expression of the gene. The type of gene combinations for a particular locus (i.e. AA, Aa
or aa) is the genotype. The appearance or expression of the genes at particular loci (i.e. black or brown) is the phenotype. The phenotypic
expression of the gene pair is determined by how the two genes in the pair interact. A dominant gene (only requiring one copy in the pair)
is always expressed, while a recessive gene requires a homozygous pair for expression. When two heterozygous carriers of a recessive
gene are bred together, on average you can expect 25% affected, 50% carrier, and 25% normal offspring. The actual observed percentages
within litters will vary. Many dominant traits are homozygous lethal during fetal development; such as Chinese Crested dogs homozygous
for the hairless gene (HH), the gene for polycystic kidney disease in Persian and related cat breeds, and the Manx gene (MM) in cats.
Co-dominance or incomplete dominance is when heterozygous alleles show an intermediate phenotype. An example is a bi-colored cat (Ss)
as an intermediate between that seen with homozygous solid color (SS) and the recessive van pattern (a white cat with color only on its
tail and the top of the head) seen with the homozygous ss genotype. The merle color pattern in dogs is also an example. Most merle dogs
have the Mm genotype, with mm producing normal coloration. Double dominant MM merle dogs are mostly white, and can be born blind,
deaf, or with other severe abnormalities.
Sex-linked (also referred to as X-linked) disorders are controlled by genes on the X-chromosome. As males have only one X chromosome,
a single defective gene on it will cause a genetic defect. For females to be affected with an X-linked recessive disorder, they have to be
homozygous for the defective gene. Hemophilia A & B are examples of X-linked recessive disorders.
Genetic traits and disorders can be caused by the action of a single gene pair (monogenetic disorders), or several pairs of genes (complex
or polygenic inheritance). Complexly inherited traits can involve qualitative genes (that can show dominance and recessiveness), or
quantitative genes (that can act in an additive fashion). Many complexly inherited disorders are threshold traits, where a genetic load of
genes and possibly additional environmental effects combine to cross a threshold level to produce the phenotype. Several musculoskeletal
disorders, heart anomalies, and eye diseases are complexly inherited threshold traits.
There are instances when gene expression does not produce the expected phenotype. When an individual has the genotype for a trait
or disorder, but does not phenotypically express it, this is referred to as incomplete penetrance. This is an all or none phenomenon; you
either show the trait or not. The easiest way to remember this concept is that the genotype does not penetrate into the phenotype. If
an individual has a certain trait or disorder, but it differs in its severity, age of onset, progression, or form, it is referred to as variable
expressivity. With this process, all genotypically affected individuals show some aspect of the trait. Polydactyly (extra toes) in cats shows
variable expressivity in the number of extra toes present. Many of the inherited disorders listed in the breed chapters show variable
expressivity. Penetrance and expressivity may be properties of the mutant gene itself, or can be due to modifying effects of other genes
and/or the environment.
Similar genetic conditions can have different genetic causes between breeds, or even within the same breed. If a genetic trait or disorder
can be caused by different genes, they are called genocopies. In this case, direct genetic tests (of the genotype) in one breed will not work
in other breeds. We know that many forms of progressive retinal atrophy (PRA) are genocopies, and expect this to be the case with many
other disorders, such as epilepsy and cardiomyopathy. Some breed-related genetic disorders can be related to a sub-population or breed
gene pool in a specific country. For this reason, much of the information presented in the breed chapters relates to the breed in the United
States in general and may not be applicable to all breed populations worldwide, or possibly all lines within the breed.
2
Breeding Systems
Mating based on phenotype is called assortative mating. Mating like to like is positive assortative mating. Mating like to unlike (i.e., bringing
a new trait in or correcting a fault) is negative assortative mating. Matings based on genotype depend on the relationship between the
two individuals being bred. If two parents within a breed are less related than the average relationship within the breed (measured as
an inbreeding coefficient), then it is an outbreeding. If the mating of two parents produces an inbreeding coefficient higher than the
breed average, it is a linebreeding or inbreeding. Linebreeding concentrates the genes of specific common ancestors behind both parents.
Inbreeding is the mating of close relatives, such as parent to offspring, or full brother x sister.
Linebreeding and inbreeding increase homozygosity, or the pairing of like genes (aa or AA) in the offspring. This can increase the expression
of both positive and negative recessive traits. Outbreeding increases heterozygosity, or the pairing of unlike genes (Aa). Outbreeding
propagates both positive and negative recessive genes in the carrier state. Linebreeding does not create deleterious genes, and outbreeding
does not eliminate them. These breeding practices only affect the expression or masking of deleterious genes through homozygosity or
heterozygosity. Selection of breeding stock is what affects the increase or decrease in the frequency of desirable and deleterious genes.
Inbreeding or tight linebreeding should only be attempted with knowledge of the range of genes that the parents may carry based on prior
matings or genetic testing.
Crossbreeding is the production of offspring by mating individuals from two or more breeds. This produces maximum heterozygosity.
Designer breeds are created through crossbreeding. Their offspring do not reproduce themselves if bred.
Genetic Diversity
Most breeds have closed gene pools, meaning that breeding individuals must have confirmed pedigrees of ancestry from the existing
breed. No new genes can be introduced into the breed, and genes can be lost to the gene pool by selective breeding (or not breeding) of
individuals. The problem with limited genetic diversity in purebred populations stems from the effects of deleterious genes. If a breed has
a high frequency of a deleterious gene, then the breed will have issues with that disorder. Deleterious genes can cause increased neonatal
death and smaller litter size, specific genetic diseases, or impaired immunity. In some cases, selection for a specific phenotype has brought
a defective gene along with it at a high frequency. The most extreme example is the linkage of spotting in Dalmatians with the autosomal
recessive gene for abnormal purine metabolism (hyperuricosuria). All Dalmatians are homozygous recessive for this defective gene, which
can predispose to bladder stones and a skin condition.
Breeds with genetic diversity issues need to determine how they can best improve their situations. Is there enough diversity of normal
genes to maintain the health and vitality of the breed? Is there a way to breed away from high frequency defective genes without losing
valuable normal genes in the process? Some breeders discourage linebreeding and promote outbreeding in an attempt to protect genetic
diversity in their breed. It is not the type of matings utilized (linebreeding or outbreeding) that causes the loss of genes from a breed gene
pool. Rather, loss of genes occurs through selection: the use and non-use of offspring. If a breed starts narrowing their focus to breeding
stock from a limited number of lines, then a loss of genetic diversity will occur.
The process of maintaining healthy lines, with many breeders crossing between lines and breeding back as they see fit, maintains diversity
in the gene pool. If some breeders outbreed, and some linebreed to certain individuals that they favor while others linebreed to others that
they favor, then breed-wide genetic diversity is maintained. It is the varied opinion of breeders as to what constitutes the ideal dog or cat,
and their selection of breeding stock based on their opinions that maintains breed diversity.
The most important factor for diminished genetic diversity in breeds is the popular sire syndrome. The overuse of a popular sire beyond
a reasonable contribution through frequent breedings significantly skews the gene pool in his direction, and reduces the diversity of the
gene pool. Any genes that he possesses - whether positive or negative - will increase in frequency. The insidious effect of the popular sire
syndrome is the loss of genetic contribution from quality, unrelated males who are not used for breeding. The loss of other quality breeding
lines causes a significant loss of breed genetic diversity. The popular sire syndrome is a significant factor in both populous breeds and
breeds with small populations.
Genetic Testing
Genetic tests vary on what they are able to identify, and therefore how they can be used in managing genetic disease. Some tests
measure the phenotype, or what can be seen in the animal. This may not directly relate to the genotype, or the genes regulating the
defect. Screening for cataracts, ausculting for heart murmurs, thyroid autoantibodies, hip and elbow radiographs, urinalysis for crystals
or metabolites, skin biopsies, and observation of behavioral traits are all tests of the phenotype. Most tests of the phenotype only identify
affected individuals, and not carriers.
Direct gene tests utilizing PCR or polymerase chain reaction, are a direct measurement of the genotype. These can be run at any age with
a blood sample or cheek swab, regardless of the age of onset of the disorder. With tests of the genotype, you can identify affected, carrier,
and genetically normal animals.
3
Some defective genes can be linked to a genetic marker, which can be tested for. Linked-marker based tests do not identify the defective
gene, but a marker that lies close on the chromosome. During the formation of egg or sperm, a crossover and trading of genes occurs
between paired chromosomes. If a crossover between the marker and the gene occurs, the marker will no longer be linked to the defective
gene. False positive and false negative results will occur in the individual, and in all of its descendants. Due to this phenomenon, linkage
test results must be compared with results from other family members to determine whether they correlate with the known genotype of
relatives. Linked marker tests include those for cerebellar ataxia in Italian Spinone and primary hyperparathyroidism in the Keeshond.
Most tests of the genotype are for genes that are the sole and direct cause of a disease or condition. Others test for susceptibility genes
that provide liability for the disease. Some of these susceptibility genes are necessary for the animal to be affected, though other yet
undiscovered genetic or environmental factors are also necessary. Examples are cord1 PRA in English Springer Spaniels and Miniature
Dachshunds, and degenerative myelopathy in several dog breeds. Other susceptibility genes are found to occur at a greater frequency in
affected animals, but are not present in all affected animals. An example is the susceptibility gene for perianal fistula/anal furunculosis in
German Shepherd Dogs.
Many owners and breeders ask what tests should be done in their cats and dogs. The answer depends on whether the cat or dog is going to
be a pet, or be used for breeding. For a pet, it is only important to know that it is not going to be affected by a health-related disorder. For
breeding animals, it is important to know if they carry disease liability genes that they can pass on to their offspring. Further information is
available in the chapter on Genetic Counseling.
The Canine Health Information Center or CHIC (www.caninehealthinfo.org) is an open health database that has been established by the
AKC Canine Health Foundation and the Orthopedic Foundation for Animals. National parent clubs decide to enroll in the CHIC program,
and determine the testable genetic disorders for their breed. (For example, hip evaluation, CERF examination, and thyroid testing.) Owners,
breeders, and prospective owners can search online for dogs in the OFA/CHIC database, and view their test results. If a dog completes the
recommended testing panel, it receives a CHIC number regardless of whether it passes all of the tests. CHIC is about health consciousness,
not health perfection. As more testable disorders are identified, few dogs will be normal for all tests. The Kennel Club in the UK has similar
Health Breeding Schemes and a searchable Health Tests Results Finder to look up individual dogs. A similar listing of tests is not currently
available for cats, however breed-related diseases are found on the Feline Advisory Bureau (FAB-UK) website: www.fabcats.org/breeders/
inherited_disorders.
Without data on the occurrence and prevalence of disorders in dog and cat breeds, breeders cannot institute measures to improve
them. Breed clubs should routinely perform health surveys (usually every 5 years) to monitor the changing health of the breed. Owners
should take the time to fill out surveys, even on healthy animals. Breeders should record the cause and age at death, reproduction rates,
dystocia, need for caesarian section, sex of offspring, litter size, number of stillborn offspring, growth rates, and the onset and nature of
abnormalities in offspring. Post mortems should be conducted for fading kittens and puppies, and for all deaths. If one does not know why
there is loss of cats or dogs, there is loss of ability to improve the welfare and health of the next generation of a breed.
4
Genetic Counseling and Management of Genetic Disease
The hallmark of genetic disease is our ability to predict its occurrence before its onset, allowing us to alter its morbidity or mortality.
The vast majority of dogs and cats are not breeding animals, but they still require genetic counseling for inherited disorders. Owners of
large-breed puppies are counseled to feed lower calorie foods to provide for a more uniform growth rate and better joint development.
Cats genetically predisposed to FLUTD (Feline Lower Urinary Tract Disorders) and obese “pre-diabetic” cats can receive specific dietary
recommendations.
We need to be knowledgeable about what genetic tests are available, and in which individuals they should be run. Dogs from breeds with
an incidence of von Willebrand’s disease should be tested early in life, so that measures can be taken to prevent excessive hemorrhage
during surgery or injury. Dogs at risk of carrying the mdr-1 mutation should be tested early in life, before drug treatment.
In high risk breeds, individual animals should be genetically tested (or verified results documented for parents) before purchase. These
include Maine Coon and Ragdoll cats for the autosomal dominant hypertrophic cardiomyopathy gene, Persian and Himalayan cats for
autosomal dominant polycystic kidney disease, Boxers for arrythmogenic right ventricular cardiomyopathy, and Doberman Pinschers for
dilated cardiomyopathy.
We need to understand the temporal periods when genetic testing will be most accurate, and allow for intervention. Puppy hips should be
palpated with a gentle Ortolani procedure at each vaccine visit, and again at spaying or neutering under anesthesia. Juvenile interventional
surgery will only benefit those with significant subluxability prior to major growth (for pubic symphysiodesis) or the development
of osteoarthritic changes (for triple pelvic osteotomy). Genetic testing for hypothyroidism is based on the presence of thyroglobulin
autoantibodies. A dog with normal TgAA levels on two tests at least two years apart between two and six years of age is phenotypically
normal. However, TgAA levels should not be measured within 2 to 3 months post-vaccination, as a transient iatrogenic rise can occur
during this period.
For most genetic diseases, we know how to either prevent their occurrence, or at least lessen the possibility of producing offspring with
genetic disease. This can occur through the genotypic testing of the parents (identification of parents carrying liability genes for genetic
disease), phenotypic testing of the parents (identification of parents affected with genetic disease), or pedigree analysis (identification of a
carrier and affected risk based on knowledge of the carrier or affected relatives).
The genetic improvement of cats and dogs will only occur through selective breeding. However, improvement will not occur unless we
all understand our roles and responsibilities. The responsibility for this improvement lies not just with the breeder; but also with breed
organizations, veterinarians, and the general public. Breeders must perform genetic testing on prospective breeding stock before breeding.
Breed organizations must identify breed specific health issues through regular breed health surveys, fund research for breed specific
disorders, and recommend genetic testing for breeding animals. Veterinarians must counsel prospective owners and breeders on breed
specific health issues. They should provide the necessary genetic testing, or direct owners to specialists (ophthalmologists, cardiologists,
etc.) that can perform the testing. The general public must become knowledgeable about what genetic tests are needed on parents of
prospective kitten and puppy purchases, and how to verify testing status.
Inherent in these responsibilities is the acknowledgement that breeding without genetic testing is irresponsible, and unethical. Genetic
testing is health quality control. It is no longer acceptable for a breeder to choose two individuals and breed them together without regard
to genetic disease control.
The best methods for ensuring the health and diversity of any breed’s gene pool are to: 1) Avoid the popular sire syndrome. 2) Utilize
quality individuals from the breadth of the population to expand the gene pool. 3) Monitor genetic health issues through regular health
surveys. 4) Do genetic testing for breed-related disorders. 5) Participate in open health registries.
The most important goal of managing genetic disease is to avoid producing affected individuals. The secondary goal is to reduce the
frequency of carriers of defective genes in the population. At the same time, recommendations should allow perpetuation of breeding
lines, in order to preserve the genetic diversity of the population. Historically, genetic counseling has ranged from recommendations to not
repeat a mating and to outbreed, to recommendations for elimination of all relatives of affected animals from the breeding pool. Neither
of these two extremes serves the best long-term interest of specific breeds. Outbreeding may prevent the production of animals affected
with rare recessive diseases, but it will propagate and further disperse the detrimental recessive genes.
5
With widely dispersed or high frequency defective genes, it must be recognized that carriers are spread across the gene pool. Eliminating
unique breeding lines because some individuals carry a single defective gene may adversely affect gene pool diversity more than a process
that allows a limited number of carriers to reproduce. Conversely, with recently mutated or low frequency defective genes, it is advisable to
strictly limit breeding, to avoid dispersion of the defective gene further in the population.
With each new generation, breeders ask, “How can I continue my line and improve it?” Aside from selecting for conformation, behavior
and general health, breeders must consider how they are going to reduce the incidence of whichever genetic disorders are present in their
breed. There are no answers that will fit every situation. There are, however, guidelines to preserve breeding lines and genetic diversity while
reducing the risk of producing animals that carry defective genes, or are affected with genetic defects.
Breeders are the custodians of their breed’s past and future. “Above all, do no harm” is a primary oath of all medical professionals. Genetic
tests are powerful tools, and their use can cause significant positive or negative changes to breed gene pools. Once a genetic test is
developed that allows breeders to determine if an animal is a carrier of a defective gene, many owners are likely to simply eliminate carriers
from breeding. Although doing so is human nature, this temptation must be overcome. If an owner would breed an individual if it tested
normal for a genetic disease, then a carrier result should not change that decision. A direct genetic test should not alter WHO gets bred,
only WHO THEY GET BRED TO. One defective gene that can be identified through a genetic test out of tens of thousands of genes is not a
reason to stop breeding. A genetic test that should be used to help maintain breed quality and diversity should not result in limiting it.
We know that most individuals carry some unfavorable recessive genes. The more genetic tests that are developed, the greater chance
there is of identifying an undesirable gene in a breeding animal. History has shown that breeders can be successful in reducing breed-wide
genetic disease through testing and making informed breeding choices. However, there are also examples of breeds that have actually
experienced more problems as a result of unwarranted culling and restriction of their gene pools. These problems include: 1) Reducing the
incidence of one disease and increasing the incidence of another by repeated use of males known to be clear of the gene that causes the
first condition. 2) Creating bottlenecks and diminishing diversity by eliminating all carriers of a gene from the breeding pool, instead of
breeding and replacing them. 3) Concentrating on the presence or absence of a single gene and not the quality of the whole animal.
The aim is to replace the carrier breeding-animal with a normal-testing offspring that equals or exceeds it in quality. Additional carrier
testing offspring should not be placed in breeding homes; as the goal is to reduce the frequency of the defective gene in the population. As
each breeder tests and replaces carrier animals with normal-testing offspring, the problem for the breed as a whole diminishes, while not
restricting gene pool diversity.
The problem with a simple autosomal recessive disorder for which no carrier test exists is the propagation and dissemination of unapparent
carriers in the gene pool. A quality individual that is found to be a carrier of a recessive gene can be retired from breeding and replaced
with a quality relative or prior-born offspring. The genes of the retired individual can thus be preserved through the selected relative, but
the carrier risk can be cut in half. To further limit the spread of the defective gene, the offspring should be used in only a limited number
of carefully planned matings, and then should also be replaced with one or two representative offspring. The rest of the litter should be
placed in non-breeding (pet) homes. With this mating scheme, you are maintaining the good genes of the line, reducing the carrier risk
with each generation, and replacing, not adding to the overall carrier risk in the breeding population.
Breeders must assess the carrier risk of each individual animal in their breeding program. An open health registry that is supported by
the parent club makes it easier for breeders to objectively assess these matters. An example is the genetic disease control program for
cerebellar abiotrophy by the Scottish Terrier Club of America (www.stca.biz/health-registries/ca-registry). By determining the average
carrier-risk for the breeding population, breeders can select matings that have a projected risk that is lower than the breed average.
Relative risk assessments only take into account the identified carrier and affected individuals in the pedigree. Therefore, these estimates
determine the minimum risk based on the information available. If additional affected relatives to the pedigree are diagnosed, the
computed risk will rise. The relative risk pedigree calculator on the Scottish Terrier website can be used for any breed to compute carrier
and affected risk for any simple autosomal recessive disorder.
If a quality breeding animal is at high risk of being a carrier, the best advice is to breed to an individual that has a low risk. Using
relative-risk assessment as a tool, breeders should replace higher-risk breeding animals with lower-risk offspring that are equal to or better
than their parents in quality. A negative aspect of pedigree analysis is that it selects against families, regardless of an individual’s normal or
carrier status. On the other hand, it allows for the objective risk assessment and continuation of lines that might otherwise be abandoned
due to high carrier-risk.
6
Autosomal Dominant Disorders
Autosomal dominant genetic disorders are usually easy to manage. Each affected animal has at least one affected parent, but it can be
expected that half of the offspring of an affected animal will be free of the defective gene. With disorders that cause death or discomfort,
the recommendation is to not breed affected animals. To produce the next generation of a line; a normal full sibling of an affected animal,
a normal close relative, or the parent that is normal can be used.
If the defective gene is at a high frequency in the gene pool, eliminating all affected breeding animals in one generation may have a
significant negative impact on genetic diversity. When a high frequency autosomal dominant disorder is first identified, some quality,
affected animals may have to be bred, and replaced with quality, normal testing offspring. However, once a few generations have gone
by and breeders have had the opportunity to replace affected with normal individuals, the continued breeding of affected animals is not
ethical.
A problem with some autosomal dominant disorders is incomplete penetrance; where some animals with the defective gene may not show
the disorder. Roughly half their offspring, however, may be affected. If a genetic test is available, this is not a problem. Otherwise, pedigree
analysis and relative-risk assessment can identify which animals are at risk of carrying incompletely penetrant dominant genes.
Sex-Linked Disorders
For sex-linked (also known as x-linked) recessive defective genes for which carrier tests exist, breeders should follow the same “breed and
replace” recommendations as are outlined above in the discussion of autosomal recessive disorders. If there is no test, the defective gene
can be traced through the pedigree. Selecting a normal male for breeding loses the defective gene in one generation, regardless of his
relationship to affected and carrier relatives. Carrier, affected, or high risk females should not be used, due to the high risk of producing
affected male offspring. If a male is affected, he would have received the defective gene from his carrier mother. All of his daughters will
be carriers, but none of his sons. Without a test for carriers, you can use relative-risk assessment to breed him to a female that is at low
risk of being a carrier. This minimizes the chance of producing affected offspring, and a quality son can be selected for replacement. Rare
sex-linked dominant disorders are managed the same way as autosomal dominant disorders. The difference is that affected males will
always produce all affected daughters.
In polygenic disorders, the phenotype of the individual does not directly represent its genotype. If phenotypically normal parents produce
affected offspring, both should be considered to carry a genetic load of liability genes that combined to cause the disorder. Breeders must
break down affected phenotypes into traits that more directly represent the genes that control them. For example, in hip dysplasia these
include clinical signs of lameness, shallow hip sockets, subluxation or remodeling on an extended leg view, and radiographic distractibility
on a PennHIP view. If a quality individual is to be bred, but has shallow hip sockets, it should be bred to an individual with deep hip sockets.
You need to select for enough genes influencing normal development, to get below the threshold where dysplasia develops.
The environment has a role in the expression of polygenic disorders. Plane of nutrition and environmental stress, especially during critical
growth periods can alter the expression of some inherited musculoskeletal disorders. You do not want to overly protect or overly stress
the development of prospective breeding animals. Breeders should evaluate prospective breeding individuals raised under fairly uniform
conditions, which will not mask or alter the expression of genetic disease.
Polygenic disorders require knowledge of the affected or normal status of full-siblings to prospective breeding animals. Individuals whose
siblings are normal and whose parents’ sibs are normal have the greatest chance of carrying a low genetic load for the condition. This
breadth of pedigree analysis is more important than normalcy in the depth of pedigree (parents and grandparents only.) This is why it is
important to screen both pet and breeding animals from litters for polygenic disorders, and report the results in open health registries,
such as the not-for profit Orthopedic Foundation for Animals (www.offa.org). Affected individuals can be replaced with a normal sib or
parent, and bred to a low-liability mate. Breeders can replace the higher risk parent with a quality, lower risk offspring, and repeat the
process. In addition, the offspring of breeding dogs should be monitored to see which are passing the disorder with higher frequency.
7
Undetermined Mode of Inheritance
For disorders without a known mode of inheritance or carrier test, breeders should be counseled to use the same control methods as with
polygenic disorders. Animals with a low genetic load for the disorder should be selected for breeding, through the results of examinations
of first-degree relatives (littermates, parents, and offspring). If there are multiple generations of normalcy in the breadth of the pedigree,
then you can have some confidence that there is less risk that liability genes are being carried.
It is distressing when a genetic disorder is confirmed. Positive and practical genetic counseling recommendations can be made to maintain
breed lines and genetic diversity, and improve the overall health of breeds. The total elimination of defective genes will probably be
impossible for most breeds. The use of these guidelines can assist breeders in making objective breeding decisions for genetic disease
management, while continuing their breeding lines. The individual breeder can use genetic tests to; 1) identify carriers, 2) work to breed
away from the defective gene(s), and 3) ensure (through testing) that the defective gene(s) is not reintroduced in future matings. Each
breeder will have their own rate of progress, depending on the frequency of the defective gene(s) in their own breeding animals, and which
desirable individuals carry liability genes.
8
Section 2 Dog Breeds
Introduction
This section contains chapters on 171 dog breeds, including all except the most recent of the AKC breeds at the date of publication. It
should be recognized that all mixed-breed and purebred or purposely bred dogs carry detrimental genes and can be affected with genetic
disorders. A generally accepted fallacy is that purebred dogs are affected with more genetic disease than mixed-breed dogs. For the most
part, this is only true for the rarer breed-specific disorders. The most common canine genetic disorders occur across all breeds, and in
practice, we see as much genetic disease in mixed-breed dogs as we do in purebred dogs. These include the most frequent canine genetic
disorders reported by the AKC Canine Health Foundation: cancer, inherited eye disease, epilepsy, hip dysplasia, hypothyroidism, heart
disease, autoimmune disease, allergies, patella luxation, and renal dysplasia.
There are defective genes that are old in the dog genome, and spread across all dogs regardless of ancestry. The development of pure
breeds has compartmentalized genes into breed gene pools. Based on the genetic load of disease causing genes, each breed has different
frequencies of common and uncommon genetic disorders. Some defective genes are ancient, and their existence preceded the differenti-
ation of breeds. The autosomal recessive, progressive rod cone degeneration (prcd) form of progressive retinal atrophy (PRA), is caused by
the exact same mutation in at least twenty-five different breeds. Other defective mutations occurred more recently, and by propagation
through foundation dogs or popular sires, have developed into breed specific genetic disorders.
A recent development in dog breeding is the rise of designer breeds – dogs produced through the purposeful crossbreeding of two
different pure breeds. These are not considered specific breeds; because they do not breed true to reproduce themselves if bred together. It
is only the original cross, which produces them as the F1 (first filial) generation. There is a general expectation that designer dogs should be
healthier, simply because they are crossbred. However, due to the presence of disease liability genes across all breeds, this is not the case.
The only way to have a realistic expectation that any purposely bred dog – purebred or crossbred – is going to be healthy is if the breeder
is actively testing and screening breeding stock for genetic disease. The purebred parents of designer dogs should be screened for their
respective breed-specific screening tests. Prospective owners should ask to see test results on the parents of dogs for sale. Many of these
test results are available to the public in online registries from the OFA (Orthopedic Foundation for Animals: www.offa.org), CHIC (Canine
Health Information Center: www.caninehealthinfo.org), and CERF (Canine Eye Registry Foundation: www.vmdb.org/cerf.html).
Medical conditions listed in the breed chapters are grouped under the following headers; Inherited Diseases (those with a defined mode of
inheritance), and Disease Predispositions (those where a mode of inheritance is not defined). Many texts that report breed related genetic
disease do not state the relative frequency of the disorders within the breed. In many instances, a “breed-related disorder” is reported due
to a single published case report for a disease in the breed. In this section, the inherited diseases and breed predispositions are ordered
based on their perceived incidence in the breed. Reported frequencies are stated based on genetic testing services, published articles, and
health surveys. This process is the same as comparing apples to oranges; as the methods, populations, and statistics of each report cannot
be adequately compared to each other. However, the disorders are ordered with the most common first, and least common last based on
the author’s experience.
Recommendations for genetic testing of breeding dogs are based on the breed-specific recommendations of the US parent club through
the CHIC program. Where there are additional tests suggested beyond the CHIC recommendations, they are also listed. In all dog breeds,
genetic testing of breeding stock for the major common inherited diseases is recommended. These include hip and elbow radiographs
for dysplasia (or Legg-Calve-Perthes disease), a CERF eye examination by a board certified veterinary ophthalmologist, a thyroid profile
including thyroglobulin autoantibodies, a cardiac evaluation, and a patella evaluation. Most of these are once-in-a-lifetime tests. It is not
ethical to breed dogs (either purebred, designer-bred, or purposely bred) without ensuring that both parents are free of testable genetic
disease.
Not every dog breed is included in the first edition, and some breed-related disorders may be missing, because there was no published
reference at the time of publication. As the book is updated, adjustments and additions will need to be made in order to keep the listings
current. Readers are encouraged to send comments to help us update the dog breed section. Use the contact address provided in the book
preface. Chapters are in alphabetical order.
9
Affenpinscher
Longevity: 14-15 years.
Weight: 7-8 lb (3.0-3.5 kg). Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Coat: The medium-short coat is black, gray, black and tan, or silver disease. Treat surgically if causing clinical signs. OFA reports 3.8%
with markings, or solid red (some have tan furnishings). They are affected.1
low shedders. They have low grooming needs except for periodic
stripping, and ears need regular plucking. The stiff, dense and Elbow Dysplasia: Polygenically inherited trait causing elbow
wiry-textured coat is about 1” (2.5 cm) in length, and the ear hair is arthritis. OFA reports 3.1% affected, but not enough Affenpinschers
trimmed short. Color is not considered too important, though large have been evaluated for statistical confidence.1
white patches are not desirable. In Europe and England, black is the
standard breed color. Legg-Calvé-Perthes Disease: Polygenically inherited aseptic
necrosis of the femoral head, resulting in degenerative joint disease
of the hip. Can be unilateral or bilateral with onset of degeneration
10
usually between 6-9 months of age. Treat surgically if causing Recommend thyroid profile including autoantibodies, elbow
lameness/discomfort. Reported in the breed with a male prevalence radiographs, and cardiac evaluation.
on The Affenpinscher Club (UK) website.
Miscellaneous
Disease Predispositions • Breed name synonyms: Affen
Distichiasis: Abnormally placed eyelashes that irritate the • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
cornea and conjunctiva. Can cause secondary corneal ulceration. ANKC (Australian National Kennel Club), NKC (National Kennel Club)
Identified in 6.38% of Affenpinschers CERF examined by veterinary • AKC rank (year 2008): 132 (171 dogs registered)
ophthalmologists between 2000-2005.2 • Internet resources: Affenpinscher Club of America:
www.affenpinscher.org
Persistent Pupillary Membranes: Strands of fetal remnant The Affenpinscher Club (UK): www.affenpinscherclubuk.com
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
later three forms can impair vision, and dogs affected with these
forms should not be bred. Identified in 6.38% of Affenpinschers References
1. OFA Website breed statistics: www.offa.org Last accessed July. 1, 2010.
CERF examined by veterinary ophthalmologists between
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
2000-2005.2 College of Veterinary Ophthalmologists. ACVO, 2007.
3. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
Retinal Dysplasia: Retinal folds, geographic, and generalized retinal for Population and Animal Health, Michigan State University. April, 2007
dysplasia with detachment are recognized in the breed. Identified in 4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
4.26% of Affenpinschers CERF examined by veterinary ophthalmol- hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
ogists between 2000-2005.2 Vet Med Assoc 2002 Feb 15;220(4):466-71.
5. Waldman L: Seasonal flank alopecia in affenpinschers. J Small Anim
Cataracts: Anterior or posterior intermediate and punctate Pract. 1995 Jun;36(6):271-3.
cataracts occur in the breed. Unknown mode of inheritance. 6. White SD: Update on Follicular Alopecias: “Pseudo-Endocrinopathies”.
Identified in 2.13% of Affenpinschers CERF examined by veterinary Proceedings, ACVIM Forum, 2005
ophthalmologists between 2000-2005.2 7. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 193. AAHA Press, 1999.
Corneal Dystrophy: Affenpinschers can have an epithelial/stromal 8. Lieb AS, Grooters AM, Tyler JW, et. al.: Tetraparesis due to vertebral
form of corneal dystrophy. Identified in 2.13% of Affenpinschers physeal fracture in an adult dog with congenital hypothyroidism. J Small
CERF examined by veterinary ophthalmologists between Anim Pract. 1997 Aug;38(8):364-7.
9. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
2000-2005.2
House, NY 2006. p. 447-449.
Hypothyroidism: Inherited autoimmune thyroiditis. Not enough
samples have been submitted for thyroid auto-antibodies to
Michigan State University to determine an accurate frequency. (Ave.
for all breeds is 7.5%).3,4
Genetic Tests
Tests of Genotype: none
11
Afghan Hound
Points of Conformation: This breed is noted for the “far-seeing
gaze”, noble carriage and fine coat. Other key characteristics
include prominent hip bones, large feet, and they appear to have
an increased stifle angle due to the overlying haircoat. The skull is
long and finely chiseled with a slight Roman nose; no pronounced
stop is present. The occipital protuberance is prominent, the ears
are long and pendulous and covered with long silky hair, and the
leather is fine. Eyes are dark, almond-shaped, and almost triangular.
The muzzle is very long in this dolichocephalic breed. The nose is
moderate in size and black in pigmentation. Neck is long, arched,
and the topline is level, though the loin is slightly arched, and
The Breed History there is a marked tuck-up in the abdomen. The thorax is deep,
The Afghan Hound was first represented in Indian works of art the forelegs straight boned and the radius is very long; tibia is
dated 1809. The origin of the breed as the name implies was in also long, and the feet are well arched with lots of hair covering
Afghanistan and surrounding regions where they were bred for at them, and large toes are present. Their gait is smooth, elastic, and
least a few thousand years by nomadic tribes. Due to the variations high stepping with strides that cover great distance and seeming
of elevation and climate in this harsh wild region, some variation effortless. High head and tail carriage is notable. The tail is low set,
in breed type evolved, distinguishing it from the original Middle curled at the end (donut tipped), and has minimal feathering.
Eastern Sight hound. The specimens that became foundation stock
for American and European breeding programs arrived in Scotland
in 1920 (desert strain), and specimens from the other founding
Recognized Behavior Issues and Traits
Traits ascribed to this breed include: Strong independent streak,
strain (mountain type) arrived in England in 1925. The AKC
strong personality, somewhat difficult to train, and generally aloof
admitted the breed in 1926.
with strangers.
Breeding for Function These dogs have high grooming needs including daily brushing and
The mountain regions of the north gave rise to Afghans with regular bathing. They are low shedders. Some resources suggest
heavier coats, more compact build and darker coat colors. The arid snoods (hoods) to protect the long hair from soiling or getting in
regions gave rise to a lighter build and color and a less dense coat. the mouth during mealtime.
Historically this breed was a guard dog, a coursing hound, and
even reportedly used for herding. As a coursing sight hound, the These dogs have high exercise needs, and they need to be restricted
dog hunted alongside horsemen. Due to their speed and stamina to fenced enclosures or they will roam. They are very sensitive dogs.
they often worked ahead of the hunters and due to their agility, Some are good with children, some not. They do best with gentle,
they were able to manage hunts over very rough terrain. The quarry quiet children and early socialization is important. It is best to
varied depending on the locale, and may have included antelope introduce them to other pets and children when the dog is young.
and leopards. More recently, Afghan Hounds have been successfully Play activities and lots of attention should be provided to alleviate
entered in lure coursing and obedience, but many are now prized boredom.
solely for their exceptional companionship qualities.
Physical Characteristics
Height at Withers: female 24-26” (61-66 cm), male 26-28” (66-71 cm).
Coat: The very fine silky, glossy and long haircoat is shorter on
the face, though a long, soft topknot is present. Hair is short also
over the topline (the Afghan saddle) in adults. They are shown
in a natural unclipped coat. Though all coat colors are accepted
except spotted pattern, the presence of white head markings is not
encouraged. Puppies have soft fuzzy short hair on their saddles and
faces (monkey whiskers) that is replaced by an adult coat at about
one year of age.
12
Normal Physiologic Variations Disease Predispositions
Sight hounds have lower normal ranges for T4 and T3 Corneal Dystrophy: A lipid, epithelial/stromal form of corneal
concentrations compared to other breeds.1 dystrophy occurs in the breed. In most cases dystrophic change
does not progress to the point of visual impairment. Reported in
Echocardiographic Normal Values2 9.15% of Afghan Hounds CERF examined by veterinary ophthalmol-
Parameter Median (Range) ogists 2000-2005.7
Weight (kg) 23 (17-36)
Heart rate (bpm) 120 (80-140) Hypothyroidism: 7.3% positive for thyroid auto-antibodies based
LVPWD (mm) 9 (7-11) on testing at Michigan State University. (Avg. for all breeds is 7.5%).
Dorn reports a 1.8x odds ratio for developing hypothyroidism versus
LVPWS (mm) 12 (9-18)
other breeds.8,9,10
LVD (mm) 42 (33-52)
LVS (mm) 28 (20-37) Persistent Pupillary Membranes: Strands of fetal remnant
FS (%) 33 (24-48) connecting; iris to iris, cornea, lens, or involving sheets of tissue.
EPSS (mm) 4 (0-10) The later three forms can impair vision, and dogs affected with
RVd (mm) 10 (5-20) these forms should not be bred. Identified in 3.43% of Afghan
IVSd (mm) 10 (8-12) Hounds CERF examined by veterinary ophthalmologists between
IVSs (mm) 13 (8-18) 2000-2005.7
AOD (mm) 26 (20-34)
LAS (mm) 26 (18-35) Cataracts: The breed can develop rapidly progressive juvenile
cataracts that begin as equatorial vacuoles between 4 months to
N 20
2 years of age and extend into the anterior and posterior cortex.
A recessive mode of inheritance is suspected. Identified in 3.20%
LVPWD, LV posterior wall dimension at end-diastole; LVPWS, LV
of Afghan Hounds CERF examined by veterinary ophthalmolo-
posterior wall thickness at end-systole; LVD, LV chamber dimension
gists between 2000-2005. CERF does not recommend breeding any
at end-diastole; LVS, LV chamber dimension at end-systole; FS,
Afghan hound with a cataract.7,11
percent fractional shortening; EPSS, E-point septal separation; RVD,
RV chamber dimension at end-diastole; IVSd, interventricular septal Laryngeal Paralysis: The breed is predisposed to acquired laryngeal
thickness at end-diastole; IVSs, interventricular septal thickness at paralysis due to reduced function of the recurrent laryngeal nerves
end-systole; AOD, aortic root at end-diastole; LAS, left atrium at in older dogs. Arytenoid lateralization achieves the best results as a
end-systole; N, number of animals. method of surgical correction in severe cases, though increasing the
risk of aspiration pneumonia.12
Drug Sensitivities
Anesthesia: Sight hounds require particular attention during Atrioventricular (Heart) Block: Afghan Hounds are found to be at
anesthesia. Their lean body conformation with high surface-ar- increased risk of high-grade second- or third-degree atrioventricular
ea-to-volume ratio predisposes them to hypothermia during block versus other breeds. Treatment is with a pacemaker.13
anesthesia. Impaired biotransformation of drugs by the liver
results in prolonged recovery from barbiturate and thiobarbiturate Chylothorax: The Afghan hound is the breed most commonly
intravenous anesthetics. Propofol, and ketamine/diazepam affected with spontaneous chylous pleural effusion, accounting
combination are recommended induction agents.3 for 37.5% of all cases. Secondary lung lobe torsion is a frequent
complication. There is no age or sex predilection for the
condition.14,15,16
Inherited Diseases
Elbow Dysplasia: Polygenically inherited trait causing elbow Lung Lobe Torsion: Lung lobe torsion is rare in dogs and develops
arthritis. OFA reports 6.4% affected.4 most frequently in large deep-chested dogs, particularly Afghan
Hounds. Most cases in this breed were secondary to chylothorax.
Hip Dysplasia: Polygenically inherited trait causing degenerative Prognosis after surgery is fair to guarded.15,16,17
joint disease and hip arthritis. OFA reports 5.8% affected.4
Demodicosis: Afghan hounds are predisposed to demodex
Patella Luxation: Polygenically inherited laxity of patellar infections. This disorder has an underlying immunodeficiency in its
ligaments, causing luxation, lameness, and later degenerative joint pathogenesis.18
disease. Treat surgically if causing clinical signs. Too few Afghan
Hounds have been screened by OFA to determine an accurate Amyloidosis, Brachygnathism, Deafness, Exocrine Pancreatic
frequency.4 Insufficiency, Fanconi Syndrome, Gastric Dilatation-Volvulus,
Glaucoma, Intervertebral Disk Disease, Megaesophagus, Mitral
Afghan Myelopathy (necrotizing myelopathy): Rare, autosomal Valve Disease, Narcolepsy, Shoulder OCD, Oligodontia, Optic
recessive disorder of spinal cord degeneration. Onset at 3-13 Nerve Hypoplasia, Perineal Hernia, Prognathism, Progressive
months of age, rapidly progressing from paraparesis to spastic Retinal Atrophy, Pulmonic Stenosis, Retinal Dysplasia, Umbilical
paraplegia. There is no genetic test available.5,6 Hernia, von Willebrand’s Disease, and Wobbler Syndrome are
reported.19
13
Isolated Case Studies 7. Ocular Disorders Presumed to be inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
Arteriosclerosis with Arterial Obstruction: A 13-year-old 8. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
female Afghan Hound with progressive left hind-limb lameness veterinary teaching hospitals. Monograph, AKC Caninte Health Foundation.
and absence of a peripheral left hind pulse was found to have 2000.
advanced arteriosclerosis of the distal aorta, and left external iliac 9. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
and femoral arteries. Diagnosis was confirmed by ultrasonographic hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
examination of the abdominal aorta and its terminal branches.20 Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
10. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
Ganglion Cysts: Case study of a 4-month-old male Afghan Hound for Population and Animal Health, Michigan State University. April, 2007.
with subcutaneous ovoid cysts around the caudal right elbow 11. Roberts SR, Helper LC: Cataracts in Afghan Hounds. J Am Vet Med Assoc.
joint and left ischiatic tuberosity. Surgical removal demonstrated 1972;160:427.
abundant mucinous fluid and internal folding, without 12. Burbidge HM: A review of laryngeal paralysis in dogs. Br Vet J. 1995
communication to the joint cavity. These ganglion cysts apparently Jan-Feb;151(1):71-82
13. Schrope DP and Kelch WJ: Signalment, clinical signs, and prognostic
resulted from the metaplasia of fibroblasts to secreting cells.21
indicators associated with high-grade second- or third-degree
atrioventricular block in dogs: 124 cases (January 1, 1997-December 31,
D-(+)-glyceric Aciduria: This rare condition was identified in a
1997). J Am Vet Med Assoc. 2006 Jun 1;228(11):1710-7.
one year old female Afghan hound with a hepatopathy (increased 14. Fossum TW, Birchard SJ, Jacobs RM: Chylothorax in 34 dogs. J Am Vet
ALT, bilirubin and bile acids). The hepatopathy resolved with Med Assoc. 1986 Jun 1;188(11):1315-8.
supportive therapy, but the aciduria remained, suggesting that this 15. Gelzer AR, Downs MO, Newell SM, et. al.: Accessory lung lobe torsion
may be a benign condition.22 and chylothorax in an Afghan hound. J Am Anim Hosp Assoc. 1997
Mar-Apr;33(2):171-6.
Congenital Central Diabetes Insipidus: Two Afghan hound sibling 16. Williams JH, Duncan NM: Chylothorax with concurrent right
puppies showing signs of polyuria and polydipsia were diagnosed cardiac lung lobe torsion in an Afghan hound. J S Afr Vet Assoc. 1986
with this disorder.23 Mar;57(1):35-7.
17. Neath PJ, Brockman DJ, King LG: Lung lobe torsion in dogs: 22 cases
Genetic Tests (1981-1999). J Am Vet Med Assoc. 2000 Oct 1;217(7):1041-4.
18. Lemarie SL, Hosgood G, Foil CS: A retrospective study of juvenile-
Tests of Genotype: Direct test for color and mask alleles is and adult-onset generalized demodicosis in dogs (1986-91). Veterinary
available from HealthGene and VetGen. Dermatology. 1996. 7(1);3-10.
19. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Tests of Phenotype: CHIC Certification: Required testing includes Ackerman. p. 193-194 AAHA Press, 1999.
hip radiographs, CERF eye examination (minimum of 1 year), and 20. Zandvliet MM, Stokhof AA, Boroffka S, et. al.: Intermittent claudication
thyroid profile including autoantibodies. (See CHIC website; www. in an Afghan hound due to aortic arteriosclerosis. J Vet Intern Med. 2005
caninehealthinfo.org). Mar-Apr;19(2):259-61.
21. Cho KO, Park NY, Kang Mil,et. Al.: Ganglion cysts in a juvenile dog. Vet
Recommend elbow radiographs, patella evaluation and cardiac Pathol. 2000 Jul;37(4):340-3.
evaluation. 22. Sewell AC, Moritz A, Duran M: D-(+)-glyceric aciduria in an Afghan
hound. J Inherit Metab Dis. 1997 Jul;20(3):395-6.
23. Post K, McNeill JR, Clark EG, et. al.: Congenital central diabetes
Miscellaneous insipidus in two sibling Afghan hound pups. J Am Vet Med Assoc. 1989 Apr
• Breed name synonyms: Tazi, Baluchi hound, Afghan. 15;194(8):1086-8.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 24. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
ANKC (Australian National Kennel Club), NKC (National Kennel Club). Book House, NY 2006. p. 133-137.
• AKC rank (year 2008): 93 (631 dogs registered)
• Internet resources: Afghan Hound Club of America Inc.:
http://clubs.akc.org/ahca/
Afghan Hound Club of Canada: www.ahcc.ca
Afghan Hound Association (UK): www.ahaonline.co.uk
References
1. Kintzer PP and Peterson ME: Progress in the Diagnosis and Treatment of
Canine Hypothyroidism. 2007. Proceedings, ACVIM 2007.
2. Morrison SA, Moise NS, Scarlett J, et. al.: Effect of breed and body
weight on echocardiographic values in four breeds of dogs of differing
somatotype. J Vet Intern Med. 1992 Jul-Aug;6(4):220-4.
3. Court:MH: Anesthesia of the sighthound. Clin Tech Small Anim Pract
1999 Feb; 14(1):38-43.
4. OFA Website breed statistics: www.offa.org Last accessed July. 1, 2010
5. Averill DR Jr, Bronson RT: Inherited necrotizing myelopathy of Afghan
hounds. J Neuropathol Exp Neurol. 1977 Jul;36(4):734-47.
6. Cummings JF, de Lahunta A: Hereditary myelopathy of Afghan hounds, a
myelinolytic disease. Acta Neuropathol (Berl). 1978 Jun 30;42(3):173-81.
14
Airedale Terrier
early. The mix of hound and terrier leads to independent thinking
traits, and they have high intelligence. They need close human
contact, and may chew or dig if left alone for extended periods. The
hound component means that they tolerate other dogs much better
than typical terriers.
They are low shedders, low allergenic dogs and need regular
grooming. They are considered high-energy dogs. They are suitable
for both town and country as long as regular exercise is provided.
Distichiasis: Abnormally placed eyelashes that irritate the Immune-Mediated Thrombocytopenia (ITP): Autoimmune
cornea and conjunctiva. Can cause secondary corneal ulceration. destruction of blood platelets. Most common presentation is in
Identified in 5.20% of Airedale Terriers CERF examined by veterinary middle aged females. Reported at a frequency of 1.5% in the
ophthalmologists between 2000-2005.7 Airedale Terrier Health Survey 2000-2001. Reported 22.5x odds ratio
for concurrent AIHA and ITP.4,10
Cancer: The following frequencies for cancer were reported in
the Airedale Terrier Health Survey 2000-2001: Melanoma 4.0%, Dilated Cardiomyopathy: Can present with ventricular
adenocarcinoma 3.3%, hemangiosarcoma 2.7%, lymphosarcoma arrhythmias, progressing to heart failure. Increased incidence
2.5%, osteosarcoma 1.2%, mast cell tumor 1.2%.4 reported in the breed. Two to one ratio of affected males to females.
Reported at a frequency of 1.4% in the Airedale Terrier Health
Pancreatitis: Inflammation of the pancreas causing vomiting Survey 2000-2001.4,12
and peritonitis. Can be life threatening if severe. Reported at a
frequency of 3.7% in the Airedale Terrier Health Survey 2000-2001.4 Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting
of the stomach within the abdomen. Requires immediate veterinary
Corneal Dystrophy: Causes opacities on the surface of the cornea. attention. Reported at a frequency of 1.0% in the Airedale Terrier
Age of onset of 9-11 months, which may progress to vision Health Survey 2000-2001.4
impairment by 3-4 years of age. Sex-linked inheritance suggested in
one report. Identified in 3.41% of Airedale Terriers CERF examined Seasonal Flank Alopecia: Bilateral, symmetrical alopecia affecting
by veterinary ophthalmologists between 1991-1999, with none the flank, dorsum and tail. Affects primarily spayed females, in the
reported between 2000-2005.7,8,9 Spring or Autumn. Mean age of onset is 3.6 years.13
Retinal Dysplasia: Focal folds and geographic retinal dysplasia Seborrheic Dermatitis: Skin disorder presenting with greasy
are seen in the breed. Focal folds were identified in 2.89%, and skin and haircoat. Dorn reports a 2.06x odds ratio of developing
geographic dysplasia in 0.58% of Airedale Terriers CERF examined seborrheic dermatitis versus other breeds.14
by veterinary ophthalmologists between 2000-2005.7
Transitional Cell Carcinoma (TCC, bladder cancer): Increased
Inherited Epilepsy: Grand-mal seizures. Control with anticonvulsant incidence of this bladder cancer cited in the breed. TCC is a
medication. Reported at a frequency of 2.3% in the Airedale Terrier malignant cancer that can be controlled with surgery and piroxicam
Health Survey 2000-2001. Unknown mode of inheritance.4 treatment.15
Autoimmune Hemolytic Anemia (AIHA): Autoimmune Diskospondylitis: Vertebral bone infection, possibly with an
destruction of red blood cells. Clinical features include pale immune component in the breed. There are multiple case reports in
mucous membranes, weakness, lethargy and collapse. Treat with related Airedale Terriers. Thought to be due to immunosuppression
immunosuppressive drugs. Reported at a frequency of 2.3% in the from decreased immunoglobulin A production.16,17
Airedale Terrier Health Survey 2000-2001. Reported 45.3x odds ratio
versus other breeds. Reported 22.5x odds ratio for concurrent AIHA Cerebellar Abiotrophy (CCA, cerebellar ataxia): Disorder causing
and ITP.4,10,11 hypermetria, a high stepping gait, and incoordination. Onset in
this breed is 12 weeks of age. Clinical signs usually progress slowly
Missing Teeth: Reported at a frequency of 2.3% in the Airedale throughout the life of the dog, however some can progress more
Terrier Health Survey 2000-2001. Unknown mode of inheritance.4 rapidly to constant stumbling. Occurs at a low frequency in Airedale
Terriers.18
Umbilical Hernia: Congenital opening in the body wall from where
the umbilical cord was attached. Unknown mode of inheritance. Chromosomal Intersex, Demodicosis, Exocrine Pancreatic
Reported at a frequency of 1.9% in the Airedale Terrier Health Insufficiency, HyperlipoProteinemia, Hypoadrenocorticism,
Survey 2000-2001.4 Intervertrbral Disk Disease, Laryngeal Paralysis, Myasthenia
Gravis, Narcolepsy, Panosteitis, Pannus, Polycystic Kidney
Progressive Retinal Atrophy (PRA): Inherited degeneration of Disease, Portosystemic Shunt, and Sebaceous Adenitis are
the retina resulting in blindness. Age of onset around 3 years of reported.19
age. Mode of inheritance presumed recessive. Reported in 1.83%
16
Isolated Case Studies 6. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs hypothyroidism. J Am
Pituitary Carcinoma: A 6-year-old Airdale terrier presented with a Vet Med Assoc 2002 Feb 15; 220(4):466-71.
one month history of progressive behavioral and neurological signs, 7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
including proprioceptive deficits, circling, anisocoria, and head College of Veterinary Ophthalmologists. ACVO, 2007
pressing. A large, invasive, pituitary carcinoma was diagnosed at 8. Dice PF: Corneal dystrophy in the Airedale. Proc Am Coll Vet Ophthalmol.
post mortem.20 1976:7:36.
9. Cooley PL, Dice PF 2nd: Corneal dystrophy in the dog and cat. Vet Clin
Multiple Myeloma: Identified in a 10-year-old neutered male North Am Small Anim Pract. 1990 May;20(3):681-92.
Airedale Terrier with inappetence, weight loss, and lameness. 10. Goggs R, Boag AK, & Chan DL: Concurrent immune-mediated
Multiple myeloma was diagnosed based on bone marrow haemolytic anaemia and severe thrombocytopenia in 21 dogs. Vet Rec.
plasmacytosis, multiple lytic bone lesions, and hyperglobulinemia 2008 Sep 13;163(11):323-7.
with a clonal gammopathy.21 11. McAlees TJ: Immune-mediated haemolytic anaemia in 110 dogs in
Victoria, Australia. Aust Vet J. 2010 Jan;88(1-2):25-8.
Mixed Germ Cell Tumor: Identified in the lumbar spinal cord of a 12. Tidholm A, Jonsson L : A retrospective study of canine dilated
two-year-old, female Airedale terrier with a history of progressive cardiomyopathy (189 cases). J Am Anim Hosp Assoc. 1997
Nov-Dec;33(6):544-50.
paraplegia. It was composed of three different types of cells: small
13. Miller MA, Dunstan RW: Seasonal flank alopecia in boxers and
round germ cells, large eosinophilic cells, and a rarer differentiated Airedale terriers: 24 cases (1985-1992). J Am Vet Med Assoc. 1993 Dec
epithelial cell.22 1;203(11):1567-72.
14. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
Unilateral Horner’s Syndrome and Masticatory Muscle Atrophy: veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Seen in a 9-year-old, spayed female, Airedale Terrier diagnosed with 2000.
polyradiculoneuritis and ganglionitis that was most severe in the 15. Norris AM, Laing EJ, Valli VE, et. al.: Canine bladder and urethral tumors:
trigeminal nerves.23 a retrospective study of 115 cases (1980-1985). J Vet Intern Med. 1992
May-Jun;6(3):145-53.
Genetic Tests 16. Turnwald GH, Shires PK, Turk MA, et. al.: Diskospondylitis in a kennel
of dogs: clinicopathologic findings. J Am Vet Med Assoc. 1986 Jan
Tests of Genotype: Direct test for Hemophilia B is available from 15;188(2):178-83.
HealthGene. 17. Barta O, Turnwald GH, Shaffer LM, et. al.: Blastogenesis-suppressing
serum factors, decreased immunoglobulin A, and increased beta
Tests of Phenotype: CHIC Certification: Required testing includes 1-globulins in Airedale Terriers with diskospondylitis. Am J Vet Res. 1985
hip radiographs, congenital cardiac examination, and renal Jun;46(6):1319-22.
disease testing. Optional recommended testing includes CERF eye 18. Inzana KD: Brain Malformation and Storage Diseases. Proceedings,
examination, thyroid profile including autoantibodies, and elbow Western Veterinary Conference, 2002.
radiographs. (See CHIC website; www.caninehealthinfo.org). 19. The Genetic Connection: A Guide To Health Problems in Purebred Dogs.
L. Ackerman. P 194, AAHA Press, 1999.
Recommend patella evaluation. 20. Puente S: Pituitary carcinoma in an Airedale terrier. Can Vet J. 2003
Mar;44(3):240-2.
21. Ramaiah SK, Seguin MA, Carwile HF, et. al.: Biclonal gammopathy
Miscellaneous associated with immunoglobulin A in a dog with multiple myeloma. Vet
• Breed name synonyms: Airedale, Bingley Terrier (historical), Clin Pathol. 2002;31(2):83-9.
Waterside Terrier (historical), King of Terriers (historical) 22. Ferreira AJ, Peleteiro MC, Carvalho T, et. al.: Mixed germ cell tumour of
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), the spinal cord in a young dog. J Small Anim Pract. 2003 Feb;44(2):81-4.
ANKC (Australian National Kennel Club), NKC (National Kennel Club) 23. Panciera RJ, Ritchey JW, Baker JE, et. al.: Trigeminal and polyradicu-
• AKC rank (year 2008): 58 (1,776 dogs registered) loneuritis in a dog presenting with masticatory muscle atrophy and
• Internet resources: Airedale Terrier Club of America: Homer’s Syndrome. Vet Pathol. 2002 Jan;39(1):146-9.
www.airedale.org 24. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p 341-344.
National Airedale Terrier Association (UK):
http://www.nationalairedale.co.uk/
Airedale Terrier Club of Canada: www.airedaleterrier.ca
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Brooks M: Transfusion Therapy for Hemostatic Defects. Proceedings,
ACVIM Forum, 2003.
3. Gu W, Brooks M, Catalfamo J, et al: Two distinct mutations cause
severe hemophilia B in two unrelated canine pedigrees. Thromb Haemost
82:1270-1275, 1999.
4. Glickman L and Glickman N: Airedale Terrier Health Survey 2000-2001.
Airedale Terrier Club of America. 2001.
5. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. Aprial,2007
17
Akita
Points of Conformation: The full tail held over the back and the
alert, pricked ears and bear-like facial expression on the large
head characterize this stocky dog. The skull is broad, with broad
muzzle and small dark brown eyes, deep set and a triangular shape.
A shallow furrow runs in a line up the head extending onto the
forehead. Triangular ears are small. Set wide, they are strongly
leathered to keep them firmly up. The nose is large and black
pigmentation is preferred. The stop is well defined, and both lip and
palpebral margins are black. The crested neck is short. The thorax
is wide and deep, and ribs are well sprung. The topline is level and
the abdomen moderately tucked up. The high set tail is carried
The Breed History over the back curled, and reaches the tarsus. They possess heavily
First written records date to the 17th century, where in the Akita boned and muscled straight limbs, and dewclaws are not generally
Prefecture of Honshu in Northern Japan (Dewa), breeding programs removed from the forelimbs but from the hind limbs they are. Feet
were instituted to produce a sensible hunting dog. At this time, are small, compact and have well knuckled up toes. They move with
ownership of Akita dogs was restricted to the aristocracy. Their a moderate stride.
esteem was held so high that in some places they were assigned
individually hired caregivers who provided special care. This ancient Recognized Behavior Issues and Traits
Japanese dog breed is also cemented in certain spiritual traditions Traits ascribed to this breed include: Adaptability and intelligence,
wherein the dog represents good health, and a statue gift of the requires close human companionship, friendly, loyal and docile.
dog for a new addition to a family represents wishes for health, They are also described as intelligent, possessing high perseverance;
happiness and a long life for the child. This statue gift is also sent an alert and a faithful companion. Will tend to show aggression
as a get-well message for those ailing. They are of Spitz type, and towards other dogs so they are best kept solo unless socialized from
the ancient progenitor genes came into Japan with migrating puppyhood, and even then they may still assert themselves. Needs
Siberian nomads a very long time ago. an experienced owner to perform successful obedience training due
to their strong personalities. Dignified carriage, active, independent,
Akitas may also include in their heritage crosses of Chow-Chows aloof with strangers but tend to bark only when a threat is real.
with Tosa (Shikoku) and Kari dogs. In spite of the special status Akitas have a strong guarding instinct, and will capably defend
of this breed, at times, the popularity fell off to the point of near home and family. Need plenty of mental stimulation to prevent
extinction. In 1931, Japan named the breed a national monument. boredom vices. They have a high shedding tendency. Should be
Helen Keller was credited with importing the first specimens of the supervised with children and pets, as they can attack members of
breed to America. The AKC first registered Akitas in 1972. their own family.
19
Genetic Tests 15. Angles JM, Famula TR, Pedersen NC, et. al.: Uveodermatologic (VKH-like)
syndrome in American Akita dogs is associated with an increased frequency
Tests of Genotype: Direct tests for color and mask alleles are of DQA1*00201. Tissue Antigens. 2005 Dec;66(6):656-65.
available from VetGen. 16. Cottrell BD, Barnett KC: Harada disease in the Japanese Akita. J Small
Anim Pract 1987;28:517.
Tests of Phenotype: CHIC Certification: Required testing includes 17. Murphy CJ, Bellhorn RW: Anti-retinal antibodies associated with
hip radiographs, CERF eye examination (annually until year 6, then Vogt-Koyanagi-Harada-like syndrome in a dog. J Am Anim Hosp Assoc
every other year), and thyroid profile including autoantibodies. 1991;27:399.
Recommended tests include elbow radiographs, and patella 18. Kuhl KA, Shofer FS, Goldschmidt MH: Comparative histopathology of
evaluation. (See CHIC website; www.caninehealthinfo.org). pemphigus foliaceus and superficial folliculitis in the dog. Vet Pathol. 1994
Jan;31(1):19-27.
Recommend cardiac evaluation. 19. Ihrke PJ, Stannard AA, Ardans AA, et. al.: Pemphigus foliaceus in dogs: a
review of 37 cases. J Am Vet Med Assoc. 1985 Jan 1;186(1):59-66.
Miscellaneous 20. Shelton GD, Schule A, Kass PH: Risk factors for acquired myasthenia
gravis in dogs: 1,154 cases (1991-1995). J Am Vet Med Assoc.1997 Dec
• Breed name synonyms: Akita Inu, Shishi Inu, Japanese Akita, 1;211(11):1428-31.
Matagiinu (historical name for the breed in Japanese meaning 21. Dougherty SA, Center SA, Shaw EE, et. al.: Juvenile-onset polyarthritis
esteemed dog hunter). syndrome in Akitas. J Am Vet Med Assoc. 1991 Mar 1;198(5):849-56.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 22. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
ANKC (Australian National Kennel Club), NKC (National Kennel Club). in pure-bred dogs in North America. Vet Ophthalmol. 2004
• AKC rank (year 2008): 52 (3,157 dogs registered) Mar-Apr;7(2):97-111.
• Internet resources: Akita Club of America: www.akitaclub.org 23. O Toole D, Roberts S: Generalized progressive retinal atrophy in two
Japanese Akita Club of America: www.the-jaca.org Akita dogs. Vet Pathol. 1984 Sep;21(5):457-62.
Akita Club of Canada: www.akitaclub.ca 1997 Dec 1;211(11):1428-31.
24. Paulsen ME, Severin GA, Young S, et al: Progressive retinal atrophy in a
Japanese Akita-Inu Club (UK): www.japaneseakita-inu.co.uk
colony of Akita dogs. Trans Am Col Vet Ophthalmol 1988;19:1-4.
25. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
References Ackerman. p. 195. AAHA Press, 1999.
1. Fujise H, Higa K, Nakayama T, et. al.: Incidence of dogs possessing 26. Laratta LJ, Riis RC, Kern TJ, et. al.: Multiple congenital ocular defects in
red blood cells with high K in Japan and East Asia. J Vet Med Sci. 1997 the Akita dog. Cornell Vet. 1985 Jul;75(3):381-92.
Jun;59(6):495-7 27. Labelle P, Roy ME, Mohr FC: Primary diffuse tracheobronchial
2. Degen M: Pseudohyperkalemia in Akitas. J Am Vet Med Assoc. 1987 Mar amyloidosis in a dog. J Comp Pathol. 2004 Nov;131(4):338-40.
1;190(5):541-3. 28. Hashizume CT: Cervical spinal arachnoid cyst in a dog. Can Vet J. 2000
3. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010. Mar;41(3):225-7.
4. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at 29. Nagata M, Shimizu H, Masunaga T, et. al.: Dystrophic form of
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation. inherited epidermolysis bullosa in a dog (Akita Inu). Br J Dermatol. 1995
2000. Dec;133(6):1000-3.
5. LaFond E, Breur GJ and Austin CC: Breed susceptibility for 30. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002 Book House, NY 2006. P. 228-231.
Sep-Oct;38(5):467-77.
6. Glickman L, Glickman N, and Raghaven M: The Akita Club of America
National Health Survey 2000-2001. 2001.
7. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
8. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
9. Glickman LT, Glickman NW, Schellenberg DB, et. al.: Incidence of and
breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet
Med Assoc. 2000 Jan 1;216(1):40-5.
10. Duval JM, Budsberg SC, Flo GL, et. al.: Breed, sex, and body weight as
risk factors for rupture of the cranial cruciate ligament in young dogs. J Am
Vet Med Assoc. 1999 Sep 15;215(6):811-4.
11. Reichler IM, Hauser B, Schiller I, et. al.: Sebaceous adenitis in the Akita:
clinical observations, histopathology and heredity. Vet Dermatol. 2001 Oct;
12(50:243-53.
12. White SD, Rosychuk RA, Scott KV, et. al.: Sebaceous adenitis in dogs and
results of treatment with isotretinoin and etretinate: 30 cases (1990-1994).
J Am Vet Med Assoc. 1995 Jul 15;207(2):197-200.
13. Hernblad Tevell E, Bergvall K, Egenvall A: Sebaceous adenitis in Swedish
dogs, a retrospective study of 104 cases. Acta Vet Scand. 2008 May
25;50(1):11.
14. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007
20
Alaskan Malamute
set high, thickly covered in hair and sits a plume over the topline.
Limbs are heavily boned and well muscled, and not bowed. Gait is
true and tireless, with long powerful stride and excellent agility.
Neck is short, muscular, and has a moderate arch. Topline is straight
but slopes down towards the rear of the dog. The feet are large and
possess large thick pads, with plenty of hair between the toes. Toes
are well arched, and compact. Dewclaws on the rear are removed.
Retinal Dysplasia: Focal folds and geographic retinal dysplasia are Cryptorchidism, Cutaneous Lupus Erythematosus, Diabetes
seen in the breed. It is questionable whether focal folds can lead Mellitus, Epilepsy, Gastric Dilatation-Volvulus, Hemivertebra,
to disease, however dogs with the geographic form should not be Keratoconjunctivitis Sicca, Macrocytosis/stomatocytosis,
bred. Identified in 1.17% of Alaskan Malamutes CERF examined by Muscular Dystrophy, Narcolepsy, OCD-shoulder, Optic nerve
veterinary ophthalmologists between 2000-2005.9 hypoplasia, Panosteitis, Patella luxation, Portosystemic shunt,
Progressive retinal atrophy, Pulmonic stenosis, Retained teeth,
Alopecia-X (Coat Funk): Progressive, symmetrical, non-pruritic Ulcerative keratitis, Uveal hypopigmentation, Uveodermato-
truncal hair loss usually beginning in early adulthood. ACTH, LDDS, logic syndrome, Ventricular septal defect, and von Willebrand’s
and thyroid panel results are normal. Elevated blood concentrations disease are reported.25
of 17-hydroxyprogesterone (17-OHP) have been seen post ACTH
stimulation. Oral trilostane reversed the condition in some cases. Genetic Tests
The disorder appears familial.13 Tests of Genotype: Direct test for color alleles is available from
VetGen.
Glaucoma: An elevation of intraocular pressure (IOP) which,
when sustained, causes intraocular damage resulting in blindness. Direct test for CD is available from Optigen.
22
Tests of Phenotype: CHIC Certification: Required tests are; hip matosis affecting the vertebrae and trachea in an Alaskan Malamute. Aust
radiograph and CERF eye examination. Optional recommended Vet J. 1999 Jan;77(1):21-3.
testing; thyroid profile including auto-antibodies. (See CHIC 17. Caporn TM ; Read RA. Osteochondromatosis of the cervical spine
website: www.caninehealthinfo.org) causing compressive myelopathy in a dog. J Small Anim Pract 37[3]:133-7
1996 Mar
Also recommend elbow radiographs, patella evaluation and cardiac 18. Vilafranca M ; Ferrer L. Juvenile nephropathy in Alaskan Malamute
littermates. Vet Pathol 31[3]:375-7 1994 May
evaluation.
19. Burk RL, Barton CL. Renal failure and hyperparathyroidism in an Alaskan
Malamute pup. J Am Vet Med Assoc. 1978 Jan 1;172(1):69-72.
Miscellaneous 20. Mills JN ; Labuc RH ; Lawley MJ. Factor VII deficiency in an Alaskan
• Breed name synonyms: Malamute, Alaskan Malemute, Malemute malamute. Aust Vet J 75[5]:320-2 1997 May
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 21. Peterson ME, Dodds WJ. Factor IX deficiency in an Alaskan Malamute. J
ANKC (Australian National Kennel Club), NKC (National Kennel Club). Am Vet Med Assoc. 1979 Jun 15;174(12):1326-7.
• AKC rank (year 2008): 57 (1,737 registered) 22. Rishniw, M, Wilkerson, MJ, de Lahunta, A. Myelodysplasia in an
Alaskan Malamute Dog With Adult Onset of Clinical Signs. Prog Vet Neurol
• Internet resources: Alaskan Malamute Club of America Inc.:
5[1]:35-38 Spring’94.
www.alaskanmalamute.org 23. Kirkby KA, Bright RM, Owen HD: Paraoesophageal hiatal hernia and
Alaskan Malamute Research Foundation: megaoesophagus in a three-week-old Alaskan malamute. J Small Anim
www.malamutehealth.org Pract. 2005 Aug;46(8):402-5.
Alaskan Malamute Club of Canada: 24. Jimenez MA, Castejon A, San Roman F, et. al.: Maxillary ameloblastic
www.quadrant.net/amcc/ carcinoma in an Alaskan Malamute. Vet Pathol. 2007 Jan;44(1):84-7.
Alaskan Malamute Club of the UK: 25. The Genetic Connection: A Guide to health Problems in Purebred Dogs. L
www.alaskanmalamute.org.uk Ackerman. P. 195-96. AAHA Press.1999.
26. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. P. 232-236.
References
1. Lilliehook I, Tvedten H: Investigation of hypereosinophilia and potential
treatments. Vet Clin North Am Small Anim Pract. 2003 Nov; 33(6):1359-78, viii
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Fletch SM, Smart ME, Pennock PW, Subden RE. Clinical and pathologic
features of chondrodysplasia (dwarfism) in the Alaskan Malamute. J Am Vet
Med Assoc. 1973 Mar 1;162(5):357-61.
4. Subden, RE, Fletch, SM, Smart, MA, et. al.: Genetics of the Alaskan
Malamute chondrodysplasia syndrome. Journal of Heredity. 1972:63:
149-152.
5. Braund KG, Shores A, Lowrie CT, Steinberg HS, Moore MP, Bagley RS,
Steiss JE. Idiopathic polyneuropathy in Alaskan malamutes. J Vet Intern
Med. 1997 Jul-Aug;11(4):243-9.
6. Moe L: Hereditary polyneuropathy of Alaskan malamutes. In: Kirk RW,
Bonagura JD (eds). Current Veterinary Therapy XI Small Animal Practice.
W.B. Saunders, Philadelphia, PA 1992:1038-1039.
7. Sidjanin DJ, Lowe JK, McElwee JL, Milne BS, Phippen TM, Sargan DR,
Aguirre GD, Acland GM, Ostrander EA. Canine CNGB3 mutations establish
cone degeneration as orthologous to the human achromatopsia locus
ACHM3. Hum Mol Genet. 2002 Aug 1;11(16):1823-33.
8. Rubin, L., Bourns, T.K.R. and Lord, L.H. Hemeralopia in Dogs: Heredity
of Hemeralopia in Alaskan Malamutes. American Journal of Veterinary
Research, Mar. 1967, pp. 355-357.
9. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007
10. Seddon JM, Hampson EC, Smith RI, et. al.: Genetic heterogeneity of day
blindness in Alaskan Malamutes. Anim Genet. 2006 Aug;37(4):407-10.
11. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
12. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
13. Leone F, Cerundolo R, Vercelli A, Lloyd DH: The use of Trilostane for
the treatment of Alopecia X in Alaskan Malamutes. J Am Anim Hosp Assoc.
2005;41:336-342.
14. Brooks, D. Nonulcerative Keratopathy and Inflammatory Keratitis.
Proceedings, Western Veterinary Conference 2002.
15. Colombini, S. Canine zinc-responsive dermatosis. Vet Clin North Am
Small Anim Pract 29[6]:1373-83 1999 Nov.
16. Beck JA, Simpson DJ, Tisdall PL. Surgical management of osteochondro-
23
American Eskimo Dog
alert, pricked small triangular ears with blunt tips, and ears are
thickly covered in fur. The tail is carried over the back and has a
well-developed plume. The stop is well defined, the skull is fairly flat
and the muzzle is only slightly tapering. The neck is medium in length,
and the head is carried high. The topline is level, the thorax is deep
with well-sprung ribs, and there is a mild abdominal tuck up. The tail
may be dropped off the back at rest in which case it reaches to the
level of the tarsus. Dewclaw removal is optional. Feet are compact,
toes are well arched, and they have thick hair growth around the toes.
The nails are white. Limbs are straight boned with moderate muscling.
The eyes are oval and wide-set; a dark brown color is preferred. Note
The Breed History that some tear staining is normal for many dogs.
The Spitz family (Nordic type) of dogs includes the American Eskimo
Dog, and also the white Keeshond, German Spitz, white Pomeranian,
Japanese Spitz, and white Italian Spitz. Some of these other breeds
Recognized Behavior Issues and Traits
Reported breed characteristics include: Agile, very high trainability,
may have contributed to the gene pool of the American Eskimo Dog
affectionate and they like to please. A good alarm barker with high
breed. Early on in America, the breed was referred to as American
barking tendency, some have tendency to excessive barking. They
Spitz. It was in 1995 that the AKC accepted the breed into the
need close human contact. Early socialization is important so that
registry. The name change to “Eskimo” was done to reflect the
they are not overly aloof with strangers. Need mental stimulation or
Northern origins of the dogs.
will develop boredom vices. Eskie dogs have moderate exercise needs.
They do well with other pets if socialized to them early. They have
Breeding for Function moderate grooming needs. If nervous, they have a tendency to bite.
In the late 19th century in North America they were popular as circus
trick dogs. Currently, their primary purpose is as a companion dog.
Normal Physiologic Variations
None reported
Physical Characteristics
Toy Drug Sensitivities
Height at Withers: 9-12” (23-30.5 cm) None reported
Weight: 6-10 pounds (2.4-4.5kg)
Disease Predispositions Direct test for pyruvate kinase deficiency is available from PennGen.
Hypothyroidism: Inherited autoimmune thyroiditis. 7.8% positive
for thyroid auto-antibodies based on testing at Michigan State Direct test for a DM susceptability gene is available from the OFA.
University. (Ave. for all breeds is 7.5%).7,8
Tests of Phenotype: CHIC Certification: Required testing includes
Hypoadrenocorticism (Addison’s Disease): Immune mediated hip radiographs, CERF eye examination at a minimum of 2 years
destruction of the adrenal gland. Typical presentation of lethargy, of age, and an Optigen prcd-PRA test. Optional testing includes
poor appetite, vomiting, weakness, and dehydration can occur a congenital cardiac evaluation, elbow radiographs, patella
from 4 months to several years of age. Treatment with DOCA evaluation, and a thyroid profile including autoantibodies. (See
injections or oral fludrocortisone. Dorn reports a 52.81x odds ratio CHIC website; www.caninehealthinfo.org).
of developing Addison’s disease versus other breeds.9
Miscellaneous
Idiopathic Epilepsy (Inherited Seizures): Control with anti-seizure • Breed name synonyms: Eskie, Spitz, Toy American Eskimo,
medication. Dorn reports an 8.75x odds ratio of developing epilepsy Miniature American Eskimo, Standard American Eskimo.
versus other breeds.9 • Registries: AKC, UKC, NKC (National Kennel Club).
• AKC rank (year 2008): 108 (384 dogs registered)
Cataracts: Anterior cortex cataracts predominate, though posterior • Internet resources: American Eskimo Dog Club of America:
intermediate and punctate cataracts also occur in the breed. www.aedca.org
Unknown mode of inheritance. Identified in 3.56% of American The National American Eskimo Dog Association:
Eskimo Dogs CERF examined by veterinary ophthalmologists www.americaneskimo.com/NAEDA/
between 2000-2005. CERF does not recommend breeding any The National American Eskimo Dog Association of Canada:
American Eskimo Dog with a cataract.1 www.naedac.ca
Kidney Disease: Dorn reports an 8.28x odds ratio of developing
kidney disease versus other breeds. A specific type of kidney disease References
is not specified. The only reported kidney disease in the breed is a 1. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
case report of Hereditary Nephropathy (see below).9 College of Veterinary Ophthalmologists. ACVO, 2007
2. Morris Animal Foundation: Morris Animal Foundation Update: Genetic
Alopecia (Endocrine or Hormonal Alopecia): Progressive, Tests Focus on Breed-Specific Vision Problems. Canine Pract 1999:24[4]:21.
symmetrical, non-pruritic, truncal hair loss usually beginning in 3. Moody JA, Famula TR, et al. Identification of microsatellite markers
early adulthood. ACTH, LDDS, and thyroid panel results are normal. linked to progressive retinal atrophy in American Eskimo Dogs. AJVR
Elevated blood concentrations of 17-hydroxyprogesterone (17-OHP) 2005:66(11):1900-1902.
have been seen post ACTH stimulation. Oral trilostane reverses the 4. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
condition in some cases. The disorder appears familial.10 5. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23
Degenerative Myelopathy (DM): Affected dogs show an insidious 6. Giger U: Regenerative anemias caused by blood loss or hemolysis. In:
onset of upper motor neuron (UMN) paraparesis. The disease Ettinger, SJ and Feldman EC. (eds.) Textbook of Veterinary Internal Medicine
eventually progresses to severe tetraparesis. Affected dogs have W. B. Saunders, Philadelphia, pp.1784-1804. 2000.
normal results on myelography, MRI, and CSF analysis. Necropsy 7. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
confirms the condition. Unknown mode of inheritance. A direct for Population and Animal Health, Michigan State University. April, 2007.
genetic test for an autosomal recessive DM susceptibility gene is 8. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
available. All affected dogs are homozygous for the gene, however hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
only a small percentage of homozygous dogs develop DM. A genetic Vet Med Assoc 2002 Feb 15;220(4):466-71.
test for the susceptibility gene is available.4,14 9. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Anasarca, Cryptorchidism, Hemivertebra, Laryngeal Paralysis, 2000.
Megaesophagus, Methemoglobin Reductase Deficiency, 10. Chastain CB: Sex Hormone Concentrations in Dogs with Alopecia. Sm
Narcolepsy, Patent Ductus Arteriosus, Prognathism, Sebaceous Anim Clin Endocrinol 2004:14[1]:37-38.
Adenitis, and Zinc-Responsive Dermatosis are reported.11 11. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 196. AAHA Press, 1999.
Isolated Case Studies 12. Lees GE: Update: Inherited Primary Glomerular Diseases in Dogs.
Proceedings ACVIM Forum, 2003
Hereditary Nephropathy (HN): A 15 month old female American
13. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
Eskimo Dog from a father-daughter mating was diagnosed with
House, NY 2006. p. 525-528.
hereditary nephropathy. The clinical and pathologic features of 14. Awano T, Johnson GS, Wade CM, et. al.: Genome-wide association
the renal disease identified in the affected dog resembled those of analysis reveals a SOD1 mutation in canine degenerative myelopathy that
autosomal recessive HN.12 resembles amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A. 2009 Feb
24;106(8):2794-9.
25
American Foxhound
narrower than the English type, ribs are well sprung and rib cage
extends well back. The back is long and level though slightly arched.
The limbs are straight, feet are compact with well-arched toes. The
tail is carried gaily and curved, with a slight brush at the tip.
Coat: Hard, medium length coat lays flat and any color is accepted.
Disease Predispositions
Hypothyroidism: Inherited autoimmune thyroiditis. 9.3% positive
Tricolors (white, tan and black) are the most common.
for thyroid auto-antibodies based on testing at Michigan State
Longevity: 11-14 years. University. (Ave. for all breeds is 7.5%).3,4
Points of Conformation: These dogs typify a dog of moderate Leishmaniasis: This infectious disease is primarily only diagnosed
proportions. The skull is long and slightly domed, ears are set in Foxhounds. Research suggests vertical transmission (mother to
moderately low, and are long and pendulous with fine leather, and offspring), though a genetic susceptibility cannot be ruled out.5,6,7,8
have rounded tips. Wide set eyes are large and brown or hazel in
Deafness: Congenital deafness can be unilateral or bilateral.
color. The muzzle is square, and a moderate stop is present. The
Diagnosed by BAER testing.9,10
neck is medium in length and not throaty. Thorax is deep and
26
Ocular Disorders: Too few American Foxhounds have been CERF
examined to determine the frequency of ocular disorders in the
breed.11
Genetic Tests
Tests of Genotype: Direct tests for coat color alleles are available
from VetGen.
Miscellaneous
• Breed name synonyms: Foxhound
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
NKC (National Kennel Club)
• AKC rank (year 2008): 158 (17 dogs registered)
• Internet resources: American Foxhound Club Inc.:
www.americanfoxhoundclub.com
Masters of Foxhounds Association of America: www.mfha.com
The Foxhound Club of North America: http://fcna.org
References
1. Bowles CA, Alsaker RD, Wolfle TL: Studies of the Pelger-Huet anomaly in
foxhounds. Am J Pathol. 1979 Jul;96(1):237-47.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
5. Rosypal AC, Troy GC, Zajac AM, et. al.: Emergence of zoonotic canine
leishmaniasis in the United States: isolation and immunohistochemical
detection of Leishmania infantum from foxhounds from Virginia. J Eukaryot
Microbiol. 2003;50 Suppl:691-3.
6. Gaskin AA, Schantz P, Jackson J, et. al.: Visceral leishmaniasis in a New
York foxhound kennel. J Vet Intern Med. 2002 Jan-Feb;16(1):34-44.
7. Grosjean NL, Vrable RA, Murphy AJ, et. al.: Seroprevalence of antibodies
against Leishmania spp among dogs in the United States. J Am Vet Med
Assoc. 2003 Mar 1;222(5):603-6.
8. Petersen CA: New means of canine leishmaniasis transmission in
north america: the possibility of transmission to humans still unknown.
Interdiscip Perspect Infect Dis. 2009;2009:802712
9. Hiraide F, Paparella MM: Histopathology of the temporal bones of deaf
dogs. Auris Nasus Larynx. 1988;15(2):97-104.
10. Adams EW: Hereditary deafness in a family of foxhounds. J Am Vet Med
Assoc. 1956 Mar 15;128(6):302-3.
11. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007
12. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 218. AAHA Press, 1999.
13. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 170-172.
27
American
Staffordshire Terrier
Longevity: 12 years.
30
American
Water Spaniel
loyal, likes to please. He is also considered a good watchdog
and has a high barking tendency. They are notable for a high
tolerance of pain; a very stoic dog. High activity and exercise
needs are evident especially when young. Early obedience training
is recommended, as is early socialization; some have a stubborn
streak. Can be possessive of toys and food, tending to dominance,
and may develop boredom vices if not adequately exercised and
challenged mentally. Slow to mature and sensitive; responds well to
positive reinforcement in training.
Coat: The haircoat may be wavy or curly and a thick undercoat Disease Predispositions
is present. Colors include liver, chocolate, or brown. Small white Mitral Valve Disease: Mitral valve prolapse and mitral
markings are accepted on the toes and chest. They are light to regurgitation was identified in 56% of American Water Spaniels
moderate shedders and have moderate grooming needs; the screened with echocardiography at the 2002 AWSC National
haircoat can be a bit oily. Specialty. This was identified in dogs both with and without a heart
murmur. (See AWSC website)
Longevity: 11-12 years
Distichiasis: Abnormally placed eyelashes that irritate the cornea
Points of Conformation: Medium size, longer than tall, and solid and conjunctiva. Can cause secondary corneal ulceration. Identified
bone and muscling characterizes this breed. The eyes are light in 30.07% of American Water Spaniels CERF examined by veterinary
brown, hazel, or dark brown. Eyes are medium-sized, moderately ophthalmologists between 2000-2005.2
deep set and the palpebral margins are tight. The skull is flat
and broad. Ears are long, wide and heavily feathered. The stop is Patent Ductus Arteriosus: Polygenically inherited congenital heart
moderate, the muzzle square and fairly long, and the nose is dark disorder, where a fetal vessel remains open after birth, causing a
brown or black. The neck is short-to-medium, and not throaty. The mixing of oxygenated and unoxygenated blood. Affected dogs are
topline is level, and the thorax moderately deep with well sprung usually stunted, and have a loud heart murmur. Diagnosis with
ribs. The tail is carried fairly level, is moderately feathered and Doppler ultrasound. Treat with surgery. Identified in 5% of American
tapers at the terminus. Limbs are straight boned, and the feet are Water Spaniels screened with echocardiography at the 2002 AWSC
webbed and compact. Front dewclaws may be left on. The gait is National Specialty. (See AWSC website)
smooth, powerful and ground covering.
Pulmonic Stenosis: Polygenically inherited congenital heart
Recognized Behavior Issues and Traits disorder, where there is a narrowing of the outflow from the
pulmonic valve. This can cause exercise intolerance, and right sided
Reported breed characteristics include: Intelligent, high trainability,
31
heart failure. Diagnosis with Doppler ultrasound. Identified in 5%
of American Water Spaniels screened with echocardiography at the
Miscellaneous
• Breed name synonyms: Brown Water Spaniel, AWS.
2002 AWSC National Specialty. (See AWSC website) • Registries: AKC, UKC, CKC, NKC (National Kennel Club).
• AKC rank (year 2008): 136 (132 dogs registered)
Hypothyroidism: Inherited autoimmune thyroiditis. 3.7% positive
• Internet resources: American Water Spaniel Club Inc.:
for thyroid auto-antibodies based on testing at Michigan State
www.americanwaterspanielclub.org
University. (Ave. for all breeds is 7.5%).3,4
AWS Partners: http://home.earthlink.net/~awspartners/
Cataracts: Posterior cortex cataracts predominate, although American Water Spaniel Field Association: www.awsfa.org
anterior intermediate and punctate cataracts also occur in the
breed. Unknown mode of inheritance. Identified in 2.61% of References
American Water Spaniels CERF examined by veterinary ophthalmol- 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
ogists between 2000-2005. CERF does not recommend breeding 2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
any American Water Spaniel with a cataract.2 College of Veterinary Ophthalmologists. ACVO, 2007.
3. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
Persistent Pupillary Membranes: Strands of fetal remnant for Population and Animal Health, Michigan State University. April, 2007.
4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
later three forms can impair vision, and dogs affected with these
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
forms should not be bred. Identified in 1.63% of American Water 5. Coates JR, Zeng R, Awano T, et. al.: An SOD1 Mutation Associated with
Spaniels CERF examined by veterinary ophthalmologists between Degenerative Myelopathy Occurs in Many Dog Breeds. Proceedings 2009
2000-2005.2 ACVIM Forum. 2009.
6. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Retinal Dysplasia: Retinal folds, geographic, and generalized retinal Ackerman. p. 197. AAHA Press, 1999.
dysplasia with detachment are recognized in the breed. Identified 7. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
in 1.63% of American Water Spaniels CERF examined by veterinary House, NY 2006. p. 76-78.
ophthalmologists between 2000-2005.2
Genetic Tests
Tests of Genotype: Direct test for DM susceptibility gene is
available from OFA.
Weight: females 80-120 lb (36.5-54.6 kg), males 110-150 lb Elbow Dysplasia: Polygenically inherited trait causing elbow
(50-68 kg). arthritis. OFA reports 4.5% affected.1
Coat: Two coat variants exist; the Short and the Rough. Rough Patella Luxation: Polygenically inherited laxity of patellar
is about 4” (10) cm in length, while Short is 1” (2.54 cm). The ligaments, causing luxation, lameness, and later degenerative joint
undercoat is dense. Some feathering may be present. Color or disease. Treat surgically if causing clinical signs. Too few Anatolian
markings are not limited in this breed, but fawn with a dark mask is Shepherds have been screened by OFA to determine an accurate
common. frequency.1
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: Anatolian, Anatolian Karabash Dog,
Coban Kopegi (Turkish for Shepherd’s dog), Karabas, Anatolian
Sheperd, Anatolian Shephard, Kangal Dog.
• Registries: AKC, UKC, KCGB (Kennel Club of Great Britain), ANKC
(Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 110 (373 dogs registered)
• Internet resources: Anatolian Shepherd Dog Club of America:
www.asdca.org
Anatolian Shepherd Dogs International: www.anatoliandog.org
Anatolian Shepherd Dog Club of Great Britain:
www.asdc-of-gb.netfirms.com
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
5. Temizsoylu MD, Avki S: Complete ventral ankyloglossia in three related
dogs. J Am Vet Med Assoc. 2003 Nov 15;223(10):1443-5, 1433.
6. Grundmann S, Hofmann A: Ankyloglossia in an Anatolian Shepherd dog.
34
Australian
Cattle Dog
toes well arched. The low set tail is slightly curved and reaches to
the tarsus. The tail has a brush. A strong smooth gait that appears
effortless, and a strong rear quarter driving effort should be
apparent.
Weight: 35-45 lb (16-20 kg). Hip Dysplasia: Polygenically inherited trait causing degenerative
joint disease and hip arthritis. OFA reports 15.3% affected.1
Coat: The moderately hard weather resistant coat is double and
straight. The undercoat is short and dense. Colors are blue (blue Elbow Dysplasia: Polygenically inherited trait causing elbow
mottled appearance acceptable) or red speckle with or without other arthritis. OFA reports 11.6% affected.1
markings. Specific markings are set out in the standard. Puppies are
born light to white because of the Dalmation breed effect. Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Longevity: 12-13 years disease. Treat surgically if causing clinical signs. OFA reports 1.6%
affected.1
Points of Conformation: A sturdy well balanced conformation
and highly energized movements characterize this working dog. Primary Lens Luxation (PLL) and Secondary Glaucoma: An
Utility has dictated points of conformation. They possess a broad autosomal recessive gene causes primary lens luxation. Homozygous
skull, a strong profile with definite stop, the muzzle is deep and affected dogs usually develop lens luxation between 4-8 years of
lips tight, and the nose is always black. They appear dingo-like in age. Rarely, heterozygous carriers can develop lens luxation, but
many regards. Dark brown eyes are oval, medium-sized, and a sharp at a later age. Lens luxation can lead to secondary glaucoma and
stare is normal. Pricked ears are wide set and small to medium in blindness. A genetic mutation has been identified, and a genetic
size, and the neck is medium in length and not throaty. The topline test is available. One study reports a 3.1x odds ratio for secondary
is level, thorax deep, ribs well sprung, and the rib cage remains glaucoma versus other breeds.4,5
deep caudally. The limbs are straight-boned, feet are round and the
35
Spongiform Leukoencephalomyelopathy (Polioencephalo- Achromatopsia (Day Blindness): Observed in a 12-month-old
myopathy): Rare maternally (mitochondrial) inherited disorder Australian cattle dog.20
causing tremors, spastic weakness, ataxia, occasionally seizures, and
eventual paralysis beginning at 2-9 weeks of age. Caused by a point Dermatomyositis, Osteochondrosis of the Hock, Pelger-Huet
mutation in the cytochrome b gene.6,7,8 Anomaly and von Willebrand’s disease are reported.21
Cataracts: Anterior and posterior cataracts are equally represented Direct test for black, brown, and yellow colors is available from
in the breed with intermediate and punctate cataracts. Identified VetGen.
in 4.95% of Australian Cattle Dogs CERF examined by veterinary
Tests of Phenotype: CHIC Certification: Required tests include
ophthalmologists between 2000-2005. CERF does not recommend
hip and elbow radiographs (2 years of age or older), CERF eye
breeding any Australian Cattle Dog with a cataract.3
examination (2 years of age or older), gene test for prcd-PRA, and
Portosystemic Shunt (PSS, Liver Shunt): Undetermined mode of BAER hearing test. Optional tests include patella evaluation (over 1
inheritance but familial pattern. Abnormal blood vessels connecting year of age), cardiac evaluation, and hock radiograph for OCD. (See
the systemic and portal blood flow. Vessels are usually intrahepatic CHIC website; www.caninehealthinfo.org).
in this breed, with a tendency to a right divisional location. Causes
Recommend thyroid profile including autoantibodies.
stunting, abnormal behavior and possible seizures. Australian
studies show significantly higher prevalence in the breed compared Bile acids and blood ammonia tests (fasting and post-feeding) if
to other breeds.12,13,14 suspect portosystemic shunt.
Primary Glaucoma: Ocular condition causing increased pressure
within the eyeball, and secondary blindness due to damage to the Miscellaneous
retina. United States study of dogs presented to veterinary teaching • Breed name synonyms: Cattle Dog, ACD, Australian Queensland
hospitals showed an increased prevalence in male Australian Heeler, Blue Heeler, Queensland Heeler, Hall’s Heelers
Cattle Dogs. Dorn reports a 2.07x odds ratio for the disorder • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
versus other breeds. Gelatt reports 1.51% Australian Cattle Dogs ANKC (Australian National Kennel Club), NKC (National Kennel Club)
affected between 1994-2002. Diagnose with IOP (tonometry) and • AKC rank (year 2008): 68 (1,294 dogs registered)
examination of the iridocorneal angle (gonioscopy).2,3,15 • Breed resources: Australian Cattle Dog Club of America:
http://acdca.org/
Cysinuria and Cystine Bladder Stones: Caused by a metabolic Australian Cattle Dog Health, Education and Welfare, Inc,
abnormality in cystine metabolism. Australian Cattle Dogs are (ACDHEW): www.acdhew.org
found to have an increased incidence.16 Australian Cattle Dog Club of Canada: www.acdcc.ca
Australian Cattle Dog Society of Great Britain:
Persistent Pupillary Membranes: Strands of fetal remnant www.acdsocietyofgb.com
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
The later three forms can impair vision, and dogs affected with
these forms should not be bred. Identified in 1.03% of Australian
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Cattle Dogs CERF examined by veterinary ophthalmologists between 2. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
2000-2005.3 veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
Ceroid Lipofucinosis: Rare storage disease causing progressive 3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
blindness and incoordination between 1 and 2 years of age.17,18 College of Veterinary Ophthalmologists. ACVO, 2007.
4. Collier L, McCalla T, Moor CP: Anterior lens luxation in Queensland
Isolated Case Studies Heeler (Australian Cattle) dogs. Proc Am Coll Vet Ophthal 1989;20:18.
5. Johnsen DA, Maggs DJ, Kass PH: Evaluation of risk factors for
Myotonia Hereditaria: An Australian Cattle Dog with generalized
development of secondary glaucoma in dogs: 156 cases (1999-2004). J Am
muscle stiffness and hypertrophy was examined, and determined to Vet Med Assoc. 2006 Oct 15;229(8):1270-4.
be homozygous recessively affected due to a mutation in the CLCN1 6. Brenner O, de Lahunta A, Summers BA, et. al.: Hereditary polioencepha-
gene. No heterozygous Australian Dogs were identified, and it is lomyelopathy of the Australian Cattle Dog. Acta Neuropath 1997;
not known if this gene is disseminated in the general population. A Jul;94(1):54-66.
direct genetic test is available from the University of Guelph AHL.19 7. Harkin KR, Goggin JM, DeBey BM, et. al.: Magnetic Resonance imaging of
36
the brain of a dog with hereditary polioencephalomyopathy. J Am Vet Med
Assoc 1999; May 1; 214(9):1342-44.
8. Li FY, Cuddon PA, Song J, Wood SL, et. al.: Canine spongiform
leukoencephalomyelopathy is associated with a missense mutation in
cytochrome b. Neurobiol Dis. 2005 Jul 15.
9. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J 2004; Jan;167(1):23-32.
10. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
11. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum
thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
12. Tisdall PL, Hunt GB, Bellenger CR, Malik R: Congenital portosystemic
shunts in Maltese and Australian cattle dogs. Aust Vet J 1994; Jun;
71(6):174-8.
13. Hunt GB: Effect of breed on anatomy of portosystemic shunts resulting
from congenital diseases in dogs and cats: a review of 242 cases. Aust Vet J
2004;Dec; 82[12]:746-9.
14. Krotscheck U, Adin CA, Hunt GB, et. al.: Epidemiologic factors associated
with the anatomic location of intrahepatic portosystemic shunts in dogs.
Vet Surg. 2007 Jan;36(1):31-6.
15. Gelatt KN and MacKay EO: Prevalence of the Breed-Related Glaucomas
in Pure-Bred Dogs in North America. Vet Ophthalmol Mar-Apr’04;
7[2]:97-111.
16. Case LC, Ling GV, Franti CE, et. al.: Cystine-containing urinary
calculi in dogs: 102 cases (1981-1989). J Am Vet Med Assoc 1992; Jul
1;201(1):129-33.
17. Sisk DB, Levesque DC, Wood PA, Styer EL: Clinical and pathological
features of ceroid lipofucinosis in two Australian cattle dogs. J Am Vet Med
Assoc 1990; Aug 1; 197(3):361-4.
18. Wood PA, Sisk DB, Styer E, et. al.: Animal model: ceroidosis
(ceroid-lipofuscinosis) in Australian cattle dogs. Am J Med Genet. 1987
Apr;26(4):891-8.
19. Finnigan DF, Hanna WJ, Poma R, et. al.: A novel mutation of the CLCN1
gene associated with myotonia hereditaria in an Australian cattle dog. J Vet
Intern Med. 2007 May-Jun;21(3):458-63.
20. Hurn SD, Hardman C, Stanley RG: Day-Blindness in Three Dogs: Clinical
and Electroretinographic Findings. Vet Ophthalmol Jun’03; 6[2]:127-130
21. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 197-8. AAHA Press, 1999.
22. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 607-611.
37
Australian Shepherd
The limbs are straight boned, feet compact and well knuckled up. Rear
dewclaws are always removed. Gait is agile, and appearing effortless.
Weight: 35-70 lb (16-32 kg). Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. OFA reports 4.3% affected.8
Coat: The coat is moderate in length and density, wavy or straight
and moderate feathering is present on the forelegs and britches; Legg-Calvé-Perthes Disease: Polygenically inherited. Can be
a mane and frill are developed. Colors include red, red merle, blue unilateral or bilateral, with onset of degeneration usually under 9
merle, and black. These may be combined with markings of specified months of age. Treat surgically if causing lameness or discomfort.
size and distribution including white and copper. Australian Shepherds found to have a 191.4x odds ratio for
developing the disease versus other breeds.9
Longevity: 12-13 years
Cataracts: A mutation in the HSF4 gene is associated with
Points of Conformation: These dogs are medium in build and slightly co-dominant cataracts in the breed, although other inherited
longer than tall. The tail is either naturally bobbed or is docked to cataracts also occur. Australian Shepherds homozygous for the
about 4” in length. A moderate stop divides the rounded muzzle mutation tend to develop bilateral nuclear cataracts, and dogs with
from skull. An alert expression emanates from almond shaped eyes. one copy of the defective gene have a 17.7x risk of developing
Iris pigment is variable and can include brown, blue and amber. Ears posterior polar subcapsular cataracts. CERF reports anterior and
are triangular and moderate in size, and break in a fold hanging posterior cataracts are equally represented in the breed, and can be
forward or backwards. The nose is black for all but red or red merle intermediate or punctate. Reported in 2.43% of Australian Shepherds
dogs, where a liver nose is evident. Neck is moderate in muscling. The CERF examined by veterinary ophthalmologists between 2000-2005.
topline is level, ending in a moderately sloping croup. The thorax is CERF does not recommend breeding any Australian Shepherd with a
deep and the ribs well sprung, and abdomen is moderately tucked up. cataract. A direct genetic test for the HSF4 mutation is available.10,11,12
38
Patella Luxation: Polygenically inherited laxity of patellar ligaments, other ocular defects. Reported at a frequency of 5.82% in the breed in
causing luxation, lameness, and later degenerative joint disease. an Australian study. Identified in 0.61% of Australian Shepherds CERF
Treat surgically if causing clinical signs. OFA reports 1.9% affected.8 examined by veterinary ophthalmologists between 2000-2005.10,14
Collie Eye Anomaly/Choroidal Hypoplasia/Coloboma (CEA/CH): Idiopathic Epilepsy (Inherited Seizures): Control with anti-seizure
Autosomal recessive disorder of eye development that can lead medication. Reported to occur at an increased frequency in the
to retinal detachment and blindness. Iris coloboma is reported 1999 ASCA Breed Health Survey.19
in 1.45% of Australian Shepherds CERF examined by veterinary
ophthalmologists between 2000-2005. A genetic test is available Chronic Superficial Keratitis (CSK)/Pannus: Corneal disease
through Optigen, that reports 1% of Australian Shepherds test that can cause vision problems due to pigmentation. Treatment
as affected, and 10% test as carriers. Reported at a frequency of with topical ocular lubricants and anti-inflammatory medication.
4.03% affected in an Australian study.10,13,14 Australian Shepherds are a breed with increased risk of developing
CSK. The disorder usually occurs between 4-7 years of age.20
Hyperuricosuria (HUU)/Urate Bladder Stones: An autosomal
recessive mutation in the SLC2A9 gene causes urate urolithiasis and Cystine Urinary Calculi: Caused by a metabolic abnormality
can predispose male dogs to urinary obstruction. Estimated at a in cystine metabolism. Australian Shepherds are a breed with
carrier frequency of 3.46% in the breed. A genetic test is available.31 increased risk of developing cystine calculi.21
Multifocal Retinopathy/Retinal Dysplasia: Autosomal recessive Microphthalmia: Microphthalmia with coloboma appears to
retinal pigment epithelial dysplasia causing localized multifocal retinal behave as an incompletely penetrant recessive trait in the merle
detachments. Age of onset from 11 to 13 weeks of age. Reported Australian Shepherd dog. Homozygous merle dogs are usually blind,
in 0.8% of Australian Shepherds CERF examined by veterinary while heterozygous dogs can be less severely affected.10,22
ophthalmologists between 2000-2005. A genetic test is available.10
Anterior Crossbite, Brachygnathism, Cerebellar Vermian
Progressive Retinal Atrophy (PRA): Autosomal recessive inherited Hypoplasia, Cutaneous Lupus Erythematosus, Diabetes Mellitus,
retinal degeneration leading to blindness. Progressive rod cone Factor VIII Deficiency, Osteochondrodysplasia, Panosteitis,
degeneration (prcd) form occurs at a very low frequency. A genetic Patent Ductus arteriosis, Pelger-Huet Anomaly, Persistent
test is available.10 Right Aortic arch, Portosystemic Shunt, Prognathism, Pulmonic
Stenosis, and von Willebrand’s Disease are reported.23
Distichiasis: Abnormally placed eyelashes that irritate the cornea Peripheral Neuroectodermal Tumor: A peripheral primitive
and conjunctiva. Can cause secondary corneal ulceration. Identified neuroectodermal tumor (pPNET), most consistent with a human
in 1.44% of Australian Shepherds CERF examined by veterinary Ewing’s sarcoma, is described in a 5-month-old male Australian
ophthalmologists between 2000-2005.10 Shepherd puppy.26
Deafness: Inherited congenital deafness associated with the merle Myofibrillar Myopathy: A 1-year-old male neutered Australian
gene. In a multi-breed study; for single merles (Mm), 2.7% were Shepherd dog was evaluated for chronic lameness, contractures,
unilaterally deaf and 0.9% were bilaterally deaf. For double merles and exercise intolerance. Cardiomyopathy, and myofibrillar
(MM), 10% were unilaterally deaf and 15% were bilaterally deaf. myopathy with accumulation of desmin was identified.27
Diagnosed by BAER testing. Unknown mode of inheritance for
Multiple Skeletal Defects: A family of Australian Shepherds was
deafness, though dominant merle gene must be present.17,18
identified with a syndrome including cleft palate, polydactyly,
Cryptorchidism (Retained Testicles): Can be unilateral or bilateral. and often syndactyly, shortened tibia-fibula, brachygnathism and
This is a sex-limited disorder with an unknown mode of inheritance. scoliosis lethal to males. The disorder may be due to an x-linked
Reported to occur at an increased frequency in the 1999 ASCA gene, or a sex-influenced autosomal gene in conjunction with
Breed Health Survey.19 instability of the merle locus.28
Persistent Hyaloid Artery (PHA): Congenital defect resulting from Anemia and Osteopetrosis: Case study of a 1-year-old, male
abnormalities in the development and regression of the hyaloid artery. Australian Shepherd Dog with severe nonregenerative anemia
Does not cause vision problems by itself, but is often associated with associated with osteopetrosis. The anemia was attributed to failure
39
to develop normal marrow cavities combined with failure of 2005 Dec;28(6):545-51.
extramedullary erythropoiesis.29 6. Neff MW, Robertson KR, Wong AK, et. al.: Breed distribution and history of
canine mdr1-1Delta, a pharmacogenetic mutation that marks the emergence
of breeds from the collie lineage. Proc Natl Acad Sci U S A. 2004 Aug
Genetic Tests 10;101(32):11725-30.
Tests of Genotype: Direct tests for CEA/CH, retinal dysplasia, and 7. Mealey KL and Meurs KM: Breed distribution of the ABCB1-1Delta
prcd-PRA are available from Optigen. (multidrug sensitivity) polymorphism among dogs undergoing ABCB1
genotyping. J Am Vet Med Assoc. 2008 Sep 15;233(6):921-4.
Direct test for MDR1 (ivermectin sensitivity) gene is available from 8. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Washington State Univ. http://www.vetmed.wsu.edu/depts-VCPL/ 9. LaFond E, Breur GJ, Austin CC: Breed susceptibility for developmental
test.asp orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
10. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Direct test for increased cataract susceptibility is available from the
College of Veterinary Ophthalmologists. ACVO, 2007.
Animal Health Trust. 11. Mellersh CS, Pettitt L, Forman OP, et. al.: Identification of mutations
in HSF4 in dogs of three different breeds with hereditary cataracts. Vet
Direct test for HUU is available from the UC-Davis VGL and the Ophthalmol. 2006 Sep-Oct;9(5):369-78.
Animal Health Trust. 12. Mellersh CS, McLaughlin B, Ahonen S, et. al.: Mutation in HSF4 is
associated with hereditary cataract in the Australian Shepherd. Vet
Direct test for skin and nose color (black, clear red, brown (red), Ophthalmol. 2009 Nov-Dec;12(6):372-8.
and dilute colors and black or brown pigmentation on the nose) is 13. Lowe JK, Kukekova AV, Kirkness EF, et. al.: Linkage mapping of the primary
available from HealthGene and VetGen. disease locus for collie eye anomaly. Genomics. 2003 Jul:82(1):86-95.
14. Munyard KA, Sherry CR, Sherry L: A retrospective evaluation of congenital
Tests of Phenotype: CHIC Certification: Required testing includes ocular defects in Australian Shepherd dogs in Australia. Vet Ophthalmol.
hip radiographs, elbow radiographs, and CERF eye examination. 2007 Jan-Feb;10(1):19-22.
15. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
Optional recommended testing for thyroid profile including
for Population and Animal Health, Michigan State University. April, 2007.
autoantibodies, and direct tests for CEA/CH, and MDR1. (See CHIC 16. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
website; www.caninehealthinfo.org). hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
Recommend BAER testing for deafness, direct test for cataract 17. Strain GM: Deafness prevalence and pigmentation and gender
succeptability, patella examination, and cardiac evaluation. associations in dog breeds at risk. The Veterinary Journal 2004; 167(1):23-32.
18. Strain GM, Clark LA, Wahl JM, et. al.: Prevalence of deafness in dogs
Miscellaneous heterozygous or homozygous for the merle allele. J Vet Intern Med. 2009
Mar-Apr;23(2):282-6.
• Breed name synonyms: Aussie, Australian Shepherd, Pastor Dog, 19. Sharp CA and Adolphson P: Results of the 1999 ASCA Breed Health
Bob-tail, New Mexican Shepherd, California Shepherd, Spanish Survey. Aussie Times. 2002 Jan-Feb.
Shepherd (historical). 20. Chavkin MJ, Roberts SM, Salman MD, et. al.: Risk factors for development
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), of chronic superficial keratitis in dogs. J Am Vet Med Assoc. 1994 May
ANKC (Australian National Kennel Club), NKC (National Kennel Club) 15;204(10):1630-4.
• AKC rank (year 2008): 29 (6,471 dogs registered) 21. Case LC, Ling GV, Franti CE, et. al.: Cystine-containing urinary calculi in
dogs: 102 cases (1981-1989). J Am Vet Med Assoc. 1992 Jul 1;201(1):129-33.
• Internet resources: Australian Shepherd Club of America Inc:
22. Gelatt KN, Powell NG, Huston K: Inheritance of microphthalmia
www.asca.org with coloboma in the Australian shepherd dog. Am J Vet Res. 1981
Australian Shepherd Health and Genetics Institute, Inc. Oct;42(10):1686-90.
(ASGI): www.ashgi.org 23. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Canadian National Australian Shepherd Association: Ackerman. p. 198. AAHA Press, 1999.
www.cnasa.ca 24. He Q, Madsen M, Kilkenney A, et. al.: Amnionless function is required for
Australian Shepherd Club of the United Kingdom: cubilin brush-border expression and intrinsic factor-cobalamin (vitamin B12)
www.ascuk.co.uk absorption in vivo. Blood. 2005 Aug 15;106(4):1447-53.
25. O’Brien DP and Katz ML: Neuronal ceroid lipofuscinosis in 3 Australian
shepherd littermates. J Vet Intern Med. 2008 Mar-Apr;22(2):472-5.
References 26. De Cock HE, Busch MD, Fry MM, et. al.: A peripheral primitive
1. Clark LA, Wahl JM, Rees CA, et. al.: Retrotransposon insertion in SILV is neuroectodermal tumor with generalized bone metastases in a puppy. Vet
responsible for merle patterning of the domestic dog. Proc Natl Acad Sci U S Pathol. 2004 Jul;41(4):437-41.
A. 2006 Jan 31;103(5):1376-81. 27. Shelton GD, Sammut V, Homma S, et. al.: Myofibrillar myopathy with
2. Hedan B, Corre S, Hitte C, et. al.: Coat colour in dogs: identification of the desmin accumulation in a young Australian Shepherd dog. Neuromuscul
merle locus in the Australian shepherd breed. BMC Vet Res. 2006 Feb 27;2:9. Disord. 2004 Jul;14(7):399-404.
3. Geyer J, Doring B, Godoy JR, et. al.: Development of a PCR-based 28. Sponenberg DP, Bowling AT: Heritable syndrome of skeletal defects in a
diagnostic test detecting a nt230(del4) MDR1 mutation in dogs: verification family of Australian shepherd dogs. J Hered. 1985 Sep-Oct;76(5):393-4.
in a moxidectin-sensitive Australian Shepherd. J Vet Pharmacol Ther. 2005 29. Lees GE, Sautter JH: Anemia and osteopetrosis in a dog. J Am Vet Med
Feb;28(1):95-9. Assoc. 1979 Oct 15;175(8):820-4.
4. Nelson OL, Carsten E, Bentjen SA, et. al.: Ivermectin toxicity in an 30. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
Australian Shepherd dog with the MDR1 mutation associated with House, NY 2006. p. 612-615.
ivermectin sensitivity in Collies. J Vet Intern Med. 2003 May-Jun;17(3):354-6. 31. Karmi N, Brown EA, Hughes SS, et. al.: Estimated frequency of the canine
5. Geyer J, Doring B, Godoy JR, et. al.: Frequency of the nt230 (del4) MDR1 hyperuricosuria mutation in different dog breeds. J Vet Intern Med. 2010
mutation in Collies and related dog breeds in Germany. J Vet Pharmacol Ther. Nov-Dec;24(6):1337-42.
40
Australian Terrier
Recognized Behavior Issues and Traits
Reported breed characteristics include: Good in rural and urban
environments, courageous, good alarm barkers, low shedding,
adaptable, loyal, and intelligent. Can be scrappy with other dogs,
enjoys close human companionship, good with other pets if
raised with them (except other dogs, especially inter-male), high
trainability, very high energy, spirited, like to dig and if off leash,
they should be in a securely fenced enclosure; may also jump a
fence. Should be socialized to pets and children since the strong
chase instinct means that small pets could be viewed as prey.
The Breed History
In Australia, the breed was first exhibited in 1899. These terriers Normal Physiologic Variations
were the first of the Aussie breeds, with the breed standard finalized None reported
in the year 1896. The AKC registry admitted Australian Terriers in
1960. Breed origins may include the Rough-coated Terrier crossed Drug Sensitivities
over many generations with other terriers such as the Skye, Dandie None reported
Dinmont, Irish, Cairn, Yorkshire, Black-and-Tan Terrier, and perhaps
the Norwich Terrier. They were first brought to North America
following the Second World War.
Inherited Diseases
Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Breeding for Function disease. Treat surgically if causing clinical signs. Reported 8.0x odds
This small terrier was bred for both companionship and as a sturdy ratio versus other breeds. OFA reports 11.9% affected. Reported at a
hunting partner. He also served as protector of sheep flocks and frequency of 9.0% in the 2002 ATCA Health Survey.1,2,3
family. Rat and snake control were common tasks for which this
terrier was bred. Hip Dysplasia: Polygenically inherited trait causing degenerative
joint disease and hip arthritis. OFA reports 2.4% affected.1
Physical Characteristics Legg-Calvé-Perthes Disease: Polygenically inherited aseptic
Height at Withers: 10-11” (25.4-28 cm).
necrosis of the femoral head, resulting in degenerative joint disease.
Weight: 12-14 lb (4-7 kg). Can be unilateral or bilateral, with onset of degeneration usually
between 6-9 months of age. Treat surgically if causing lameness/
Coat: The double coat is water resistant. Outer coat is straight, discomfort. Reported at a frequency of 1.6% in the 2002 ATCA
harsh and broken, and 2-1/2” (6 cm) long except furnishings. Inner Health Survey.2
coat is dense and short. Colors include blue and tan, sandy, and red.
The hairs form a distinct topknot, apron and ruff. White markings Elbow Dysplasia: Polygenically inherited trait causing elbow
on feet and chest are faults. arthritis. Too few Australian Terriers have been screened by OFA to
determine an accurate frequency.1
Longevity: 14 years
Deafness: Congenital deafness can be unilateral of bilateral. Primitive Neuroectodermal Tumour: An 18-month-old female
Diagnosed by BAER testing. Reported at a frequency of 2.3% in the Australian terrier that died of central nervous system disease was
2002 ATCA Health Survey. Not listed as a breed at risk by Strain.2,10 found to have a large hemorrhagic primitive neuroectodermal
tumour with ependymal differentiation replacing the thalamus and
Idiopathic Epilepsy (inherited seizures): Control with anti-seizure part of the hypothalamus of the brain.14
medication. Reported at a frequency of 2.1% in the 2002 ATCA
Health Survey.2 Genetic Tests
Tests of Genotype: none
Hyperadrenocorticism (Cushing’s disease): Hyperfunction of the
adrenal gland caused by a pituitary or adrenal tumor. Clinical signs Tests of Phenotype: CHIC Certification: Required testing includes
may include increased thirst and urination, symmetrical truncal CERF eye examination, patella evaluation, and thyroid profile
alopecia, and abdominal distention. Reported at a frequency of including autoantibodies. (See CHIC website; www.caninehealthinfo.
1.9% in the 2002 ATCA Health Survey.2 org). Recommend hip and elbow radiographs, cardiac evaluation,
blood and urine glucose tests for diabetes.
Cryptorchidism (Retained Testicles): Can be unilateral or bilateral.
This is a sex-limited disorder with an unknown mode of inheritance.
Reported at a frequency of 1.6% in the 2002 ATCA Health Survey.2 Miscellaneous
• Breed name synonyms: Aussie, Broken-coated Toy Terrier
Distichiasis: Abnormally placed eyelashes that irritate the cornea (Historical).
and conjunctiva. Can cause secondary corneal ulceration. Identified • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
in 1.48% of Australian Terriers CERF examined by veterinary ANKC (Australian National Kennel Club), NKC (National Kennel Club).
ophthalmologists between 2000-2005.6 • AKC rank (year 2008): 113 (330 dogs registered)
• Internet resources: Australian Terrier Club of America:
Persistent Pupillary Membranes: Strands of fetal remnant http://australianterrier.org
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
later three forms can impair vision, and dogs affected with these References
forms should not be bred. Identified in 1.48% of Australian Terriers 1. OFA Website breed statistics: www.offa.org Last accessed July. 1, 2010.
CERF examined by veterinary ophthalmologists between 2000-2005.6 2. Australian Terrier Club of America: 2002 ATCA Health Survey. 2002.
3. LaFond E, Breur GJ and Austin CC: Breed susceptibility for
Mast Cell Tumor (MCT): Skin tumors that can reoccur locally or developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
with distant metastasis. Reported at a frequency of 1.3% in the Sep-Oct;38(5):467-77.
4. Chastain BD and Panciera D: Risk Factors for Diabetes Mellitus in Dogs.
2002 ATCA Health Survey.2
Sm Anim Clin Endocrinol 2004:14[2]:11.
5. Fall T, Hamlin HH, Hedhammar A, et. al.: Diabetes mellitus in a population
Keratoconjunctivitis Sicca (KCS, Dry Eye): Ocular condition of 180,000 insured dogs: incidence, survival, and breed distribution. J Vet
causing lack of tear production and secondary conjunctivitis, Intern Med. 2007 Nov-Dec;21(6):1209-16.
corneal ulcerations, and vision problems. Reported at a frequency of 6. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
1.1% in the 2002 ATCA Health Survey.2 College of Veterinary Ophthalmologists. ACVO, 2007.
7. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
8. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
42
for Population and Animal Health, Michigan State University. April, 2007.
9. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
10. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32
11. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 198. AAHA Press, 1999
12. Hughes SM: Canine gastrinoma: a case study and literature review of
therapeutic options. N Z Vet J. 2006 Oct;54(5):242-7
13. Reimer ME, Leib MS, Reimer MS, et. al.: Rectal ganglioneuroma in a dog.
J Am Anim Hosp Assoc. 1999 Mar-Apr;35(2):107-10
14. Headley SA, Koljonen M, Gomes LA, et. al.: Central primitive
neuroectodermal tumour with ependymal differentiation in a dog. J Comp
Pathol. 2009 Jan;140(1):80-3.
15. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 348-351.
43
Basenji
including children. They like to be kept busy, and will do best with a
household that provides lots of playtime, exercise and attention.
Longevity: 10-12 years. Pyruvate Kinase Deficiency (PK, Basenji Hemolytic Anemia):
Autosomal recessive disorder causing severe hemolytic anemia,
Points of Conformation: The tail is carried over the straight topline progressive osteomyelosclerosis, and hemosiderosis. Death occurs
in a curled position, head carriage is high, and the medium-sized due to anemia or hepatic failure usually at less than five years of age.
ears are carried pricked up, with a furrowed brow. Eyes are hazel to Occurs at a low frequency in the breed. A genetic test is available.7,8,9
brown. They have short backs, a definite waist and are well muscled
with strong bone. They have a horse-like smooth running trot.
Disease Predispositions
Persistent Pupillary Membranes: Strands of fetal remnant
Recognized Behavior Issues and Traits connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
Reported characteristics of these high activity dogs include: Playful, later three forms can impair vision, and dogs affected with these
smart, and are known to be courageous hunters. They tend to be forms should not be bred. PPMs can be associated with corneal
fastidious about staying clean, washing themselves with their opacity or coloboma in this breed. Dorn reports a 110.61x odds ratio
tongues like a cat. They are independently minded, and cautious in Basenjis versus other breeds. Identified in 47.64% of Basenjis
around strangers, while being calm and friendly with family, CERF examined by veterinary ophthalmologists between 2000-2005.
44
Of these, 9.47% were iris to cornea, 3.71% were iris to lens, and
0.47% were iris sheets. PPMs are shown to be inherited in this
Genetic Tests
Tests of Genotype: Phenotypic test for Fanconi Syndrome is
breed, but the mode of inheritance has not been determined.3,10,11,12 available from PennGen.
Hypothyroidism: Inherited autoimmune thyroiditis. 10.8% positive Linked marker test for Fanconi Syndrome is available from the OFA.
for thyroid auto-antibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5%).1,13,14 Direct test for pyruvate kinase deficiency is available from
HealthGene, Optigen, PennGen, University of Missouri, and VetGen.
Corneal Dystrophy: The endothelial form is associated with
persistant papillary membranes in this breed, and can cause edema, Direct tests for color alleles is available from VetGen.
keratits, and loss of vision. Basenjis with the endothelial form
should not be bred. The epithelial-stromal form causes opacities Tests of Phenotype: CHIC Certification: Required testing includes
on the surface of the cornea. Unknown mode of inheritance. The hip radiographs, thyroid profile including autoantibodies, CERF eye
endothelial form is identified in 2.70%, and the epithelial-stromal examination (each year until 6, thereafter every 2 years), and linked
form is identified in 2.23% of Basenjis CERF examined by veterinary marker test for Fanconi syndrome from OFA. (See CHIC website;
ophthalmologists between 2000-2005.10 www.caninehealthinfo.org).
Cataracts: Posterior and capsular punctate cataracts predominate Recommend patella evaluation, elbow radiographs, and cardiac
in the breed. Identified in 2.41% of Basenjis CERF examined by evaluation.
veterinary ophthalmologists between 2000-2005. CERF does not
recommend breeding any Basenji with cataracts.10
Miscellaneous
Progressive Retinal Atrophy (PRA): Progressive degeneration • Breed name synonyms: Barkless dog, Congo dog, Congo Terrier
of the retina, eventually causing blindness. Typical age of onset • Registries: AKC, CKC, UKC (provisional), KCGB (Kennel Club
between 4 to 10 years, with some reported between ages 3 and of Great Britain), ANKC (Australian National Kennel Club), NKC
13. Presumed autosomal recessive inheritance. CERF recommends (National Kennel Club)
that any Basenji with PRA should not be bred. 1.62% of Basenjis • AKC rank (year 2008): 85 (774 dogs registered)
CERF examined by veterinary ophthalmologists between 2000-2005 • Internet resources: The Basenji Club of America:
are labeled suspicious for PRA, and 0.65% are identified with http://basenji.org
generalized PRA. No genetic test is available.10 Basenji Club of Canada: www.basenjiclubofcanada.com
The Basenji Club of Great Britain: www.basenjiclubofgb.org
Demodicosis: Dorn reports a 2.07x odds ratio of developing The Basenji Health Endowment: www.basenjihealth.org
demodectic mange versus other breeds. This disorder has an
underlying immunodeficiency in its pathogenesis.3 References
1. Seavers A, Snow DH, Mason KV, et. al.: Evaluation of the thyroid status of
Optic Nerve Coloboma: Congenital cavity in the optic nerve that Basenji dogs in Australia. Aust Vet J. 2008 Nov;86(11):429-34.
can cause blindness or vision impairment. Affected dogs should 2. Latimer KS, Prasse KW: Neutrophilic movement of a Basenji with
not be bred. Identified in 0.79% of Basenjis CERF examined by Pelger-Huet anomaly. Am J Vet Res. 1982 Mar;43(3):525-7.
3. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary ophthalmologists between 2000-2005. Can be associated veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
with persistent pupillary membranes in this breed.10 2000.
4. Noonan CH, Kay JM: Prevalence and geographic distribution of Fanconi
Immunoproliferative Enteropathy (IPEB, IPSID, syndrome in Basenjis in the United States. J Am Vet Med Assoc. 1990 Aug
Lymphangiectasia): Inherited disorder causing chronic diarrhea, 1;197(3):345-9.
progressive emaciation, malabsorption and maldigestion. Biopsy 5. Bovee KC, Joyce T, Reynolds R, et. al.: The fanconi syndrome in Basenji
dogs: a new model for renal transport defects. Science. 1978 Sep
findings include villous clubbing and fusion, increased tortuosity of 22;201(4361):1129-31.
intestinal crypts, and diffuse infiltration of mononuclear inflammatory 6. OFA Website breed statistics: www.offa.org Last accessed July. 1, 2010.
cells. Lymphangectasia may be secondary. Treatment with 7. Whitney KM, Goodman SA, Bailey EM, et. al.: The molecular basis of
immunosuppressive drugs and diet. Unknown mode of inheritance.15,16 canine pyruvate kinase deficiency. Exp Hematol. 1994 Aug;22(9):866-74.
8. Burman SL, Ferrara L, Medhurst CL, et. al.: Pyruvate kinase deficiency
Cystine Urinary Calculi: Seen at an increased frequency in the anaemia in a Basenji dog. Aust Vet J. 1982 Oct;59(4):118-20.
9. Whitney KM, Lothrop CD Jr: Genetic test for pyruvate kinase deficiency
breed secondary to cystinuria from Fanconi syndrome.17
of Basenjis. J Am Vet Med Assoc. 1995 Oct 1;207(7):918-21.
10. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Epilepsy, Retinal Dysplasia and Umbilical Hernia are reported.18 College of Veterinary Ophthalmologists. ACVO, 2007
11. James RW: Persistent pupillary membrane in basenji dogs. Vet Rec. 1991
Isolated Case Studies Mar 23;128(12):287-8.
12. Mason TA: Persistent pupillary membrane in the Basenji. Aust Vet J.
Intrahepatic Venous Obstruction: Intrahepatic post-sinusoidal 1976 Aug;52(8):343-4.
obstruction, similar to congenital Budd-Chiari syndrome in human 13. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
patients, was diagnosed in a young Basenji dog.19 for Population and Animal Health, Michigan State University. April, 2007.
14. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
45
15. Spohr A, Koch J, Jensen AL: Ultrasonographic findings in a basenji
with immuno-proliferative enteropathy. J Small Anim Pract. 1995
Feb;36(2):79-82.
16. MacLachlan NJ, Breitschwerdt EB, Chambers JM, et. al: Gastroenteritis
of basenji dogs. Vet Pathol. 1988 Jan;25(1):36-41
17. Case LC, Ling GV, Franti CE, et. al.: Cystine-containing urinary calculi in
dogs: 102 cases (1981-1989). J Am Vet Med Assoc. 1992 Jul 1;201(1):129-33.
18. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 199, AAHA Press, 1999.
19. Cohn LA, Spaulding KA, Cullen JM, et. al.: Intrahepatic postsinusoidal
venous obstruction in a dog. J Vet Intern Med. 1991 Nov-Dec;5(6):317-21.
20. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 12006. pp 138-141.
46
Basset Hound
are often removed. The topline is level and tail carriage is typical
for hounds— carried high when on a scent. The tail is thick, slightly
curved and reaches almost to the ground at rest. The gait is easy,
and movement of limbs is parallel.
Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting Persistent Mullerian Duct Syndrome: Diagnosed in a male dog
of the stomach within the abdomen. Requires immediate veterinary with oviducts, a uterus, and cranial vaginal tract. Usually caused by
attention. Occurs at an increased frequency in the breed.13 a defective mullerian inhibiting substance (MIS) receptor.24
Intervertebral Disk Disease: The breed is at increased risk for acute Congenital Hypotrichosis: Four 4 week-old Basset Hound
paralysis/pain from intervertebral disk extrusion and spinal cord littermates with predominantly mahogany coats had congenital
damage. This is an emergency situation that requires immediate focal alopecia especially affecting the head and dorsal pelvic region.
veterinary attention.14 Histologic diagnosis was hypotrichosis.25
50
Drug Sensitivities Disease Predispositions
None reported Periodontal Disease: Beagles are predisposed to periodontal
disease, with 44% by two years of age, and up to 81% of older dogs
Inherited Diseases affected. The maxillary premolars are most frequently affected.
Hip Dysplasia: Polygenically inherited trait causing degenerative Few affected Beagles are clinically impaired, though halitosis and
joint disease and hip arthritis. OFA reports 17.8% affected.2 gingivitis are usually present.12,13
Patella Luxation: Polygenically inherited trait causing stifle Distichiasis: Abnormally placed eyelashes that irritate the cornea
instability and arthritis. OFA reports 1.4% affected.2 and conjunctiva. Can cause secondary corneal ulceration. Identified
in 17.30% of Beagles CERF examined by veterinary ophthalmolo-
Elbow Dysplasia: Polygenically inherited trait causing elbow gists between 2000-2005.3
arthritis. Too few Beagles have been evaluated by OFA to determine
an accurate frequency.2 Hypothyroidism: Inherited autoimmune thyroiditis. 16.5% positive
for thyroid autoantibodies based on testing at Michigan State
Primary (Narrow and Open Angle) Glaucoma: Autosomal University. (Ave. for all breeds is 7.5).14,15,16
recessive glaucoma causes bilateral increased pressure within the
eyeball between 1-2 years of age. Secondary blindness occurs due Retinal Dysplasia: Focal folds are seen in the breed. Identified in
to damage to the retina. Diagnose with tonometry and gonioscopy. 2.70% of Beagles CERF examined by veterinary ophthalmologists
Diagnosed in 1.10% of Beagles presented to veterinary teaching between 2000-2005.3
hospitals. Beagles with open angle glaucoma have increased
Cataracts: Anterior and posterior cataracts are equally represented
myocilin protein levels in the aqueous humor, with intermediate
in the breed, and can be intermediate or punctate. Reported in
levels in heterozygous carriers. A genetic test is not available. CERF
2.16% of Beagles CERF examined by veterinary ophthalmologists
does not recommend breeding any Beagle with glaucoma.3,4,5,6
between 2000-2005. CERF does not recommend breeding any
Factor VII Deficiency: An autosomal recessive, mild to moderate Beagle with a cataract.3
bleeding disorder occurs in the breed due to a mutation in the cFVII
Intervertebral Disc Disease (IVDD): Spinal cord disease due to
gene. A genetic test is available.7,8
prolapsed disk material. Clinical signs include back pain, scuffing of
Chondrodystrophy (Dwarfism): An autosomal recessive paws, spinal ataxia, limb weakness, and paralysis. Almost all dogs
dwarfism occurs in the breed. Affected dogs have a small and with IVDD have calcified disk material. Beagles are significantly
disproportionate body size, a shortened neck, curved, deformed over-represented with cervical IVDD. Dorn reports a 1.39x odds
legs, a broadened skull, and chronic arthritis. They can be diagnosed ratio versus other breeds.17,18
by by x-ray stippling (i.e., punctate bright spots) of the wrist bones
Cryptorchidism (Retained Testicles): Can be unilateral or bilateral.
under 3 months of age, or by a compressed L7 vertebrae at over 6
This is a sex-limited disorder with an unknown mode of inheritance.
months. Genetic research is ongoing to identify the defective gene
Reported as a breed issue on the National Beagle Club website.
at the Mark Neff lab.
Diabetes Mellitus (Sugar Diabetes): Almost exclusively female
Musladin-Leuke Syndrome (MLS, Chinese Beagle Syndrome):
Beagles are at increased risk of developing diabetes due to immune
An autosomal recessive disease that affects the development
mediated destruction of the pancreatic beta cells. Treat with insulin
and structure of connective tissue. It is multi-systemic, with
injections, dietary management, and glucose monitoring.19
involvement of multiple organs, including bone, heart, skin,
and muscle. Affected dogs walk up on their toes due to tendon Corneal Dystrophy: The breed can form oval epithelial corneal
contracture. They often have tighter skin with limited “scruff”. They opacities that can progressively block vision. They do not lead to
have a flat skull, higher ear set and slanted eyes. The disease shows corneal edema.3,20
variable expressivity, and affected dogs live a normal lifespan. See
the National Beagle Club and UV-Davis VGL websites for more Persistent Pupillary Membranes: Strands of fetal remnant
information. A genetic test is available. connecting; iris to iris, cornea, lens, or involving sheets of tissue.
The later three forms can impair vision, and dogs affected with
Pyruvate Kinase Deficiency (PK): A rare, autosomal recessive these forms should not be bred. Identified in 1.62% of Beagles CERF
disease of red blood cells causing exercise intolerance with a examined by veterinary ophthalmologists between 2000-2005.3
persistent, severe, and highly regenerative anemia, splenomegaly,
and progressive osteosclerosis. A genetic test is available.9,10 Prolapsed Gland of the Nictitans (Cherry Eye): This condition
occurs secondary to inflammation of the gland. Identified in 1.35%
Tapetal Degeneration: A rare, autosomal recessive degeneration of of Beagles CERF examined by veterinary ophthalmologists between
the tapetum occurs as a result of abnormal postnatal melanosome 2000-2005.3
development. The degeneration of the tapetum does not affect
vision and does not result in functional or structural damage to the Idiopathic Epilepsy (Inherited Seizures): Control with anti-seizure
retina.3,11 medication. Seizures generally start under one year of age. Reported
as a breed issue on the National Beagle Club website.21
51
Pulmonic Stenosis: Narrowing of the right ventricular outflow concentrations, anaemia, leucopenia and methylmalonic aciduria.
tract/pulmonary artery. Clinical signs in severely affected dogs The disorder responded to parenteral vitamin B12 therapy. This has
include exercise intolerance, stunting, dyspnea, syncope and ascites. been identified as an autosomal recessive disorder in other breeds.32
A left systolic murmur is present on auscultation. Beagles are
over-represented.22,23 Cerebellar Cortical Abiotrophy/Ataxia: Two of five 4-1/2 month
old Beagle littermates (a male and a female) presented with
Juvenile Polyarteritis (Beagle Pain Syndrome): A naturally cerebellar ataxia, intension tremor, and nystagmus. Purkinje cell
occurring vasculitis and perivasculitis of unknown etiology occurs degeneration in the cerebellar cortex was seen on necropsy. This has
in 6-40 month old Beagles, presenting with episodes of fever been identified as an autosomal recessive disorder in other breeds.33
and neck pain that last 3-7 days. Histologically, the small-to
medium-sized muscular arteries of the heart, cranial mediastinum, Membranoproliferative Glomerulonephropathy: 5 of 7 adult
and cervical spinal meninges are consistently involved. Beagles from the same litter developed polyuria, polydipsia,
Undetermined mode of inheritance.24 proteinuria, and azotemia by 8 years of age. Membranoproliferative
glomerulonephritis was diagnosed on light and electron microscopy
Bladder and Urethral Tumors: Beagles are over-represented with of renal biopsies.34
tumors of the bladder and urethra versus other breeds.25
Renal Agenesis: Cases of unilateral kidney agenesis have been
Microphthalmia with Multiple Congenital Ocular Defects: documented in the literature. Compensatory renal hyperplasia
Several congenital unilateral and bilateral microphthalmia occurs in the opposite kidney, with normal kidney values.35,36
syndromes are recognized in the breed with associated corneal, lens,
and retinal defects. Reported in 0.54% of Beagles CERF examined Vetricular Septal/Conotruncal Defect: A family of Beagle dogs
by veterinary ophthalmologists between 2000-2005. CERF does not was identified with congenital heart disease characterized by
recommend breeding any Beagle with microphthalmia.3,26 ventricular septal defect and ventricular outflow abnormalities.
Breeding studies suggested an autosomal recessive mode of
Deafness: Congenital deafness can be unilateral or bilateral. inheritance.37
Associated with extreme piebald pigmentation. Diagnose by BAER
testing. Unknown mode of inheritance.27 Genetic Tests
Tests of Genotype: Direct test for MLS is available from UC-Davis
Renal Amyloidosis: Beagles were over-represented in a study of
VGL.
renal amyloidosis. Affected dogs were over 6 years of age, with a
female preponderance. Clinical signs were consistent with renal Direct tests for PK and Factor VII deficiencies are available from
failure. Histopathology showed moderate to severe diffuse global PennGen.
glomerular amyloidosis without tubular or glomerular lesions.28
Direct test for Factor VII deficiency is available from VetGen.
Progressive Myoclonic Epilepsy (Lafora’s Disease): Older affected
Beagles show progressive, intermittent seizures that can progress Direct test for coat color alleles is available from VetGen.
to status epilepticus. The seizures are often elicited by external
stimuli, especially a change in noise or light in the surroundings. Tests of Phenotype: CHIC certification: Required testing includes hip
Electroencephalographic findings show myoclonus epilepsy. radiographs, CERF eye examination a direct test for MLS, and either
Postmortem histopathological findings include multiple periodic a cardiac evaluation by a cardiologist, or a thyroid profile including
acid-Schiff-positive inclusion bodies consistent with Lafora’s autoantibodies. (See CHIC website; www.caninehealthinfo.org).
disease.29,30
Recommend patella evaluation and elbow radiographs.
Black Hair Follicular Dysplasia, Brachygnathism, Cervical
Vertebral Instability, Cleft Lip/Palate, Copper Hepatopathy, Urine test for Cobalamine Malabsorption/Methylmalonic Aciduria is
Cutaneous Asthenia, Demodicosis, Dilated Cardiomyopathy, available from PennGen.
Dysfibrinogenemia, Ectodermal Defect, Elongated Soft Palate,
Factor VIII Deficiency, Globoid Cell Leukodystrophy, GM-1 Miscellaneous
Gangliosidosis, Hyperlipidemia, Hypotrichosis, IgA Deficiency, • Breed name synonyms: English Beagle, Pocket beagle and Glove
Lissencephaly, Mitral Valve Disease, Narcolepsy, Non-Sphero- beagle are historical nicknames for the smallest of the small variety.
cytic Hemolytic Anemia, Optic Nerve Hypoplasia, Panosteitis, • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
Peripheral Vestibular Disease, Prognathism, Progressive Retinal ANKC (Australian National Kennel Club), NKC (National Kennel Club).
Atrophy, Shaker Disease, Spina Bifida, Vertebral Stenosis, and • AKC rank (year 2008): 5 (33,722 dogs registered)
XX Sex Reversal are reported.31 • Internet resources: The National Beagle Club:
http://clubs.akc.org/NBC/
Isolated Case Studies The Beagle Club (UK): www.thebeagleclub.org
Cobalamin Malabsorption (Methylmalonic Aciduria): A
six-month-old beagle was presented with a three-month history
of failure to gain weight, lethargy, intermittent vomiting and
seizures. Laboratory results showed low serum cobalamin (Cbl)
52
References a retrospective study of 115 cases (1980-1985). J Vet Intern Med. 1992
May-Jun;6(3):145-53.
1. Crippa L, Ferro E, Melloni E, et. al.: Echocardiographic parameters and
26. Rubin LF: Hereditary microphakia and microphthalmia syndrome in the
indices in the normal beagle dog. Lab Anim. 1992 Jul;26(3):190-5.
beagle. Trans Am Coll Vet Ophthalmol 1971;2:50.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
27. Strain GM: Deafness prevalence and pigmentation and gender
3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
College of Veterinary Ophthalmologists. ACVO, 2007.
28. DiBartola SP, Tarr MJ, Parker AT, et. al.: Clinicopathologic findings in
4. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas in
dogs with renal amyloidosis: 59 cases (1976-1986). J Am Vet Med Assoc.
pure-bred dogs in North America. Vet Ophthalmol. 2004 Mar-Apr;7(2):97-111.
1989 Aug 1;195(3):358-64.
5. Mackay EO, Källberg ME, and Gelatt KN: Aqueous humor myocilin protein
29. Hegreberg GA and Padgett GA: Inherited progressive epilepsy of
levels in normal, genetic carriers, and glaucoma Beagles. Vet Ophthalmol.
the dog with comparisons to Lafora’s disease of man. Fed Proc. 1976
2008 May-Jun;11(3):177-85.
Apr;35(5):1202-5.
6. Gelatt KN and Gum GG: Inheritance of primary glaucoma in the beagle.
30. Gredal H, Berendt M, and Leifsson PS: Progressive myoclonus epilepsy
Am J Vet Res. 1981 Oct;42(10):1691-3.
in a beagle. J Small Anim Pract. 2003 Nov;44(11):511-4.
7. Spurling NW, Burton LK, Peacock R, et. al.: Hereditary factor-VII
31. The Genetic Connection: A Guide to Health Problems in Purebred Dogs.
deficiency in the beagle. Br J Haematol. 1972 Jul;23(1):59-67.
L Ackerman. p. 199-200. AAHA Press, 1999.
8. Callan MB, Aljamali MN, Margaritis P, et. al.: A novel missense mutation
32. Fordyce HH, Callan MB, and Giger U: Persistent cobalamin deficiency
responsible for factor VII deficiency in research Beagle colonies. J Thromb
causing failure to thrive in a juvenile beagle. J Small Anim Pract. 2000
Haemost. 2006 Dec;4(12):2616-22.
Sep;41(9):407-10.
9. Prasse KW, Crouser D, Beutler E, et. al.: Pyruvate kinase deficiency anemia
33. Kent M, Glass E, and deLahunta A: Cerebellar cortical abiotrophy in a
with terminal myelofibrosis and osteosclerosis in a beagle. J Am Vet Med
beagle. J Small Anim Pract. 2000 Jul;41(7):321-3.
Assoc. 1975 Jun 15;166(12):1170-5.
34. Rha JY, Labato MA, Ross LA, et. al.: Familial glomerulonephropathy in a
10. Giger U, Mason GD, and Wang P: Inherited erythrocyte pyruvate kinase
litter of beagles. J Am Vet Med Assoc. 2000 Jan 1;216(1):46-50, 32.
deficiency in a beagle dog. Vet Clin Pathol. 1991;20(3):83-86.
35. Diez-Prieto I, García-Rodríguez MB, Ríos-Granja MA, et. al.: Diagnosis of
11. Burns MS, Bellhorn RW, Impellizzeri CW, et. al.: Development of
renal agenesis in a beagle. J Small Anim Pract. 2001 Dec;42(12):599-602.
hereditary tapetal degeneration in the beagle dog. Curr Eye Res. 1988
36. Robbins GR: Unilateral renal agenesis in the beagle. Vet Rec. 1965 Nov
Feb;7(2):103-14.
13;77(46):1345-7.
12. Kortegaard HE, Eriksen T, and Baelum V: Periodontal disease in
37. Diez-Prieto I, García-Rodríguez B, Ríos-Granja A, et. al.: Cardiac
research beagle dogs - an epidemiological study. J Small Anim Pract. 2008
conotruncal malformations in a family of beagle dogs. J Small Anim Pract.
Dec;49(12):610-6.
2009 Nov;50(11):597-603.
13. Saxe SR, Greene JC, Bohannan HM, et. al.: Oral debris, calculus,
38. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
and periodontal disease in the beagle dog. Periodontics. 1967
Book House, NY 2006. p. 147-151.
Sep-Oct;5(5):217-25.
14. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
15. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
16. Musser E and Graham WR: Familial occurrence of thyroiditis in
purebred beagles. Lab Anim Care. 1968 Feb;18(1):58-68.
17. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
18. Dallman MJ, Palettas P, and Bojrab MJ: Characteristics of dogs admitted
for treatment of cervical intervertebral disk disease: 105 cases (1972-1982).
J Am Vet Med Assoc. 1992 Jun15;200(12):2009-11.
19. Fall T, Hamlin HH, Hedhammar A, et. al.: Diabetes mellitus in a
population of 180,000 insured dogs: incidence, survival, and breed
distribution. J Vet Intern Med. 2007 Nov-Dec;21(6):1209-16.
20. Ekins MB, Sgoutas DS, Waring GO 3rd, et. al.: Oval lipid corneal opacities
in beagles: VI. Quantitation of excess stromal cholesterol and phospholipid.
Exp Eye Res. 1983 Feb;36(2):279-86.
21. Morita T, Shimada A, Ohama E, et. al.: Oligodendroglial vacuolar
degeneration in the bilateral motor cortices and astrocytosis in epileptic
beagle dogs. J Vet Med Sci. 1999 Feb;61(2):107-11.
22. McCaw D and Aronson E: Congenital cardiac disease in dogs. Mod Vet
Pract. 1984 Jul;65(7):509-12.
23. Patterson DF, Haskins ME, and Schnarr WR: Hereditary dysplasia of
the pulmonary valve in beagle dogs. Pathologic and genetic studies. Am J
Cardiol. 1981 Mar;47(3):631-41.
24. Snyder PW, Kazacos EA, Scott-Moncrieff JC, et. al.: Pathologic features
of naturally occurring juvenile polyarteritis in beagle dogs. Vet Pathol. 1995
Jul;32(4):337-45.
25. Norris AM, Laing EJ, Valli VE, et. al.: Canine bladder and urethral tumors:
53
Bearded Collie
can be independent, sometimes a bit stubborn perhaps, but make
an exceptional pet for the right owner. They are also reported to be
loving, active (bouncy is a word commonly used), and friendly. They
have a strong chase instinct, so should not run off-leash out of an
enclosure. They like close contact with their family. They are strong
alarm barkers and very loyal. Early training and socialization are
important. Exercise should include lots of play to help keep them fit
and mentally challenged. They may try to herd children by nipping
at heels.
55
Beauceron
feet are large, round, and compact with black nails. Hind double
dewclaws form well separated “thumbs” with nails, placed rather
close to the foot. Movement is fluid and effortless, covering ground
in long reaching strides (extended trot).
Coat: Outer coat is 1.25” to 1.5”, coarse, dense and lying close to Inherited Diseases
the body. It is short and smooth on the head, ears and lower legs. Hip Dysplasia: Polygenically inherited trait causing degenerative
The hair is somewhat longer around the neck. Acceptable coat joint disease and hip arthritis. OFA reports 14.7% affected.3
colors are: Black and Rust, Black and Tan, Grey Black and Tan, and
Harlequin. Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. OFA reports 5.5% affected.3
Longevity: 10-12 years.
Patella Luxation: Polygenically inherited laxity of patellar
Points of Conformation: The Beauceron is medium in all its ligaments, causing luxation, lameness, and later degenerative joint
proportions. The length of body, measured from the point of the disease. Treat surgically if causing clinical signs. Too few Beaucerons
shoulder to the point of the buttock, is slightly greater than the have been screened by OFA to determine an accurate frequency.3
height at the withers. The head must be in proportion with the
body, measured from the tip of the nose to the occiput it is about
40% of the height at the withers. The eyes are horizontal and
Disease Predispositions
Hypothyroidism: Inherited autoimmune thyroiditis. 4.0% positive
slightly oval in shape, and dark brown. The ears are set high, and for thyroid autoantibodies based on testing at Michigan State
may be cropped (upright) or natural. The skull is flat or slightly University. (Ave. for all breeds is 7.5%).4,5
rounded near the sides of the head. The muzzle must not be narrow,
pointed, or excessively broad in width. The lips are well pigmented. Gastric Dilation/Volvulus (GDV, Bloat): Polygenically inherited,
The teeth meet in a scissors bite. The tail is strong at the base, life-threatening twisting of the stomach within the abdomen.
carried down, descending at least to the point of the hock, forming Requires immediate veterinary attention. Reported as a breed
into a slight J without deviating to the right or to the left. The problem on the Beauceron Club of Canada website.
56
Dermatomyositis-like Disease: Juvenile-onset (usually by 6 4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
months of age) disease that initially presents with papules, pustules, hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
and vesicles eventuating in crusted erosions, ulcers, and alopecia. Vet Med Assoc 2002 Feb 15;220(4):466-71.
Chronically affected Beaucerons show scarring, and either hyper or 5. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
hypopigmentation. Unknown mode of inheritance.6
6. Ihrke P: Ischemic Skin Disease in the Dog. Proceedings, 2006 World Small
Animal Veterinary Association World Congress. 2006.
Epidermolysis Bullosa: Cutaneous blistering in response to trauma.
7. Scott DW, Miller WH and Griffin CE: Muller and Kirks’s Small Animal
Junctional form: Affected Beaucerons show crusted papules and Dermatology, 5th Ed., WB Saunders, p756-757. 1995.
erosions in genital region and at mucocutanoeuos junctions at 6 8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
weeks. Spreads to face, pinnae, medial thighs, perianal regions, feet College of Veterinary Ophthalmologists. ACVO, 2007.
and tail.7 9. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 201, AAHA Press, 1999.
Ocular Disorders: Too few Beaucerons have been CERF examined 10. Clercx C, McEntee K, Gilbert S, et. al.: Nonresponsive generalized
by veterinary ophthalmologists to determine accurate frequencies bacterial infection associated with systemic lupus erythematosus in a
for inherited ocular disorders. Entropion, ectropion, and progressive Beauceron. J Am Anim Hosp Assoc. 1999 May-Jun;35(3):220, 222, 224-8.
retinal atrophy are reported.8 11. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 695-699.
Inhalant Allergies are reported.9
Genetic Tests
Tests of Genotype: None available.
Miscellaneous
• Breed name synonyms: Berger de Beauce, Bas Rouge, Beauce
Shepherd.
• Registries: AKC, UKC, KCGB (Kennel Club of Great Britain), ANKC
(Australian National Kennel Club), NKC (National Kennel Club), FCI.
• AKC rank (year 2008): 139 (117 dogs registered.)
• Internet resources: American Beauceron Club: www.beauce.org
Beauceron Club UK: www.beauceronclubuk.com
The Beauceron Club in Canada: www.beauceronscanada.com
References
1. Clark LA, Wahl JM, Rees CA, et. al.: Retrotransposon insertion in SILV is
responsible for merle patterning of the domestic dog. Proc Natl Acad Sci U
S A. 2006 Jan 31;103(5):1376-81.
2. O’Sullivan N, Robinson R: Harlequin colour in the Great Dane dog.
Genetica. 1988-1989;78(3):215-8.
3. OFA Website breed statistics: www.offa.org Last accessed July. 1, 2010.
57
Bedlington Terrier
allergy dogs. Regular exercise is important, and one should introduce
other dogs or cats with care when the dog is young. Though a
fearless fighter, these dogs are playful and gentle with the family.
Drug Sensitivities
None reported
Points of Conformation: This is a moderately sized dog with Patella Luxation: Polygenically inherited congenital laxity of
an alert demeanor. The head is narrow with no stop, skull is patellar ligaments, causing medial luxation, lameness, and later
dolichocephalic, and the profile is slightly convex (Roman-nosed). degenerative joint disease. Treated surgically if causing clinical
Eyes are almond-shaped, and blue dogs have dark eyes, while signs. OFA reports 12.3% affected. Reported at a frequency of 1.4%
others may have a range including hazel. Pendulous ears reach in the BTCA Health Survey 2003-2004.8,9
to the lateral commissure of the lips. Nose is pigmented black or
brown. They have a long, tapered neck and have a deep thorax, with Elbow Dysplasia: Polygenically inherited trait causing elbow
moderate arch and obvious tuck. Dewclaws are usually removed. arthritis. Too few Bedlington Terriers have been screened to
The low-set tail reaches to the tarsus. These dogs move straight and determine an accurate frequency.9
true, with a springy gait.
Retinal Dysplasia: Autosomal recessive disorder, present at birth,
with concurrent retinal detachment and cataract. Present at a low
Recognized Behavior Issues and Traits frequency in the breed.10,11,12
Reported traits include: Enjoys company, but can be aloof with
strangers. The dog will also do alarm barking, and enjoys barking
in general. They are average in activity level, and are low shed, low
58
Disease Predispositions Hyperadrenocorticism (Cushing’s Disease): Hyperfunction of the
adrenal gland caused by a pituitary or adrenal tumor. Clinical signs
Hypothyroidism: Inherited autoimmune thyroiditis. 12.7% positive
for thyroid auto-antibodies based on testing at Michigan State may include increased thirst and urination, symmetrical truncal
University. (Ave. for all breeds is 7.5%). Reported at a frequency of alopecia, and abdominal distention. Reported at a frequency of
4.3% in the BTCA Health Survey 2003-2004. 8,13,14 1.6% in the BTCA Health Survey 2003-2004.8
Pancreatic Acinar Atrophy (Exocrine Pancreatic Insufficiency): Keratoconjunctivitis Sicca (KCS, Dry Eye): Ocular condition
Immune-mediated pancreatic acinar atrophy. Clinical signs are causing lack of tear production and secondary conjunctivitis,
poor weight gain, and steatorrhea. Treatment is with enzyme corneal ulcerations, and vision problems. Age of onset 2-5 years.
supplementation. Reported at a frequency of 8.9% in the BTCA Reported at an increased frequency verses other breeds. Reported
Health Survey 2003-2004.8 at a frequency of 1.1% in the BTCA Health Survey 2003-2004.8,18
Cataracts: Anterior, equatorial or posterior intermediate and Cryptorchidism (Retained Testicles): Can be unilateral or bilateral.
punctate cataracts occur in the breed. Age of onset 3-24 months. This is a sex-limited disorder with an unknown mode of inheritance.
Reported in 8.49% of Bedlington Terriers presented to veterinary Reported at a frequency of 1.1% in the BTCA Health Survey
teaching hospitals. Identified in 8.41% of Bedlington Terriers CERF 2003-2004.8
examined by veterinary ophthalmologists between 2000-2005.
Entropion: Rolling in of eyelids, often causing corneal irritation
Reported at a frequency of 7.8% in the BTCA Health Survey
or ulceration. Reported at a frequency of 1.1% in the BTCA Health
2003-2004. CERF Does not recommend breeding any Bedlington
Survey 2003-2004.8
Terrier with a cataract.8,11,15,16
Corneal Dystrophy: Causes opacities on the surface of the
Persistent Pupillary Membranes: Strands of fetal remnant
cornea. Identified in 1.08% of Belington Terriers CERF examined by
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
veterinary ophthalmologists between 2000-2005.11
The later three forms can impair vision, and dogs affected with
these forms should not be bred. Identified in 6.47% of Bedlington Glaucoma, Microphthalmia, Osteogenesis Imperfecta,
Terriers CERF examined by veterinary ophthalmologists between Progressive Retinal Atrophy, and Renal Dysplasia are reported.19
2000-2005.11
Distichiasis: Abnormally placed eyelashes that irritate the cornea Isolated Case Studies
and conjunctiva. Can cause secondary corneal ulceration. Identified None reported
in 4.96% of Bedlington Terriers CERF examined by veterinary
ophthalmologists between 2000-2005. Reported at a frequency of Genetic Tests
20.0% in the BTCA Health Survey 2003-2004.8,11 Tests of Genotype: Direct test for Copper Toxicosis is available
from VetGen and the Animal Health Trust.
Deafness: Congenital deafness can be unilateral of bilateral.
Diagnosed by BAER testing. Reported at a frequency of 3.3% in Direct test for the brown color allele is available from VetGen.
the BTCA Health Survey 2003-2004. Not listed as a breed at risk by
Strain.8,17 Tests of Phenotype: CHIC Certification: Required testing includes
patella evaluation, CERF eye examination at a minimum of 1 year of
Heart Murmur/Valvular Heart Disease: Reported at a frequency age. and genetic test for copper toxicosis. (See CHIC website; www.
of 3.1% in the BTCA Health Survey 2003-2004. No specific valve caninehealthinfo.org).
involvement reported.8
Recommend hip and elbow radiographs, thyroid profile including
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis autoantibodies, and cardiac evaluation.
and pyotraumatic dermatitis. Reported at a frequency of 2.7% in
the BTCA Health Survey 2003-2004.8
Miscellaneous
Idiopathic Epilepsy (Inherited Seizures): Control with • Breed name synonyms: Rothbury Terrier (historical)
anticonvulsant medication. Reported at a frequency of 2.4% in the • Registries: CKC, AKC, UKC, KCGB (Kennel Club of Great Britain),
BTCA Health Survey 2003-2004.8 ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 126 (226 dogs registered)
Dental Issues: The BTCA Health Survey 2003-2004 reports 2.4% • Internet resources: Bedlington Terrier Club of America:
of Bedlington Terriers with undershot bites, and 1.2% with missing http://bedlingtonamerica.com/
teeth.8 The National Bedlington Terrier Club of England:
www.bedlingtons.org.uk
Aggression: Reported at a frequency of 2.3% in the BTCA Health The Bedlington Terrier Association (UK): www.thebta.info/
Survey 2003-2004.8 The Bedlington Terrier Health Group (UK):
www.bedlingtonterrierhealthgroup.org.uk
Imperforate Nasolacrimal Puncta: Blocked or malformed tear
duct. This defect usually results in excessive tearing. Reported at a
frequency of 2.1% in the BTCA Health Survey 2003-2004.8,11
59
References
1. Forman OP, Boursnell ME, Dunmorec BJ: Characterization of the
COMMD1 (MURR1) mutation causing copper toxicosis in Bedlington
terriers. Anim Genet. 2005 Dec; 36(6); 497-501.
2. Coronado VA, Damaraju D, Kohijoki R, et. al.: New haplotypes in the
Bedlington terrier indicate complexity in copper toxicosis. Mamm Genome.
2003 Jul;14(7):483-91.
3. van de Sluis B, Peter AT, Wijmenga C: Indirect molecular diagnosis of
copper toxicosis in Bedlington terriers is complicated by haplotype diversity.
J Hered. 2003 May-Jun;94(3):256-9.
4. Koskinen MT, Bredbacka P: Assessment of the population structure of five
Finnish dog breeds with microsatellites. Anim Genet. 2000 Oct;31(5):310-7.
5. Hultgren BD, Stevens JB, Hardy RM: Inherited, chronic, progressive
hepatic degeneration in Bedlington terriers with increased liver copper
concentrations: clinical and pathologic observations and comparison with
other copper-associated liver diseases. Am J Vet Res. 1986 Feb;47(2):365-77.
6. Ubbink GJ, Van den Ingh TS, Yuzbasiyan-Gurkan V, et. al.: Population
dynamics of inherited copper toxicosis in Dutch Bedlington terriers
(1977-1997). J Vet Intern Med. 2000 Mar-Apr;14(2):172-6.
7. Haywood S: Copper toxicosis in Bedlington terriers. Vet Rec. 2006 Nov
11;159(20):687.
8. Bedlington Terrier Club of America: Bedlington Terrier Club of America
Health Survey 2003-2004. 2004.
9. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
10. Dietz HH: Retinal dysplasia in dogs--a review. Nord Vet Med. 1985
Jan-Feb;37(1):1-9.
11. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
12. Rubin LF: Heredity of retinal dysplasia in the Bedlington terrier. Journal
of the American Veterinary Medical Association 1968;152:260-262.
13. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
14. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
15. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
16. Nasisse MP: Diseases of the Lens and Cataract Surgery. Proceedings
Waltham/OSU Symposium, Small Animal Ophthalmology, 2001.
17. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
18. Westermeyer HD, Ward DA, Abrams K: Breed predisposition to
congenital alacrima in dogs. Vet Ophthalmol. 2009 Jan-Feb;12(1):1-5.
19. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 203. AAHA Press, 1999.
20. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 352-354.
60
Belgian Malinois
tucked up, and the tail reaches the tarsus and is carried below
horizontal in a curve. Limbs are straight with an oval cross section;
dewclaws may be removed in front, and on the hind limbs are
usually removed. Foreleg feet are compact and possess strong black
nails, though a white nail may accompany a white toe marking. Rear
feet may be a bit more elongated. The gait is long, ground covering
and smooth. In the breed standard, reference is made to the fact
that the breed likes to circle rather than move in a straight line. This
is likely a characteristic that derives from their herding behavior.
Genetic Tests
Tests of Genotype: Direct tests are available for presence of
black-and-tan and sable coat colors from HealthGene and VetGen.
62
Belgian Sheepdog
reaches the tarsus at rest, and is held low. Limbs are straight boned,
with oval cross section, the feet are small, round, toes well knuckled
up and well padded, though the rear feet are longer. Nails are black,
unless a white toe marking is adjacent in which case they are white.
Rear dewclaws should be removed. The gait is springy and low, and
ground covering. The breed standard describes a tendency to circle
rather than move in a straight line, perhaps referring to the natural
herding movements.
63
Disease Predispositions non-weight bearing lameness and stifle effusion. Rapid progression
produced marked periosteal new bone formation. Cytology of a stifle
Idiopathic Epilepsy (inherited seizures): Control with anti-seizure
medication. In the Belgian Sheepdog, seizures can be partial or joint aspirate revealed numerous large polygonal neoplastic cells
generalized. Prevalence of 9.5% in Denmark with an average age with considerable anisocytosis and anisokaryosis. The deep form of
of onset of 3.3 years. Epilepsy has a high heritability in the breed malignant fibrous histiocytoma was diagnosed at necropsy.18
of 0.76 with a polygenic mode of inheritance, though influenced
by a single autosomal recessive gene of large effect. Genome-wide Eosinophilic Myositis: A 2-year-old male Belgian sheepdog with
linkage scan identifies multiple chromosomal locations for possible eosinophilic myositis, which particularly affects the masticatory
epilepsy liability genes.8,9,10,11 muscles, tested positive for the presence of muscle-specific
auto-antibodies. Treatment with immunosuppressive drugs.19
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. Synovial hemangioma: An 8-year-old castrated male Belgian
The later three forms can impair vision, and dogs affected with Sheepdog with lameness of 3 months’ duration was diagnosed with
these forms should not be bred. Identified in 6.34% of Belgian synovial hemangioma. Pain, soft-tissue swelling, and hemarthrosis
Sheepdogs CERF examined by veterinary ophthalmologists between were localized to the left stifle joint. The dog was free of detectable
2000-2005.2 neoplasia 6 months after amputation of the affected hind leg.20
Cataracts: Anterior and posterior cortex cataracts predominate, Tests of Phenotype: CHIC Certification: Required testing includes
though intermediate and punctate cataracts also occur in the hip and elbow radiographs, and CERF eye examination. (See CHIC
breed. Unknown mode of inheritance. Identified in 2.75% of Belgian website; www.caninehealthinfo.org).
Sheepdogs CERF examined by veterinary ophthalmologists between
2000-2005. CERF does not recommend breeding any Belgian Recommend thyroid profile including autoantibodies, patella
Sheepdog with a cataract.2 evaluation and cardiac evaluation.
65
Belgian Tervuren
muzzle is pointed, the stop is moderately well defined, and the nose
is black. The neck is long, well muscled, and not throaty. The topline
is level, the thorax deep, and the abdomen moderately tucked up.
The tail is high set and reaches to the tarsus at rest; in action it may
be held horizontal to the topline. Limbs are straight boned, and the
bone is oval in cross section. Dewclaws may be removed in front,
and are usually removed in the rear. Feet are small, compact and
well knuckled up with strong nails. The gait is springy and ground
covering. As for the Malinois, the standard stipulates a preference
to move in a circle over a straight line. This may reflect the herding
heritage of this breed.
The Breed History
This is one of four coat types of the Belgian Shepherd type dog.
This breed originated in the town of Tervuren, Belgium. The other
Recognized Behavior Issues and Traits
Reported breed characteristics include: Defensive-protective,
haircoat types are Malinois, Groenendael, and Laekenois. Their
devoted (even possessive), courageous, may be snappy, and has
common ancestor is the Belgian Sheepdog. The Tervuren are the
high exercise needs and a high base activity level. Grooming needs
longhaired, colored other than black variety, though hairs are black
are low, and moderate shedding occurs. They are generally good
tipped. The Tervuren is considered a later variety that the Malinois,
with other dogs in the household, and have variable tolerance to
and may be derived from the Groenendaels since matings of the
other smaller pets. Not the best choice of dog for a household with
latter can produce the Tervuren coat type. Though these coat types
a child; they do best with experienced owners.
share a single breed standard outside the AKC and America, the
types are split into separate breeds here, with minor distinguishing
characteristics. The first breed standard for the Tervuren was drawn Normal Physiologic Variations
up in 1893. The AKC registered these dogs first in 1959. Leukopenia: Physiologic leukopenia, resulting from low numbers
of neutrophils, lymphocytes, and monocytes, may be a typical
finding in a large percentage of healthy Belgian Tervuren and is not
Breeding for Function of clinical importance in otherwise healthy dogs. Healthy Belgian
Very high intelligence and trainability are a breed hallmark.
Tervuren may also have RBC counts and hematocrits higher than
Obedience, herding, tracking, sledding, drug detection, and
expected for healthy dogs. In one study of 180 healthy Belgian
Schutzhund represent some of their talents. Historically, herding
Tervuren in the United States, total WBC counts ranged from 2,610
was their primary purpose, with farm protection running second.
to 16,900. All dogs were otherwise clinically normal. In a study in
Currently, they serve as service dogs, police and security dogs, and
Belgium, only 1 of 94 Tervuren was identified with the condition.
are widely used in agility trials. Many are also companion dogs.
Reported at a frequency of 1.3% in the 2003 American Belgian
Tervuren Club Health Survey.1,2,3,4
Physical Characteristics
Height at Withers: female 22-24” (56-61 cm), male 24-26” (61-66 cm).
Drug Sensitivities
Weight: Average 62 lb (28 kg). None reported
Coat: The outer coat is long, dense and straight. Hairs are hard but Inherited Diseases
not wiry. The undercoat is dense and soft. Furnishings are more Elbow Dysplasia: Polygenically inherited trait causing elbow
developed in males. Facial hair is short. A non-black longhaired arthritis. OFA reports 4.4% affected.5
Belgian Shepherd-type dog is the distinguishing characteristic of a
Tervuren. Black masking and a fawn to mahogany base color with Hip Dysplasia: Polygenically inherited trait causing degenerative
black tipping is the preferred combination, but other non-black joint disease and hip arthritis. OFA reports 3.6% affected. Reported
colors are accepted. The dogs tend to get darker with age. A small at a frequency of 2.2% in the 2003 American Belgian Tervuren Club
white chest patch is accepted. Health Survey.4,5
67
• Internet resources: American Belgian Tervuren Club Inc.:
www.abtc.org
Belgian Shepherd Dog Club of Canada: www.bsdcc.org
Belgian Shepherd Dog Association of Great Britain:
www.bsdaofgb.co.uk
References
1. Greenfield CL, Messick JB, Solter PF, et. al.: Leukopenia in six healthy
Belgian Tervuren. J Am Vet Med Assoc. 1999 Oct 15;215(8):1121-2.
2. Greenfield CL, Messick JB, Solter PE: Results of Hematologic Analyses and
Prevalence of Physiologic Leukopenia in Belgian Tervuren. J Am Vet Med
Assoc 2000:216[6]:866-871.
3. Gommeren K, Duchateau L, Paepe D, et. al.: Investigation of
physiologic leukopenia in Belgian Tervuren dogs. J Vet Intern Med. 2006
Nov-Dec;20(6):1340-3.
4. Evans, R and ABTC: 2003 American Belgian Tervuren Club Health Survey.
2004.
5. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
6. Oberbauer AM, Grossman DI, Irion DN, et. al.: The genetics of epilepsy in
the Belgian tervuren and sheepdog. J Hered. 2003 Jan-Feb;94(1):57-63.
7. Famula TR, Oberbauer AM: Reducing the incidence of epileptic
seizures in the Belgian Tervuren through selection. Prev Vet Med. 1998
Jan;33(1-4):251-9.
8. Berendt M, Gulløv CH, & Fredholm M: Focal epilepsy in the Belgian
shepherd: evidence for simple Mendelian inheritance. J Small Anim Pract.
2009 Dec;50(12):655-61.
9. Berendt M, Gulløv CH, Christensen SL, et. al.: Prevalence and
characteristics of epilepsy in the Belgian shepherd variants Groenendael
and Tervueren born in Denmark 1995-2004. Acta Vet Scand. 2008 Dec
22;50:51.
10. Oberbauer AM, Belanger JM, Grossman DI, et. al.: Genome-wide linkage
scan for loci associated with epilepsy in Belgian shepherd dogs. BMC Genet.
2010 May 4;11:35.
11. MacManus D: 1998 Tervuren Health Survey. 1998.
12. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
13. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
14. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
15. Lubbes D, Mandigers PJ, Heuven HC, et. al.: Incidence of gastric
carcinoma in Dutch Tervueren shepherd dogs born between 1991 and 2002.
Tijdschr Diergeneeskd. 2009 Jul 15-Aug 1;134(14-15):606-10.
16. Mahaffey MB, Yarbrough KM, Munnell JF: Focal loss of pigment in the
Belgian Tervuren dog. J Am Vet Med Assoc. 1978 Aug 15;173(4):390-6.
17. Chavkin MJ, Roberts SM, Salman MD, et. al.: Risk factors for
development of chronic superficial keratitis in dogs. J Am Vet Med Assoc.
1994 May 15;204(10):1630-4.
18. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 202. AAHA Press, 1999.
19. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 629-634.
68
Bernese
Mountain Dog
ribs. The tail is carried low when resting and is heavily haired. It
reaches to the tarsus or a bit lower. Legs are straight boned, and
dewclaws may be removed. Feet are compact and the toes are well
arched. Rear dewclaws are removed.
Points of Conformation: Sturdily built, large, but agility has Hip Dysplasia: Polygenically inherited trait causing degenerative
not been compromised. Heavy bone and musculature are bred joint disease and hip arthritis. Reported 7.2x odds ratio versus other
into these dogs. The eyes have a gentle expression and are a dark breeds. OFA reports 16.0% affected. Reported at a frequency of
brown, oval shaped and have tight fitting eyelids. Ears are high set, 14.0% in the 2005 BMDCA Health Survey.1,3,6
triangular and hang close to the cheek. The skull has a moderate
stop and a slight furrow runs up along the midline. The square Patella Luxation: Polygenically inherited laxity of patellar ligaments,
muzzle ends in a large black nose. Lips are free of flews; they are a causing luxation, lameness, and later degenerative joint disease.
dry-mouthed breed. Neck is of medium length, well muscled and Treat surgically if causing clinical signs. OFA reports 3.2% affected.2
the topline is level. The thorax is deep and possesses well-sprung
69
von Willebrand’s Disease Type 1 (vWD): Autosomal recessive Cranial Cruciate Ligament Rupture (ACL): Traumatic tearing of
genetic disorder causing a mild bleeding syndrome. A direct genetic the anterior cruciate ligament. Treatment is surgery. Reported at
test is available from VetGen, reporting 1% affected, and 16% a frequency of 7.3% in the 2005 BMDCA Health Survey. Unknown
carrier in the breed. mode of inheritance.1
Progressive Retinal Atrophy (PRA): An autosomal recessive Malignant Histiocytosis: The breed is predisposed to develop
early retinal degeneration is identified in the breed, with an onset malignant histiocytomas in any area of the body. The most common
of night blindness around one year of age. Identified in 0.12% of clinical signs are anorexia, weight loss, lethargy, anemia, and
Bernese Mountain Dogs CERF examined by veterinary ophthalmolo- dyspnea and/or coughing. Radiographs in affected dogs usually
gists between 2000-2005, with an additional 0.24% labeled reveal either pulmonary nodules or consolidation, mediastinal mass,
suspicious for PRA. Confirm with an electroretinogram. A genetic pleural effusion, or hepatomegaly and splenomegaly. The average
test is not available. CERF does not recommend breeding any age of diagnosis is 6.5 years, with an average life expectancy
Bernese Mountain Dog with PRA.7,8 post-diagnosis of 49 days. Dorn reports a 15.07x odds ratio for
the disorder versus other breeds. The trait appears to have a major
Juvenile Renal Dysplasia: Rare, membranoproliferative Mendelian gene in its transmission, with a heritability of 0.298.
glomerulonephritis with concomitant interstitial nephritis. Affected One study in France reported an affected frequency of up to 25%.
dogs present initially with polyuria and polydipsia, which progresses Reported as the cause of death of 10.7% of Bernese Mountain Dogs
to clinical renal failure. Affected dogs are identified from months of in Denmark at an average age of 6.9 years. Reported at a frequency
age to 2-7 years of age. The renal expression of megalin is reduced or of 4.0% in the 2005 BMDCA Health Survey, though listed as the #1
completely absent. One study suggests an inherited susceptibility to cause of death.1,16,17,18,19,20,21,22,23
Borrelia infection as a precipitating factor. The mode of inheritance
is polygenic, with a major autosomal recessive gene, and possibly an Hypothyroidism: Inherited autoimmune thyroiditis. 4.8% positive
additional sex-linked gene influencing its expression.9,10,11,12,13 for thyroid auto-antibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5%). Reported at a frequency of
Hepatocerebellar Degeneration: A rare, autosomal recessive 7.0% in the 2005 BMDCA Health Survey.1,24,25
disease seen in 4-6 week old Bernese Mountain Dogs characterized
by progressive cerebellar and hepatic disease. Histologically, Cataracts: Anterior cortex punctate cataracts predominate, through
degeneration and depletion of Purkinje’s cells and vacuolation, posterior, nuclear, and capsular cataracts also occur in the breed.
degeneration, and nodular regeneration of hepatic tissues are Age of onset at 1 year. Identified in 4.03% of Bernese Mountain
evident.14 Dogs CERF examined by veterinary ophthalmologists between
2000-2005. Reported at a frequency of 4.7% in the 2005 BMDCA
Health Survey. CERF does not recommend breeding any Bernese
Disease Predispositions Mountain Dog with a cataract.1,7
Mortality/Longevity: Bernese Mountain Dogs are found to have
diminished longevity, with a yearly breed-specific mortality risk of Idiopathic Epilepsy: Grand-mal or petit-mal (partial) seizures
6.5%. The probability for survival by 5 years of age is 83%, and by are seen in this breed, with an average onset of 1-3 years of
ten years of age is 30%. The 2005 BMDCA Health Survey found age. There is a male predominance. Treat with anticonvulsant
an average age at death of 7.8 years. A danish study showed an medication. Pedigree studies in the breed indicate a polygenic
average life span of 7.1 years. Mortality studies in Sweden show mode of inheritance for grand-mal seizures, with the influence of
a significantly increased risk of death due to tumors, especially in a major recessive gene. Fly-Biting Petit-Mal Seizures are reported
male dogs, versus other breeds.1,15,16,17 at a frequency of 4.0%, and Grand-mal seizures are reported at a
frequency of 1.9% in the 2005 BMDCA Health Survey.1,26
Umbilical Hernia: Congenital umbilical hernias are reported at a
frequency of 24.0% in the 2005 BMDCA Health Survey.1 Gastric Dilatation-Volvulus (Bloat, GDV): Polygenically inherited,
life-threatening twisting of the stomach within the abdomen.
Osteoarthritis: Bernese Mountain Dogs have an increased
Requires immediate veterinary attention. Reported at a frequency
incidence of arthritis. Dorn reports a 1.58x odds ratio versus other
of 4.0% in the 2005 BMDCA Health Survey, with an average age of
breeds. Reported at a frequency of 17.0% in the BMDCA 2005
5 years, and a 23% fatality.1
Health Survey, with an average age of onset of 5.5 years.1,18
Persistent Pupillary Membranes: Strands of fetal remnant
Allergic Dermatitis (Atopy): Inhalant or food allergy. Presents
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
with pruritis and pyotraumatic dermatitis (hot spots). Reported at a
The later three forms can impair vision, and dogs affected with
frequency of 16.0% in the 2005 BMDCA Health Survey.1
these forms should not be bred. Identified in 3.49% of Bernese
Panosteitis: A self-limiting disease of young, large breed dogs Mountain Dogs CERF examined by veterinary ophthalmologists
involving the diaphyseal and metaphyseal areas of the tubular between 2000-2005.8
long bones, characterized by medullary fibrosis and both endosteal
Mast Cell Tumor (MCT): Skin tumors that can reoccur locally or
and subperiosteal new bone deposition. Affected dogs show
with distant metastasis. Mast cell tumors produce histamine, which
intermittent lameness. Treatment is with non-steroidal anti-inflam-
can cause inflammation and ulceration. Reported at a frequency of
matory drugs and rest. Reported at a frequency of 7.3% in the 2005
3.0% in the 2005 BMDCA Health Survey.1
BMDCA Health Survey, with an average age of onset of 1.1 years.1
70
Lymphoma/Lymphosarcoma: Malignant lymphatic cancer that with age. An autosomal recessive mode of inheritance is suggested.31
most commonly presents in the lymph nodes, spleen, liver, or heart.
Reported at a frequency of 3.0% in the 2005 BMDCA Health Survey.1 Cervical Vertebral Instability (Wobbler Syndrome): Presents
with UMN spasticity and ataxia. Imaging studies suggest that the
Humeral Osteochondritis Dissecans (OCD): Polygenically inherited primary lesion is foramenal stenosis and intervertebral instability at
cartilage defect of the humeral head. Causes shoulder joint pain C3-7. MRI is superior to myelography in determining site, severity,
and lameness in young growing dogs. Mild cases can resolve with and nature of the spinal cord compression. Treatment is with
rest, while more severe cases require surgery. 2.24:1 male to female surgery. Undetermined mode of inheritance. Reported as a sporadic
ratio in the breed. Age of onset usually 2-4 months. 50% of cases finding in the breed.32
are bilateral. Reported 47.1x odds ratio versus other breeds. Dorn
reports a 4.40x odds ratio for OCD versus other breeds. Reported at Rosenthal Fiber Encephalopathy (Alexander’s Disease): Fatal,
a frequency of 2.9% in the 2005 BMDCA Health Survey. Unknown neonatal degenerative neurological disease presenting with rapidly
mode of inheritance.1,6,18 progressive nonambulatory tetraparesis, generalized tremors, and
depressed mental status. Macroscopically the brain shows moderate
Entropion: Rolling in of eyelids, often causing corneal irritation enlargement of the lateral ventricles. Histologically there are GFAP
or ulceration. Entropion is reported in 1.89% of Bernese Mountain positive staining eosinophilic deposits consistent with Rosenthal
Dogs CERF examined by veterinary ophthalmologists between fibers (RFs) throughout the white matter of the central nervous
2000-2005. Reported at a frequency of 2.4% in the 2005 BMDCA system, and a marked proliferation of abnormally large astrocytes.33,34
Health Survey.1,8
Color Dilution Alopecia, Fibrinoid Leukodystrophy, Hypertrophic
Cleft Palate: Congenital disorder of incomplete closure of the Osteodystrophy, Hypoadrenocorticism, and Sebaceous Adenitis
maxillary processes to form the roof of the mouth. Reported as the are reported.35
#1 most frequent birth defect in the 2005 BMDCA Health Survey.1
71
Recommend thyroid profile including autoantibodies, patella Feb 13;166(7):199-202.
evaluation and bile acids or blood ammonia for liver shunt. 18. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Miscellaneous 2000.
19. Paterson S, Boydell P, Pike R: Systemic histiocytosis in the Bernese
• Breed name synonyms: Berner Sennenhund, Berner, Bernese
mountain dog. J Small Anim Pract. 1995 May;36(5):233-6.
Cattle Dog, Durrbachler (historical).
20. Schmidt ML, Rutteman GR, van Niel MH, et. al.: Clinical and
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
radiographic manifestations of canine malignant histiocytosis. Vet Q. 1993
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
Sep;15(3):117-20.
• AKC rank (year 2008): 40 (3,338 dogs registered) 21. Affolter VK, Moore PF:Localized and desiminated histiocytic sarcoma of
• Internet resources: Bernese Mountain Dog Club of America: dendritic cell origin in dogs. Vet Pathol. 2002. Jan;39(1):74-83.
www.bmdca.org 22. Padgett GA, Madewell BR, Keller ET,et. Al,: Inheritance of histiocytosis in
Bernese Mountain Dog Club of Canada: www.bmdcc.ca Bernese mountain dogs. J Small Anim Pract. 1995 Mar;36(3):93-8.
Bernese Mountain Dog Club of Great Britain: 23. Abadie J, Hédan B, Cadieu E, et. al.: Epidemiology, pathology, and genetics
www.bernese.co.uk of histiocytic sarcoma in the Bernese mountain dog breed. J Hered. 2009
Berner-Garde Foundation: www.bernergarde.org Jul-Aug;100 Suppl 1:S19-27.
24. Nachreiner R and Refsal K: Personal communication, Diagnostic Center for
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14. Carmichael KP, Miller M, Rawlings CA, et. al.: Clinical, hematologic, causing spinal cord compression in a mature Bernese mountain dog. J Small
and biochemical features of a syndrome in Bernese mountain dogs Anim Pract. 2001 Feb;42(2):79-81.
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Apr 15;208(8):1277-9. with an intrahepatic portosystemic shunt in a dog. J Am Vet Med Assoc. 2006
15. Egenvall A, Bonnett BN, Shoukri M, et. al.: Age pattern of mortality in Feb 1; 228(3):389-91.
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16. Egenvall A, Bonnett BN, Hedhammar A, et. al.: Mortality in over juvenile dog. J Am Vet Med Assoc. 1995 Sep 1;207(5):596-8.
350,000 insured Swedish dogs from 1995-2000: II. Breed-specific age 39. Welle MM, Sutter E, Malik Y, et. al.: Fibromatosis in a young Bernese
and survival patterns and relative risk for causes of death. Acta Vet Scand. Mountain Dog: clinical, imaging, and histopathological findings. J Vet Diagn
2005;46(3):121-36. Invest. 2009 Nov;21(6):895-900.
17. Nielsen L, Andreasen SN, Andersen SD, et. al.: Malignant histiocytosis and 40. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
other causes of death in Bernese mountain dogs in Denmark. Vet Rec. 2010 House, NY 2006. p. 240-243.
72
Bichon Frisé
Recognized Behavior Issues and Traits
This type of dog is ascribed as: Friendly, with an outgoing
temperament. Fear biter or separation anxiety may occur in some
shy dogs, but breeding of dogs that deviate from the typical playful
Bichon personality is not accepted. They are alarm barkers but not
considered watchdogs. They need close human contact, and are
considered moderately trainable. They are fine for city life, as they
are active dogs with average exercise needs.
Urinary Calculi: The breed is found to be at an increased risk of Diabetes Mellitus: Caused by a lack of insulin production by
developing struvite, oxalate, and cystine calculi (due to cystinuria). the pancreas. Controlled by insulin injections, diet, and glucose
Dorn reports a 4.68x odds ratio in Bichon Frise versus other breeds. monitoring. Dorn reports a 3.24x odds ratio in Bichon Frise
Reported at a frequency of 5% in the 2007 BFCA Health Survey for versus other breeds. Unknown mode of inheritance. Reported at a
Breeders.2,4,12,13,14,15 frequency of 1% in the 2007 BFCA Health Survey for Breeders.2,4
Umbilical Hernia: Congenital opening in the body wall from where Motor Dyskinesia: A rare disorder presenting with episodic
the umbilical cord was attached. Reported at a frequency of 5% involuntary skeletal muscle activity with normal levels of
in the 2007 BFCA Health Survey for Breeders. Unknown mode of consciousness, similar to paroxysmal dystonic choreoathetosis. The
inheritance.2 disorder is differentiated from partial motor seizure activity by the
character of the episodes, absence of identifiable preceding aura,
Distichiasis: Abnormally placed eyelashes that irritate the cornea absence of autonomic signs and the fact that multiple limbs are
and conjunctiva. Can cause secondary corneal ulceration. Identified affected in a varying pattern without generalization and loss of
in 3.33% of Bichon Frise CERF examined by veterinary ophthalmol- consciousness.24
ogists between 2000-2005.9
Brachygnathism, Deafness, Entropion, Epilepsy, Factor IX
Corneal Dystrophy: The epithelial/stromal form occurs in the breed, Deficiency, Prognathism, Progressive Retinal Atrophy, Retinal
causing opacities on the surface of the cornea. Average age of Dysplasia, Shaker Syndrome, Ventricular Septal Defect, and von
onset is 2 years. Unknown mode of inheritance. Identified in 2.74% Willebrand’s Disease are reported.25
of Bichon Frise CERF examined by veterinary ophthalmologists
between 2000-2005.9
Isolated Case Studies
Ciliary Dyskinesia: Inherited abnormal anatomy and function Congenital Alopecia: A Bichon Frise puppy was born with an
of cilia. Causes chronic secondary respiratory infections due absence of hair follicles, erector pili muscles, sebaceous glands,
to abnormal respiratory ciliary clearance, and infertility due and sweat glands. This defect was not associated with abnormal
to abnormal sperm motility. Unknown mode of inheritance. pigmentation, normal black and brown pigmentation developed
Reported at a frequency of 2% in the 2007 BFCA Health Survey for independently of the alopecic pattern.26
Breeders.2,16
Hydrocephalus and Antidiuretic Hormone Deficiency: A
Persistent Pupillary Membranes: Strands of fetal remnant 13-month-old male bichon frise with a domed skull was examined for
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The the investigation of intermittent seizures, ataxia, abnormal behavior,
later three forms can impair vision, and dogs affected with these polyuria, and polydipsia. Severe hyponatremia and hypoosmolality
forms should not be bred. Identified in 1.95% of Bichon Frise CERF were identified, and diagnostic testing indicated inappropriate
examined by veterinary ophthalmologists between 2000-2005.9 antidiuretic hormone secretion. MRI revealed severe hydrocephalus.27
Hypothyroidism: Inherited autoimmune thyroiditis. 1.7% positive Episodic Ataxia/Ion Channelopathy: A four-year-old neutered
for thyroid auto-antibodies based on testing at Michigan State male Bichon Frise developed chronic, progressive, episodic cerebellar
University. (Ave. for all breeds is 7.5%).17,18 ataxia. All testing was normal. Treatment with 4-aminopyridine
resolved all signs, suggesting an ion channelopathy.28
Primary (Narrow Angle) Glaucoma: Ocular condition causing
increased pressure within the eyeball, and secondary blindness due Genetic Tests
to damage to the retina. Diagnose with tonometry and gonioscopy. Tests of Genotype: none
Diagnosed in 1.59% of Bichon Frises presented to veterinary
teaching hospitals.19 Tests of Phenotype: CHIC Certification: Required testing includes
hip radiographs, patella evaluation (after 12 months, and then
Portosystemic Shunt (PSS, Liver Shunt): Congenital disorder, annually), and CERF eye examination (annually). Optional testing
where abnormal blood vessels connecting the systemic and includes congenital cardiac evaluation, and bile acids for liver shunt.
portal blood flow. Vessels can be intrahepatic or extrahepatic. (See CHIC website; www.caninehealthinfo.org).
Causes stunting, abnormal behavior and possible seizures. A case
study documented secondary pruritis that resolved with surgical Recommend thyroid profile including autoantibodies and elbow
correction of the shunt. One study showed a significantly higher radiographs.
74
Miscellaneous 22. Tobias KM & Rohrbach BW: Association of breed with the diagnosis of
congenital portosystemic shunts in dogs: 2,400 cases (1980-2002). J Am
• Breed name synonyms: Bichon, Bichon Teneriffe, Teneriffe Vet Med Assoc. 2003 Dec 1;223(11):1636-9.
(historical), Bichon a Poil Frise 23. Miller SA, Hohenhaus AE, Hale AS: Case-control study of blood type,
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), breed, sex, and bacteremia in dogs with immune-mediated hemolytic
ANKC (Australian National Kennel Club), NKC (National Kennel Club) anemia. J Am Vet Med Assoc. 2004 Jan 15;224(2):232-5.
• AKC rank (year 2008): 35 (4,675 dogs registered) 24. Penderis J, Franklin RJ: Dyskinesia in an adult bichon frise. J Small Anim
• Internet resources: Bichon Frise Club of America: Pract. 2001 Jan;42(1):24-5.
www.bichon.org 25. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Bichon Frise Club of Canada: www.bichonfriseclubofcanada.com Ackerman. p.202-3, AAHA Press, 1999.
Bichon Frise Club of Great Britain: 26. Grieshaber TL, Blakemore JC, Yaskulski S: Congenital alopecia in a
www.bichonfriseclubofgb.info/ Bichon Frise. J Am Vet Med Assoc. 1986 May 1;188(9):1053-4
27. Shiel RE, Pinilla M, & Mooney CT: Syndrome of inappropriate
antidiuretic hormone secretion associated with congenital hydrocephalus
References in a dog. J Am Anim Hosp Assoc. 2009 Sep-Oct;45(5):249-52.
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010. 28. Hopkins AL & Clarke J: Episodic cerebellar dysfunction in a bichon frise:
2. BFCA Health Committee: 2007 BFCA Health Survey for Breeders. 2008. a canine case of episodic ataxia? J Small Anim Pract. 2010 Aug;51(8):444-6.
3. LaFond E, Breur GJ and Austin CC: Breed susceptibility for 29. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002 Book House, NY 2006. p. 529-532.
Sep-Oct;38(5):467-77.
4. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
5. Adkins EA, Hendrix DV: Outcomes of dogs presented for cataract
evaluation: a retrospective study. J Am Anim Hosp Assoc. 2005
Jul-Aug;41(4):235-40.
6. Wallace MR, MacKay EO, Gelatt KN, et. al.: Inheritance of cataract in the
Bichon Frise. Vet Ophthalmol. 2005 May-Jun;8(3):203-5.
7. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
8. Gelatt KN, MacKay EO: Secondary glaucomas in the dog in North
America. Vet Ophthalmol. 2004 Jul-Aug;7(4):245-59.
9. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
10. Gelatt, KN, Wallace MR. Andrew SE, et. al: Cataracts in the Bichon Frise:
Vet Ophthalmol:2003;6;1;3-9.
11. White SD: Update on Allergies: Atopic Dermatitis. Proceedings,
Northeast Veterinary Conference 2004.
12. Jones BR, Kirkman JH, Hogan J, et. al.: Analysis of uroliths from cats and
dogs in New Zealand, 1993-96. N Z Vet J. 1998 Dec;46(6):233-6.
13. Case LC, Ling GV, Franti CE, et. al.: Cystine-containing urinary
calculi in dogs: 102 cases (1981-1989). J Am Vet Med Assoc. 1992 Jul
1;201(1):129-33.
14. Houston DM, Moore AE, Favrin MG, et. al.: Canine urolithiasis: a look at
over 16 000 urolith submissions to the Canadian Veterinary Urolith Centre
from February 1998 to April 2003. Can Vet J. 2004 Mar;45(3):225-30.
15. Houston DM & Moore AE: Canine and feline urolithiasis: examination of
over 50 000 urolith submissions to the Canadian veterinary urolith centre
from 1998 to 2008. Can Vet J. 2009 Dec;50(12):1263-8.
16. Maddux JM, Edwards DF, Barnhill MA, et. al.: Neutrophil function in
dogs with congenital ciliary dyskinesia. Vet Pathol. 1991 Sep;28(5):347-53.
17. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
18. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
19. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
in pure-bred dogs in North America. Vet Ophthalmol. 2004
Mar-Apr;7(2):97-111.
20. Hunt GB: Effect of breed on anatomy of portosystemic shunts resulting
from congenital diseases in dogs and cats: a review of 242 cases. Aust Vet J.
2004 Dec;82(12):746-9.
21. Waisglass SE, Gillick A, Cockshutt J, et. al.: Pruritus possibly associated
with a portosystemic shunt in a bichon frise puppy. Can Vet J. 2006
Nov;47(11):1109-11.
75
Black Russian Terrier
The palpebral margins are tight and black, as are the lips. No
flews. Small triangular ears are high set, and just reach the lateral
canthus. Gingival surface is pigmented, and spots of pigment may
occur on the tongue. Neck thick, well muscled, the thorax is wide
and deep with oval cross section, pronounced withers merge with
level topline. The abdomen is well tucked up, loin is short. Limbs
are straight, with very short straight metacarpals/metatarsals, and
large rounded feet. Nails dark and rear dewclaws often removed.
The thick tail is high set, and usually docked to the length of 3-5
vertebrae. Gait is springy, smooth and long.
Coat: Color must be black, or black intermixed with a few other Patella Luxation: Polygenically inherited laxity of patellar
gray hairs. A thick double coat, with a coarse overcoat and ligaments, causing luxation, lameness, and later degenerative
undercoat thick and soft in texture. Length of hairs 1.5-4” (4-10 joint disease. Treat surgically if causing clinical signs. Too few
cm) and has a tousled appearance—not wiry, not curly. Hair in and Black Russian Terriers have been screened by OFA to determine an
around the ears is trimmed for show. Fairly easy keeping coat. accurate frequency.1
Genetic Tests
Tests of Genotype: Direct test for hyperuricosuria is available from
the UC-Davis VGL and Animal Health Trust.
Miscellaneous
• Breed name synonyms: Black Terrier, Chornyi, Terrier Noir Russe,
Russian Bear Schnauzer, Tchiorny Terrier
• Registries: AKC, CKC, FCI, SKC, ANKC (Australian National Kennel
Club), NKC (National Kennel Club)
• AKC rank (year 2008): 121 (245 dogs registered)
• Breed resources: Black Russian Terrier Club of America:
www.brtca.org
Black Russian Terrier Club of Canada: www.brtcc.ca
Black Russian Terrier Club (UK): www.rbtclub.co.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Bende B, Nemeth T: High prevalence of urate urolithiosis in the Russian
black terrier. Vet Rec. 2004 Aug 21;155(8):239-40.
3. Bannasch D, Safra N, Young A, et. al.: Mutations in the SLC2A9 Gene
Cause Hyperuricosuria and Hyperuricemia in the Dog. PLoS Genet. 2008.
4(11): e1000246. doi:10.1371/journal.pgen.1000246
4. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
77
Black and
Tan Coonhound
Recognized Behavior Issues and Traits
Reported breed traits include: Friendly, though some individuals are
reserved, watchful, and obedient. Noted to be very intelligent, with
an independent streak, and when off leash, need to be restricted to
a fenced enclosure. They have high exercise needs, though exhibit
low activity levels around the home.
78
Persistent Pupillary Membranes: Strands of fetal remnant • Internet resources: American Black and Tan Coonhound Club:
connecting; iris to iris, cornea, lens, or involving sheets of tissue. www.abtcc.com
The later three forms can impair vision, and dogs affected with American Black and Tan Coonhound Association:
these forms should not be bred. Identified in 3.01% of Black and www.abtcha.net
Tan Coonhounds CERF examined by veterinary ophthalmologists
between 2000-2005.7 References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Ectropion: Rolling out of eyelids, often with a medial canthal 2. Dodds WJ: Bleeding Disorders in Animals. Proceedings World Small
pocket. Can also cause conjunctivitis. Ectropion is reported in Animal Veterinary Association Congress. 2005
1.91% of Black and Tan Coonhounds CERF examined by veterinary 3. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
ophthalmologists between 1991-1999. None were reported for Population and Animal Health, Michigan State University. April, 2007.
between 2000-2005.7 4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Entropion: Rolling in of eyelids, often causing corneal irritation Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
or ulceration. Entropion is reported in 1.91% of Black and Tan 5. Cummings JF, Haas DC: Coonhound paralysis. An acute idiopathic
Coonhounds CERF examined by veterinary ophthalmologists polyradiculoneuritis in dogs resembling the Landry-Guillain-Barre
syndrome. J Neurol Sci. 1966 Jan-Feb;4(1):51-81.
between 1991-1999. None were reported between 2000-2005.7
6. Holmes DF, Schultz RD, Cummings JF, et. al.: Experimental coonhound
paralysis: animal model of Guillain-Barre syndrome. Neurology. 1979
Distichiasis: Abnormally placed eyelashes that irritate the cornea
Aug;29(8):1186-7.
and conjunctiva. Can cause secondary corneal ulceration. Identified 7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
in 1.20% of Black and Tan Coonhounds CERF examined by College of Veterinary Ophthalmologists. ACVO,2007
veterinary ophthalmologists between 2000-2005.7 8. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 203. AAHA Press, 1999.
Progressive Retinal Atrophy (PRA): Inherited degeneration of 9. Kim DY, Royal AB, and Villamil JA: Disseminated melanoma in a dog
the retina leading to blindness. Clinically evident by 2 years of age. with involvement of leptomeninges and bone marrow. Vet Pathol. 2009
There may be more than one form of PRA in the breed. Unknown Jan;46(1):80-3.
mode of inheritance.7 10. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 152-155.
Cryptorchidism, Gastric Dilatation-volvulus, and Pelger-Huet
Anomaly are reported.8
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: Coonhound, Black and Tan, American
Black and Tan Coonhound.
• Registries: AKC, CKC, UKC, (Here known as the American Black
and Tan Coonhound), NKC.
• AKC rank (year 2008): 42 (3,222 dogs registered)
79
Bloodhound
of the flews everts the lower lids. Eye colors match the coat, with
hazel and yellow being common pigmentation. Ears are very low
set, long and pendulous, but the leather is fairly fine textured. The
flews are extensive and merged with neck folds, forming the large
dewlap. Body skin is loose. The neck is long, the thorax is rounded
and deep, and the loin is mildly arched. The tail is large, long
and tapered and carried high. Gait is smooth and elastic on this
muscular dog. Legs are straight and solid. Feet are compact and
well knuckled.
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: Bluetick
• Registries: AKC, UKC, CKC, ANKC (Australian National Kennel
Club), NKC (National Kennel Club)
• AKC rank: (none) AKC recognized in Dec. 2009. Entire stud book
entered.
• Internet resources: American Bluetick Hound Association:
www.akc.org/akc_clubs/?AmericanBluetickHoundAssociation
Bluetick Coonhound Breeders of America:
www.bluetickbreedersofamerica.com
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Cummings JF, Haas DC: Coonhound paralysis. An acute idiopathic
polyradiculoneuritis in dogs resembling the Landry-Guillain-Barre
syndrome. J Neurol Sci. 1966 Jan-Feb;4(1):51-81.
5. Holmes DF, Schultz RD, Cummings JF, et. al.: Experimental coonhound
paralysis: animal model of Guillain-Barre syndrome. Neurology. 1979
Aug;29(8):1186-7.
6. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
7. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 203. AAHA Press, 1999.
8. Boysen BG, Tryphonas and L, Harries NW: Globoid cell leukodystrophy
in the bluetick hound dog. I. Clinical manifestations. Can Vet J. 1974
Nov;15(11):303-8.
9. AKC Breed Website: www.akc.org/breeds/bluetick_coonhound Last
accessed July 1, 2010.
83
Border Collie
well-sprung ribs characterize these dogs. The tail reaches to at least
their tarsus, and though usually carried low, may be held level when
excited. The body is a bit longer than high and dewclaws may be
removed. Compact feet, straight limbs, and a smooth, long, low, way
of going is characteristic.
Coat: Very dense smooth, rough, or medium coats are found; rough Inherited Diseases
and smooth are the only permitted forms in the AKC standard. Hip Dysplasia: Polygenically inherited trait causing degenerative
Colors include black and tan, tri-color, merle, sable, and black, joint disease and hip arthritis. OFA reports 10.9% affected. Reported
usually with white markings. Solid white is not accepted. These at a frequency of 7.1% in the 2007 BCSA Health Survey.1,6
dogs are average shedders, and should be brushed very regularly.
The dense undercoat sheds out in Spring. Collie Eye Anomaly/Choroidal Hypoplasia/Coloboma (CEA/CH):
Autosomal recessive disorder of eye development that can lead
Longevity: 12-15 years. to retinal detachment and blindness. A genetic test is available
through Optigen, that reports 2% of Border Collies test as affected,
Points of Conformation: The physical characteristics of the Border and 28% test as carriers. Worldwide test results on the Border
Collie are not considered a high priority, except how they contribute Collie Health website reports 0.7% affected and 24.8% carrier.
to their ability to work. These dogs are medium sized, and they Reported 0.7% affected in Switzerland. Reported in 1.64% of Border
possess a very alert expression. Their skull is broad with a moderate Collies CERF examined by veterinary ophthalmologists between
stop. Ears are set up and semi-erect, oval eyes are dark brown 2000-2005. CERF does not recommend breeding any Border Collie
usually, though blue is acceptable in the merle, and their nose is with CH.7,8,9,10,11
black. A moderately arched long neck, level topline, deep thorax and
84
Elbow Dysplasia: Polygenically inherited trait causing elbow Lens Luxation: Breed predisposition identified in the Border Collie.
arthritis. OFA reports 1.4% affected.6 Age of onset 3-5 years of age. Often progresses to secondary
glaucoma. CERF does not recommend breeding any Border Collie
Patella Luxation: Polygenically inherited laxity of patellar with lens luxation.7,27,28
ligaments, causing luxation, lameness, and later degenerative joint
disease. Treat surgically if causing clinical signs. OFA reports 1.1% Deafness: Congenital deafness can be unilateral or bilateral.
affected.6 Diagnosed by BAER testing. OFA reports 0.6% of Border Collies
BAER test as affected. A study in the United Kingdom showed 2.0%
Trapped Neutrophil Syndrome (TNS, Static Neutropenia): unilaterally deaf, and 0.4% bilaterally deaf. Correlated with blue
Congenital autosomal recessive disorder causing mature eyes, with white head pigmentation, and/or the merle gene. In a
neutrophils to become trapped in the bone marrow. Affected pups multi-breed study; for single merles (Mm), 2.7% were unilaterally
have recurrent infections and fail to thrive. Reported in Border deaf and 0.9% were bilaterally deaf. For double merles (MM), 10%
Collies worldwide. This disorder is distinct from cyclic neutropenia. were unilaterally deaf and 15% were bilaterally deaf.6,29,30,31,32
Worldwide test results on the Border Collie Health website reports
0.8% affected and 19.2% carrier. A linked marker genetic test is Portosystemic Shunt (PSS, Liver Shunt): Abnormal blood
available.10,12,13,14 vessels connecting the systemic and portal blood flow. Causes
stunting, abnormal behavior and possible seizures. Seen at a higher
Progressive Retinal Atrophy (PRA): X-linked recessive mode prevalence in the breed compared to other breeds. Undetermined
of inheritance. Age of onset 1-2 years of age. Reported in 0.45% mode of inheritance.33
of Border Collies CERF examined by veterinary ophthalmologists
between 2000-2005. CERF does not recommend breeding any Osteochondrosis of the Shoulder/Stifle: Age of onset of
Border Collie with PRA. The causative mutation is not known, and lameness usually 4-7 months of age. Male predominance. One
a genetic test is not available. There may be more than one form of study identified three affected out of five Border Collie littermates.
PRA in the breed.7,15 Reported 15.0x odds ratio for shoulder OCD versus other breeds.
Reported at a frequency of 1.9% in the 2007 BCSA Health Survey.
Neuronal Ceroid Lipofuscinosis (NCL): Autosomal recessive, Unknown mode of inheritance.1,34,35
degenerative progressive neurological disease causing hyperactivity
and later aggression, gait abnormalities, blindness and dementia. Cataracts: Anterior or posterior punctate cataracts predominate
Onset between 16 months and 2 years of age. Dogs do not survive in the breed. Reported in 1.34% of Border Collies presented
more than 6 months from the onset of clinical signs. Worldwide to veterinary teaching hospitals. Identified in 1.23% of Border
test results on the Border Collie Health website reports 2.6% Collies CERF examined by veterinary ophthalmologists between
carriers. A genetic test is available.10,16,17,18,19,20 2000-2005. CERF does not recommend breeding any Border Collie
with a cataract.7,36
Cobalamin Malabsorption (Methylmalonic Aciduria): Autosomal
recessive disorder presenting with chronic, nonregenerative anemia, Diabetes Mellitus: Caused by a lack of insulin production by
and methylmalonic aciduria. The disorder responds to parenteral the pancreas. Controlled by insulin injections, diet, and glucose
vitamin B12 therapy, and affected animals have a good prognosis monitoring. Age of onset 6-12 years. A Swedish study showed an
with treatment. A phenotypic urine test is available.21,22 increased incidence in the breed, with the majority of affected
Border Collies being female. Unknown mode of inheritance.37
Disease Predispositions Separation Anxiety: The breed may have a tendency towards
Hypothyroidism: Inherited autoimmune thyroiditis. 11.2% positive
separation anxiety.38
for thyroid auto-antibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5%). Reported at a frequency of Retinal Dysplasia: Focal folds and geographic retinal dysplasia
2.9% in the 2007 BCSA Health Survey.1,23,24 are seen in the breed. Dogs with the geographic form should not
be bred. Identified in 0.75% of Border Collies CERF examined by
Persistent Pupillary Membranes: Strands of fetal remnant
veterinary ophthalmologists between 2000-2005.7
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
later three forms can impair vision, and dogs affected with these Cerebellar Abiotrophy (CA, Ataxia): Identified in multiple
forms should not be bred. Identified in 6.31% of Border Collies CERF siblings of Border Collies presenting with signs of progressive
examined by veterinary ophthalmologists between 2000-2005.7 ataxia and hypermetria beginning at 6-8 weeks of age. Pathology
demonstrates extensive loss of the cerebellar granular cell layer,
Epilepsy (Inherited Seizures): Studies show a strong founder
with relative sparing of Purkinje cells. Presumptive autosomal
effect with a major recessive mode of inheritance. Epilepsy in the
recessive mode of inheritance.39,40
Border Collie often has a severe clinical course, with dogs who first
seizure under 2 years of age having a diminished life expectancy. Ciliary Dyskenesia, Corneal Dystrophy, Cyclic Hematopoiesis,
Cluster seizures and status epilepticus occur at a higher frequency Malignant Hyperthermia, Neuroaxonal Dystrophy, Pannus,
in the breed. Up to 71% of Border Collies can show anticonvulsant Patent Ductus Arteriosis, and Pelger-Huet Anomaly are
resistance. Dorn reports an 8.79x odds ratio of developing epileptic reported.41
seizures versus other breeds. Reported at a frequency of 3.3% in the
2007 BCSA Health Survey.1,25,26
85
Isolated Case Studies Linked marker test for Trapped Neutrophil Syndrome (TNS) is
available from University of New South Wales
Sensory and Motor Neuropathy: A 5-month-old female Border
Collie was evaluated because of progressive hind limb ataxia. http://www.bordercollie.org.au/pdf/TNSsamplinginternational.pdf
Sensory nerve conduction velocity was absent in the tibial, common
Tests of Phenotype: CHIC Certification: Required testing includes
peroneal, and radial nerves and was decreased in the ulnar nerve;
hip radiographs, CERF eye examination (annually until age 7),
motor nerve conduction velocity was decreased in the tibial,
and participation in the CHIC DNA repository. Optional tests
common peroneal, and ulnar nerves. Pathology included nerve
include elbow and shoulder radiographs, thyroid profile including
fiber depletion and axonal degeneration in remaining fibers. A
autoantibodies, BAER test for deafness, cardiac evaluation, and
littermate was similarly affected. In another study, two Border Collie
gene tests for CEA/CH, NCL, and TNS. (See CHIC website; www.
littermates were diagnosed with a purely sensory distal peripheral
caninehealthinfo.org).
neuropathy.42,43
Recommend patella evaluation.
Superficial Necrolytic Dermatitis (Hepatocutaneous Syndrome):
Two Border Collies were identified in a study of 36 dogs with Urine test for Methylmalonic Aciduria is available from PennGen.
diagnoses of superficial necrolytic dermatitis, suggesting a breed
prevalence. Affected dogs present with erythema, crusting,
exudation, ulceration and alopecia involving footpads, peri-ocular Miscellaneous
or peri-oral regions, anal–genital regions, and pressure points • Breed name synonyms: BC
on the trunk and limbs. Average age of presentation is 10 years. • Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain),
Diagnosis is by biopsy.44 ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 53 (2,104 dogs registered)
Aortic Elastin Dysplasia (Dissecting Hematoma): Two cases • Internet resources: Border Collie Society of America:
of sudden death in a Border Collie and a Border Collie cross. www.bordercolliesociety.com
Pathological findings were pericardial tamponade with dissection of American Border Collie Association:
the ascending aorta, and unusual splitting of the elastin within the www.americanbordercollie.org
wall of the aorta, as described in Marfan syndrome.45 United States Border Collie Club (working collies):
www.bordercollie.org
Nemaline Rod Myopathy: Case study of a 10 month old Border United States Border Collie Handlers Association:
Collie with exercise intolerance, abnormal electromyography, and www.usbcha.com
the presence of nemaline rods in fresh, frozen, and glutaraldehyde- Canadian Border Collie Association:
fixed biopsies from proximal appendicular limb muscles.46 www.canadianbordercollies.org
Border Collie Club of Great Britain: www.bordercollieclub.com
Cervical Syringomyelia and Hydrocephalus with Scoliosis: Border Collie Health: www.bordercolliehealth.com
Case study of a 6-month-old female Border Collie with a 1-month
history of progressive curvature of the cervical spine. Suboccipital
craniotomy and laminectomy of the first cervical vertebra were
References
1. Border Collie Society of America: 2007 BCSA Health Survey. 2008.
performed, improved the scoliosis and syringomyelia.47 2. Clark LA, Wahl JM, Rees CA, et. al.: Retrotransposon insertion in SILV is
responsible for merle patterning of the domestic dog. Proc Natl Acad Sci U
Myasthenia Gravis and Dysautonomia: A two year old male intact S A. 2006 Jan 31;103(5):1376-81.
border collie with diarrhea, coughing, vomiting and stranguria 3. Nelson OL, Carsten E, Bentjen SA, et. al.: Ivermectin toxicity in
had megaoesophagus, flaccid bladder, poor pupillary light reflexes, an Australian Shepherd dog with the MDR1 mutation associated
an absent gag reflex, poor anal tone, and aspiration pneumonia. with ivermectin sensitivity in Collies. J Vet Intern Med. 2003
Testing revealed coexisting autoimmune myasthenia gravis and May-Jun;17(3):354-6.
dysautonomia.48 4. Geyer J, Doring B, Godoy JR, et. al.: Frequency of the nt230 (del4) MDR1
mutation in Collies and related dog breeds in Germany. J Vet Pharmacol
Ther. 2005 Dec;28(6):545-51.
Genetic Tests 5. Mealey KL & Meurs KM: Breed distribution of the ABCB1-1Delta
Tests of Genotype: Direct test for Collie Eye Anomaly/Choroidal (multidrug sensitivity) polymorphism among dogs undergoing ABCB1
Hypoplasia is available from Optigen. (Recommended for breeding genotyping. J Am Vet Med Assoc. 2008 Sep 15;233(6):921-4.
dogs) 6. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Direct test for Neuronal Ceroid Lipofuscinosis (NCL) is available College of Veterinary Ophthalmologists. ACVO, 2007
from Optigen and the Animal Health Trust. 8. Bedford PG: Collie eye anomaly in the border collie. Vet Rec. 1982 Jul
10;111(2):34-5.
Direct test for MDR1 Mutation is available from Washington 9. Lowe JK, Kukekova AV, Kirkness EF, et. al.: Linkage mapping of the primary
State Univ. http://www.vetmed.wsu.edu/depts-VCPL/test.aspx. disease locus for collie eye anomaly. Genomics. 2003 Jul:82(1):86-95.
(Recommended for all dogs) 10. Border Collie Health website genetic testing statistics. www.
bordercolliehealth.com Last accessed July 1, 2010.
Direct tests for black, brown (red) and true red coat colors, and 11. Walser-Reinhardt L, Hässig M, & Spiess B: Collie eye anomaly in
black and brown nose are available from VetGen and HealthGene. Switzerland. Schweiz Arch Tierheilkd. 2009 Dec;151(12):597-603.
12. Allan FJ, Thompson KG, Jones BR, et. al.: Neutropenia with a probable
86
hereditary basis in Border Collies. N Z Vet J. 1996 Apr;44(2):67-72. the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
13. Shearman JR, Zhang QY, Wilton AN: Exclusion of CXCR4 as the cause of 37. Fall T, Hamlin HH, Hedhammar A, et. al.: Diabetes mellitus in a
Trapped Neutrophil Syndrome in Border Collies using five microsatellites on population of 180,000 insured dogs: incidence, survival, and breed
canine chromosome 19. Animal Genetics 2006;37(1):89. distribution. J Vet Intern Med. 2007 Nov-Dec;21(6):1209-16.
14. Shearman JR, Wilton AN: Elimination of neutrophil elastase and adaptor 38. Bradshaw JW, McPherson JA, Casey RA, et. al.: Aetiology of separation-
protein complex 3 subunit genes as the cause of trapped neutrophil related behaviour in domestic dogs. Vet Rec. 2002 Jul 13;151(2):43-6.]
syndrome in Border collies. Animal Genetics 2007;38 (2):188–189. 39. Sandy JR, Slocombe RE, Mitten RW, et. al.: Cerebellar abiotrophy in a
15. Vilboux T, Chaudieu G, Jeannin P, et. al.: Progressive retinal atrophy in family of Border Collie dogs. Vet Pathol. 2002 Nov;39(6):736-8.
the Border Collie: a new XLPRA. BMC Vet Res. 2008 Mar 3;4:10. 40. Gill JM, Hewland M: Cerebellar degeneration in the Border collie. N Z Vet
16. Melville SA, Wilson CL, Chiang CS, et. al.: A mutation in canine CLN5 J. 1980 Aug;28(8):170.
causes neuronal ceroid lipofuscinosis in Border collie dogs. Genomics. 2005 41. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Sep;86(3):287-94. Ackerman. p.203, AAHA Press, 1999.
17. Koie H, Shibuya H, Sato T, et. al.: Magnetic resonance imaging of 42. Harkin KR, Cash WC, Shelton GD: Sensory and motor neuropathy in a
neuronal ceroid lipofuscinosis in a border collie. J Vet Med Sci. 2004 Border Collie. J Am Vet Med Assoc. 2005 Oct 15;227(8):1263-5, 1250.
Nov;66(11):1453-6. 43. Vermeersch K, Van Ham L, Braund KG, et. al.: Sensory neuropathy in two
18. Taylor RM, Farrow BR: Ceroid-lipofuscinosis in border collie dogs. Acta Border collie puppies. J Small Anim Pract. 2005 Jun;46(6):295-9.
Neuropathol (Berl). 1988;75(6):627-31. 44. Outerbridge CA, Marks SL, Rogers QR: Plasma amino acid
19. Studdert VP, Mitten RW: Clinical features of ceroid lipofuscinosis in concentrations in 36 dogs with histologically confirmed superficial
border collie dogs. Aust Vet J. 1991 Apr;68(4):137-40. necrolytic dermatitis. Vet Dermatol. 2002 Aug;13(4):177-86.
20. Taylor RM, Farrow BR: Ceroid lipofuscinosis in the border collie dog: 45. Boulineau TM, Andrews-Jones L, Van Alstine W: Spontaneous aortic
retinal lesions in an animal model of juvenile Batten disease. Am J Med dissecting hematoma in two dogs. J Vet Diagn Invest. 2005 Sep;17(5):492-7.
Genet. 1992 Feb 15;42(4):622-7. 46. Delauche AJ, Cuddon PA, Podell M, et. al.: Nemaline rods in canine
21. Morgan LW, McConnell J: Cobalamin deficiency associated with myopathies: 4 case reports and literature review. J Vet Intern Med. 1998
erythroblastic anemia and methylmalonic aciduria in a border collie. J Am Nov-Dec;12(6):424-30.
Anim Hosp Assoc. 1999 Sep-Oct;35(5):392-5. 47. Takagi S, Kadosawa T, Ohsaki T, et. al.: Hindbrain decompression in a dog
22. Battersby IA, Giger U, Hall EJ: Hyperammonaemic encephalopathy with scoliosis associated with syringomyelia. J Am Vet Med Assoc. 2005 Apr
secondary to selective cobalamin deficiency in a juvenile Border collie. J 15;226(8):1359-63, 1347.
Small Anim Pract. 2005 Jul;46(7):339-4 48. Gajanayake I, Niessen SJ, Cherubini GB, et. al.: Autoimmune
23. Nachreiner R and Refsal K: Personal communication, Diagnostic Center myasthenia gravis and dysautonomia in a dog. J Small Anim Pract. 2008
for Population and Animal Health, Michigan State University. April, 2007. Nov;49(11):593-5.
24. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of 49. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
serum thyroid hormone autoantibodies in dogs with clinical signs of Book House, NY 2006. p. 635-639.
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
25. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
26. Hülsmeyer V, Zimmermann R, Brauer C, et. al.: Epilepsy in Border Collies:
clinical manifestation, outcome, and mode of inheritance. J Vet Intern Med.
2010 Jan-Feb;24(1):171-8.
27. Curtis R: Lens luxation in the dog and cat. Vet Clin North Am Small Anim
Pract. 1990 May;20(3):755-73.
28. Foster SJ, Curtis R, Barnett KC: Primary lens luxation in the Border collie.
J Small Anim Pract 1986;27:1.
29. Platt S, Freeman J, di Stefani A, et. al.: Prevalence of unilateral and
bilateral deafness in border collies and association with phenotype. J Vet
Intern Med. 2006 Nov-Dec;20(6):1355-62
30. De Risio L, Freeman J, Blott S, et. al.: Prevalence, Heritability and Genetic
Correlations of Congenital Sensorineural Deafness and Pigmentation
Phenotypes in 4143 Border Collies. Proceedings, 2009 ACVIM Forum. 2009.
31. Strain GM, Clark LA, Wahl JM, et. al.: Prevalence of deafness in dogs
heterozygous or homozygous for the merle allele. J Vet Intern Med. 2009
Mar-Apr;23(2):282-6.
32. De Risio L, Lewis T, Freeman J, et. al.: Prevalence, heritability and genetic
correlations of congenital sensorineural deafness and pigmentation
phenotypes in the Border Collie. Vet J. 2011 Jun;188(3):286-90.
33. Hunt GB: Effect of breed on anatomy of portosystemic shunts resulting
from congenital diseases in dogs and cats: a review of 242 cases. Aust Vet J
2004;Dec; 82[12]:746-9.
34. Knecht CD, Van Sickle DC, Blevins WE, et. al.: Osteochondrosis of the
shoulder and stifle in 3 of 5 Border Collie littermates. J Am Vet Med Assoc.
1977 Jan 1;170(1):58-60.
35. LaFond E, Breur GJ and Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
36. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
87
Border Terrier
Recognized Behavior Issues and Traits
Reported breed characteristics include: Friendly, good family dog,
high trainability, good natured, high energy and activity levels, and
game in the field when hunting (showing perseverance, tenacity,
courageous). Should not be off leash unless in a fenced enclosure.
May exhibit inter-male aggression but considered less scrappy than
most other terriers. Introduce early to children and cats. The Border
Terrier will view small pets as prey. Good alarm barkers but may
bark excessively, chew, or dig if bored. Likes close human contact.
Adaptable to city or country living.
The Breed History
The name “border” arises from the breed’s region of origin, along Normal Physiologic Variations
the border between England and Scotland. They are one of the None reported
oldest British terrier breeds, pictured in artwork dating back as far
as the year 1869. First AKC registrations occurred in the year 1930. Drug Sensitivities
None reported
Breeding for Function
In England, these working terriers helped farmers protect their Inherited Disease
sheep from predators including foxes. As a valued protector of Elbow Dysplasia: Polygenically inherited trait causing elbow
sheep herds, they were selected for stamina and water resistant arthritis. OFA reports 4.5% affected.1
coats, which helped them work long days in a harsh environment.
Hip Dysplasia and Legg-Calve Perthes Disease: Polygenically
They also served as ratters. Today, they are entered in competitions
inherited traits causing degenerative joint disease and hip arthritis.
such as flyball, earthdog tests, agility and tracking.
OFA reports 3.6% affected.1
89
Borzoi
from the front, but are straight. The feet are well knuckled up and
the dewclaws are generally removed. Hindquarters are wider than
forequarters. Their long tail is set low and carried low in a curve. A
powerful springy gait is desired.
90
the cervical spinal cord. Clinical signs include limb weakness, Microphthalmia, Optic Nerve Hypoplasia, Stifle OCD,
proprioceptive deficits, and paralysis. Evidence of an autosomal Dysfibrinogenemia, Hypertrophic Osteodystrophy, Lymphedema,
recessive trait was found in this breed.9 Methemoglobin Reductase Deficiency, and Oligodontia are
reported.14
Disease Predispositions
Multifocal Chorioretinopathy: Borzoi’s can develop a retinopathy Isolated Case Studies
that does not progress once developed, and does not cause visual Multisystemic Inflammatory Disease: Report of a 6 week-old
abnormalities. Various studies have found 5.6% to 12% of adult dog developing anorexia, temporary intention tremor, seizures,
dogs with this lesion. Pedigree analysis and breeding studies rule episodic pyrexia, tachypnea, conjunctivitis, otitis and neck pain.
out a sex-linked or autosomal dominant mode of inheritance, Hematological abnormalities included an inflammatory leukogram
although male dogs predominate. CERF does not recommend and regenerative anemia. Post mortem examination revealed a
breeding any Borzoi with chorioretinopathy.10,11 multisystemic inflammatory disease involving thyroids, lymph
nodes, spleen, pancreas, bladder and lung, but no lesions to account
Mammary Cancer: Dorn reports a 17.06x odds ratio of developing for the neurological signs.15
mammary cancer versus other breeds.12
Cutaneous Malignant Histiocytosis: Report of a 4 year-old dog.
Gastric Dilation/Volvulus (Bloat): Life-threatening twisting of This is a multi-system, rapidly progressive disease in which there is
the stomach within the abdomen. Requires immediate veterinary simultaneous involvement of multiple organs such as spleen, lymph
attention. Dorn reports a 13.47x odds ratio of developing GDV nodes, lung, bone marrow, skin and subcutis. The disease is poorly
versus other breeds.12 responsive to treatment. A canine cell line (CCT) was established
from this dog.16
Cataracts: Anterior cortex punctate, and capsular cataracts
predominate in the breed. Unknown mode of inheritance. Identified
in 3.40% of Borzois CERF examined by veterinary ophthalmolo- Genetic Tests
gists between 2000-2005. CERF does not recommend breeding any Tests of Genotype: Direct test of K coat color alleles is available
Borzoi with a cataract.11 from VetGen.
Persistent Pupillary Membranes: Strands of fetal remnant Direct tests for a DM susceptability gene is available from the OFA.
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
Tests of Phenotype: CHIC Certification: Required tests are; CERF
The later three forms can impair vision, and dogs affected with
eye examination, thyroid profile including autoantibodies, cardiac
these forms should not be bred. Identified in 1.44% of Borzois CERF
certification, and direct gene test for DM. Optional recommended
examined by veterinary ophthalmologists between 2000-2005.11
tests are; hip and elbow radiographs. (See CHIC website: www.
Progressive Retinal Atrophy (PRA): Inherited degeneration of the caninehealthinfo.org)
retina. Autosomal recessive inheritance in most breeds. 1.03% of
Recommend patella evaluation.
Borzois CERF examined by veterinary ophthalmologists between
2000-2005 are labeled suspicious for PRA.11
Miscellaneous
Congenital Malformation of the Canine Tricuspid Valve: • Breed name synonyms: Russian wolfhound, Psowaya Barsaya.
Affected Borzois have a mild right-sided heart murmer with this • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
congenital condition. It is inherited as an autosomal dominant trait ANKC (Australian National Kennel Club), NKC (National Kennel Club).
with reduced penetrance in the Labrador Retriever. OFA reports • AKC rank (year 2008): 94 (630 dogs registered)
0.8% of Borzois have heart disease through cardiac evaluation.8,13 • Internet resources: Borzoi Club of America:
www.borzoiclubofamerica.org
Dilated Cardiomyopathy: Primary disease of heart muscle causing Borzoi Canada: www.borzoicanada.ca
arrythmias and heart failure. Unknown mode of inheritance. The Borzoi Club UK: www.theborzoiclub.org.uk
Reported at an increase frequency in the breed. OFA reports 0.8% of
Borzois have heart disease through cardiac evaluation.8
References
1. Kintzer PP and Peterson ME: Progress in the Diagnosis and Treatment of
Degenerative Myelopathy (DM): Affected dogs show an insidious
Canine Hypothyroidism. 2007. Proceedings, ACVIM 2007.
onset of upper motor neuron (UMN) paraparesis. The disease
2. Court MH: Anesthesia of the sighthound. Clin Tech Small Anim Pract
eventually progresses to severe tetraparesis. Affected dogs have 1999 Feb;14(1):38-43.
normal results on myelography, MRI, and CSF analysis. Necropsy 3. Conaway DH, Padgett GA, Nachreiner RF. The familial occurrence
confirms the condition. Unknown mode of inheritance. A direct of lymphocytic thyroiditis in borzoi dogs. Am J Med Genet. 1985
genetic test for an autosomal recessive DM susceptibility gene is Oct;22(2):409-14.
available. All affected dogs are homozygous for the gene, however 4. Conaway DH, Padgett GA, Bunton TE, et al. Clinical and histological
only a small percentage of homozygous dogs develop DM. OFA features of primary progressive, familial thyroiditis in a colony of Borzoi
reports DM susceptibility gene frequencies of 25% carrier, and 2% dogs. Vet Path 1985;22: 439-446.
homozygous “at-risk”.8,18 5. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
6. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
91
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
7. Kapatkin AS, Gregor TP, Hearon K, Richardson RW, McKelvie PJ,
Fordyce HH, Smith GK. Comparison of Two Radiographic Techniques for
Evaluation of Hip Joint Laxity in 10 Breeds of Dogs. J Am Vet Med Assoc
224[4]:542-543 Feb 15’04
8. OFA Website breed statistics: www.offa.org Last accessed July. 1, 2010.
9. Olby, N. Update on Canine Wobbler Surgery. Proceedings ACVIM 2003.
10. Storey ES, Grahn BH, Alcorn J: Multifocal chorioretinal lesions in Borzoi
dogs. Vet Ophthalmol. 2005 Sep-Oct;8(5):337-47.
11. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
12. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
13. Wright, KN. New Findings in Congenital Malformation of the Canine
Tricuspid Valve. Proceedings: ACVIM 2003
14. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 204. AAHA Press, 1999.
15. Cheeseman MT, Kelly DF, Horsfall KL. Multisystemic inflammatory
disease in a borzoi dog. J Small Anim Pract. 1995 Jan;36(1):22-4.
16. Sakai H, Nakano H, Yamaguchi R, Yonemaru K, Yanai T, Masegi T.
Establishment of a new canine cell line (CCT) originated from a cutaneous
malignant histiocytosis. \J Vet Med Sci. 2003 Jun;65(6):731-5.
17. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 160-163.
18. Awano T, Johnson GS, Wade CM, et. al.: Genome-wide association
analysis reveals a SOD1 mutation in canine degenerative myelopathy that
resembles amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A. 2009 Feb
24;106(8):2794-9.
92
Boston Terrier
Recognized Behavior Issues and Traits
Boston terriers are described as being of high intelligence with a
stubborn streak, alert, very active, playful, and having a very gentle
disposition. Moderate exercise requirements, low grooming needs,
ability to get along with gentle children and other pets are hallmarks
of the breed. Will alarm bark, but they are not considered protectors.
Boston terriers are suitable for home and apartment living, and they
do not tolerate temperature extremes. They may snore and snort.
Some may be picky eaters. They are minimal shedders.
Dystocia: Boston terriers are prone to difficult birthing, due to both Atresia Ani (Imperforate Anus): An increased incidence of this
a dorsoventrally flattened pelvic canal and large fetuses with big congenital condition is reported in the breed, with a frequency of
heads.12 0.07%, and an odds ratio of 13.77x. Treatment is surgery.24
Distichiasis: Abnormally placed eyelashes that irritate the Cleft Lip and Palate: Boston terriers may have an increased
cornea and conjunctiva. Can cause secondary corneal ulceration. frequency of cleft lip and palate versus other breeds.25
Identified in 3.82% of Boston terriers CERF examined by veterinary
ophthalmologists between 2000-2005.6 Hemivertebra and Butterfly Vertebra: May cause scoliosis, pain or
spinal cord compression if severe. Unknown mode of inheritance.26
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The Perineal Hernia: Boston terriers have a predisposition to
later three forms can impair vision, and dogs affected with these developing perineal hernias. Treatment is surgery.27,28
forms should not be bred. Identified in 3.61% of Boston Terriers CERF
examined by veterinary ophthalmologists between 2000-2005.6 Uveal Cysts: Boston terriers have a higher frequency of uveal cysts
than other breeds, with a mean age of cyst development of 6.8 years.29
Glaucoma: Ocular condition causing increased pressure within
the eyeball, and secondary blindness due to damage to the Cataract Resorption-induced Uveitis: Spontaneous cataract
retina. Diagnose with tonometry and gonioscopy. Can be a resorption, and associated lens-induced uveitis primarily occurs
primary condition or secondary to cataract or lens luxation. Dorn in young Boston Terriers. Medical control of the lens-induced
reports a 2.12x odds ratio for developing glaucoma versus other uveitis by use of mydriatics and, infrequently, topical and systemic
breeds. Another report found a 4.1x odds ratio for secondary corticosteroids is essential.30
glaucoma versus other breeds. Diagnosed in 2.88% of Boston
Vascular Ring Anomaly: Reported at an increased frequency in the
terriers presented to veterinary teaching hospitals. CERF does not
breed. Causes regurgitation and megaesophagus when solid food is
recommend breeding any Boston Terrier with glaucoma.3,6,13,14,15
first fed. Correct with surgery.31
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis
Glial Tumors: Boston terriers may have a predisposition to nervous
and pyotraumatic dermatitis. Reported at an increased frequency in
tissue tumors of glial origin.32
Boston terriers.16
Anasarca, Calcinosis Circumscripta, Cerebellar Vermian
Corneal Dystrophy: Epithelial-stromal, and endothelial forms occur
Hypoplasia, Craniomandibular Osteopathy, Cryptorchidism,
in the breed. Endothelial form is associated with progressive corneal
Demodicosis, Entropion, Hydrocephalus, Keratoconjunctivitis
edema, which can lead to bullous keratopathy and corneal erosions. Age
Sicca, Mitral valve Disease, Pelger-Huet Anomaly, Progressive
of onset 6-13 years. Treatment is symptomatic and palliative. Epithelial-
Retinal Atrophy, Prolapsed Gland of Nictitans, Pyloric Stenosis,
stromal form is identified in 2.63% of Boston terriers, and endothelial
Sacrocaudal Dysgenesis, Spina Bifida, Ulcerative Keratitis, and
form in 0.21% of Boston Terriers CERF examined by veterinary
Wry Mouth are reported.33
ophthalmologists between 2000-2005. CERF does not recommend
breeding any Boston Terrier with endothelial corneal dystrophy.6,17
Isolated Case Studies
Hypothyroidism: Inherited autoimmune thyroiditis. 1.9% positive Muscular Dystrophy: Sarcoglycan-deficient muscular dystrophy
for thyroid auto-antibodies based on testing at Michigan State has been reported in several young, male and female Boston
University. (Ave. for all breeds is 7.5%).18,19 Terriers. Affected dogs present with muscle atrophy or hypertrophy,
gait abnormalities, dysphagia, and dramatically increased CK, AST,
Hyperadrenocorticism (Cushing’s Disease): Caused by a functional and ALT activities.34
adrenal or pituitary tumor. Clinical signs may include increased
thirst and urination, symmetrical truncal alopecia, and abdominal Dandy-Walker-Like Syndrome: Case report of an affected
distention. Dorn reports a 5.60x odds ratio versus other breeds.3,20,21 Boston terrier puppy. Congenital disorder causing cerebellar ataxia
and other CNS signs due to cysts arising from the 4th ventricle,
Deafness: Congenital deafness can be unilateral or bilateral. Associated dysgenesis of the cerebellar vermis, and hydrocephalus of the 3rd
with Irish pattern and piebald pigmentation. Diagnose by BAER testing. and lateral ventricles. A previous report of this syndrome in Boston
Unknown mode of inheritance.OFA reports 1.9% affected.2,22 terriers suggests the problem may be inherited in this breed.35
Vitreous Degeneration: Liquefication of the vitreous gel which Tubular Colonic Duplication: A six-month-old, intact female
may predispose to retinal detachment, glaucoma, and blindness. Boston terrier presented with clinical signs of increased frequency of
Identified in 1.22% of Boston Terriers CERF examined by veterinary defecation, tenesmus, and constipation, which had been present since
ophthalmologists between 2000-2005.6 birth. A diagnosis of tubular colonic duplication was made via contrast
radiography and colonoscopy. The condition was corrected surgically.36
Hypospadias: Almost 25% of all diagnoses of hypospadias (an
abnormal opening of the urethra) occur in Boston terriers. There is
94
Choroid Plexus Carcinoma and Meningeal Carcinomatosis: A 12. Eneroth A, Linde-Forsberg C, Uhlhorn M, et. al.: Radiographic pelvimetry
6-year-old neutered female Boston terrier had a slow onset of bilateral for assessment of dystocia in bitches: a clinical study in two terrier breeds.
visual loss. On magnetic resonance imaging (MRI) there were multiple J Small Anim Pract. 1999 Jun;40(6):257-64.
cyst-like structures found in the parenchyma of the cerebrum, 13. Gelatt KN, MacKay EO: Secondary glaucomas in the dog in North
America. Vet Ophthalmol. 2004 Jul-Aug;7(4):245-59.
cerebellum and brainstem. Histopathologically the diagnosis was a
14. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas in
choroid plexus carcinoma with meningeal carcinomatosis.37 pure-bred dogs in North America. Vet Ophthalmol. 2004 Mar-Apr;7(2):97-111.
15. Johnsen DA, Maggs DJ, Kass PH, et. al.: Evaluation of risk factors for
Neuroblastoma: A mediastinal neuroblastoma was found in a development of secondary glaucoma in dogs: 156 cases (1999-2004). J Am
15-mth-old Boston terrier with dyspnea. The tumor compressed Vet Med Assoc. 2006 Oct 15;229(8):1270-4.
adjacent lung and invaded the cervical spinal cord.38 16. Ackerman, L: Managing Inhalant Allergies I: Proceedings, 2004 Atlantic
Coast Veterinary Conference. 2004.
Genetic Tests 17. Cooley PL, Dice PF 2nd: Corneal dystrophy in the dog and cat. Vet Clin
Tests of Genotype: Direct test for early-onset hereditary cataract North Am Small Anim Pract. 1990 May;20(3):681-92.
(EHC) is available from the Animal Health Trust (UK) and VetGen. 18. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
Direct test for coat color alleles is available from VetGen. 19. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
Tests of Phenotype: CHIC Certification: Required testing includes hypothyroidism. J Am Vet Med Assoc. 2002 Feb 15;220(4):466-71.
CERF eye examination, patella examination, and BAER test for 20. McManus JL, Nimmons GB, Buchta W: Case report. Surgical and medical
deafness. See CHIC website (www.caninehealthinfo.org). management of hyperadrenocorticalism in a Boston Terrier. Can Vet J. 1970
Apr;11(4):78-80.
Recommended tests include hip and elbow radiographs, thyroid 21. Kaufman J: Diseases of the adrenal cortex of dogs and cats. Mod Vet
profile including autoantibodies, and cardiac evaluation. Pract. 1984 Jun;65(6):429-34.
22. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J 2004; Jan;167(1):23-32.
Miscellaneous 23. Hayes HM Jr, Wilson GP: Hospital incidence of hypospadias in dogs in
• Breed Name Synonyms: Boston, Boston Bulldog, Boston Bull, North America. Vet Rec. 1986 May 31;118(22):605-7.
American Bull Terrier (historical name before 1891). The American 24. Vianna ML, Tobias KM: Atresia ani in the dog: a retrospective study. J
Gentleman (nickname) Am Anim Hosp Assoc. 2005 Sep-Oct;41(5):317-22.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 25. Edmonds L, Stewart RW, Selby L: Cleft lip and palate in Boston terrier
ANKC (Australian National Kennel Club), NKC (National Kennel Club) pups. Vet Med Small Anim Clin. 1972 Nov;67(11):1219
• AKC rank (year 2008): 17 (10,930 dogs registered) 26. Done SH, Drew RA, Robins GM, et. al: Hemivertebra in the dog: clinical
• Internet resources: Boston Terrier Club of America: and pathological observations. Vet Rec. 1975 Apr 5;96(14):313-7.
27. Hosgood G, Hedlund CS, Pechman RD, et. al.: Perineal herniorrhaphy:
www.bostonterrierclubofamerica.org
perioperative data from 100 dogs. J Am Anim Hosp Assoc. 1995
Boston Terrier Club of Canada: Jul-Aug;31(4):331-42.
www.bostonterrierclubofcanada.com 28. Robertson JJ: Perineal hernia repair in dogs. Mod Vet Pract. 1984
May;65(5):365-8.
References 29. Corcoran KA, Koch SA: Uveal cysts in dogs: 28 cases (1989-1991). J Am
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by Vet Med Assoc. 1993 Aug 15;203(4):545-6.
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8. 30. Gelatt KN: Spontaneous cataract resorption and lens-induced uveitis in
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010. the dog. Mod Vet Pract. 1975 May;56(5):331-5.
3. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at 31. Fossum TW: Surgery of Cardiac Disease. Proceedings, 2009 WSAVA
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation. 2000. World Congress. 2009.
4. Adkins EA, Hendrix DV: Outcomes of dogs presented for cataract 32. Hayes HM, Priester WA Jr, Pendergrass TW: Occurrence of
evaluation: a retrospective study. J Am Anim Hosp Assoc. 2005 nervous-tissue tumors in cattle, horses, cats and dogs. Int J Cancer. 1975
Jul-Aug;41(4):235-40. Jan 15;15(1):39-47.
5. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in 33. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11. Ackerman. p. 204-05 AAHA Press, 1999.
6. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American 34. Deitz K, Morrison JA, Kline K, et. al.: Sarcoglycan-deficient muscular
College of Veterinary Ophthalmologists. ACVO, 2007 dystrophy in a Boston Terrier. J Vet Intern Med. 2008 Mar-Apr;22(2):476-80.
7. Mellersh CS, Graves KT, McLaughlin B, et. al.: Mutation in HSF4 associated 35. Noureddine C, Harder R, Olby NJ, et. al.: Ultrasonographic appearance
with early but not late-onset hereditary cataract in the Boston Terrier. J of Dandy Walker-like Syndrome in a Boston Terrier. Vet Radiol Ultrasound.
Hered. 2007;98(5):531-3. 2004 Jul-Aug;45(4):336-9.
8. LaFond E, Breur GJ and Austin CC: Breed susceptibility for 36. Shinozaki JK, Sellon RK, Tobias KM, et. al.: Tubular colonic duplication in
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002 a dog. J Am Anim Hosp Assoc. 2000 May-Jun;36(3):209-13.
Sep-Oct;38(5):467-77. 37. Lipsitz D, Levitski RE, Chauvet AE: Magnetic resonance imaging of a
9. Coyne BE, Fingland RB: Hypoplasia of the trachea in dogs: 103 cases choroid plexus carcinoma and meningeal carcinomatosis in a dog. Vet
(1974-1990). J Am Vet Med Assoc. 1992 Sep 1;201(5):768-72. Radiol Ultrasound. 1999 May-Jun;40(3):246-50.
10. Monnet M: Brachycephalic Airway Syndrome. Proceedings, 2004 World 38. Kelly DF: Neuroblastoma in the dog. J Pathol. 1975 Aug;116(4):209-12.
Small Animal Veterinary Association Congress. 2004. 39. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
11. Lorinson D, Bright RM, White RAS: Brachycephalic Airway Obstruction Book House, NY 2006. p. 533-537.
Syndrome - A Review of 118 Cases. Canine Pract 1997: 22(5/6):18-21.
95
Bouvier des Flandres
substantial in the middle, there is a slightly tucked up abdomen. The
high set tail is usually docked to leave only 2-3 vertebrae. Limbs are
straight and fairly heavily boned and well muscled, they have short
metacarpals and metatarsals. Feet are compact and the toes are
well knuckled up, nails are black and the pads are thick. Dewclaws
may be taken off.
Subaortic Stenosis (SAS): Affected dogs present with a left heart Eosinophilic Granulomatous Colitis with Ulceration: A
base murmur, aortic velocities greater than 1.5 m/second on Doppler 3-year-old Bouvier de Flandres dog was identified with hemorrhagic
echocardiography, aortic regurgitation, and mitral regurgitation. diarrhea, anorexia, weight loss and anemia. Abdominal palpation
Can cause exercise intolerance, syncope, and progress to heart revealed a palpable thickened large intestine. Histopathology
failure. Diagnose by auscultation and echocardiography. The breed revealed eosinophilic granulomatous colitis with ulceration.29
is one predisposed to subaortic stenosis. Reported at a frequency of
1.30% in the 2004 Bouvier Health Survey. Considered polygenically Primary Lymphedema and Lymphangiosarcoma: A 4-year-old,
inherited.6,14 spayed female fawn Bouvier des Flandres presented to the Ontario
Veterinary College Veterinary Teaching Hospital with a lifelong
97
history of bilateral hind limb edema, and a recently discovered in pure-bred dogs in North America. Vet Ophthalmol. 2004
inguinal mass. Based on history, clinical, and histopathological Mar-Apr;7(2):97-111.
findings, the dog was diagnosed with primary lymphedema and 14. Fuentes VL: Methods Of Screening for Subaortic Stenosis. Proceedings,
secondary lymphangiosarcoma.30 14th ECVIM-CA Congress. 2004.
15. Breton K: Death and Derm: Deadly Dermatologic Diseases. Proceedings,
2004 ACVIM Forum. 2004.
Genetic Tests 16. Sjollema BE, van Sluijs FJ: Perineal hernia in the dog: developments in
Tests of Genotype: Direct test for K allele color genes is available its treatment and retrospective study in 197 patients. Tijdschr Diergeneeskd.
from VetGen. 1991 Feb 1;116(3):142-7.
17. van der Gaag I, Happe RP: The histological appearance of peroral small
Tests of Phenotype: CHIC Certification: Required testing includes intestinal biopsies in clinically healthy dogs and dogs with chronic diarrhea.
hip and elbow radiographs, congenital cardiac evaluation, and CERF Zentralbl Veterinarmed A. 1990 Jul;37(6):401-16.
eye examination. (See CHIC website;www.caninehealthinfo.org). 18. Teske E, Naan EC, van Dijk EM, et. al.: Canine prostate carcinoma:
epidemiological evidence of an increased risk in castrated dogs. Mol Cell
Recommend thyroid profile including autoantibodies and patella Endocrinol. 2002 Nov 29;197(1-2):251-5.
evaluation. 19. Van Rensburg IBJ, Petrick S, Van der Lagt J, Smit M: Multiple inherited
eye anomalies including persistent hyperplastic tunica vasculosa lentis in
the Bouvier des Flandres. Prog Vet Comp Ophthal 1992;2:143,.
Miscellaneous 20. Peeters ME, Ubbink GJ: Dysphagia-associated muscular dystrophy:
• Breed Name Synonyms: Bouvier, Belgian Cattle Dog, and a familial trait in the bouvier des Flandres. Vet Rec. 1994 Apr
historically, toucheur de boeuf, Viulbaard, or koehond. 23;134(17):444-6.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 21. Braund KG, Steinberg HS, Mehta JR: Investigating a degenerative
ANKC (Australian National Kennel Club), NKC (National Kennel Club) polymyopathy in four related Bouvier des Flandres dogs. Vet
• AKC Rank (Year 2008): 83 (821 dogs registered) Med1990:85(6):558,562-566,568-570.
22. Poncelet L, Gilbert S, Jauniaux T, Balligand M: Swimming Puppy
• Internet resources: The American Bouvier des Flandres Club:
Syndrome in a Litter of Bouvier-Des-Flandres. Annales de
www.bouvier.org
23. Braund KG, Steinberg HS, Shores A, et. al.: Laryngeal paralysis in
Bouvier des Flandres Club of Canada: www.bouviercanada.com immature and mature dogs as one sign of a more diffuse polyneuropathy. J
Bouvier Des Flandres Club of Great Britain: Am Vet Med Assoc. 1989 Jun 15;194(12):1735-40.
www.bouvierclub.co.uk 24. O’Brien J: Spontaneous laryngeal disease in the canine. Laryngoscope.
Bouvier Health Foundation: www.bouvierhealthfoundation.org 1975 Dec;85(12 pt 1):2023-5.
25. Venker-Van Haagen AJ, Bouw J, Hartmann W: Hereditary transmission
References of laryngeal paralysis in Bouviers. Journal of the American Animal Hospital
Association 1981;17: 75-76.
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
26. Venker-van Hagen AJ: Laryngeal paralysis in Bouvier dogs and
2. LaFond E, Breur GJ and Austin CC: Breed susceptibility for
breeding advice to prevent this condition. Tijdschrift voor Diergeneeskunde
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
1981;107: 21-22.
Sep-Oct;38(5):467-77.
27. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
3. Ruhli MB, Spiess BM: Goniodysplasia in the Bouvier des Flandres.
Ackerman. p. 205. AAHA Press, 1999.
Schweiz Arch Tierheilkd. 1996;138(6):307-11.
28. House A: Atresia of the distal external acoustic meatus in a Bouvier des
4. van der Linde-Sipman JS: Dysplasia of the pectinate ligament and
Flandres. J Small Anim Pract. 2001 Feb;42(2):88-9.
primary glaucoma in the Bouvier des Flandres dog. Vet Pathol. 1987
29. van der Gaag I, van der Linde-Sipman JS:Eosinophilic granulomatous
May;24(3):201-6.
colitis with ulceration in a dog. J Comp Pathol. 1987 Mar;97(2): 179-85.
5. da Costa RC, Parent J, Poma R: Adult-Onset Distal Sensorimotor
30. Webb JA, Boston SE, Armstrong J, et.al: Lymphangiosarcoma in a
Polyneuropathy in Bouvier des Flandres Dogs. Proceedings, 2005 ACVIM
Bouvier des Flandres. J Vet Intern Med. 2004 Jan-Feb; 18(1): 122-4.
Forum. 2005.
31. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
6. The Bouvier Health Foundation, Slater M: The 2004 Bouvier Health
Book House, NY 2006. P. 640-644.
Survey. 2005.
7. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007
9. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
10. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71
11. Glickman LT, Glickman NW, Schellenberg DB, et. al.: Incidence of and
breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet
Med Assoc. 2000 Jan 1;216(1):40-5.
12. Wilkie DA: Glaucoma in the Dog I. Proceedings, Western Veterinary
Conference 2003.
13. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
98
Boxer
Recognized Behavior Issues and Traits
Boxer breed characteristics reported include: A dog with high
intelligence, independent minded, and possessing excellent strength
and stamina. He is a watchdog and a good defender and loves to
be around children. This breed is sometimes aloof with strangers,
but enjoys close human contact. They are bred for a stable
temperament and can be very playful, even boisterous. They are
considered high-energy dogs and should be given daily exercise
and play sessions to help them keep fit and mentally challenged.
Training and socialization should be consistent and start early. These
The Breed History dogs may snore and can drool. They have low grooming needs, and
are low shedders. They tolerate temperature extremes poorly. They
This breed originates from Tibetan lines of mastiff dogs; progressive
should not be off-leash because of their well developed chase and
development of the modern breed type has occurred since the 16th
fight instincts.
century, primarily in Germany. A breed club established the first
breed standard in Munich in the late 1800s. The breed is a bulldog
type, and these trace back to Molossus bloodlines. Other bloodlines Normal Physiologic Variations
bred into the boxer include terrier and perhaps English Bulldogs. Heart size, based on the vertebral heart scale is normally larger than
The boxer is thought to get his name from the way he used his other breeds.1
front paws during fights since it resembled a human boxing action.
Others feel the name is a derivative of the Germanic word boxl. The Boxer dogs may have an increased relative thickness of the LVW
year 1904 marked the first AKC registry. and IVS that is independent of aortic size, aortic velocity, or
arterial blood pressure, and this morphology should be taken into
consideration when screening Boxers by echocardiography.2
Breeding for Function
In Germany, the boxer was a top choice for police work. Before A natural bob-tail Boxer line has been developed due to the
fighting and baiting were outlawed, this breed was also used for heterozygous dominant expression of the T gene. Homozygous
these old sports. In Germany, the breed was used for hunting large dominant individuals are pre-natally lethal.3
game such as boars or bears and their powerful jaws were used
to secure the catch. They were also used in theater and circus. The
boxer was also used as a watchdog, assistance dog, and has become
Drug Sensitivities
Boxers have reportedly had severe reactions to injectable (IV or
a very popular companion and obedience dog.
IM) acepromazine, including profound hypotension, collapse,
respiratory arrest, and profound bradycardia.
Physical Characteristics
Height at Withers: female 21-23.5” (53.5-60 cm), male 22.5-25”
(57-63.5 cm).
Inherited Diseases
Boxer Cardiomyopathy (Arrhythmogenic Right Ventricular
Weight: females 55-65 lb (25-29.5 kg), males 65-80 lb (29.5-36.5 kg). Cardiomyopathy, ARVC): Autosomal dominant disorder with
Males are heavier boned. incomplete penetrance, characterized by sudden death, ventricular
premature complexes (VPCs), ventricular tachycardia, syncope,
Coat: The short glossy coat is brindle or fawn. White marking dilated cardiomyopathy, and heart failure. The primary disease
(“flash”) is allowed over up to one third of the coat. All-white pups process is ventricular arrhythmia, which is reported in over
can be born, but are not used for breeding. The mask is usually black. 30% of all Boxers. Diagnose with 24 hour Holter ECG. Greater
than 100 VPCs in 24 hours is abnormal for this breed. VPCs
Longevity: 11-13 years. are generally positive in Lead II, suggesting a right ventricular
origin. Echocardiogram is generally normal until heart failure/
Points of Conformation: This dog is a medium-built athletic cardiomyopathy develops. Treat with anti-arrhythmic drugs.
dog with well-developed musculature, and a springy stride. The One study showed that fish oils (omega 3 fatty acids) reduced
brachycephalic head is broad and the muzzle is blunt and broad. Eyes arrhythmias in affected Boxers. A direct genetic test is available
are dark brown, and the forehead wrinkles when ears are pricked. Ears showing homozygous affected dogs more severely affected than
are usually cropped and the nose is black, a distinct stop is present, heterozygotes. Genetic testing shows 41% heterozygotes and 6%
and a slight prognathism is the standard. The topline slopes slightly homozygous for the gene.4,5,6,7,8,9
down towards the back end, they have a deep thorax with a short
back and a slight tuck-up is standard. Dewclaws may be removed and Hip Dysplasia: Polygenically inherited trait causing degenerative
tails are generally docked. Feet are compact, with well-knuckled toes. joint disease and hip arthritis. OFA reports 11.1% affected.10
99
Elbow Dysplasia: Polygenically inherited trait causing elbow developing cutaneous mast cell tumors. Mast cell tumors produce
arthritis. One study found Boxers to be one of the most commonly histamine, and can cause inflammation and ulceration. These are
affected breeds with the fragmented medial coronoid process form typically more benign in Boxers, but they are at higher risk to develop
of elbow dysplasia. OFA reports 0.7% affected.10,11,12 additional MCTs at distant sites (outside the surgical margins).31,32
Patella Luxation: Polygenically inherited laxity of patellar Histiocytic Ulcerative Colitis (Boxer Colitis): Inflammatory bowel
ligaments, causing luxation, lameness, and later degenerative joint disease (IBD) that occurs predominantly in Boxers. The lesions are
disease. Treat surgically if causing clinical signs. Too few Boxers characterized by mucosal ulceration and a mixed inflammatory
have been screened by OFA to determine an accurate frequency.10 cell infiltrate. Treatment is with medication and diet. Enrofloxacin
therapy against intramucosal E. coli improves clinical signs in some
Progressive Axonopathy (Boxer Axonopathy): Rare, autosomal cases, reflecting an infectious role in the pathogenesis. Some severe
recessive disorder presenting with a slowly progressive weakness cases cannot be controlled. Unknown mode of inheritance.33,34,35,36
and incoordination of the hind limbs. Age of onset 2-3 months.
Progresses to all four limbs, eventually causing severe paresis and Gingival Hypertrophy: Older Boxers can develop a proliferative
ataxia. No genetic test is available.13 gingival hypertrophy affecting all gum surfaces. Treat with
gingivectomy.37
Disease Predispositions
Dystocia (Difficult Whelpings): Dystocia presents more commonly Atopic Dermatitis/Inhalant Allergies: Presents with pruritis,
in Boxers than other breeds. In a Swedish study, 27.7% of whelpings pyotraumatic dermatitis (hot spots), and often hives. Reported at an
developed dystocia, with the majority requiring caesarian section. increased frequency in the breed versus other breeds. White Boxers
The most common reasons for dystocia were primary uterine have a higher risk.38
inertia (60%) and malpresentation of the fetus (26%).14
Cranial Cruciate Ligament Rupture (ACL): Traumatic tearing
Hypothyroidism: Inherited autoimmune thyroiditis. 18.0% positive of the anterior cruciate ligament. The breed is found to have an
for thyroid auto-antibodies based on testing at Michigan State increased incidence versus other breeds. Treatment is surgery.
University. (Ave. for all breeds is 7.5%).15,16 Found to be moderately (28%) heritable, with a frequency of 5.7%
in the breed in a Danish study.25,27
Distichiasis: Abnormally placed eyelashes that irritate the cornea
and conjunctiva. Can cause secondary corneal ulceration. Identified Stifle Osteochondritis Dessicans (OCD): Polygenically inherited
in 12.90% of Boxers CERF examined by veterinary ophthalmologists cartilage defect. Causes stifle joint pain and lameness in young
between 2000-2005. Because the condition causes significant corneal growing dogs. Mild cases can resolve with rest, while more severe
disease in the Boxer, CERF discourages breeding affected dogs.17 cases require surgery. Reported 56.3x odds ratio versus other breeds.12
Aortic Stenosis (Subaortic Stenosis, SAS): Affected dogs present Ectropion: Rolling out of eyelids, often with a medial canthal
with a left heart base murmur, and aortic velocities greater than pocket. Can also cause conjunctivitis. Dorn reports a 7.97X odds
1.5 m/second on Doppler echocardiography, aortic regurgitation, ratio in Boxers versus other breeds. Ectropion is reported in 4.52%
and mitral regurgitation. Can cause exercise intolerance, syncope, of Boxers CERF-examined by veterinary ophthalmologists between
and progress to heart failure. Occurring in 10% of Boxers screened 2000-2005.17
in one study. Identified in 8.50% of screened Boxers in Italy.
Pulmonic Stenosis (PS): Congenital cardiac disorder of restricted
Reported at a frequency of 8.1% in Switzerland. Odds ratio of 8.6x
pulmonic outflow. Echocardiogram findings of restriction of right
versus other breeds. Unknown mode of inheritance – considered
ventricular outflow tract, pulmonic valve and/or main pulmonary
polygenic.18,19,20,21,22,23,24
artery on transthoracic imaging from the right parasternal and left
Cryptorchidism (Retained Testicles): Can be unilateral or bilateral. cranial parasternal short-axis views. Identified in 3.12% of screened
Boxers have an increased prevalence of the disorder. Found to be Boxers in Italy. Reported at a frequency of 3.3% in Switzerland.
moderately (24%) heritable in the breed in a Danish study. Identified Unknown mode of inheritance.20,21,23,24
in 9.8% of male pups in a Swedish study. Reported at a frequency
Cataracts: Anterior cortex intermediate and nuclear punctate
of 10.7% with a heritability of 0.24 in a Dutch study.14,25,26,27
cataracts predominate in the breed. Identified in 2.71% of Boxers
Persistent Corneal Erosion/Corneal Dystrophy (Ulcerative CERF examined by veterinary ophthalmologists between 2000-2005.
Keratitis, Indolent Ulcer, Boxer Ulcer): Inherited breed prevalence. CERF does not recommend breeding any Boxer with a cataract.17
Treat with topical medications, keratectomy, flap +/- contact
Epilepsy: Inherited seizures. Can be generalized or partial. Treat
lens. Reported in 9.05% of Boxers CERF examined by veterinary
with anticonvulsants. Dorn reports a 7.17x odds ratio in Boxers
ophthalmologists between 2000-2005.17,28,29
versus other breeds. Found to be moderately (36%) heritable in a
Cancer/Neoplasia: A Danish study shows a higher standard Danish study, with a frequency of 2.4%.25,27,39
morbidity rate (SMR) for both malignant and benign cancers in
Chronic Pancreatitis: Often subclinical inflammation of the
Boxers versus other breeds.30
pancreas that can cause intermittent discomfort and gastrointes-
Mast Cell Tumor (MCT): Boxers are a predisposed breed for tinal upsets. Can possibly lead to pancreatic insufficiency or diabetes
mellitus. Boxers have a 3.0x relative risk versus other breeds.40
100
Demodicosis: Dorn reports a 2.66x odds ratio of developing Oral Cancer: One study found that Boxers were a breed with a
demodectic mange versus other breeds. This disorder has an significantly higher risk of developing oral and pharyngeal tumors,
underlying immunodeficiency in its pathogenesis. One study shows as compared with all breeds combined.58
that a DLA haplotype imparts a 5x odds ratio for the disorder.39,41
Intracranial Meningioma: One study found that Boxers are
Follicular Dysplasia: Alopecia primarily to the flank region, overrepresented compared to other breeds for intracranial
beginning at 2-4 years of age. Melatonin may help alleviate clinical meningiomas. These are the most common brain tumor in dogs, and
signs. Unknown mode of inheritance.42 can be benign, or malignant.59
Osteosarcoma (Bone Cancer): Boxers have an increased incidence Juvenile Necrotizing Vasculitis/Sterile Meningitis: Affected
of developing malignant osteosarcoma versus other breeds. Occurs Boxers are all under 2 years of age, presenting with apathy, fever,
primarily in the extremities.43 delayed proprioception, ataxia, and increased head and cervical
pain. Histopathology shows necrotizing vasculitis in the CNS, with
Inflammatory Myopathies: Boxers are a breed at increased risk perivascular granulomatous inflammation. 40% of all dogs with
of developing inflammatory myopathies, including polymyositis, this diagnosis are Boxers. Treat with steroids. Unknown mode of
masticatory muscle myositis, dermatomyositis-like myopathy, and inheritance.60
extraocular myositis. A high proportion of affected Boxers have
muscle-specific circulating autoantibodies against sarcolemma Calcinosis Circumspecta, Central PRA, Cervical Vertebral
antigens. A serum antigen assay can be used as a diagnostic test.44,45 Instability, Cutaneous Asthenia, Cystinuria, Deafness, Dermoid
Sinus, Elongated Soft Palate, Factor II Deficiency, Factor
Seasonal Flank Alopecia: Bilateral, symmetrical alopecia affecting VII Deficiency, Gastric Dilatation-Volvulus, Hyperadreno-
the flank, dorsum and tail. Affects primarily spayed females in the corticism, Hypoplastic Trachea, Lupoid Onychopathy,
Spring or Autumn. Mean age of onset is 3.6 years.46 Nodular Dermatofibrosis, Polydontia, Progressive Retinal
Atrophy, Prolapsed Gland of Nictitans, Pyloric Stenosis,
Spondylosis Deformans: A study of spondylosis deformans and Sphingomyelinosis, Spina Bifida, Supernumerary Teeth,
osteophyte development in Boxers showed that it is a heritable Tricuspid Valve Dysplasia, and von Willebrand’s Disease are
condition, especially at specific vertebral sites. Spondylosis reported.61
deformans does not usually cause spinal problems for the dog.47
Atrial Septal Defect (ASD): Congenital cardiac disorder of the Isolated Case Studies
wall between the left and right atria. Causes a left heart base Neuroblastoma: A 2 year old Boxer presenting renal disease
systolic murmur that must be differentiated from subaortic stenosis and a palpable abdominal mass was diagnosed with a peripheral
by echocardiography. Affected dogs show exercise intolerance, neuroblastoma.62
syncope, dyspnea, and/or a cough. Reported at a frequency
of 0.16% in a Swedish study, but identified at a much higher Polyglandular Syndrome: An 8-year-old spayed female boxer dog,
frequency in a French study.2,48 presented because of progressive symmetrical truncal alopecia,
lethargy, and intolerance to cold. Pathological findings were
Degenerative Myelopathy: Degenerative condition of the spinal immune thyroiditis and lymphocytic adrenalitis.63
cord in older Boxers presenting with progressive weakness and
incoordination of the hind limbs. No treatments have been found Type C Niemann-Pick Disease (Lipid Storage Disease):
to be effective. Unknown mode of inheritance. A direct genetic A 9-month-old boxer dog was presented with progressive
test for an autosomal recessive DM susceptibility gene is available. neurological deterioration. The brain showed increased levels of
All affected dogs are homozygous for the gene, however, only a lactosylceramide and two gangliosides, GM3 and GM2.64
small percentage of homozygous dogs develop DM. OFA reports
Neuronal Vacuolation: Two 6-month-old Boxer littermates
DM susceptibility gene frequencies of 38% carrier and 45%
presented with progressive pelvic limb paresis and ataxia, upper
homozygous “at risk”.10,49,50,51
airway stridor, and visual deficits. Pathology revealed neuronal
Cleft Lip/Palate: Congenital disorder of facial formation. Found vacuolation and spinocerebellar degeneration, analogous to the
to be moderately (27%) heritable, with a frequency of 2.3% in the syndrome reported in Rottweilers.65
breed in a Danish study.25,27
Genetic Tests
Juvenile Nephropathy: Rare disorder in young Boxers presenting Tests of Genotype: Direct test for ARVC is available from North
with severe polyuria and polydipsia, and progressing to chronic Carolina State University - Meurs Lab.
renal failure. Histopathology includes immature glomeruli and/or
tubules, and persistent mesenchyme. A reflux nephropathy may be A direct genetic test for an autosomal recessive DM susceptibility
involved in the disease process.52,53,54,55 gene is available from the OFA.
T-Cell Lymphoma (Mycosis Fungoides): Boxers have an increased Direct test for coat color alleles is available from VetGen.
incidence of developing this more malignant form of cutaneous
lymphoma versus other breeds.56,57 Tests of Phenotype: Recommend hip and elbow radiographs,
CERF eye examination, cardiac evaluation (echocardiogram +/- 24
101
hour Holter ECG), patella evaluation, and thyroid profile including with aortic stenosis among boxer dogs in Norway and Sweden. Vet Rec.
autoantibodies. 2000 Aug 5;147(6):152-6.
20. Vollmar AC, Fox PR: Assessment of Cardiovascular Disease in 527 Boxers.
Proceedings, 2005 ACVIM Forum. 2005.
Miscellaneous 21. Bussadori C, Pradelli D, Borgarelli M, et. al.: Congenital heart
• Breed name synonyms: Bullenbeisser (historical) disease in boxer dogs: Results of 6years of breed screening Vet J. 2009
• Registries: CKC, AKC, UKC, KCGB (Kennel Club of Great Britain), Aug;181(2):187-92.
ANKC(Australian National Kennel Club), NKC (National Kennel Club. 22. Kienle RD, Thomas WP & Pion PD: The natural clinical history of canine
• AKC rank (year 2008): 6 (29,705 dogs registered) congenital subaortic stenosis. J Vet Intern Med. 1994 Nov-Dec;8(6):423-31.
• Internet resources: The American Boxer Club: 23. Jenni S, Gardelle O, Zini E, et. al.: Use of auscultation and Doppler
http://americanboxerclub.org echocardiography in Boxer puppies to predict development of subaortic or
Boxer Club of Canada: http://boxerclubofcanada.com pulmonary stenosis. J Vet Intern Med. 2009 Jan-Feb;23(1):81-6.
24. Höpfner R, Glaus T, Gardelle O, et. al.: Prevalence of heart murmurs,
The British Boxer Club: www.thebritishboxerclub.co.uk
aortic and pulmonic stenosis in boxers presented for pre-breeding exams in
Switzerland. Schweiz Arch Tierheilkd. 2010 Jul;152(7):319-24.
References 25. Nielen AL, Knol BW, van Hagen MA, et. al.: Genetic and epidemiological
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the vertebral heart scale as an aid to the radiographic diagnosis of cardiac 1;128(19):586-90.
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2. Cunningham SM, Rush JE, Freeman LM, et. al.: Echocardiographic ratio dogs and cats. Vet Rec. 2003 Apr 19;152(16):502-4.
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3. Haworth K, Putt W, Cattanach B, et. al.: Canine homolog of the T-box problems in boxer dogs. Prev Vet Med. 2004 Apr 30;63(1-2):39-50.
transcription factor T; failure of the protein to bind to its DNA target leads 28. Chavkin MJ, Riis RC, Scherlie PH: Management of a persistent corneal
to a short-tail phenotype. Mamm Genome. 2001 Mar;12(3):212-8. erosion in a boxer dog. Cornell Vet. 1990 Oct;80(4):347-56.
4. Meurs KM: Boxer dog cardiomyopathy: an update. Vet Clin North Am 29. Cooley PL, Dice PF 2nd: Corneal dystrophy in the dog and cat. Vet Clin
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5. Spier AW, Meurs KM: Assessment of heart rate variability in Boxers with 30. Brønden LB, Nielsen SS, Toft N, et. al.: Data from the Danish veterinary
arrhythmogenic right ventricular cardiomyopathy. J Am Vet Med Assoc. 2004 cancer registry on the occurrence and distribution of neoplasms in dogs in
Feb 15;224(4):534-7. Denmark. Vet Rec. 2010 May 8;166(19):586-90.
6. Smith CE, Freeman LM, Rush JE, et. al.: Omega-3 fatty acids in Boxer dogs 31. Kiupel M, Webster JD, Miller RA, et. al.: Impact of tumour depth, tumour
with arrhythmogenic right ventricular cardiomyopathy. J Vet Intern Med. location and multiple synchronous masses on the prognosis of canine
2007 Mar-Apr;21(2):265-73. cutaneous mast cell tumours. J Vet Med A Physiol Pathol Clin Med. 2005
7. Meurs KM, Spier AW, Miller MW, et. al.: Familial ventricular arrhythmias in Aug;52(6):280-6.
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8. Meurs KM, Spier AW, Wright NA, et. al.: Comparison of in-hospital versus 2004 Dec;26(4):156-69.
24-hour ambulatory electrocardiography for detection of ventricular 33. German AJ, Hall EJ, Kelly DF, et. al.: An immunohistochemical study
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9. Meurs KM, Mauceli E, Acland G, et. al.: Genome-Wide Association 34. Churcher RK, Watson AD: Canine histiocytic ulcerative colitis. Aust Vet J.
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in the Boxer Dog. Proceedings, 2009 ACVIM Conference. 2009. 35. Hostutler RA, Luria BJ, Johnson SE, et. al.: Antibiotic-responsive
10. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010. histiocytic ulcerative colitis in 9 dogs. J Vet Intern Med. 2004
11. Meyer-Lindenberg A, Langhann A, Fehr M, et. al.: Prevalence of Jul-Aug;18(4):499-504.
fragmented medial coronoid process of the ulna in lame adult dogs. Vet Rec. 36. Mansfield CS, James FE, Craven M, et. al.: Remission of histiocytic
2002 Aug 24;151(8):230-4. ulcerative colitis in Boxer dogs correlates with eradication of invasive
12. LaFond E, Breur GJ & Austin CC: Breed susceptibility for intramucosal Escherichia coli. J Vet Intern Med. 2009 Sep-Oct;23(5):964-9.
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Acta Vet Scand. 2007 Mar 21;49:8. veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
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Vet Med Assoc 2002 Feb 15;220(4):466-71. of chronic pancreatitis at post-mortem examination in first-opinion dogs. J
16. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for Small Anim Pract. 2007 Nov;48(11):609-18.
Population and Animal Health, Michigan State University. April, 2007. 41. It V, Barrientos L, López Gappa J, et. al.: Association of canine juvenile
17. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American generalized demodicosis with the dog leukocyte antigen system. Tissue
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18. French A, Luis Fuentes V, Dukes-McEwan J, et. al.: Progression of aortic 42. Rachid MA, Demaula CD, Scott DW, et. al.: Concurrent follicular
stenosis in the boxer. J Small Anim Pract. 2000 Oct;41(10):451-6. dysplasia and interface dermatitis in Boxer dogs. Vet Dermatol. 2003
19. Heiene R, Indrebo A, Kvart C, et. al.: Prevalence of murmurs consistent Jun;14(3):159-66.
102
43. Misdorp W, Hart AA: Some prognostic and epidemiologic factors in
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44. Evans J, Levesque D, Shelton GD: Canine Inflammatory Myopathies: A
Review of 200 Cases. Proceedings, 2003 ACVIM Forum. 2003.
45. Hankel S, Shelton GD, Engvall E, et. al.: Sarcolemma-specific
autoantibodies in canine inflammatory myopathy. Vet Immunol
Immunopathol. 2006 Sep 15;113(1-2):1-10.
46. Miller MA, Dunstan RW: Seasonal flank alopecia in boxers and
Airedale terriers: 24 cases (1985-1992). J Am Vet Med Assoc. 1993 Dec
1;203(11):1567-72.
47. Carnier P, Gallo L, Sturaro E, et. al: Prevalence of spondylosis deformans
and estimates of genetic parameters for the degree of osteophytes
development in Italian Boxer dogs. J Anim Sci. 2004 Jan;82(1):85-92.
48. Chetbuul V, Trolle JM, Nicolle A, et. al,:Congenital heart diseases in the
boxer dog: A retrospective study of 105 cases (1998-2005). J Vet Med A
Physiol Pathol Clin Med. 2006 Sept; 53(7): 346-51.
49. Olby NJ: Decreased Mobility in Old Dogs: Causes and Treatment.
Proceedings, 2004 ACVIM Forum. 2004.
50. Miller AD, Barber R, Porter BF, et. al.: Degenerative myelopathy in two
Boxer dogs. Vet Pathol. 2009 Jul;46(4):684-7.
51. Awano T, Johnson GS, Wade CM, et. al.: Genome-wide association
analysis reveals a SOD1 mutation in canine degenerative myelopathy that
resembles amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A. 2009 Feb
24;106(8):2794-9.
52. Peeters D, Clercx C, Michiels L, et. al.: Juvenile nephropathy in a boxer, a
rottweiler, a collie and an Irish wolfhound. Aust Vet J. 2000 Mar;78(3):162-5.
53. Hoppe A, Karlstam E: Renal dysplasia in boxers and Finnish harriers. J
Small Anim Pract. 2000 Sep;41(9):422-6.
54. Kolbjornsen O, Heggelund M, Jansen JH, et. al,: End-stage kidney disease
probably due to reflux nephropathy with segmental hypoplasia (Ask-Upmark
kidney) in young boxer dogs in Norway.A retrospective study. Vet Pathol.
2008 Jul;45(4)::467-74.
55. Chandler ML, Elwood C, Murphy KF, et. al.: Juvenile nephropathy in 37
boxer dogs. J Small Anim Pract. 2007 Dec;48(12):690-4.
56. Lurie DM, Lucroy MD, Griffey SM: T-Cell-Derived Malignant Lymphoma
in the Boxer Breed. Vet Comp Oncol 2004: 2[3]:171-175.
57. Pastor M, Chalvet-Monfray K, Marchal T, et. al.: Genetic and
environmental risk indicators in canine non-Hodgkin’s lymphomas: breed
associations and geographic distribution of 608 cases diagnosed throughout
France over 1 year. J Vet Intern Med. 2009 Mar-Apr;23(2):301-10.
58. Dorn CR, Priester WA: Epidemiologic analysis of oral and pharyngeal
cancer in dogs, cats, horses, and cattle. J Am Vet Med Assoc. 1976 Dec
1;169(11):1202-6.
59. Sturges BK, Dickinson PJ, Bollen AW, et. al.: Magnetic resonance imaging
and histological classification of intracranial meningiomas in 112 dogs. J Vet
Intern Med. 2008 May-Jun;22(3):586-95
60. Behr S & Cauzinille L: Aseptic suppurative meningitis in juvenile
boxer dogs: retrospective study of 12 cases. J Am Anim Hosp Assoc. 2006
Jul-Aug;42(4):277-82.
61. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p 205, AAHA Press, 1999.
62. Forrest LJ,, Galbreath EJ, Dubielzig RR,et. Al,:Peripheral neuroblastoma in
a dog. Vet Radiol Ultrasound. 1997 Nov-Dec;38(6):457-60.
63. Kooistra HS, Rijnberk A, van den Ingh TS, et. al.: Polyglandular deficiency
syndrome in a boxer dog: thyroid hormone and glucocorticoid deficiency.
Vet Q. 1995 Jun;17(2):59-63.
64. Kuwamura M, Awakura T, Shimada A, et. al.: Type C Niemann-Pick
disease in a boxer dog. Acta Neuropathol (Berl). 1993;85(3):345-8.
65. Geiger DA, Miller AD, Cutter-Schatzberg K, et. al.: Encephalomyelopathy
and polyneuropathy associated with neuronal vacuolation in two Boxer
littermates. Vet Pathol. 2009 Nov;46(6):1160-5.
66. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 248-253.
103
Boykin Spaniel
strong driving power. As speed increases it is natural for the legs to
fall to a center line of travel.
Genetic Tests
Tests of Genotype: Direct test for exercise induced collapse (EIC) is
available from the University of Minnesota Veterinary Diagnostic Lab.
Miscellaneous
• Breed name synonyms: Boykin
• Registries: AKC, UKC, CKC, FCI, NKC (National Kennel Club)
• AKC rank (none): AKC Recognized in December, 2009. Entire
stud book entered.
• Internet resources: Boykin Spaniel Club and Breeders
Association of America: www.boykinspanielclub.org
Boykin Spaniel Society: www.boykinspaniel.org
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Tsai KL & Murphy KE: Clinical and genetic assessments of hip joint laxity
in the Boykin spaniel. Can J Vet Res. 2006 Apr;70(2):148-50.
3. Minor KM, Patterson EE, Gross SD, et. al.: Frequency of the Canine
105
Briard
their guarding and watchdog talents, they are considered a gentle
dog. They require lots of exercise.
Drug Sensitivities
The Breed History None reported
The first written records of this breed originated in the 12th century
in France. Napoleon and Charlemagne are reported to have kept Inherited Diseases
Briards. The first breed standard was laid out in 1897. Often referred Hip Dysplasia: Polygenically inherited trait causing degenerative
to as a “heart wrapped in fur”, both the Marquis de Lafayette and joint disease and hip arthritis. OFA reports 14.5% affected. Reported
Thomas Jefferson are credited with bringing the breed to America, at a frequency of 19.4% in France. Reported at a frequency of
and first AKC registrations occurred in 1922. UKC registration 14.14% in the BCA Health Survey.3,4,5
occurred in 1948.
Congenital Stationary Night Blindness/Retinal dysplasia (CSNB,
Breeding for Function RPE65 Mutation): Autosomal recessive disorder causing night
They were originally used to defend home and farm, but later they blindness and varying degrees of day blindness from birth. A
became widely used as sheep herding dogs. They have also been mutation test is available from Optigen, that reports 1% affected,
used for tracking and hunting, and have served in times of war. and 10% carrier in the breed. CERF does not recommend breeding
any Briard affected with CSNB.6,7,8,9
Physical Characteristics Central Progressive Retinal Atrophy (CPRA): Autosomal recessive
Height at Withers: female 22-25.5” (56-65 cm), male 23 to 27” disease of slowly progressive retinal degeneration, caused by a
(58.5-68.5 cm). defect in Vitamin E metabolism. Used to be seen in high numbers
of Briards, especially in Europe when on Vitamin E poor diets.
Weight: females 50-80 lb. (22.5-36.5 kg), males 60-100 lb. Now seen infrequently as diets have improved. CERF does not
(27.5-45.5 kg). recommend breeding any Briard with RPED/CPRA.9,10
Coat: The long (6”) wavy double coat is solid colored. All colors Elbow Dysplasia: Polygenically inherited trait causing elbow
are accepted except white. Black, gray and shades of tawny are arthritis. OFA reports 0.2% affected.3
common. The coat requires frequent grooming; they are moderate
shedders. Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Longevity: 10-12 years. disease. Treat surgically if causing clinical signs. Too few Briards
have been screened by OFA to determine an accurate frequency.3
Points of Conformation: The Briard is a large solidly built powerful
dog, with distinctive eyebrows and beard. Their ears are high set
and pendulous. Each rear limb carries double dewclaws. The tail has Disease Predispositions
a distinctive tip called a crochet, which is a small hook. The tail is Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting
carried low and reaches to the tarsus. Eyes are black or brown with of the stomach within the abdomen. Requires immediate veterinary
dark palpebral margins; lips and nose are pigmented black. Topline is attention. Reported at a frequency of 11.69% in the BCA Health
slightly inclined down towards the croup. They have a deep thorax. Survey.4
Miscellaneous
• Breed name synonyms: Chien Berger de Brie, Chien d’Aubry
(historical).
• Registries: CKC, AKC, UKC, KCGB (Kennel Club of Great Britain),
ANKC(Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank in year 2008: 123 (237 dogs registered)
107
Brittany
over its length towards the rear. They possess a deep thorax with
well-sprung ribs, and rib cage stays deep well back. They have a
slight abdominal tuck up. Dewclaws may be taken off. Feet are
intermediate in size and shape, and limbs are straight. Gait is
smooth, low and elastic, with minimal apparent effort.
109
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Cork LC, Price DL, Griffin JW, et. al.: Hereditary canine spinal muscular
atrophy: canine motor neuron disease. Can J Vet Res. 1990 Jan;54(1):77-82.
3. Sack GH Jr, Cork LC, Morris JM, et. al.: Autosomal dominant inheritance
of hereditary canine spinal muscular atrophy. Ann Neurol. 1984 Apr;
15(4):369-73.
4. Richtsmeier JT, Sack GH Jr, Grausz HM, et. al.: Cleft palate with autosomal
recessive transmission in Brittany spaniels. Cleft palate with Craniofacial J.
1994 Sep; 31(5):364-71.
5. Johnson JP, McLean RH, Cork LC, et. al.: Genetic analysis of an inherited
deficiency of the third component of complement in Brittany spaniel dogs.
Am J Med Genet. 1986 Nov;25(3):557-62.
6. Cork LC, Morris JM, Olson JL, et. al.: Membranoproliferative Glomerulone-
phritis in Dogs with a Genetically Determined Deficiency of the Third
Component of Complement. Clinical Immunology and Immunopathology
1991;60: 455-470.
7. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
8. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
9. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
10. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
11. Saridomichelakis MN, Farmaki R, Leontides LS, et. al.: Aetiology of
canine otitis externa: a retrospective study of 100 cases. Vet Dermatol. 2007
Oct;18(5):341-7.
12. Patterson EN: Clinical Characteristics and Inheritance of Idiopathic
Epilepsy.Proceedings, Tufts’ Canine and Feline Breeding and Genetics
Conference. 2007.
13. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing
lens luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
14. Marcellin-Little DJ, DeYoung DJ, Ferris KK, et. al.: Incomplete ossification
of the humeral condyle in spaniels. Vet Surg. 1994 Nov-Dec;23(6):475-87.
15. Scott DW: Cutaneous Lupus Erythematosus 2008: Presentation &
Management. Proceedings, 2008 ACVIM Forum. 2008.
16. Higgins RJ, LeCouteur RA, Kornegay JN , et. al.: Late-onset progressive
spinocerebellar degeneration in Brittany Spaniel dogs. Acta Neuropathol
(Berl). 1998 Jul;96(1):97-101.
17. Tatalick LM, Marks SL, Baszler TV: Cerebellar abiotrophy characterized by
granular cell loss in a Brittany. Veterinary Pathology 1993;30(4):385-8.
18. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 206. AAHA Press, 1999.
19. Olsen D, Harkin KR, Banwell MN, et. al.: Postoperative rupture of an
aortic aneurysmal dilation associated with a patent ductus arteriosus in a
dog. Vet Surg. 2002 May-Jun;31(3):259-65.
20. Eyster GE, Dalley JB, Chaffee A, et. al.: Aorticopulmonary septal defect in
a dog. J Am Vet Med Assoc. 1975 Dec 15;167(12):1094-6.
21. Larcher T, Abadie J, Roux FA, et. al.: Persistent left cranial vena cava
causing oesophageal obstruction and consequent megaoesophagus in a
dog. J Comp Pathol. 2006 Aug-Oct;135(2-3):150-2.
22. Anderson DM, White RA: Nasal dermoid sinus cysts in the dog. Vet Surg.
2002 Jul-Aug;31(4):303-8.
23. Beningo KE, Scott DW: Idiopathic linear pustular acantholytic
dermatosis in a young Brittany Spaniel dog. Vet Dermatol. 2001
Aug;12(4):209-13.
24. English RV, Breitschwerdt EB, Grindem CB, et. al.: Zollinger-Ellison
syndrome and myelofibrosis in a dog. J Am Vet Med Assoc. 1988 May
15;192(10):1430-4.
25. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 15-19.
110
Brussels Griffon
Recognized Behavior Issues and Traits
Reported breed characteristics include: Requires early leash and
obedience training. The Brussels Griffon has a plucky but sensitive
nature and is somewhat shy with strangers. The wire coats need
hand stripping but on a maintenance basis, these dogs have
average grooming needs. This breed is considered to be a bit
slower to housetrain than some other breeds. Intelligent but easily
bored, they respond best to positive reinforcement and a patient
approach. Good alarm barkers; high barking tendency. Some do
not recommend these dogs for those with children under 5 years
The Breed History of age; they can be quite assertive. Brussels Griffon dogs have low
to moderate exercise requirements. These little dogs are fearless if
Arising from Afffenpinscher and Belgian street dogs (chiens barbus),
threatened. They require close human contact.
the Brussels Griffon is packed with personality plus. Later on in the
breed development, first Pug then Ruby Spaniel crosses occurred.
It was likely from the Pug crosses that the smooth coated variety Normal Physiologic Variations
arose. Some also place Yorkshire terriers and French Barbet in the Cesarean Section: According to a British study, 39% of Brussels
breed development tree. Some confusion exists regarding Belgian Griffon litters are delivered via C-section.1
vs. Brussels Griffons as they are classified differently in Belgium
than elsewhere. The AKC first registered the breed in 1910. Drug Sensitivities
None reported
Breeding for Function
Bred early on for ratting, the recent focus of breeders was for a Inherited Diseases
companion dog. Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Physical Characteristics disease. Treat surgically if causing clinical signs. Reported in 7.0%
Height at Withers: 7-8” (18-20 cm). of dogs in the 2004 ABGA Health Survey. Average age of onset 2.3
years. OFA reports a high incidence, but too few Brussels Griffon
Weight: 8-10 lb (3.5-4.5 kg). have been screened to determine an accurate frequency.2,3
Coat: There are two distinct coats—Wirehaired and Smooth-coated Hip Dysplasia and Legg-Calve-Perthes Disease: Polygenically
(Brabancon) types. The rough coat is about 3-4” (7.5-10 cm) inherited traits causing degenerative joint disease and hip arthritis.
in length, dense, with emphasis on maximum wire texture. The OFA reports a high incidence, but too few Brussels Griffon have
Brabancon coat is smooth, short and glossy. Colors include black been screened to determine accurate frequencies.2
and tan, black, belge (a mix of black and ruddy brown) with black
whiskers and mask, and red. Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. OFA reports a high incidence, but too few Brussels Griffon
Longevity: 13-14 years have been screened to determine an accurate frequency.2
Syringomyelia (SM): Syringomyelia is a condition where fluid Hypothyroidism: Inherited autoimmune thyroiditis. 1.7% positive
filled cavities develop within the spinal cord. The majority of for thyroid auto-antibodies based on testing at Michigan State
affected dogs do not show clinical signs. Clinical signs of SM can University. (Ave. for all breeds is 7.5%).8,9
present usually between 5 months and 3 years of age, and include
persistent scratching at the shoulder region with apparent neck, Progressive Retinal Atrophy (PRA): Inherited degeneration of the
thoracic limb, or ear pain and thoracic limb lower motor neuron retina progressing to blindness. Autosomal recessive inheritance in
deficits. Diagnosis is by MRI. In a study skewed toward affected most breeds. Identified in 1.41% of Brussels Griffon CERF examined
families, SM was diagnosed in 37.5% of Brussels Griffon, with by veterinary ophthalmologists between 2000-2005. CERF does not
5.8% showing clinical signs. Chiari-like malformation (CM) is a recommend breeding any Brussels Griffon with PRA.4
predisposing factor for SM (61.7% with CM had SM, though 22.7%
of dogs without CM had SM in this study).6 Corneal Dystrophy: Brussels Griffon can have an epithelial/
stromal form of corneal dystrophy. Identified in 1.41% of Brussels
Vitreous Degeneration: Liquefaction of the vitreous gel which may Griffon CERF examined by veterinary ophthalmologists between
predispose to retinal detachment occurs in the breed. Identified 2000-2005.4
in 14.49% of Brussels Griffon CERF examined by veterinary
ophthalmologists between 2000-2005.4 Optic Nerve Coloboma: A congenital cavity in the optic nerve
which, if large, may cause blindness or vision impairment.
Persistent Pupillary Membranes: Strands of fetal remnant Identified in 0.71% of Brussels Griffon CERF examined by veterinary
connecting; iris to iris, cornea, lens, or involving sheets of tissue. ophthalmologists between 2000-2005. CERF does not recommend
The later three forms can impair vision, and dogs affected with breeding any Brussels Griffon with a coloboma.4
these forms should not be bred. Identified in 5.65% of Brussels
Cleft Lip, Retained Primary Teeth, and Ulcerative Keratitis are
Griffon CERF examined by veterinary ophthalmologists between
reported.10
2000-2005.4
Cleft Palate: Congenital disorder of midline closure of palate. Isolated Case Studies
Reported in 5% of puppies born in the 2003 ABGA Puppy Mortality Sry-negative XX Sex Reversal (Hermaphrodism): A Brussels
Survey.7 Griffon is documented with this autosomal recessive disorder,
where outwardly male dogs are chromosomal females (XX), and
Allergic Dermatitis: Presents with pruritis and pyotraumatic there is an absence of “male” causing SRY.11
dermatitis (hot spots). Reported in 3.9% of dogs in the 2004 ABGA
Health Survey. Average age of onset 3.6 years.3
Genetic Tests
Epilepsy: Inherited seizures. Can be generalized or partial. Seizures Tests of Genotype: Direct test for rough or smooth coat is
are reported in 2.9% of dogs in the 2004 ABGA Health Survey. The available from VetGen.
cause of the seizures was not defined.3
Tests of Phenotype: CHIC Certification: Required testing includes
Cryptorchidism: Unilateral or bilateral undescended testicles. CERF eye examination and patella evaluation (after age 2). Optional
Reported in 2.8% of dogs in the 2004 ABGA Health Survey. This is a recommended testing includes hip radiographs, thyroid profile
sex-limited disorder with an undetermined mode of inheritance.3 including autoantibodies, electroretinogram for PRA, and MRI for
syringomyelia. (See CHIC website; www.caninehealthinfo.org)
Persistent Hyaloid Artery (PHA): Congenital defect resulting
from abnormalities in the development and regression of the American Brussels Griffon Association “Champions For Health”
hyaloid artery. Does not cause vision problems by itself, but is often program recommends Patella and Hip radiographs, CERF eye exam
associated with other ocular defects. Identified in 2.47% of Brussels and ERG for PRA, thyroid profile including autoantibodies, and MRI
Griffon CERF examined by veterinary ophthalmologists between for SM.
2000-2005.4
Recommend elbow radiographs and cardiac evauation.
Heart Murmur: Reported in 2.1% of dogs in the 2004 ABGA Health
Survey. Average age of onset 5.0 years. The anatomical cause of the Miscellaneous
heart murmur was not defined, though mitral valvular disease is • Breed name synonyms: Griffon Bruxellois, Griffon Belge, Belgian
reported in the breed.3 Griffon, or Griffons d’Ecurie (historical).
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
Bladder Stones: Reported in 2.1% of dogs in the 2004 ABGA ANKC (Australian National Kennel Club), NKC (National Kennel Club).
Health Survey. Average age of onset 5.4 years. The mineral content • AKC rank (year 2008): 67 (1,320 dogs registered)
(type) of the bladder stone was not defined.3 • Internet resources: American Brussels Griffon Association:
www.brussels-griffon.info/
Distichiasis: Abnormally placed eyelashes that irritate the
112
The Griffon Bruxellois Club (UK): www.griffonclub1897.co.uk
National Brussels Griffon Club: www.brussels-griffon.net
References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. American Brussels Griffon Association: 2004 ABGA Health Survey. 2004.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
5. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
6. Rusbridge C, Knowler SP, Pieterse, et. al.: Chiari-like malformation in the
Griffon Bruxellois. J Small Anim Pract. 2009 Aug;50(8):386-93.
7. American Brussels Griffon Association: 2003 ABGA Puppy Mortality
Survey 2003.
8. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
9. Nachreiner RF, Refsal KR, Graham PA, et. al,: Prevalence of serum thyroid
hormaone autoantibodies in dogs with clinical signs of hypothyroidism, J
Am Vet Med Assoc 2002 Feb 15;220(4): 466-71.
10. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 206 , AAHA Press, 1999.
11. Meyers-Wallen VN: Inherited Disorders of Sexual Development in Dogs
and Cats. Proceedings, 2007 Tufts’ Canine and Feline Breeding and Genetics
Conference. 2007.
12. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 450-453.
113
Bull Terrier
Recognized Behavior Issues and Traits
Reported breed attributes include: Playful, friendly, active. If they
bite, they are reluctant to let go and so must never be teased.
Dominant personalities are common. Bull Terriers were bred for
fighting so will ably defend and may not get along with all dogs
(watch especially for inter-male aggression). They are generally
deeply attached to their human family. High activity and exercise
needs must be met. If left alone without companionship and mental
exercise, they may develop boredom vices. Need to be socialized
well to children, and also socialized so that they do not become
The Breed History possessive. They are alarm barkers, not nuisance barkers generally.
If off leash, they must be in a fenced enclosure. They may consider
First records for the Bull Terrier date back to 1835 in Britain.
small pets as prey. Obedience training is important but keep
Crossing a Bulldog with a White English Terrier (now extinct) is
sessions short to prevent boredom.
thought to have provided the foundation for the breed. Later, a
documented outcross to Spanish Pointer was done to increase size.
The white variety was first bred around 1860, and the breed was Normal Physiologic Variations
formally split into the white and colored in 1936. The bull terrier May vocalize in grumbles and groans and this is distinct from
in AKC is registered as the standard size breed, (Bull Terrier) and a growling.
miniature size, the Miniature Bull Terrier.
Echocardiography: In 14 normal bull terriers, the left ventricular
Breeding for Function wall thickness was greater and the aortic root diameter smaller than
those reported as normal for other breeds of comparable body size.
This breed was valued as a pit fighter. A very strong constitution,
Left atrial dimensions were also larger, however this may have been
agility and tenacity were bred into them. Over the years, the
due to the “maximizing” method of measurement. These dogs also
breeders have worked to make the dog more companionable.
had higher aortic velocities than those reported for other breeds.
While these dogs were selected to be as close to normal as possible,
Physical Characteristics the breed may have a particular anatomy that produces abnormal
Height at Withers: 21-22“ (53-56 cm). left ventricular echocardiographic parameters. Inaccurate diagnoses
of left ventricular hypertrophy and left ventricular outflow tract
Weight: 52-62 lb (24-28 kg). obstruction may result if breed-specific values are not used.1
Coat: The breed is divided into white and colored types. Hairs are
short and hard, lie flat, and have good sheen. For white variety:
Echocardiographic Normal Values:1
all white or white with limited markings on the head. For colored Parameter Mean SD 95% CI
variety: other base colors than white, may have white markings; Ao l/a (cm) 1.9 0.3 1.3-2.5
brindle is preferred. They are moderate shedders and have low Ao s/a (cm) 2 0.2 1.6-2.4
grooming needs. LVld (cm) 3.8 0.3 3.2-4.4
IVSa (cm) 1.3 0.2 0.9-1.7
Longevity: 11-13 years
IVSd (cm) 1 0.2 0.6-1.4
Points of Conformation: The distinctive head is long, and the LVFWa (cm) 1.2 0.1 1.0-1.4
face is full and a curve over the top of the skull to the tip of the LFVWd (cm) 1 0.1 0.8-1.2
nose is present. Ears are close set and small, the leather is thin, and FS% 32.5 4.5 24-41
they prick erect when dog is alert. Small dark eyes are deep-set, SV (mL) 38.2 7.3 24-53
close-set, and piercing in expression. Oblique in shape, blue eyes HR (beats/min) 130.9 22.5 86-176
disqualify. The nose is black, and the neck is very muscular, long, Weight (kg) 22.9 3.7 *
and not throaty. The thorax is round and deep with very well sprung AoV (m/s) 1.9 0.2 1.5-2.3
ribs. The back is short and only slightly arched at the loins. Limbs
are straight boned, and moderately long. The feet are compact and SD standard deviation, CI confidence interval, Ao aortic annular
well-knuckled. The tapering tail is low set, short, and carried parallel diameter, l/a long axis, s/a short axis, LVl left ventricular internal
to the topline. The gait is smooth and ground covering. dimension, d diastolic, IVS interventricular septum, s systolic, LVFW
left ventricular free wall thickness, FS% fractional shortening, SV
stroke volume, HR heart rate, AoV aortic velocity
114
Parameter Weight (kg) However a neurological partial seizure disorder cannot be ruled out,
20 25 30 as some dogs have abnormal electroencephalograms and respond
LA l/a (cm) 2.5-3.4 2.8-3.7 3.1-4.0 to anticonvulsants. Compulsion was reported at a frequency of
LA s/a (cm) 2.2-3.5 2.5-3.8 2.8-4.1 18.05%, and spinning 17.65% in the 1997 BTCA Health Survey.
LVls (cm) 1.9-3.0 2.2-3.2 2.4-3.5 Unknown mode of inheritance.3,13,14
LA is left atrium diameter, l/a is long axis view, s/a is short axis view, Deafness: Congenital deafness can be unilateral or bilateral.
LVls is left ventricular internal dimension during systole Diagnosed by BAER testing: Strain reports total (uni or bilateral)
deafness frequency of 19.9% in white Bull Terriers, and 1.3% in
colored Bull Terriers based on BAER testing. 9.9% of all Bull Terriers
Drug Sensitivities test unilaterally deaf, and 1.1% test bilaterally deaf.15
None reported
Persistent Pupillary Membranes: Strands of fetal remnant
Inherited Diseases connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
Hip Dysplasia: Polygenically inherited trait causing degenerative later three forms can impair vision, and dogs affected with these
joint disease and hip arthritis. OFA reports 6.7% affected.2 forms should not be bred. Identified in 7.84% of Bull Terriers CERF
examined by veterinary ophthalmologists between 2000-2005.16
Patella Luxation: Polygenically inherited laxity of patellar ligaments,
causing luxation, lameness, and later degenerative joint disease. Hypothyroidism: Inherited autoimmune thyroiditis. 7.0% positive
Treat surgically if causing clinical signs. OFA reports 2.1% affected. for thyroid autoantibodies based on testing at Michigan State
Reported at a frequency of 2.84% in the 1997 BTCA Health Survey.2,3 University. (Ave. for all breeds is 7.5%).17,18
Hereditary Nephritis: Autosomal dominant disorder causing renal Primary Lens Luxation: Occurs in the breed due to abnormalities
failure at variable ages in affected dogs due to abnormal kidney of the suspensory apparatus of the lens (zonule). Often progresses
basement membrane protein and structure. Dorn reports a 8.16x to secondary glaucoma. Relative risk of 65.88x versus other breeds.
odds ratio for kidney disease versus other breeds. No genetic test is Identified in 5.88% of Bull Terriers CERF examined by veterinary
available.4,5 ophthalmologists between 2000-2005. Unknown mode of
inheritance. CERF does not recommend breeding any Bull Terrier
Polycystic Kidney Disease (PKD): Autosomal dominant caused with lens luxation.16,19
by an undetermined mutation in the PKD 1 gene. Renal cysts are
diagnosed by ultrasound. They are usually bilateral, from less than 1 Cataracts: Anterior, posterior, intermediate and punctate cataracts
mm to over 2.5 cm in diameter, and occur in the cortex and medulla. occur in the breed. Identified in 3.92% of Bull Terriers CERF
Causes chronic renal failure. Dorn reports a 8.16x odds ratio for examined by veterinary ophthalmologists between 2000-2005. CERF
kidney disease versus other breeds. No genetic test is available.4,6,7,8,9 does not recommend breeding any Bull Terrier with a cataract.16
Elbow Dysplasia: Polygenically inherited trait causing elbow Mitral Valvular Stenosis/Left Ventricular Outflow Tract
arthritis. Too few Bull Terriers have been screened by OFA to Obstruction (LVOTO): Found at an increased frequency in Bull
determine an accurate frequency.2 Terriers. Echocardiography is a much more sensitive test than
auscultation for murmurs. Pathological findings can include
Lethal Acrodermatitis: An autosomal recessive disease. Affected thickened, nodular, and stiff mitral valves with short, thickened, and
dogs present with stunting, splayed digits, eating difficulties, fused chordae tendineae. Myxomatous valvular degeneration, small
skin disease of the face and feet, and increased susceptibility to vessel arteriosclerosis in the myocardium and fibrosis of cardiac
microbial infections. In older dogs, paronychia, nail disease and conduction tissue were common histologic findings in Bull Terriers
hyperkeratosis of the footpads develops, becoming severe in dogs with clinical cardiac disease. An increased incidence was found in
over six months of age. Median survival time is 7 months. Although Bull Terriers affected with PKD, though it could not be identified if
many of the clinical signs and the pathology of this condition there is a direct genetic correlation between the two disorders.20,21,22
suggest zinc deficiency, the measurement of blood zinc levels as a
diagnostic aid is of limited value, and the dogs do not respond to Aortic Stenosis: Found at an increased frequency in Bull Terriers.
zinc treatment. Reported at a frequency of 0.81% in the 1997 BTCA Clinical signs can include syncope, exercise intolerance/fatigue, or
Health Survey. No genetic test is available.3,10,11 heart murmur. Cardiac ultrasound shows thickened and/or poorly
opening aortic valve leaflets, and an elevated blood flow velocity
Disease Predispositions through the aortic valve annulus (mean v=5.2m/s; range=4.8-5.9).
Varying degrees of concentric LVH and mitral valve thickening can
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis
be seen. Many affected bull terriers have concurrent severe mitral
and pyotraumatic dermatitis (hot spots). Bull Terriers are at an
valve stenosis.23
increased risk versus other breeds, especially white Bull Terriers.
Reported at a frequency of 25.56% in the 1997 BTCA Health Survey.3,12 Demodicosis: Demodectic mange dermatitis has an underlying
immunodeficiency in its pathogenesis. Dorn reports a 2.14x odds
Compulsive Tail Chasing and Spinning: Disorder of persistent
ratio versus other breeds. Unknown mode of inheritance.9
spinning observed in the breed. Possibly a behavioral compulsion,
as 75% of affected dogs respond to clomipramine administration. Actinic Keratosis: Affected dogs present with alopecia, erythema,
115
comedones, scales, excoriation, pustules, epidermal collarettes,
crusts and scars, with pathologic development of epidermal
References
1. O’Leary CA, Mackay BM, Taplin RH, et. al.: Echocardiographic parameters
hyperplasia, parakeratosis, and orthokeratosis. Lesions occur in 14 healthy English Bull Terriers. Aust Vet J. 2003 Sep;81(9):535-42.
secondary to prolonged UV/sunlight exposure, and may be a 2. OFA Website breed statistics: www.offa.org Last accessed July. 1, 2010.
precursor to squamous cell carcinoma. Seen at an increased 3. Bull Terrier Club of America & Slater M: 1997 BTCA Health Survey. 1997.
frequency in the breed.24 4. O’Leary CA, Ghoddusi M, Huxtable CR: Renal pathology of polycystic
kidney disease and concurrent hereditary nephritis in Bull Terriers. Aust Vet
J. 2002 Jun;80(6):353-61.
Retinal Dysplasia: Focal dysplasia and retinal folds are recognized
5. Hood JC, Dowling J, Bertram JF, et. al.: Correlation of histopathological
in the breed, which can lead to retinal detachment. Reported in features and renal impairment in autosomal dominant Alport syndrome in
1.96% of Bull Terriers CERF-examined by veterinary ophthalmolo- Bull terriers. Nephrol Dial Transplant. 2002 Nov;17(11):1897-908.
gists between 2000-2005.16 6. O’Leary CA, Turner S: Chronic renal failure in an English bull terrier with
polycystic kidney disease. J Small Anim Pract. 2004 Nov;45(11):563-7.
Vitreous Degeneration: Liquefaction of the vitreous gel which may 7. O’Leary CA, Mackay BM, Malik R, et. al.: Polycystic kidney disease in
predispose to retinal detachment. Identified in 1.96% of Bull Terriers bull terriers: an autosomal dominant inherited disorder. Aust Vet J. 1999
CERF examined by veterinary ophthalmologists between 2000-2005.16 Jun;77(6):361-6.
8. O’Leary CA, Duffy D, Biros I, et. al.: Linkage confirms canine pkd1
orthologue as a candidate for bull terrier polycystic kidney disease. Anim
Inverted Canines: In affected Bull Terriers, the mandibular canine
Genet. 2009 Aug;40(4):543-6.
teeth are tipped (curved) caudally and impact at the mesio-palatal 9. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
gingival margin of the maxillary canine teeth.25 veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
Cerebellar Abiotrophy, Cerebellar Vermian Hypoplasia, Cleft Lip/ 10. McEwan NA, McNeil PE, Thompson H, et. al.: Diagnostic features,
Palate, Deep Pyoderma, Ectropion, Entropion, Inguinal Hernia, confirmation and disease progression in 28 cases of lethal acrodermatitis
Keratoconjunctivitis Sicca, Laryngeal Paralysis, Osteochondritis of bull terriers. J Small Anim Pract. 2000 Nov;41(11):501-7.
Dessicans-Hock and Stifle, Progressive Retinal Atrophy, 11. Jezyk PF, Haskins ME, MacKay-Smith WE, et. al.: Lethal acrodermatitis in
bull terriers. J Am Vet Med Assoc. 1986 Apr 15;188(8):833-9.
Prognathism, Prolapsed Nictitans, Retained Primary Teeth, and 12. Nødtvedt A, Egenvall A, Bergvall K, et. al.: Incidence of and risk factors
Wry Mouth are reported.26 for atopic dermatitis in a Swedish population of insured dogs. Vet Rec.
2006 Aug 19;159(8):241-6.
Isolated Case Studies 13. Moon-Fanelli AA, Dodman NH: Description and development of
compulsive tail chasing in terriers and response to clomipramine treatment.
Sick Sinus Syndrome: A 6.5-year-old, spayed female bull terrier J Am Vet Med Assoc. 1998 Apr 15;212(8):1252-7.
was investigated for episodic weakness and a syncopal episode. 14. Dodman NH, Knowles KE, Shuster L, et. al.: Behavioral changes
Resting ECG revealed bradycardia (40 to 60 bpm), sinus pauses of associated with suspected complex partial seizures in bull terriers. J Am Vet
typically 2-4s, atrial premature contractions (APCs), and junctional Med Assoc. 1996 Mar 1;208(5):688-091.
escape beats. Vagal maneuvers did not result in significant 15. Strain GM: Deafness prevalence and pigmentation and gender
sinus pauses, and atropine response was normal in rate but not associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
16. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
rhythm, implying a conduction disturbance rather than excessive
College of Veterinary Ophthalmologists. ACVO, 2007.
parasympathetic tone.27 17. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
Genetic Tests hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
18. Nachreiner R and Refsal K: Personal communication, Diagnostic Center
Tests of Genotype: Direct test for color alleles is avaiable from
for Population and Animal Health, Michigan State University. April, 2007.
VetGen. 19. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing
lens luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
Tests of Phenotype: CHIC certification: Required testing 20. O’Leary CA, Mackay BM, Taplin RH, et. al.: Auscultation and echocardio-
includes patella examination, cardiac evaluation (recommend graphic findings in Bull Terriers with and without polycystic kidney disease.
echocardiogram), BAER test for deafness, and kidney disease Aust Vet J. 2005 May;83(5):270-5.
screening with urine protein:creatinine ratio. (See CHIC website; 21. Lehmkuhl LB, Ware WA, Bonagura JD: Mitral stenosis in 15 dogs. J Vet
www.caninehealthinfo.org). Intern Med. 1994 Jan-Feb;8(1):2-17.
22. O’Leary CA & Wilkie I: Cardiac valvular and vascular disease in Bull
Terriers. Vet Pathol. 2009 Nov;46(6):1149-55.
Recommended tests include CERF eye examination, hip and elbow 23. Oyama MA, Sisson DD, Behr MJ, et. al.: Severe Valvular Aortic Stenosis
radiographs, and thyroid profile including autoantibodies. in Bull Terriers: Clinical, Anatomic and Histopathologic Characteristics.
Proceedings, 2003 ACVIM Forum. 2003.
Miscellaneous 24. Costa SS, Munhoz TD, Calazans SG, et. al.: Clinical and Epidemiological
Evaluation of Actinic Keratosis in Seven Dogs. Proceedings, 2009 WSAVA
• Breed name synonyms: English Bull Terrier, White Cavalier (for World Congress. 2009.
white variety) 25. Pavlica Z, Cestnik V: Management of lingually displaced mandibular
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), canine teeth in five bull terrier dogs. J Vet Dent 1995: 12[4]:127-9.
ANKC (Australian National Kennel Club), NKC (National Kennel Club) 26. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
• AKC rank (year 2008): 57 (1,900 dogs registered) Ackerman. p. 206-07. AAHA Press, 1999.
• Internet resources: Bull Terrier Club of America: www.btca.com 27. Kavanagh K: Sick sinus syndrome in a bull terrier. Can Vet J. 2002
Jan;43(1):46-8.
The Bull Terrier Club of Canada: http://thebullterrierclub.ca
28. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
The Bull Terrier Club (UK): www.thebullterrierclub.com Book House, NY 2006. p. 358-361.
116
Bulldog
and well arched. The back is somewhat roached (wheel-backed). The
thorax is deep with rounded ribs. The abdomen is moderately tucked
up. A low set tail is carried low, and the tail tapers and is straight
or screwed, but a curly tail is a fault. Limbs are stout and short
but fairly straight boned. The elbows stand away from the chest
wall. The feet are moderate in size and compact, and are straight
ahead but especially the metatarsals deviate outward. This is due
to so-called cow hocked conformation. Toes are well knuckled and
nails are stubby and strong. The loins sit higher than the shoulder.
The rolling gait is loose-jointed and ambling.
Coat: The short, flat glossy coat is straight, the hairs are fine, and Inherited Diseases
the skin is quite loose especially around the neck area. Colors Hip Dysplasia: Polygenically inherited trait causing degenerative
include brindle, white, red, fawn, and piebald. A small white chest joint disease and hip arthritis. OFA reports 73.2% affected.3
patch is accepted.
Elbow Dysplasia: Polygenically inherited trait causing elbow
Longevity: 10-12 years arthritis. OFA reports a high incidence, but too few Bulldogs have
been screened to determine an accurate frequency.3
Points of Conformation: These dogs are medium-sized, massive
both across the chest and throughout the body. The dark eyes Patella Luxation: Polygenically inherited laxity of patellar
are front facing, set low in the skull, are wide set and round, and ligaments, causing luxation, lameness, and later degenerative joint
moderate in size, the palpebral margins are dark and no nictitans disease. Treat surgically if causing clinical signs. OFA reports 6.2%
or sclera should show. The ears are very high and wide set, small affected. Reported 6.1x odds ratio versus other breeds.3,4
and thin in leather; termed a rose ear in shape and carriage, which
means the folded portion is splayed so that the front is further from Hyperuricosuria (HUU)/Urate Urolithiasis: An autosomal
the head than the back. This feature helps distinguish the English recessive disease caused by a mutation in the SLC2A9 gene causes
Bulldog from the French Bulldog because the latter has erect bat hyperuricosuria and predisposes to urate bladder stones. Stone
ears, and is also smaller in stature. formation is predominantly seen in males. Bulldogs have a 7.9x
Odds Ratio of forming urate bladder stones versus other breeds. A
The head is massive, being both broad and square with a direct genetic test is available.5,6,7
pronounced stop forming a hollow between the eyes. The muzzle
is very short, upturned, and the nose is broad and colored black. Anasarca (Lethal Congenital Edema): Anasarca occurs in
The flews are very well developed and overhang the lower jaws. the breed. Puppies are born dead and edematous. Can also be
A dewlap is well developed, and the head and face are heavily associated with cleft palate. Segregation analysis indicates an
wrinkled. The lower jaw is considerably prognathic and prominent autosomal recessive mode of inheritance.8
(referred to as chops). The neck is very short and thick, muscular
117
Disease Predispositions Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
Brachycephalic Complex: Stenotic nares, elongated soft palate,
everted laryngeal saccules, laryngeal collapse, and occasionally later three forms can impair vision, and dogs affected with these
hypoplastic trachea. Reported to cause obstructive sleep apnea forms should not be bred. Identified in 1.64% of Bulldogs CERF
in the breed. Can cause secondary bronchial collapse. Dorn reports examined by veterinary ophthalmologists between 2000-2005.16
a 29.27x odds ratio for elongated soft palate versus other breeds.
Cataracts: Anterior, posterior, equatorial, and capsular cataracts
Identified in 19.2% of Bulldogs in an Australian study. One study
occur in the breed. Identified in 1.31% of Bulldogs CERF examined
showed the Bulldog as the most frequently affected breed, and an
by veterinary ophthalmologists between 2000-2005. CERF does not
overall surgical curative rate of 94.2%.9,10,11,12,13,14,15
recommend breeding any Bulldogs with a cataract.16
Distichiasis: Abnormally placed eyelashes that can cause secondary
Pododermatitis/Interdigital Cysts: Affected dogs can present
corneal ulceration. Identified in 15.74% of Bulldogs CERF examined
with erythema. thickening of the skin, alopecia, pyoderma, nodules,
by veterinary ophthalmologists between 2000-2005. CERF states
ulcers haemorrhagic bullae, and draining tracts. Increased risk
that breeding of affected animals should be discouraged. Dorn
versus other breeds.21
reports a 1.48x odds ratio versus other breeds.9,16
Pulmonic Stenosis: Bulldogs are the most common breed to have
Entropion: Rolling in of the eyelids, which can predispose to
pulmonic stenosis, with an odds ratio of 19.2x versus other breeds.
corneal irritation and ulceration. Reported in 14.43% of Bulldogs
This congenital heart abnormality in Bulldogs frequently is caused
CERF examined by veterinary ophthalmologists between 2000-2005.
by a circumpulmonary left coronary artery originating from a single
Dorn reports a 4.37x odds ratio versus other breeds.9,16
right coronary artery.22,23
Ectropion: A rolling out of the eyelids, that can cause tear pooling,
Demodicosis: Generalized demodicosis has an underlying
conjunctivitis, and frequent infection. Reported in 8.85% of
immunodeficiency in its pathogenesis. Dorn reports a 3.0x odds
Bulldogs CERF examined by veterinary ophthalmologists between
ratio versus other breeds.9
2000-2005. Dorn reports a 4.37x odds ratio versus other breeds.9,16
Hiatal Hernia: The Bulldog has the highest incidence of hiatal
Retinal Dysplasia: Focal folds and geographic retinal dysplasia are
hernia for all breeds. The most common presentation is reflux
seen in the breed. Dogs with the geographic form should not be
esophagitis. Treatment is with surgery.24
bred. Reported in 7.54% of Bulldogs CERF examined by veterinary
ophthalmologists between 2000-2005.16 Spina Bifida: Review of cases to veterinary teaching hospitals
suggests a high incidence of spina bifida in the English Bulldog.
Prolapsed Gland of the Nictitans (Cherry Eye): Occurs at a high
Urinary and fecal incontinence is the most common clinical sign.
frequency in the breed. This condition is secondary to chronic
Radiographs and myelography confirm the diagnosis.25
conjunctivitis, usually of an allergic nature.17
Urethrorectal Fistula: Several case reports are in the literature
Hypothyroidism: Inherited autoimmune thyroiditis. 4.2% positive
of Bulldogs with congenital urethrorectal fistulas. Affected
for thyroid auto-antibodies based on testing at Michigan State
dogs present with urine dribbling the anus, and chronic cystitis.
University. (Ave. for all breeds is 7.5%.).18,19
Treatment is with surgery.26,27,28
Stifle Osteochondritis Dessicans (OCD): Polygenically inherited
Cryptorchidism, Deafness, Factor VII Deficiency, Factor VIII
cartilage defect. Causes stifle joint pain and lameness in young
Deficiency, Fold Dermatitis, Hemivertebra, Hydrocephalus,
growing dogs. Mild cases can resolve with rest, while more severe
Laryngeal Paralysis, Myelodysplasia, Sacrocaudal Dysgenesis,
cases require surgery. Reported 44.2x odds ratio versus other breeds.4
Seasonal Flank Alopecia, Subaortic Stenosis, Supernumerary
Keratoconjunctivitis Sicca (KCS, Dry Eye): An abnormality of the Teeth, Tetralogy of Fallot, Ventricular Septal Defect, von
tear film, resulting in ocular irritation and/or vision impairment. Age Willebrand’s Disease, and Wry Mouth are reported.29
of onset 2-5 years. Treatment with topical ocular lubricants and
anti-inflammatory medication. CERF does not recommend breeding Isolated Case Studies
any Bulldogs with KCS.16,20 Cerebellar Cortical Degeneration: Three young full-sibling Bulldogs
presented with a wide-based stance, marked hypermetria, spasticity,
Cystine Urolithiasis: Bulldogs have a higher incidence of Cystine and intention tremors of the head and trunk with loss of balance.
(32.3x OR) bladder stones compared to other breeds. Cystine stones Pathology showed a loss of cerebellar Purkinje and granule cells.30
are due to a defect in cystine metabolism.5,6
Acrochordonous Skin Plaques: Clinical report of numerous, closely
Chronic Superficial Keratitis (Pannus): Corneal disease that can associated acrochordons forming a plaque, preferentially located at
cause vision problems due to pigmentation. Treatment with topical the dorsal neck of two Bulldogs.31
ocular lubricants and anti-inflammatory medication. Identified
in 1.97% of Bulldogs CERF examined by veterinary ophthalmolo- Cor Triatriatum Dexter: A 3.5 month old male Bulldog with ascites
gists between 2000-2005. CERF does not recommend breeding any and a history of respiratory distress was diagnosed at autopsy with
Bulldogs with pannus.16 the heart anomaly cor triatriatum dexter.32
118
Parotid Duct Sialolithiasis: Two case reports are in the literature; Australia. J Small Anim Pract. 2006 Mar;47(3):150-4.
a 7 year old male Bulldog and a 3 year old male Bulldog. Blockage 11. Veasey SC, Chachkes J, Fenik P, et. al.: The effects of ondansetron
of the parotid duct with a sialolith causes chronic facial swelling. on sleep-disordered breathing in the English bulldog. Sleep. 2001 Mar
Surgical removal of the sialolith, or of the salivary gland and duct is 15;24(2):155-60.
12. Coyne BE, Fingland RB: Hypoplasia of the trachea in dogs: 103 cases
curative.33,34
(1974-1990). J Am Vet Med Assoc. 1992 Sep 1;201(5):768-72.
13. Riecks TW, Birchard SJ, & Stephens JA: Surgical correction of
Sperm Tail Defects: A 2 year old Bulldog was identified with 93.3%
brachycephalic syndrome in dogs: 62 cases (1991-2004). J Am Vet Med
of spermatozoa with morphological tail defects, including strong Assoc. 2007 May 1;230(9):1324-8.
folding, coiling and fracture of sperm midpieces and tails, axonemal 14. Torrez CV & Hunt GB: Results of surgical correction of abnormalities
defects and the presence of swollen and unevenly distributed associated with brachycephalic airway obstruction syndrome in dogs in
mitochondria. The defect was considered to be genetic in origin.35 Australia. J Small Anim Pract. 2006 Mar;47(3):150-4.
15. De Lorenzi D, Bertoncello D, & Drigo M: Bronchial abnormalities found
Genetic Tests in a consecutive series of 40 brachycephalic dogs. J Am Vet Med Assoc.
2009 Oct 1;235(7):835-40.
Tests of Genotype: Direct test for HUU is available from the
16. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
UC-Davis VGL and the Animal Health Trust. College of Veterinary Ophthalmologists. ACVO, 2007
17. Abrams K: Selected Adnexal Diseases in the Dog. Proceedings, 2004
Tests of Phenotype: CHIC Certification: Required testing includes Western Veterinary Conference. 2004.
patella evaluation (minimum 1 year of age) and congenital cardiac 18. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
exam (by a cardiologist, preferably by echocardiography). (See CHIC for Population and Animal Health, Michigan State University. April, 2007.
website; www.caninehealthinfo.org). 19. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
Recommended: hip and elbow radiographs, CERF eye examination, hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
and thyroid profile including autoantibodies. 20. Colitz CMH: Keratoconjunctivitis Sicca: Cause, Effect & Treatment.
Proceedings, 2004 Western Veterinary Conference. 2004.
Miscellaneous 21. Breathnach R: Intractable Pododermatitis. Proceedings, British Small
Animal Veterinary Congress 2006.
• Breed name synonyms: English Bulldog 22. Buchanan JW: Pathogenesis of single right coronary artery
• Registries: **AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), and pulmonic stenosis in English Bulldogs. J Vet Intern Med. 2001
ANKC (Australian National Kennel Club)-as British bulldog, NKC Mar-Apr;15(2):101-4.
(National Kennel Club) **Just termed Bulldog in AKC 23. Buchanan JW: Causes and prevalence of cardiovascular diseases. In Kirk
• AKC rank (year 2008): 8 (23,413 dogs registered) RW, Bonagura JD, eds: Current veterinary therapy XI, Philadelphia, 1992,
• Internet resources: The Bulldog Club of America: WB Saunders.
http://thebca.org/ 24. Lorinson D, Bright RM: Long-term outcome of medical and surgical
The British Bulldog Club: www.britishbulldogclub.co.uk treatment of hiatal hernias in dogs and cats: 27 cases (1978-1996). J Am
Bulldog Club of Central Canada: Vet Med Assoc. 1998 Aug 1;213(3):381-4.
www.bulldogclubofcentralcanada.net/ 25. Wilson JW, Kurtz HJ, Leipold HW, et. al.: Spina bifida in the dog. Vet
Pathol. 1979 Mar;16(2):165-79
26. Silverstone AM, Adams WM: Radiographic diagnosis of a rectourethral
References fistula in a dog. J Am Anim Hosp Assoc. 2001 Nov-Dec;37(6):573-6.
1. Moon PF, Erb HN, Ludders JW, et. al.: Perioperative risk factors for 27. Ralphs SC, Kramek BA: Novel perineal approach for repair of a
puppies delivered by cesarean section in the United States and Canada. J urethrorectal fistula in a bulldog. Can Vet J. 2003 Oct;44(10):822-3.
Am Anim Hosp Assoc. 2000 Jul-Aug;36(4):359-68. 28. Cruse AM, Vaden SL, Mathews KG, et. al.: Use of computed tomography
2. Evans KM and Adams VJ: Proportion of litters of purebred dogs born by (CT) scanning and colorectal new methylene blue infusion in evaluation
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8. of an English Bulldog with a rectourethral fistula. J Vet Intern Med. 2009
3. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010. Jul-Aug;23(4):931-4.
4. LaFond E, Breur GJ & Austin CC: Breed susceptibility for developmental 29. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002 Sep-Oct;38(5): Ackerman. p. 215-16. AAHA Press, 1999.
467-77. 30. Gandini G, Botteron C, Brini E, et. al.: Cerebellar cortical degeneration
5. Ling GV, Franti CE, Ruby AL, et. al.: Urolithiasis in dogs. II: Breed in three English bulldogs: clinical and neuropathological findings. J Small
prevalence, and interrelations of breed, sex, age, and mineral composition. Anim Pract. 2005 Jun;46(6):291-4.
Am J Vet Res. 1998 May;59(5):630-42. 31. Bidaut AP, Gross TL, Noli C, et. al.: Acrochordonous plaques in two
6. Bartges JW, Osborne CA, Lulich JP, et. al.: Prevalence of cystine and urate Bulldogs and a Pug dog. Vet Dermatol. 2003 Jun;14(3):177-9.
uroliths in bulldogs and urate uroliths in dalmatians. J Am Vet Med Assoc. 32. Duncan RB Jr, Freeman LE, Jones J, et. al.: Cor triatriatum dexter in an
1994 Jun 15;204(12):1914-8. English Bulldog puppy: case report and literature review. J Vet Diagn Invest.
7. Bannasch D, Safra N, Young A, et. al.: Mutations in the SLC2A9 Gene 1999 Jul;11(4):361-5.
Cause Hyperuricosuria and Hyperuricemia in the Dog. PLoS Genet 4(11) 33. Trumpatori BJ, Geissler K, Mathews KG: Parotid duct sialolithiasis in a
2008: e1000246. doi:10.1371/journal.pgen.1000246. dog. J Am Anim Hosp Assoc. 2007 Jan-Feb;43(1):45-51.
8. Ladds PW, Dennis SM, Leipold HW: Lethal congenital edema in Bulldog 34. Tivers MS & Moore AH: Surgical treatment of a parotid duct sialolith in
pups. J Am Vet Med Assoc. 1971 Jul 1;159(1):81-6. a bulldog. Vet Rec. 2007 Aug 25;161(8):271-2.
9. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at 35. Rota A, Manuali E, Caire S, et. al.: Severe tail defects in the spermatozoa
veterinary teaching hospitals. MonographAKC6. ejaculated by an English bulldog. J Vet Med Sci. 2008 Jan;70(1):123-5.
10. Torres CV, Hunt GB: Results of surgical correction of abnormalities 36. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
associated with brachycephalic airway obstruction syndrome in dogs in Book House, NY 2006. p. 538-542.
119
Bullmastiff
Recognized Behavior Issues and Traits
Reported breed attributes include: Gentle, self assured, courageous,
sensitive to temperature extremes, intelligent, and some are a bit
overprotective and may resist obedience training. Very aloof with
strangers so early socialization and obedience training is important.
Low to moderate exercise needs, good for town or country, low
grooming needs, moderate shedders, and have a high drooling and
snoring tendency. Good dog for experienced dog handlers.
120
within the deep cerebellar nuclei. This disorder is most likely Lymphoma/Lymphosarcoma: Malignant cancer of lymphoid
inherited in an autosomal recessive manner.7,8 tissue. An increased prevalence is seen in the breed. In one study, a
large family of Bullmastiffs was identified, where 15% of the dogs
Disease Predispositions developed lymphosarcoma over a three year period.15,16
Entropion: Rolling in of eyelids, often causing corneal irritation
Optic Nerve Hypoplasia: A congenital defect of the optic nerve
or ulceration. Entropion is reported in 7.12% of Bullmastiffs CERF
which causes blindness and abnormal pupil response in the affected
examined by veterinary ophthalmologists between 2000-2005.4
eye. CERF does not recommend breeding affected dogs. Identified in
Hypothyroidism: Inherited autoimmune thyroiditis. 5.8% positive 1.57% of Bullmastiffs CERF examined by veterinary ophthalmolo-
for thyroid auto-antibodies based on testing at Michigan State gists between 1991-1999, though none were reported between
University. (Ave. for all breeds is 7.5%).9,10 2000-2005.4
Distichiasis: Abnormally placed eyelashes that irritate the cornea Calvarial Hyperostotic Syndrome (CHS): A clinical syndrome
and conjunctiva. Can cause secondary corneal ulceration. Identified is identified in young male Bullmastiffs of progressive and often
in 4.02% of Bullmastiffs CERF examined by veterinary ophthalmolo- asymmetric cortical thickening of the calvaria with irregular,
gists between 2000-2005.4 bony proliferation over the frontal, temporal, and occipital bones.
Osteopathy is diagnosed based on radiographs and biopsy. In 80%
Persistent Pupillary Membranes: Strands of fetal remnant of the cases presented, the lesion is self-limiting.17
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
later three forms can impair vision, and dogs affected with these Oligodendroglial Dysplasia (Spinal Cord Leukodystrophy):
forms should not be bred. Identified in 3.10% of Bullmastiffs CERF Affected Bullmastiffs show a young adult onset, slowly progressive,
examined by veterinary ophthalmologists between 2000-2005, with moderate to severe ataxia of all limbs, spastic tetraparesis that is
1.55% being iris to cornea.4 worse in the pelvic limbs, and a diffuse, action-related, whole-body
tremor. Histopathological lesions include white matter myelin
Ectropion: A rolling out of the eyelids, that can cause tear pooling, plaques, and proliferation of oligodendroglial processes.18
conjunctivitis, and frequent infection. Can be secondary to
macroblepharon; an abnormally large eyelid opening. Ectropion is Anasarca, Cervical Vertebral Instability, Epilepsy, Panosteitis,
reported in 3.10%, and macroblepharon in 2.79% of Bullmastiffs Seasonal Flank Alopecia, and Supernumerary Teeth are reported.19
CERF examined by veterinary ophthalmologists between
2000-2005.4 Isolated Case Studies
Craniomandibular Osteopathy (CMO): A 6-month-old bullmastiff
Osteochondritis Desicans (OCD): Polygenically inherited joint was presented with bilateral painful swellings of the mandible.
cartilage defect. Causes joint pain and lameness in young growing Craniomandibular osteopathy was diagnosed based on radiographs
dogs. Mild cases can resolve with rest, while more severe cases and biopsy. The condition resolved with palliative care.20
require surgery. Reported 85.9x odds ratio for hock OCD, and 6.7x
odds ratio for shoulder OCD versus other breeds.3 Primary Ciliary Dyskinesia: A 2.5-year-old male Bullmastiff with
a history of chronic bronchopneumonia and chronic rhinitis was
Cranial Cruciate Ligament Rupture (ACL): Traumatic tearing of found to have primary ciliary dyskinesia. Diagnostic evaluations
the anterior cruciate ligament. Dorn reports a 2.80x odds ratio in included tracheal mucociliary clearance, functional and ultrastruc-
Bullmastiffs versus other breeds. Treatment is surgery.11 tural ciliary examination, induction of ciliogenesis in cell culture,
and sperm evaluation.21
Cataracts: Capsular cataracts predominate, though anterior,
posterior, and nuclear cataracts also occur in the breed. Identified in Juvenile Renal Dysplasia: A 15-week-old female Bull Mastiff
2.79% of Bullmastiffs CERF examined by veterinary ophthalmolo- which presented with clinical signs of chronic renal failure. Renal
gists between 2000-2005. CERF does not recommend breeding any dysplasia and concurrent pyelonephritis were diagnosed by
Bullmastiff with a cataract.4 ultrasound, clinical pathology, and biopsy.22
Gastric Dilatation-Volvulus (bloat, GDV): Polygenically inherited, Muscle Tumors: Primary skeletal muscle lymphoma and muscle
life-threatening twisting of the stomach within the abdomen. hemangiosarcoma have been diagnosed in individual case studies
Requires immediate treatment. Reported at an increased frequency of Bullmastiffs.23,24
in the breed.12
Medulloepithelioma: A 6-month-old Bullmastiff presented
Dilated Cardiomyopathy (DCM): Dilated cardiomyopathy with clinical signs of incomplete upper motor neuron transverse
causing heart failure is identified in the breed. Unknown mode of myelopathy involving the hindlimbs. An embryonal medulloepithe-
inheritance.13 lioma was found involving the L1 spinal cord.25
Cystine Urinary Calculi: Bullmastiffs are a breed with increased Lymphangiosarcoma: A 3.5-year-old Bullmastiff presented
risk of developing cystine calculi, due to an abnormality of cystine with vaginal bleeding 3 weeks after cessation of estrus, during
metabolism.14 which intromission by the male had been unsuccessful. During
ovariohysterectomy a large multi-cystic, proliferative, spongy,
121
fluid-filled, brownish-red mass surrounding the cervix and Jan;62(1):67-71.
projecting into the abdominal space was removed with the cervix. 14. Case LC, Ling GV, Franti CE, et. al.: Cystine-containing urinary
Histopathology revealed malignant lymphangiosarcoma that had calculi in dogs: 102 cases (1981-1989). J Am Vet Med Assoc. 1992 Jul
invaded into the surrounding tissues.26 1;201(1):129-33.
15. Onions DE: A prospective survey of familial canine lymphosarcoma. J
Natl Cancer Inst. 1984 Apr;72(4):909-12.
Genetic Tests 16. Edwards DS, Henley WE, Harding EF, et. al.: Breed Incidence of
Tests of Genotype: Direct tests for PRA and Multifocal Retinopathy Lymphoma in a UK Population of Insured Dogs. Vet Comp Oncol 2003:
are available from Optigen. 1[4]:200-206.
17. Pastor KF, Boulay JP, Schelling SH, et. al.: Idiopathic hyperostosis
Tests of Phenotype: CHIC certification: Required testing includes of the calvaria in five young bullmastiffs. J Am Anim Hosp Assoc. 2000
hip and elbow radiographs, CERF eye examination, congenital cardiac Sep-Oct;36(5):439-45.
evaluation (by a cardiologist or by echocardiography), and thyroid 18. Morrison JP, Schatzberg SJ, De Lahunta A, et. al.: Oligodendroglial
profile including autoantibodies. Optional tests include direct test for dysplasia in two bullmastiff dogs. Vet Pathol. 2006 Jan;43(1):29-35.
19. The Genetic Connection: A Guide to Health Problems in Purebred Dogs.
PRA, and kidney tests. (See CHIC website; www.caninehealthinfo.org).
L Ackerman. p. 207-8. AAHA Press, 1999.
20. Huchowski SL: Craniomandibular osteopathy in a bullmastiff. Can Vet J.
Recommend patella evaluation.
2002 Nov; 43(11):883-5.
21. Clercx C, Peeters D, Beths T, et. al.: Use of Ciliogenesis in the Diagnosis
Miscellaneous of Primary Ciliary Dyskinesia in a Dog. J Am Vet Med Assoc 2000:
• Breed name synonyms: Gamekeeper’s Night Dog (historical). 217[11]:1681-1685.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 22. Abraham LA, Beck C, Slocombe RF: Renal dysplasia and urinary tract
ANKC (Australian National Kennel Club), NKC (National Kennel Club). infection in a Bull Mastiff puppy. Aust Vet J. 2003 Jun; 81(6):336-9.
• AKC rank (year 2008): 39 (3,447 dogs registered) 23. Tucker DW, Olsen D, Kraft SL, et. al.: Primary hemangiosarcoma of the
iliopsoas muscle eliciting a peripheral neuropathy. J Am Anim Hosp Assoc.
• Internet resources: American Bullmastiff Association:
2000 Mar-Apr;36(2):163-7.
http://bullmastiff.us/
24. Harkin KR, Kennedy GA, Moore WE, et. al.: Skeletal muscle lymphoma in
Bullmastiff Fanciers of Canada: www.bmfc.ca a bullmastiff. J Am Anim Hosp Assoc. 2000 Jan-Feb;36(1):63-6.
British Bullmastiff League: www.britishbullmastiffleague.com 25. Kennedy FA, Indrieri RJ, Koestner A: Spinal cord medulloepithelioma in a
dog. J Am Vet Med Assoc. 1984 Oct 15;185(8):902-4.
References 26. Williams JH, Birrell J, Van Wilpe E: Lymphangiosarcoma in a
3.5-year-old Bullmastiff bitch with vaginal prolapse, primary lymph
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8. node fibrosis and other congenital defects. J S Afr Vet Assoc. 2005
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010 . Sep;76(3):165-71.
3. LaFond E, Breur GJ & Austin CC: Breed susceptibility for 27. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002 Book House, NY 2006. p.. 254-257.
Sep-Oct;38(5):467-77.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
5. Kijas JW, Miller BJ, Pearce-Kelling SE, et. al.: Canine models of
ocular disease: outcross breedings define a dominant disorder present
in the English mastiff and bull mastiff dog breeds. J Hered. 2003
Jan-Feb;94(1):27-30.
6. Casal ML, Dambach DM, Meister T, et. al.: Familial glomerulonephropathy
in the Bullmastiff. Vet Pathol. 2004 Jul;41(4):319-25.
7. Johnson RP, Neer TM, Partington BP, et. al.: Familial cerebellar ataxia
with hydrocephalus in bull mastiffs. Vet Radiol Ultrasound. 2001
May-Jun;42(3):246-9.
8. Carmichael S, Griffiths IR, Harvey MJ: Familial cerebellar ataxia with
hydrocephalus in bull mastiffs. Vet Rec. 1983 Apr 9;112(15):354-8.
9. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
10. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
11. Dorn CR: Canine breed-specific risks of frequently diagnosed
diseases at veterinary teaching hospitals. Monograph. AKC Canine Health
Foundation. 2000.
12. Glickman LT, Glickman NW, Schellenberg DB, et. al.: Incidence of and
breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet
Med Assoc. 2000 Jan 1;216(1):40-5.
13. Spier AW, Meurs KM, Coovert DD, et. al.: Use of western immunoblot for
evaluation of myocardial dystrophin, alpha-sarcoglycan, and beta-dystro-
glycan in dogs with idiopathic dilated cardiomyopathy. Am J Vet Res. 2001
122
Cairn Terrier
Normal Physiologic Variations
None reported
Drug Sensitivities
None reported
Inherited Diseases
Hip Dysplasia and Legg-Calve-Perthes Disease: Polygenically
inherited traits causing degenerative hip joint disease and arthritis.
Both disorders are reported at high frequencies by OFA, but too
The Breed History few Cairn Terriers are screened to determine accurate frequencies.
A highly valued working terrier type dog was developed on the Isle Reported 17.9x odds ratio for Legg-Calve-Perthes versus other
of Skye in Scotland that possessed courage fending off unwanted breeds.1,2
pests, including foxes and otters larger than themselves. In the
1870s, the Dandie Dinmont and Skyes (included Westies, Scotties, Patella Luxation: Polygenically inherited laxity of patellar
and Cairn) were split off into separate types, and by 1912, the ligaments, causing luxation, lameness, and later degenerative joint
Cairns had their own registry and classes. AKC registry began in disease. Treat surgically if causing clinical signs. Too few Cairn
1913. From that decade forward, no intermingling of the Westies Terriers are screened by OFA to determine accurate frequencies.
and Cairns took place. The name cairn means a rock pile used to Padgett reports a frequency of 3.2% in the breed. Reported at a
mark landmarks, and the Cairn terriers would effectively clear these high frequency in the 2005 CTCA Health Survey.1,3,4
of vermin. As “Toto” in the Wizard of Oz, this likeable dog became a
popular pet. Ocular Melanosis and Glaucoma: Cairn terriers can have a familial
form of ocular melanosis that slowly progresses to melanocytic
Breeding for Function glaucoma and blindness. The disease is characterized by diffuse
intraocular infiltration of heavily pigmented melanocytes. Age of
A hardy, courageous terrier-type, it was bred to control vermin
onset 2-14 years. Diagnosed in 1.82% of Cairn terriers presented
and this is still emphasized in the breed. They are now valued as a
to veterinary teaching hospitals. Pedigree studies suggest
companion dog. The breeding community favors retention of the
an autosomal dominant mode of inheritance. CERF does not
historical type.
recommend breeding any Cairn Terrier with ocular melanosis.5,6,7,8,9
124
Base narrow Canines, Cleft Lip/Palate, Factor VIII Deficiency,
Factor IX Deficiency, Hydrocephalus, Pancreatitis, Progressive
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Retinal Atrophy, Retinal Dysplasia, Vitamin A Responsive 2. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
Dermatosis, von Willebrand’s Disease, and Wry Mouth are developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
reported.32 Sep-Oct;38(5):467-77.
3. Control of Canine Genetic Diseases. Padgett GA. pp. 164-165. Howell
Isolated Case Studies Book House, NY. 1998.
4. Cairn Terrier Club of America: 2005 CTCA Health Survey. 2005.
Juvenile Polycystic Kidney and Liver Disease: Three related 5. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
puppies with abdominal distention caused by nephromegaly and in pure-bred dogs in North America. Vet Ophthalmol. 2004
hepatomegaly had gross and histologic polycystic lesions in the Mar-Apr;7(2):97-111.
kidney and liver.33 6. Hanselman BA: Melanocytic glaucoma in a cairn terrier. Can Vet J. 2002
Apr;43(4):296-8.
Pseudohermaphrodite: A 6 1/2-month-old Cairn terrier, considered 7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
to be a bilateral cryptorchid male, was presented with dysuria and College of Veterinary Ophthalmologists. ACVO, 2007.
urinary incontinence. This was found to be due to a congenital 8. Petersen-Jones SM, Forcier J, & Mentzer AL: Ocular melanosis in the
communication between the urinary bladder and uterus and resulted Cairn Terrier: clinical description and investigation of mode of inheritance.
in distention of the uterus with urine which could not be voided. Vet Ophthalmol. 2007 Nov-Dec;10 Suppl 1:63-9.
An ovariohysterectomy was performed. The dog was found to be a 9. Petersen-Jones SM, Mentzer AL, Dubielzig RR, et. al.: Ocular
melanosis in the Cairn Terrier: histopathological description of the
genetic female with what resembled external male genitalia.34
condition, and immunohistological and ultrastructural characterization
of the characteristic pigment-laden cells. Vet Ophthalmol. 2008
Anury (congenital taillessness): Two related Cairn Terriers were
Jul-Aug;11(4):260-8.
born without tails, and abnormality of the sacral and caudal
10. van Straten G, Leegwater PA, de Vries M, et. al.: Inherited congenital
vertebra. Both dogs had fecal incontinence. A mating of the two extrahepatic portosystemic shunts in Cairn terriers. J Vet Intern Med. 2005
dogs produced two normal offspring.35 May-Jun;19(3):321-4.
11. Schermerhorn T, Center SA, Dykes NL, et. al: Characterization of
Multiple Myeloma/Plasmacytoma: A 13 month old female Cairn hepatoportal microvascular dysplasia in a kindred of cairn terriers. J Vet
terrier was diagnosed with multiple myeloma. Radiographically, pelvic Intern Med. 1996 Jul-Aug;10(4):219-30.
tumor masses and characteristic systemic osteolysis were found.36 12. Tobias KM, Rohrbach BW: Association of breed with the diagnosis of
congenital portosystemic shunts in dogs: 2,400 cases (1980-2002). J Am
Bronchoesophageal Fistula: A 1-year-old male Cairn terrier was Vet Med Assoc. 2003 Dec 1;223(11):1636-9.
evaluated for chronic coughing that was aggravated by eating 13. Wenger DA, Victoria T, Rafi MA, et. al.: Globoid cell leukodystrophy in
or drinking. Radiography revealed an esophageal diverticulum, cairn and West Highland white terriers. J Hered. 1999 Jan-Feb;90(1):138-42.
regional megaesophagus, and focal interstitial densities in the 14. Victoria T, Rafi MA, Wenger DA, et. al.: Cloning of the canine GALC cDNA
right caudal and middle lunglobes. Radiographic diagnosis was and identification of the mutation causing globoid cell leukodystrophy
bronchoesophageal fistula. This report references two other cases of in West Highland White and Cairn terriers. Genomics. 1996 May
1;33(3):457-62.
bronchoesophageal fistula in the breed.37
15. Skelly BJ, Wallace M, Rajpurohit YR, et. al.: Identification of a 6 base pair
insertion in West Highland White Terriers with erythrocyte pyruvate kinase
Genetic Tests deficiency. Am J Vet Res. 1999 Sep;60(9):1169-72.
Tests of Genotype: Direct test for Globoid Leukodystrphy is 16. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
available from the Jefferson Medical College (215-955-1666) and for Population and Animal Health, Michigan State University. April, 2007.
HealthGene. 17. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
Direct test for Pyruvate Kinase Deficiency is available from hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
PennGen. 18. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Tests of Phenotype: Recommend hip and elbow radiographs, 2000.
19. Schick RO, Fadok VA: Responses of atopic dogs to regional allergens:
patella examination, CERF eye examination, thyroid profile including
268 cases (1981-1984). J Am Vet Med Assoc. 1986 Dec 1;189(11):1493-6.
autoantibodies and cardiac evaluation.
20. Catchpole B, Ristic JM, Fleeman LM, et. al.: Canine diabetes mellitus: can
old dogs teach us new tricks? Diabetologia. 2005 Oct;48(10):1948-56.
Miscellaneous 21. Catchpole B, Kennedy LJ, Davison LJ, et. al.: Canine diabetes mellitus:
• Breed name synonyms: Short-Haired Skye (historical), Cairn from phenotype to genotype. J Small Anim Pract. 2008 Jan;49(1):4-10.
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), 22. Short AD, Catchpole B, Kennedy LJ, et. al.: T cell cytokine gene
ANKC (Australian National Kennel Club), NKC (National Kennel Club) polymorphisms in canine diabetes mellitus. Vet Immunol
23. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
• AKC rank (year 2008): 51 (2,161 registered)
in pure-bred dogs in North America. Vet Ophthalmol. 2004
• Internet resources: Cairn Terrier Club of America:
Mar-Apr;7(2):97-111.
www.cairnterrier.org 24. Miller SA, Hohenhaus AE, Hale AS: Case-control study of blood type,
Cairn Terrier Club of Canada: www.cairnterrierclub.ca breed, sex, and bacteremia in dogs with immune-mediated hemolytic
The Cairn Terrier Club (UK): www.thecairnterrierclub.co.uk anemia. J Am Vet Med Assoc. 2004 Jan 15;224(2):232-5.
25. Watson PJ: Chronic Hepatitis in Dogs. Proceedings, 2009 British Small
125
Animal Veterinary Congress. 2009.
26. Ling GV, Franti CE, Ruby AL, et. al.: Urolithiasis in dogs. II: Breed
prevalence, and interrelations of breed, sex, age, and mineral composition.
Am J Vet Res. 1998 May;59(5):630-42.
27. Weaver AD: Survey with follow-up of 67 dogs with testicular sertoli cell
tumours. Vet Rec. 1983 Jul 30;113(5):105-7.
28. Zaal MD, van den Ingh TS, Goedegebuure SA, et. al: Progressive
neuronopathy in two Cairn terrier litter mates. Vet Q. 1997 Mar;19(1):34-6.
29. Palmer AC, Blakemore WF: Progressive neuronopathy in the cairn terrier.
Vet Rec. 1988 Jul 2;123(1):39.
30. Cummings JF, De Lahunta A, Moore JJ 3rd: Multisystemic chromatolytic
neuronal degeneration in a Cairn terrier pup. Cornell Vet. 1988
Jul;78(3):301-14.
31. Cummings JF, de Lahunta A, Gasteiger EL: Multisystemic chromatolytic
neuronal degeneration in Cairn terriers. A case with generalized cataplectic
episodes. J Vet Intern Med. 1991 Mar-Apr;5(2):91-4.
32. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 208, AAHA Press, 1999.
33. McKenna SC, Carpenter JL: Polycystic disease of the kidney and liver in
the Cairn Terrier. Vet Pathol. 1980 Jul;17(4):436-42.
34. van Schouwenburg SJ, Louw GJ: A case of dysuria as a result of a
communication between the urinary bladder and corpus uteri in a Cairn
Terrier. J S Afr Vet Assoc. 1982 Mar;53(1):65-6.
35. Hall DS, Amann JF, Constantinescu GM, et. al.: Anury in two Cairn
terriers. J Am Vet Med Assoc. 1987 Nov 1;191(9):1113-5.
36. Tuch E, Tuch K: Multiple myeloma/plasmacytoma in a young dog.
Tierarztl Prax. 1992 Jun;20(3):292-5.
37. Basher AW, Hogan PM, Hanna PE, et. al.: Surgical treatment of a
congenital bronchoesophageal fistula in a dog. J Am Vet Med Assoc. 1991
Aug 15;199(4):479-82.
38. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p 362-365.
126
Canaan Dog
the tarsus at rest. Limbs are straight boned, and dewclaws may be
removed. The Canaan dogs have compact feet with well-knuckled
toes. Gait is agile, quick, powerful.
Coat: The flat short (0.5-1.5”) harsh outer coat is straight and the Disease Predispositions
inner coat is flat, short and soft. The ruff is more obvious in the Cataracts: Posterior and nuclear intermediate cataracts
male dog. The accepted colors are: predominate in the breed. Identified in 4.35% of Canaan Dogs CERF
1. Solid (black, brown) with or without specified markings. examined by veterinary ophthalmologists between 2000-2005. CERF
2. Mostly solid white, with or without body patches of color, and does not recommend breeding any Canaan Dog with a cataract.2
with a matching symmetrical mask. The mask may contain a small
blaze of white only. Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
Longevity: 12-13 years later three forms can impair vision, and dogs affected with these
forms should not be bred. Identified in 3.86% of Canaan Dogs CERF
Points of Conformation: There are 2 subtypes of dogs, the examined by veterinary ophthalmologists between 2000-2005.2
so –called “stockdog” type and a longer coated, heavier type
dog. Overall, the standard requires a medium-sized dog with Distichiasis: Abnormally placed eyelashes that irritate the cornea
medium-large erect ears, a long wedge-shaped head and square and conjunctiva. Can cause secondary corneal ulceration. Identified
conformation. Almond-shaped dark colored eyes are slightly in 2.42% of Canaan Dogs CERF examined by veterinary ophthalmol-
slanted up. Palpebral rims are colored liver or black, and the stop ogists between 2000-2005.2
is moderate. The neck is moderate in muscling and length and
well arched, not throaty. The topline is level except for a slight Progressive Retinal Atrophy (PRA): Progressive degeneration of
loin arch. The thorax is moderately deep and ribs are well sprung, the retina, eventually causing blindness. 1.93% of Canaan Dogs
and abdomen well tucked up. The “bottle brush” tail may be curled CERF examined by veterinary ophthalmologists were diagnosed
once over the back when excited, and the length of the tail is to with generalized PRA, and 1.93% were labeled suspicious for PRA
127
between 2000-2005. Undetermined mode of inheritance. CERF does 6. Coates JR, Zeng R, Awano T, et. al.: An SOD1 Mutation Associated with
not recommend breeding any Canaan Dog with PRA.2,3 Degenerative Myelopathy Occurs in Many Dog Breeds.Proceedings, 2009
ACVIM Forum. 2009.
Idiopathic Epilepsy: Generalized or partial seizures. Control with 7. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
anti-seizure medication. Seen at an increased frequency in the House, NY 2006. p. 650-653.
breed. Unknown mode of inheritance.3
Genetic Tests
Tests of Genotype: Direct test for a DM susceptibility gene is
available from OFA.
Miscellaneous
• Breed name synonyms: Kelef K’naani, Kelev Cana’ani, Canaan.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
• AKC rank (year 2008): 150 (61 dogs registered)
• Internet resources: The Canaan Dog Club of America:
www.cdca.org (the AKC parent club)
The Israel Canaan Dog Club of America:
www.itb.it/canaan/icdca/ (UKC parent club)
British Canaan Dog Society: www.thecanaandog.co.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Israel Canaan Dog Club of America: ICDCA Health Database. 2007.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
128
Cane Corso
Recognized Behavior Issues and Traits
The Cane Corso is a protector of his property and owners.
Intelligent, the Cane Corso is easily trained. As a large and athletic
breed, they need a lot of exercise. They are affectionate to their
owner and bond closely with children and family. They can be
aggressive to other dogs and to strangers, including other children.
Cane Corsos are light shedders, which make grooming simple – all
they need is an occasional brushing.
129
Prolapsed Gland of the Nictitans (Cherry Eye): This condition is 8. AKC Breed Website: www.akc.org/breeds/cane_corso Last accessed July
secondary to chronic conjunctivitis, usually of an allergic nature. 1, 2010.
Reported as a breed health issue on the CCAA website.
Inherited Ocular Disorders: Too few Cane Corsos have been CERF
examined by veterinary ophthalmologists to determine an accurate
frequency of inherited ocular disorders.6
Genetic Tests
Tests of Genotype: Direct test for retinal dysplasia is available from
Optigen.
Miscellaneous
• Breed name synonyms: Cane Corso Italiano, Cane di Macellaio,
Sicilian Branchiero, Italian Mastiff
• Registries: AKC, UKC, FCI, NKC (National Kennel Club)
• AKC rank: (none) AKC recognized in June 2010. Entire stud book
entered.
• Internet resources: Cane Corso Association of America:
www.canecorso.org
Society In America For Cane Corso Italiano: www.thesacci.com
The British Cane Corso Society: www.canecorso.org.uk
Cane Corso Club of Canada: www.canecorsoclubofcanada.ca
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Genevois JP, Remy D, Viguier E, et. al.: Prevalence of hip dysplasia
according to official radiographic screening, among 31 breeds of dogs in
France. Vet Comp Orthop Traumatol. 2008;21(1):21-4.
3. Cristina RT & Dégi J: Studies on Otitis Externa in Dogs. Proceedings, 17th
ECVIM-CA Congress. 2007.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
6. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
7. Stefanello D, Romussi S, Signorelli P, et. al.: Primary osseous melanoma in
the tibia of a dog. J Am Anim Hosp Assoc. 2008 May-Jun;44(3):139-43.
130
Cardigan Welsh Corgi
ears are smaller and more pointed, and the tail is docked short in
comparison.
Retinal Dysplasia: Focal folds and geographic retinal dysplasia are Tests of Phenotype: CHIC Certification: Required tests are; CERF
seen in the breed. It is questionable whether focal folds can lead eye examination, genetic test for rcd3-PRA, and hip radiographs.
to disease, however dogs with the geographic form should not be (See CHIC website: www.caninehealthinfo.org)
bred. Reported in 0.76% of Cardigan Welsh Corgis CERF examined
by veterinary ophthalmologists between 2000-2005.7 Recommend patella evaluation, elbow radiographs, thyroid profile
including autoantibodies, and cardiac evaluation.
Cystinuria/Cystine Bladder Stones: Caused by a metabolic
abnormality in cystine metabolism. Welsh Corgis have an Miscellaneous
increased risk for developing cystine bladder stones. Treat with • Breed name synonyms: Cardigan, Corgi, Cardi
surgical removal and life-long medical therapy. Unknown mode of • Registries: AKC, UKC, CKC , KCGB (Kennel Club of Great Britain),
inheritance in this breed. Dorn reports a 4.14x increased odds ratio ANKC (Australian National Kennel Club), NKC (National Kennel Club)
for bladder stones versus other breeds.11,12,13,14 • AKC rank (year 2008): 82 (845 dogs registered)
• Internet resources: Cardigan Welsh Corgi Club of America:
Perineal Hernia: An Australian study identified the Corgi breed as
www.cardigancorgis.com
most commonly affected with perineal hernias. The mean age of
Cardigan Welsh Corgi Association (UK):
affected dogs was 9.4 years. Treatment is herniorrhaphy surgery.15
www.cardiganwelshcorgiassoc.co.uk
Glaucoma: Primary, narrow angle glaucoma occurs in the breed. Canadian Cardigan Corgi Club: www.cardigancorgi.ca
Can cause blindness due to retinal damage, or secondary lens
luxation. Screen with gonioscopy and tonometry. Frequency and References
mode of inheritance in the breed has not been determined.16 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Petersen-Jones SM, Entz DD: An improved DNA-based test for detection
Intervertebral Disc Disease (IVDD): Serious neurological condition of the codon 616 mutation in the alpha cyclic GMP phosphodiesterase
where disk degeneration and rupture into spinal nerves and the gene that causes progressive retinal atrophy in the Cardigan Welsh Corgi.
spinal cord causes pain and possible paralysis. Requires immediate Vet Ophthalmol. 2002 Jun;5(2):103-6.
veterinary care. Dorn reports a 1.70x increased odds ratio versus 3. Petersen-Jones SM, Entz DD, Sargan DR: cGMP phosphodiesterase-alpha
mutation causes progressive retinal atrophy in the Cardigan Welsh corgi
other breeds.14
dog. Invest Ophthalmol Vis Sci. 1999 Jul;40(8):1637-44.
4. Keep JM: Clinical aspects of progressive retinal atrophy in the Cardigan
Central progressive Retinal Atrophy, Ceroid Lipofuscinosis, and
Welsh Corgi. Aust Vet J. 1972 Apr;48(4):197-9.
Methemaglobin Reductase Deficiency are reported.17 5. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
Isolated Case Studies 6. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
X-linked Severe Combined Immunodeficiency (XSCID): X-linked hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
recessive disorder was identified in one family of Cardigan Welsh Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
Corgis. Affected dogs cannot generate antigen-specific immune 7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
responses. A genetic test was developed to identify carrier females.18
8. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
Mucopolysaccharidosis VI (MPS VI): PennGen reports MPS VI
9. Coates JR, Zeng R, Awano T, et. al.: An SOD1 Mutation Associated with
132
Degenerative Myelopathy Occurs in Many Dog Breeds.Proceedings, 2009
ACVIM Forum. 2009.
10. Coates JR & Wade C: Update on the Genetic Basis of Canine
Degenerative Myelopathy. Proceedings, 2008 ACVIM Forum. 2008.
11. Weichselbaum RC, Feeney DA, Jessen CR, et. al.: Evaluation of the
morphologic characteristics and prevalence of canine urocystoliths from a
regional urolith center. Am J Vet Res. 1998 Apr;59(4):379-87.
12. Bovee KC, McGuire T: Qualitative and quantitative analysis of uroliths in
dogs: definitive determination of chemical type. J Am Vet Med Assoc. 1984
Nov 1;185(9):983-7.
13. Case LC, Ling GV, Franti CE, et. al.: Cystine-containing urinary
calculi in dogs: 102 cases (1981-1989). J Am Vet Med Assoc. 1992 Jul
1;201(1):129-33.
14. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
15. Bellenger CR: Perineal hernia in dogs. Aust Vet J. 1980 Sep;56(9):434-8.
16. Ketring KL: Schirmer Testing & Tonometry Are “Good Medicine”.
Proceedings, 2005 Western Veterinary Conference. 2005.
17. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 242-43, AAHA Press, 1999
18. Pullen RP, Somberg RL, Felsburg PJ, et. al.: X-linked severe combined
immunodeficiency in a family of Cardigan Welsh corgis. J Am Anim Hosp
Assoc. 1997 Nov-Dec;33(6):494-9.
19. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 654-658.
133
Cavalier King
Charles Spaniel
It is held level with the topline or a bit lower. They possess straight
legs and compact feet, and dewclaws may be removed. Their
movement is smooth and low, and straight with long strides.
Coat: The silky, soft, slightly wavy moderately long coat is lightly Patella Luxation: Polygenically inherited laxity of patellar
feathered. Blenheim color is a white dog with chestnut markings ligaments, causing luxation, lameness, and later degenerative joint
and a specific chestnut mark on the forehead in a white blaze is disease. Treat surgically if causing clinical signs. Reported 9.1x odds
favored (Blenheim mark). Other colors include tri-color in red, white ratio versus other breeds. OFA reports 2.3% affected. Reported at a
and black. Ruby, a red solid, and black and tan are other coat color frequency of 6.2% in the ACKCSC, Inc. Health Survey 2004-2005.6,7,8
variants.
Elbow Dysplasia: Polygenically inherited trait causing elbow
Longevity: 9-14 years. arthritis. OFA reports 0.7% affected.6
Points of Conformation: They have very soft expressions, and Episodic Collapse (Paroxysmal Hypertonicity, Hyperexplexia):
their large dark brown eyes are set wide apart on a broad face. Autosomal recessive disorder in the breed. Collapse with increased
The skull is not domed and a moderate stop is present, the nose is limb extensor tone triggered by excitement and characterized by a
large, square and black. The ears are pendulous and feathering is brief period of bunny hopping with the head held down and the rear
moderate. Slightly longer than tall, they are moderately boned, and end raised. Affected dogs may show signs starting at three months
the neck is long and slightly arched. The topline is level and chest of age. Treatment is with clonazepam. The condition resolves over
is moderately deep with ribs well sprung. Their tail may be docked. time in some dogs. A genetic test is available.36,52,53
134
Muscular Dystrophy: X-linked recessive muscular dystrophy due Retinal Dysplasia: Focal retinal dysplasia with retinal folds is
to a mutation in the dystrophin gene has been identified in the reported in 9.30%, and geographic retinal dysplasia is reported in
breed. Affected dogs show clinical signs from a few months of 3.18% of Cavalier King Charles spaniels CERF examined by veterinary
age, including weakness, muscle atrophy, exercise intolerance, ophthalmologists between 2000-2005. Severe cases can progress to
dysphagia and macroglossia (enlarged tongue). Serum creatine retinal detachment. CERF does not recommend breeding any CKCS
kinase is usually markedly elevated. Male dogs with the mutation with retinal dysplasia. Reported at 3.0% in the ACKCSC, Inc. Health
are clinically affected and female dogs with the mutation are Survey 2004-2005.7,30
silent carriers. Affected males with the same mutation have been
identified in the UK and the USA.9,10 Distichiasis: Abnormally placed eyelashes that irritate the cornea
and conjunctiva. Can cause secondary corneal ulceration. Identified
Congenital Keratoconjunctivitis Sicca (KCS) and Ichthyosiform in 9.16% of Cavalier King Charles spaniels CERF examined by
Dermatosis: Rare autosomal recessive, congenital disorder in the veterinary ophthalmologists between 2000-2005. Reported at 2.7%
breed of lack of tear production and scaly skin. In affected dogs, in the ACKCSC, Inc. Health Survey 2004-2005.7,30
the coat appears curly at birth, and the skin deteriorates as the dog
matures. The eye condition is treatable with lubricants. A genetic Corneal Dystrophy: The breed can have an epithelial/stromal form
test is available.58 of corneal dystrophy. Age of onset 2-5 years. Identified in 8.24%
of Cavalier King Charles spaniels CERF examined by veterinary
ophthalmologists between 2000-2005. Reported at 2.7% in the
Disease Predispositions ACKCSC, Inc. Health Survey 2004-2005.7,30,31
Chronic Mitral Valve Disease/Mitral Prolapse: Systolic heart
murmurs caused by chronic mitral valve disease are common in the Deafness: Can be congenital or progressive in the breed, and can be
breed, with an average age of diagnosis of 6.25 years. Left atrial unilateral or bilateral. The progressive form results in deafness by
enlargement, and not heart enlargement, should be used to evaluate 3-5 years of age. Diagnosed by BAER testing. Reported at 6.2% in
the heart size and indirectly the severity of mitral regurgitation on the ACKCSC, Inc. Health Survey 2004-2005.7,32,33
radiographs. Left atrial enlargement is found to occur only in the
last year prior to congestive heart failure. Echocardiographic studies Cataracts: In the Cavalier King Charles spaniel, onset is at an early
suggest that mitral regurgitation and prolapse may be present in age (less than 6 months), affecting the cortex and nucleus with
most affected dogs by 5 years of age. Predisposition may be related rapid progression to complete cataract, resulting in blindness.
to serotonin (5HT) metabolism. Heritability estimates of 0.67 for Punctate cataracts also occur. Reported in 3.90% of Cavalier
the grade of murmur and 0.33 for the presence/absence of murmur King Charles spaniels presented to veterinary teaching hospitals.
have been calculated in the breed. Heart murmurs are reported Identified in 2.98% of Cavalier King Charles spaniels CERF examined
at a frequency of 30.7%, and mitral valve disease at 27.0% in the by veterinary ophthalmologists between 2000-2005. Reported at
ACKCSC, Inc. Health Survey 2004-2005. Mode of inheritance has not 6.0% in the ACKCSC, Inc. Health Survey 2004-2005. CERF does not
been determined.7,11,12,13,14,15,16 recommend breeding any CKCS with a cataract.7,30,34
Chiari-like Malformation (Occipital Bone Hypoplasia): This Keratoconjunctivitis Sicca (KCS, Dry Eye): Ocular condition
condition is characterized by a shortening of the basicranium and causing lack of tear production and secondary conjunctivitis, corneal
supra-occipital bone with a compensatory lengthening of the cranial ulcerations, and vision problems. Age of onset 2-5 years. Treat
vault, especially the parietal bone. CM can be diagnosed with MRI. with topical ocular lubricants and anti-inflammatory medication.
CM can strongly predispose, but is not necessary for the brain Reported at 5.3% in the ACKCSC, Inc. Health Survey 2004-2005.7,35
disease syringomyelia.17,18,19,20,21,22,23,24,25,26,27
Allergic Dermatitis: Presents with pruritis and pyotraumatic
Pancreatic Acinar Atrophy (Exocrine Pancreatic Insufficiency): dermatitis (hot spots). Inhalant allergies were identified in 5.0%,
Cavalier King Charles Spaniels are found to have an increased Food Allergy was identified in 3.5%, and Hot Sports were identified
incidence of for immune-mediated pancreatic acinar atrophy. in 4.8% of Cavalier King Charles spaniels in the ACKCSC, Inc. Health
Clinical signs are poor weight gain, and steatorrhea. One study in Survey 2004-2005.7
the UK found a prevalence of 26.3%. Median age of onset is 6 years.
Treat with pancreatic enzyme supplementation. Breeding studies Sebaceous Cysts: Benign sebaceous skin cysts are reported at 5.0%
suggest an autosomal recessive mode of inheritance in German in the ACKCSC, Inc. Health Survey 2004-2005.7
shepherd dogs, another breed found at risk.28
Syringomyelia (SM): Syringomyelia is a condition where fluid filled
Brachycephalic Complex: Includes elongated soft palate, stenotic cavities develop within the spinal cord. The majority of affected
nares, hypoplastic trachea, and everted laryngeal saccules. dogs do not show clinical signs. Morphological variation of the
Causes dyspnea, and can cause collapse and death with extreme atlantoaxial spine found in the breed does not correlate to the
stress. Identified in 20.5% of Cavalier King Charles spaniels in an occurrence of SM. Chiari-like malformation (CM) is a predisposing
Australian study. Surgery is indicated in severe cases.29 factor, but not always present with SM. Crowding of the caudal
cranial fossa can be a predisposing factor for developing SM.
Umbilical Hernias: Congenital inherited umbilical hernias are Ultrasonography through the atlantoccipital junction can identify
reported at 12.1% in the ACKCSC, Inc. Health Survey 2004-2005.7 cerebellar herniation through the foramen magnum, but not a
syrinx. Clinical signs of SM can present usually between 5 months
135
and 3 years of age, and include persistent scratching at the shoulder intact, tympanic membrane is found in most cases with a viscous
region with apparent neck, thoracic limb, or ear pain and thoracic mucus plug filling the middle ear on myringotomy. Treatment
limb lower motor neuron deficits. Diagnosis is by MRI. The size of consists of repeated removal of the mucus plug, flushing of the
the syrinx on MRI, and dorsal horn location are positively correlated middle ear, and local and systemic medical therapy. Tympanostomy
to the amount of pain exhibited. Corticosteroid or NSAID treatment tubes may be helpful for chronic recurrent cases. The disorder must
can improve, but not resolve the clinical signs. The percentage of be differentiated from syringomyelia in the breed.49,50
Cavalier King Charles Spaniels in the general population with an
MRI identified syrinx is not determined, but is expected to be high. Fly Catching Behavior: Behavioral disorder identified in the breed
Clinical signs of SM are reported at 3.9% in the ACKCSC, Inc. Health with classic clinical signs as if watching, and then catching a fly.
Survey 2004-2005. One study computed a heritability of 0.37, with Some affected dogs may behave as if their ears or feet are irritated,
the influence of multiple genes involved.17,18,19,20,21,22,23,24,25,26,27,36,37,38,39 and some may also chase their tail. Fly catching has previously been
classified as a complex partial seizure, however non-responsiveness
Intervertebral Disc Disease (IVDD): Cavalier King Charles spaniels to anticonvulsants makes it more likely that this is a compulsive
have an increased risk of developing spinal cord disease due to disorder.51
prolapsed disk material. Clinical signs include back pain, scuffing of
paws, spinal ataxia, limb weakness, and paralysis. Reported at 3.2% Diabetes Mellitus: Caused by a lack of insulin production by
in the ACKCSC, Inc. Health Survey 2004-2005.7 the pancreas. Controlled by insulin injections, diet, and glucose
monitoring. Cavalier King Charles spaniels have a 1.45x risk of
Chronic Pancreatitis: Often subclinical inflammation of the developing the disorder. However, members of the breed with a
pancreas that can cause intermittent discomfort and gastrointes- specific IL-10 allele have a 4.05x risk of developing the disorder.
tinal upsets, and can possibly lead to pancreatic insufficiency or Unknown mode of inheritance.54,55
diabetes mellitus. Cavalier King Charles spaniels have a 3.2x relative
risk versus other breeds.40 Immunoglobulin Deficiency with Pneumocystis Pneumonia:
Cavalier King Charles spaniels can have a defect in immunity that
Idiopathic Epilepsy: Generalized or parital seizures. Control with makes them susceptible to infection with pneumocystosis. IgG
anti-seizure medication. Seizures are reported at a frequency of concentrations are lower, and IgM concentrations are significantly
3.0% in the ACKCSC, Inc. Health Survey 2004-2005. Unknown mode higher in the affected dogs.56
of inheritance.6,36
Microphthalmia: Congenital disorder of a small eye (globe)
Femoral Artery Occlusion/Aortic Thromboembolism: Observed associated with cataract, and posterior lenticonus. Identified in
in 2.3% Cavalier King Charles spaniels examined. Femoral artery 0.11% of Cavalier King Charles spaniels CERF examined by veterinary
occlusion is not clinically important in dogs because of adequate ophthalmologists between 2000-2005. CERF does not recommend
collateral circulation. The higher frequency in the breed may be due breeding any CKCS with this condition.57
to a primary femoral artery abnormality, or secondary to thrombus
formation from heart disease.41,42 Brachgnathism, Hydrocephalus, Mitochondrial Myopathy,
Prognathism, Progressive Retinal Atrophy, Renal Dysplasia, and
Hypothyroidism: Inherited autoimmune thyroiditis. 2.2% positive Wry Mouth are reported.59
for thyroid auto-antibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5%).43,44 Isolated Case Studies
Bilateral Renal Agenesis: Two one-day-old littermates were found
Persistent Pupillary Membranes: Strands of fetal remnant
to have a complete absence of both kidneys. Littermates and the
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
parents had normal kidneys.60
The later three forms can impair vision, and dogs affected with
these forms should not be bred. Identified in 1.62% of Cavalier King Ventricular Septal Defect (VSD): A ventricular septal defect was
Charles Spaniels CERF examined by veterinary ophthalmologists diagnosed in a 3-month-old male Cavalier King Charles spaniel and
between 2000-2005.30 corrected surgically.61
Eosinophilic Disease: The breed may have a predisposition to Juvenile Masticatory Muscle Myositis: Three of four 12-week-old
eosinophilic disorders. Several case reports of unrelated Cavalier cavalier King Charles spaniel littermates presented with difficulty in
King Charles spaniels with eosinophilic stomatitis, enteritis, opening the mouth. Diagnosis was established immunohistochem-
bronchopneumonopathy, or oral granulomas are reported. All istry and histopathology. Corticosteroid treatment resolved the
responded to corticosteroid therapy.45,46,47 condition in all the affected pups.62
Xanthinuria, Xanthine Urolithiasis: Several affected Cavalier King Organic Aciduria with Seizures: A 6-month-old, female Cavalier
Charles spaniels have been reported with urethral obstruction and King Charles spaniel exhibited seizures due to an organic aciduria
renal insufficiency. Xanthinuria is caused by an inherited deficiency with excessive excretion of hexanoylglycine. Cluster seizures were
of the enzyme xanthine oxidase. An autosomal recessive mode of controlled with anticonvulsants.63
inheritance is suggested.48
Points of Conformation: A broad skull, large jaws and soft mouth von Willebrand’s Disease (vWD): Severe, autosomal recessive
provide the capacity for bird fetching. The face has a moderate stop, bleeding disorder, Type III von Willebrand’s disease occurs in the
and eyes are yellow to amber. The ears are high set, triangular and breed. A genetic test has not been developed.5
medium length and pendulous, with medium leather. This medium
sized dog has a deep thorax, and is well muscled with strong bones, Patella Luxation: Polygenically inherited laxity of patellar
though not coarsely built. The topline is level or mildly ascending ligaments, causing luxation, lameness, and later degenerative
towards the rear. Working dogs would normally have any rear joint disease. Treat surgically if causing clinical signs. Too few
dewclaws removed; fronts as well. Chesapeake Bay Retrievers have been screened by OFA to determine
an accurate frequency.1
139
Disease Predispositions a frequency of 0.83% in Chesapeake Bay Retrievers. Unknown mode
of inheritance. A direct genetic test for an autosomal recessive DM
Hypothyroidism: Inherited autoimmune thyroiditis. 12.9% positive
for thyroid auto-antibodies based on testing at Michigan State susceptibility gene is available. All affected dogs are homozygous
University. (Ave. for all breeds is 7.5%).6,7 for the gene, however, only a small percentage of homozygous dogs
develop DM. OFA testing shows 45% carrier and 12% homozygous
Distichiasis: Abnormally placed eyelashes that irritate the cornea “at risk” for the DM susceptibility gene.14,15,16
and conjunctiva. Can cause secondary corneal ulceration. Dorn
reports a 1.53x odds ratio in Chesapeake Bay Retrievers versus Entropion/Ectropion: Rolling in or out of the eyelids. Can cause
other breeds. Identified in 5.98% of Chesapeake Bay Retrievers CERF corneal irritation or conjunctivitis. Dorn reports a 1.40x odds ratio
examined by veterinary ophthalmologists between 2000-2005.2,8 in Chesapeake Bay Retrievers versus other breeds. Entropion is
reported in 0.55% and Entropion in 0.09% of Chesapeake Bay
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis Retrievers CERF examined by veterinary ophthalmologists between
and pyotraumatic dermatitis (hot spots). Reported at a frequency of 2000-2005.2,8
4.5% in the 2004 ACC Health Survey.9
Adult-onset Hair Loss (Endocrine Hair Loss): Young adult
Umbilical Hernia: Congenital opening in the body wall from where Chesapeake Bay Retrievers present with nonpruritic, non-inflam-
the umbilical cord was attached. Reported at a frequency of 4.3% in matory, hair loss affecting the axillae, latero-ventral thorax,
the 2004 ACC Health Survey. Unknown mode of inheritance.9 flanks, ventrum, dorsum, rump and/or the caudal part of the
thighs in both male and female dogs. Hormonal investigations
Cataracts: Posterior cortical, axial, triangular opacities are the showed increased adrenal and sex steroid concentration in seven
major inherited cataract in the breed, though anterior, capsular, and cases. Histopathology revealed follicular hyperkeratosis and
nuclear cataracts also occur. Age of onset around one year of age. plugging, follicular atrophy, and occasional melanin clumping with
Identified in 4.23% of Chesapeake Bay Retrievers CERF examined malformed hair shafts. Unknown mode of inheritance.17
by veterinary ophthalmologists between 2000-2005. Early reports
suggest dominant inheritance with incomplete penetrance. CERF Anterior Crossbite, Brachygnathism, Central PRA, Prognathism,
does not recommend breeding any Chesapeake Bay Retriever with a Retinal Dysplasia, and Wry Mouth are reported.18
cataract.2,10
Isolated Case Studies
Idiopathic Epilepsy: Generalized or partial seizures. Control with Tricuspid Stenosis: A 3-year-old castrated male Chesapeake
anti-seizure medication. Reported at a frequency of 3.5% in the Bay Retriever was referred for evaluation of tachypnea, exercise
2004 ACC Health Survey. Unknown mode of inheritance.9 intolerance, and cyanosis. On echocardiographs, there was severe
tricuspid stenosis and right-to-left atrial-level shunting of blood.
Humeral Osteochondritis Dissecans (OCD): Polygenically inherited
Balloon dilation of the stenotic tricuspid valve was palliative.19
cartilage defect of the humeral head. Causes shoulder joint pain
and lameness in young growing dogs. Mild cases can resolve with Lymphangiosarcoma: Case study of a a three-year-old, neutered
rest, while more severe cases require surgery. 50% of cases are male Chesapeake Bay Retriever presented for acute swelling of the
bilateral. Reported 7.7x odds ratio versus other breeds.11 head, neck, and cranial trunk. Diffuse lymphangiosarcoma involving
the superficial and deep dermis and subcutaneous tissue was
Cranial Cruciate Ligament Rupture (ACL): Traumatic tearing of
observed on skin biopsies.20
the anterior cruciate ligament. The breed is found to be one with an
increased incidence. Dorn reports a 2.01x odds ratio in Chesapeake
Bay Retrievers versus other breeds. Treatment is surgery.8,12 Genetic Tests
Tests of Genotype: Direct test for prcd-PRA is available from
Persistent Pupillary Membranes: Strands of fetal remnant Optigen.
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
later three forms can impair vision, and dogs affected with these Direct test for EIC is available from the University of Minnesota
forms should not be bred. Identified in 1.55% of Chesapeake Bay Veterinary Diagnostic Lab.
Retrievers CERF examined by veterinary ophthalmologists between
2000-2005.2 Direct genetic test for an autosomal recessive DM susceptibility
gene is available from the OFA.
Gastric Dilatation-Volvulus (bloat, GDV): Polygenically inherited,
life-threatening twisting of the stomach within the abdomen. Tests of Phenotype: CHIC Certification: Required testing includes
Requires immediate treatment. Reported at an increased frequency hip and elbow radiographs, and CERF eye examination (after 12
in the breed.13 months of age). Optional recommended testing for prcd-PRA,
thyroid profile including autoantibodies, and congenital cardiac
Degenerative Myelopathy (DM): Affected dogs show an insidious examination. (See CHIC website; www.caninehealthinfo.org).
onset of upper motor neuron (UMN) paraparesis at an average
age of 11.4 years. The disease eventually progresses to severe Recommend patella evaluation.
tetraparesis. Affected dogs have normal results on myelography,
MRI, and CSF analysis. Necropsy confirms the condition. Reported at
140
Miscellaneous 21. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p 33-37.
• Breed name synonyms: Chessie
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 48 (2,463 dogs registered)
• Internet resources: The American Chesapeake Club:
www.amchessieclub.org/
Chesapeake Bay Retriever Club of Canada: www.cbrcc.ca
Chesapeake Bay Retriever Club (UK):
www.chesapeakebayretrieverclub.co.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Morris Animal Foundation: Morris Animal Foundation Update: Genetic
Tests Focus on Breed-Specific Vision Problems. Canine Pract 1999:24(4):21.
4. Minor KM, Patterson EE, Gross SD, et. al.: Frequency of the Canine
Exercise Induced Collapse Gene in Diverse Breeds. Proceedings, 2009 ACVIM
Forum. 2009.
5. Johnson GS, Lees GE, Benson RE, et. al.: A bleeding disease (von
Willebrand’s disease) in a Chesapeake Bay Retriever. J Am Vet Med Assoc.
1980 Jun 1;176(11):1261-3.
6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
7. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
8. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
9. American Chesapeake Club: 2004 American Chesapeake Club Health
Survey. 2004.
10. Gelatt KN, Whitley RD, Lavach JD, et. al.: Cataracts in Chesapeake Bay
Retrievers. J Am Vet Med Assoc. 1979 Dec 1;175(11):1176-8.
11. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
12. Duval JM, Budsberg SC, Flo GL, et. al.: Breed, sex, and body weight as
risk factors for rupture of the cranial cruciate ligament in young dogs. J
Am Vet Med Assoc. 1999 Sep 15;215(6):811-4.
13. Glickman LT, Glickman NW, Schellenberg DB, et. al.: Incidence of and
breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet
Med Assoc. 2000 Jan 1;216(1):40-5.
14. Coates JR: Degenerative Myelopathy of Pembroke Welsh Corgi Dogs.
Proceedings, 2005 ACVIM Forum. 2005.
15. Coates JR & Wade C: Update on the Genetic Basis of Canine
Degenerative Myelopathy. Proceedings, 2008 ACVIM Forum. 2008.
16. Awano T, Johnson GS, Wade CM, et. al.: Genome-wide association
analysis reveals a SOD1 mutation in canine degenerative myelopathy that
resembles amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A. 2009 Feb
24;106(8):2794-9.
17. Cerundolo R, Mauldin EA, Goldschmidt MH, et. al.: Adult-onset hair loss
in Chesapeake Bay retrievers: a clinical and histological study. Vet Dermatol.
2005 Feb;16(1):39-46.
18. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 209, AAHA Press, 1999.
19. Kunze P, Abbott JA, Hamilton SM, et. al.: Balloon valvuloplasty for
palliative treatment of tricuspid stenosis with right-to-left atrial-level
shunting in a dog. J Am Vet Med Assoc. 2002 Feb 15;220(4):491-6, 464.
20. Fossum TW, Miller MW, Mackie JT: Lymphangiosarcoma in a dog
presenting with massive head and neck swelling. J Am Anim Hosp Assoc.
1998 Jul-Aug;34(4):301-4.
141
Chihuahua
pink in blonde dogs. The neck is short and the topline is level, ribs
are well sprung and the thorax is moderate in depth. The tail is
sickle shaped and rests out or up over the back (just touching).
Limbs are straight, and feet are very small with toes set well apart.
Longevity: 12-14 years. Hip Dysplasia and Legg-Calve Perthes Disease: Polygenically
inherited traits causing degenerative hip joint disease and arthritis.
Points of Conformation: Their build is compact and well muscled, Too few Chihuahuas have been screened by OFA to determine an
and they are longer than tall, with fine bones. They have a domed accurate frequency. Reported 26.8x odds ratio for Legg-Calve-
skull, large wide-set dark eyes, though in light dogs, the eye color Perthes versus other breeds.5,7
may match the coat. Domed skulls in some dogs leads to an open
fontanelle termed molera. Ears are erect when alert, and folded Elbow Dysplasia: Polygenically inherited trait causing elbow
back when resting. They are large and triangular. The muzzle is arthritis. Too few Chihuahuas have been screened by OFA to
moderately short and tapers. The nose is black or self-colored, or determine an accurate frequency.5
142
Disease Predispositions Progressive Retinal Atrophy (PRA): Inherited degeneration
of the retina. Presumed autosomal recessive inheritance. 1.9%
Hydrocephalus: Congenital increased volume of cerebrospinal
fluid (CSF), with a concurrent dilation of the ventricular system of Chihuahuas CERF examined by veterinary ophthalmologists
and reduction of brain tissue. Can cause behavior changes, visual between 2000-2005 are identified as affected, and 1.27% as
defects, impaired motor function, or seizures. Not all Chihuahuas suspicious for PRA.9,16
with an open fontanel are hydrocephalic. Dorn reports a 62.63x
Urinary Calculi: The breed is found to be at an increased risk of
odds ratio versus other breeds.6,8
developing oxalate, and cystine bladder stones. Cystine calculi are
Dental Issues: A high frequency of undershot bites, overshot bites. secondary to a defect in cystine metabolism.17,18,19
and wry mouth are reported in the 2009 CCA Health Survey.3
Corneal Dystrophy: Endothelial form is associated with progressive
Vitreous Degeneration: Liquefaction of the vitreous gel which may corneal edema, which can lead to bullous keratopathy and corneal
predispose to retinal detachment and blindness. Identified in 5.70% erosions. Onset 6-13 years, with an average of 9.5 years. Treatment
of Chihuahuas CERF examined by veterinary ophthalmologists is symptomatic and palliative. Identified in 0.63% of Chihuahuas
between 2000-2005.9 CERF examined by veterinary ophthalmologists between
2000-2005.9,20
Collapsing Trachea: Caused by diminished integrity of the cartilage
rings in the trachea. Can produce increased coughing, stridor, and Pulmonic Stenosis: Inherited congenital malformation of the
respiratory distress. Dorn reports a 5.57x odds ratio versus other pulmonic valve. Causes stricture of the right ventricular outflow
breeds.6 tract or stricture of the pulmonary artery. The Chihuahua is
identified as a breed at increased risk. Undetermined mode of
Persistent Pupillary Membranes: Strands of fetal remnant inheritance.21
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
later three forms can impair vision, and dogs affected with these Acquired Myasthenia Gravis: Chihuahuas are a breed at increased
forms should not be bred. Identified in 5.06% of Chihuahuas CERF risk of developing generalized or focal acquired myasthenia gravis.
examined by veterinary ophthalmologists between 2000-2005.9 The most common presenting signs were generalized weakness,
with or without megaesophagus. Diagnosis is by identifying serum
Canine Pattern Baldness: Progressive alopecia developing at acetylcholine receptor antibodies.22
the post- and/or pre-auricular regions, along the ventral neck,
thorax and abdomen, and on the caudomedial thighs. The hair loss Necrotizing Meningoencephalitis: A non-suppurative acute to
starts around 6 months of age and gradually progresses over the chronic necrotizing meningoencephalitis is identified in Chihuahuas,
following year, but remains restricted to the described areas.10 similar to that seen in the Pug and Maltese breeds. Genetic research
suggests different genetic causes between breeds. Affected dogs
Umbilical Hernia/Cleft Palate: Both of these congenital anomalies present with seizures, blindness and mentation changes from 1 to
are reported at an increased frequency in the breed.3 10 years of age.23,24,25
Cryptorchidism (Retained Testicles): Can be bilateral or unilateral. Color Dilution Alopecia, Demodicosis, Factor VIII Deficiency,
Chihuahuas have an increased prevalence of the disorder.3,11 Glaucoma, Keratoconjunctivitis Sicca, Methemoglobin
Reductase Deficiency, Myelodysplasia, Neuroaxonal Dystrophy,
Cataracts: Anterior and posterior cortex intermediate cataracts Osteochondritis Dessicans-Shoulder, Patent Ductus Arteriosus,
predominate in the breed, although nuclear and capsular cataracts Retained Primary Teeth, and Spina Bifida, are reported.26
also occur. Identified in 4.43% of Chihuahuas CERF examined by
veterinary ophthalmologists between 2000-2005. CERF does not Isolated Case Studies
recommend breeding any Chihuahua with a cataract.3,9 Primary Hypoparathyroidism: Two Chihuahuas were diagnosed in
a 15 year study in Australia. Affected dogs presented with Seizures,
Chronic Valvular Disease/Endocardiosis: Thickening of the heart
muscle tremors and fasciculations due to hypocalcemia. Treatment
valves with age, leading to congestive heart disease. Reported
with calcium supplementation.27
increased frequency in the breed. Dorn reports a 3.11x odds ratio
versus other breeds.6,12 Leiomyosarcoma: A 2 month-old female Chihuahua had a
3-week history of progressive disorientation, left-sided circling,
Hypothyroidism: Inherited autoimmune thyroiditis. 2.6% positive
and incessant whimpering. Necropsy revealed a primary
for thyroid auto-antibodies based on testing at Michigan State
leiomyosarcoma in the midline of the posterior thalamus with
University. (Ave. for all breeds is 7.5%).13,14
secondary obstructive hydrocephalus of the lateral ventricles.28
Portosystemic Shunt (PSS, liver shunt): Congenital disorder,
Narcolepsy: A two-year-old male Chihuahua suffered paroxysmal
where abnormal blood vessels connecting the systemic and portal
attacks of muscle weakness and immobility elicited by stimulation,
blood flow. Vessels can be intrahepatic or extrahepatic. Causes
such as feeding. Low CSF levels of hypocretin provided a diagnosis
stunting, abnormal behavior and possible seizures. Tobias reports
of hypocretin-deficient narcolepsy. The dog responded to treatment
a 4.9x Odds Ratio versus other breeds. Undetermined mode of
with imipramine.29
inheritance.15
143
Ceroid-Lipofuscinosis: A two-year-old, female chihuahua 8. Axlund TW: Managing the Hydrocephalic Patient: Medical and Surgical
presented with a six-month history of visual dysfunction. Options. Proceedings, 2004 Atlantic Coast Veterinary Conference. 2004.
Histologically, swollen neurons possessing yellowish pigment 9. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
granules in the cytoplasm were observed throughout the CNS. College of Veterinary Ophthalmologists. ACVO, 2007.
10. White SD: Update on Follicular Alopecias: ‘Pseudo-Endocrinopathies’.
These storage materials stained positively for ceroid-lipofuscinosis.
Proceedings, 2005 ACVIM Forum. 2005.
There was a concurrent hydrocephalus.30 11. Yates D, Hayes G, Heffernan M, et. al: Incidence of cryptorchidism in
dogs and cats. Vet Rec. 2003 Apr 19;152(16):502-4.
Esophagobronchial Fistula: A 10-month-old, intact male 12. Keene BW, Hamlin RL, Rush JE, et. al.: Diagnosis and Management of
Chihuahua presented for a 7-month history of regurgitation and Canine Chronic Valvular Disease. Proceedings, 2004 Northeast Veterinary
coughing. Survey radiographs revealed a soft-tissue opacity within Conference. 2004.
the distal esophagus. A contrast study confirmed the presence of an 13. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
esophagobronchial fistula.31 for Population and Animal Health, Michigan State University. April, 2007.
14. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
Cardiac Fibrosarcoma: A 6-year-old Chihuahua dog presented serum thyroid hormone autoantibodies in dogs with clinical signs of
with dyspnea, cyanosis, and pleural effusion. At necropsy, primary hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71
cardiac fibrosarcoma of the right atrium was diagnosed.32 15. Tobias KM & Rohrbach BW: Association of breed with the diagnosis of
congenital portosystemic shunts in dogs: 2,400 cases (1980-2002). J Am
Absence Seizures with Myoclonus: An eight-month-old Vet Med Assoc. 2003 Dec 1;223(11):1636-9.
Chihuahua was reported with recurrent episodes of head and nose 16. Hurn SD, Hardman C, Stanley RG: Day-blindness in three dogs: clinical
twitching lasting one to two seconds, multiple times per day. EEG and electroretinographic findings. Vet Ophthalmol. 2003 Jun;6(2):127-30.
confirmed epilepsy.33 17. Jones BR, Kirkman JH, Hogan J, et. al.: Analysis of uroliths from cats and
dogs in New Zealand, 1993-96. N Z Vet J. 1998 Dec;46(6):233-6.
18. Dolinsek D: Calcium oxalate urolithiasis in the canine: surgical
Genetic Tests management and preventative strategies. Can Vet J. 2004 Jul;45(7):607-9.
Tests of Genotype: Direct tests for color alleles and coat length are 17. Ling GV, Franti CE, Ruby AL, et. al.: Urolithiasis in dogs. II: Breed
available from VetGen. prevalence, and interrelations of breed, sex, age, and mineral composition.
Am J Vet Res. 1998 May;59(5):630-42.
Tests of Phenotype: CHIC Certification: Required testing includes 20. Cooley PL, Dice PF 2nd: Corneal dystrophy in the dog and cat. Vet Clin
congenital cardiac evaluation, CERF eye examination (minimum 1 North Am Small Anim Pract. 1990 May;20(3):681-92.
year of age), and patella evaluation (minimum 1 year of age). (See 21. McCaw D, Aronson E: Congenital cardiac disease in dogs. Mod Vet Pract.
CHIC website; www.caninehealthinfo.org). 1984 Jul;65(7):509-12.
22. Shelton GD, Schule A, Kass PH: Risk factors for acquired myasthenia
Additional recommended tests are hip and elbow radiographs, and gravis in dogs: 1,154 cases (1991-1995). J Am Vet Med Assoc. 1997 Dec
1;211(11):1428-31.
thyroid profile including autoantibodies.
23. Kube SA, Dickinson PJ, Affolter TW, et. al.: Necrotizing Meningoenceph-
alitis in Chihuahua Dogs. Proceedings, 2005 ACVIM Forum. 2005.
Miscellaneous 24. Pedersen NC, Vernau K, Dickinson P, et. al.: DLA Association in Various
• Breed name synonyms: Teacup, Chi, Chihauhau Toy Breeds with Immune Mediated Encephalopathies. Proceedings, 4th
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), Tufts’ Canine and Feline Breeding and Genetics Conference. 2009.
ANKC (Australian National Kennel Club), NKC (National Kennel Club) 25. Higgins RJ, Dickinson PJ, Kube SA, et. al.: Necrotizing meningoencepha-
• AKC rank (year 2008): 12 (15,985 dogs registered) litis in five Chihuahua dogs. Vet Pathol. 2008 May;45(3):336-46.
26. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
• Internet resources: Chihuahua Club of America:
Ackerman. p. 209. AAHA Press, 1999.
http://www.chihuahuaclubofamerica.com/ 27. Russell NJ, Bond KA, Robertson ID, et. al.: Primary hypoparathy-
British Chihuahua Club: www.the-british-chihuahua-club.org.uk roidism in dogs: a retrospective study of 17 cases. Aust Vet J. 2006
Aug;84(8):285-90.
References 28. Zabka TS, Lavely JA, Higgins RJ: Primary intra-axial leiomyosarcoma
1. Vroom MW, Slappendel RJ: Transient juvenile hypoglycaemia in a with obstructive hydrocephalus in a young dog. J Comp Pathol. 2004
Yorkshire terrier and in a Chihuahua. Vet Q. 1987 Apr;9(2):172-6. Nov;131(4):334-7.
2. Clark LA, Wahl JM, Rees CA, et. al.: Retrotransposon insertion in SILV is 29. Tonokura M, Fujita K, Morozumi M, et. al.: Narcolepsy in a hypocretin/
responsible for merle patterning of the domestic dog. Proc Natl Acad Sci U orexin-deficient chihuahua. Vet Rec. 2003 Jun 21;152(25):776-9.
S A. 2006 Jan 31;103(5):1376-81. 30. Kuwamura M, Hattori R, Yamate J, et. al.: Neuronal ceroid-lipofus-
3. Chihuahua Club of America: 2009 Chihuahua Club of America Health cinosis and hydrocephalus in a chihuahua. J Small Anim Pract. 2003
Survey. 2009. May;44(5):227-30.
4. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by 31. Nawrocki MA, Mackin AJ, McLaughlin R, et. al.: Fluoroscopic and
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8. endoscopic localization of an esophagobronchial fistula in a dog. J Am
5. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010. Anim Hosp Assoc. 2003 May-Jun;39(3):257-61.
6. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at 32. Madarame H, Sato K, Ogihara K, et. al.: Primary cardiac fibrosarcoma in
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation. a dog. J Vet Med Sci. 2004 Aug;66(8):979-82.
2000. 33. Poma R, Ochi A, & Cortez MA: Absence seizures with myoclonic features
7. LaFond E, Breur GJ & Austin CC: Breed susceptibility for in a juvenile Chihuahua dog. Epileptic Disord. 2010 Jun;12(2):138-41.
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002 34. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Sep-Oct;38(5):467-77. Book House, NY 2006. p. 458-461.
144
Chinese Crested
at the tip. In action the tail is held high or even over the back.
Dewclaws may be removed. The finely boned limbs are straight, the
feet are elongated with a “hare” conformation. The gait is quick and
agile, but smooth. Skin may have a mottled pigmentation.
Physical Characteristics Chinese crested dogs are very sensitive to heat and cold. The skin
Height at Withers: 11-13“ (28-33 cm) is thin, and prone to lacerations and dryness. They sweat through
their skin so they do not pant as much as other breeds.
Weight: 5-12 lb (2-5.5 kg)
Coat: Two coat types exist: Hairless and Powderpuff. Hairless have
Drug Sensitivities
None reported
no body hair. It is present only on the extremities and the head hair
is called the crest. From the metacarpals and going distally, and
from the tarsus distally they have socks of hair. The tail has a plume Inherited Diseases
of hair as well. In all dogs the hair is silky, but the Powderpuff has a Incomplete Dentition: It is common to have variable expression of
double coat. Any color is accepted, as is any color combination. missing premolars with the autosomal dominant hairless phenotype.1,2
Powderpuff is a full-coated variety. Mixed haircoat litters are born Patella Luxation: Polygenically inherited laxity of patellar ligaments,
to Powderpuff X hairless and hairless X hairless crosses. These two causing luxation, lameness, and later degenerative joint disease.
varieties are generally crossed because the hairless dogs are not Treat surgically if causing clinical signs. OFA reports 4.5% affected.3
as vigorous (breeding, integument, missing teeth). The hairless
type is AD, and homozygotes are not viable, so hairless dogs are Primary Lens Luxation (PLL) and Secondary Glaucoma:
heterozygotes. An autosomal recessive gene causes primary lens luxation.
Homozygous affected dogs usually develop lens luxation between
Longevity: 12-13 years. 4-8 years of age. Rarely, heterozygous carriers can develop lens
luxation, but at a later age. Lens luxation can lead to secondary
Points of Conformation: A fine-boned toy dog with almost square glaucoma and blindness. A genetic mutation has been identified,
proportions. Eyes are wide set and nose and eyes are colored to and a genetic test is available. OFA testing shows 27% carrier, and
match the coat, and almond shaped. Erect ears are large, the skull 2% affected.4
is wedge shaped, the stop distinct, and the muzzle tapers. In the
hairless variety, missing teeth are not faulted but in Powderpuff they Progressive Retinal Atrophy (PRA): More than one form of
are. The slightly arched neck provides for high head carriage. The PRA occurs in the breed. The autosomal recessive prcd form (age
topline is level though the croup slopes down slightly. The thorax of onset between 3-8 years) occurs, and a genetic test exists but
is moderately shallow and there is a moderate abdominal tuck. The prcd-PRA does NOT appear to be the predominant PRA disease type.
tapered tail reaches the tarsus at rest, and is slender with a curve (See Optigen website: www.optigen.com) 0.56% of Chinese Crested
145
Dogs CERF examined by veterinary ophthalmologists between
2000-2005 are identified as affected, and 1.55% as suspicious for
Isolated Case Studies
None reported
PRA. CERF does not recommend breeding Chinese Crested Dogs
affected with PRA.5
Genetic Tests
Hip Dysplasia and Legg-Calve Perthes Disease: Polygenically Tests of Genotype: Direct test for prcd-PRA test is available from
inherited traits causing degenerative hip joint disease and arthritis. Optigen.
Too few Chinese Crested Dogs have been screened by OFA to
determine an accurate frequency.3 Direct test for PLL is available from the OFA and the Animal Health
Trust.
Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. Too few Chinese Crested Dogs have been screened by OFA Tests of Phenotype: CHIC Certification: Required testing includes
to determine an accurate frequency.3 CERF eye examination (annually), patella evaluation (at a minimum of
1 year of age), and a congenital cardiac evaluation. Optional testing
Canine Multiple System Degeneration (CMSD): This rare, includes genetic tests for PLL and prcd-PRA, BAER hearing test, and
autosomal recessive disorder causes progressive cerebellar hip radiographs. (See CHIC website; www.caninehealthinfo.org).
ataxia, with its onset between nine and sixteen weeks of age.
Histopathology shows loss of Purkinje’s cells, then bilateral Recommend elbow radiographs and thyroid profile including
symmetric degeneration of the olivary nuclei, followed by autoantibodies.
degeneration of the substantia nigra and caudate nucleus. Affected
dogs do not survive beyond 5-6 months of age.1 Miscellaneous
• Breed name synonyms: Crested, Crestie, Powderpuff, Chinese
Disease Predispositions Edible dog (historical), Chinese Hairless, Chinese Royal Hairless,
Vitreous Degeneration: Liquefaction of the vitreous gel Chinese Ship Dog (historical), South African Hairless (historical in
which may predispose to retinal detachment and blindness. Africa), Pyramid or Giza Hairless (historical name in Egypt)
Vitreous Degeneration is reported in 7.69% of Chinese crested • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
dogs CERF-examined by veterinary ophthalmologists between ANKC (Australian National Kennel Club), NKC (National Kennel Club)
2000-2005.5 • AKC rank (year 2008): 54 (2,098 dogs registered)
• Internet resources: American Chinese Crested Club Inc.:
Hypothyroidism: Inherited autoimmune thyroiditis. 7.4% positive www.accc.chinesecrestedclub.info/
for thyroid auto-antibodies based on testing at Michigan State Chinese Crested Club of Great Britain:
University. (Ave. for all breeds is 7.5%).6,7 www.thechinesecrestedclubofgb.co.uk
Chinese Crested Club of Canada:
Sunburn: Chinese crested dogs are very sensitive to sunlight www.chinesecrestedclubcanada.com
(ultraviolet radiation). Sun block should be used when exposed to
direct sunlight. References
1. O’brien DP, Johnson GS, Schnabel RD, et. al.: Genetic mapping of canine
Cataracts: Anterior and posterior cortex intermediate cataracts multiple system degeneration and ectodermal dysplasia Loci. J Hered. 2005
predominate in the breed, although nuclear and capsular cataracts Nov-Dec;96(7):727-34.
also occur. Reported in 5.92% of Chinese Cresteds presented to 2. Drögemüller C, Karlsson EK, Hytönen MK, et. al.: A mutation in hairless
veterinary teaching hospitals. Identified in 2.02% of Chinese Crested dogs implicates FOXI3 in ectodermal development. Science. 2008 Sep
Dogs CERF examined by veterinary ophthalmologists between 12;321(5895):1462.
2000-2005. CERF does not recommend breeding any Chinese 3. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Crested Dogs with a cataract.5,8 4. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing
lens luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
Persistent Pupillary Membranes: Strands of fetal remnant 5. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
later three forms can impair vision, and dogs affected with these Population and Animal Health, Michigan State University. April, 2007.
forms should not be bred. Identified in 1.85% of Chinese Crested Dogs 7. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
CERF examined by veterinary ophthalmologists between 2000-2005.5 hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
Comedomes (Blackheads): The skin of Chinese crested dogs 8. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
are prone to spontaneous comedome formation throughout the the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
dorsal skin, on the limbs and prepuce. Plugged follicles containing 9. Kimura T, Doi K: Spontaneous comedones on the skin of hairless
abundant sebum and keratic substances resembles human acne.9 descendants of Mexican hairless dogs. Exp Anim. 1996 Oct;45(4):377-84.
10. Strain GM: Deafness prevalence and pigmentation and gender
Deafness: Unilateral or bilateral congenital deafness is reported by associations in dog breeds at risk. Vet J 2004; Jan;167(1):23-32.
Strain. Diagnosed by BAER testing.10 11. The Genetic Connection: A Guide to Health Problems in Purebred Dogs.
L Ackerman. p. 209-10. AAHA Press, 1999.
12. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Brachygnathism and Prognathism are reported.11
Book House, NY 2006. p. 462-465.
146
Chinese Shar-pei
broad and flattened, the butterfly nose is black or matching the
coat color, nostrils are wide. The tail is thick at its origin, tapers to
the tip and is very high set. It curls over the back when the dog
is alert. Metatarsals are short, and rear dewclaws are removed.
Forelimbs are straight and moderately boned and muscled, feet
are medium-sized and toes are arched (not splayed). Their gait is
smooth and ground covering.
Coat: The straight, short standoff coat is very unusual in texture, Hip Dysplasia: Polygenically inherited trait causing degenerative
being very short (< 1”) and very rough (bristles). Solid colors such as joint disease and hip arthritis. OFA reports 13.4% affected.3
black, cream and red and sable are accepted, but some shading of
solids is often present and is acceptable. Patella Luxation: Polygenically inherited laxity of patellar ligaments,
causing luxation, lameness, and later degenerative joint disease. Treat
Longevity: 11-12 years. surgically if causing clinical signs. Reported 11.4x odds ratio versus
other breeds. OFA reports 9.9% affected.3,4
Points of Conformation: Blue-black tongue, palate, gingivae and
lips/flews are present. Significant skin wrinkles are also a unique Primary Lens Luxation: Autosomal recessive inherited disorder
characteristic of this breed. Note that puppies have much more in the Shar Pei. The average age of onset of affected dogs is 4.9
extensive wrinkles than the adult. In the adult the wrinkles may years (range 3-6 years). Relative risk of 44.66x versus other breeds.
remain on the head, neck, and anterior thorax. Their dark eyes are Identified in 1.89% of Shar Peis CERF examined by veterinary
small, deep set and almond shaped, and the expression is defined ophthalmologists between 2000-2005. CERF does not recommend
as scowling. Irises may be lighter in light coated dogs. The neck breeding any Shar Pei with lens luxation. No genetic test is
is short and strong, with a well-developed dewlap, the topline is available.5,6,7
fairly level though a dip behind the withers should be present. The
thorax has moderate depth. Square, compact conformation, and Disease Predispositions
medium in size, the head is large for the body, and their triangular Entropion: Entropion, a rolling in of the eyelids, can cause corneal
thick-leathered clamshell ears are small and lying folded flat irritation and ulceration. It is reported in 38.68% of Shar Peis CERF
forward against the head. Prick ears are a disqualification. Their examined by veterinary phthalmologists between 2000-2005.
muzzle has a shape described as “hippopotamus” because of its Reported at a frequency of 34.9% in the CSPCA Health Through
fullness. Soft tissue may even cause a slight bulging or fold of Education Health Survey. CERF does not recommend breeding any
the nose on top of the muzzle. The stop is moderate, and skull is Shar Pei with entropion.6,8
147
Ear Disease: Bacterial ear infection was identified in 16.0% of in some dogs by intermittent fever and joint swelling (Shar Pei
Shar Peis, Yeast ear infection was identified in 31.8%, and Stenotic fever). Pathological findings include deposition of amyloid in the
(narrowed) ear canals was identified in 9.2% of Shar Peis in the renal medulla, with possible deposition in glomeruli, liver, spleen,
CSPCA Health Through Education Health Survey.8 stomach, small intestine, myocardium, lymph node, prostate
gland, thyroid gland, and pancreas. Shar Pei dogs under 7 years
Shar Pei Fever, Recurrent Fever of Unknown Origin (RFUO): of age have a 10x odds ratio of developing RA. The prevalence of
Breed-related disorder causing high fever, swollen joints (especially RA among littermates is between 25% and 50%. Reported at a
hocks), and predisposing to renal amyloidosis and renal failure. An frequency of 4.5% in the CSPCA Health Through Education Health
epidemiological survey of privately owned dogs indicated a RFUO Survey.8,23,24
prevalence of 23% in Shar Pei dogs. Reported at a frequency of
23.0% in the CSPCA Health Through Education Health Survey.8,9,10 Demodicosis: Focal or generalized demodectic mange has an
underlying immunodeficiency in its pathogenesis. Reported at a
Allergies: Inhalant allergies were identified in 7.7%, and Food frequency of 3.5% in the CSPCA Health Through Education Health
Allergy was identified in 14.1% of Shar Peis in the CSPCA Health Survey.8
Through Education Health Survey.8
Primary (Narrow Angle) Glaucoma: Ocular condition causing
Cutaneous Mucinosis: Breed-related disorder of dermatitis increased pressure within the eyeball, and secondary blindness due
secondary to mucin accumulation in skin. Studies show a defect to damage to the retina. Diagnose with tonometry and gonioscopy.
in hyaluronic acid metabolism associated with the HAS2 gene. Diagnosed in 4.40% of Shar Peis presented to veterinary teaching
This condition may be related to abnormal mast cell function hospitals.25
or accumulation. Treatment is with steroids. Reported at a
frequency of 12.1% in the CSPCA Health Through Education Health Megaesophagus: Dilated esophagus resulting in regurgitation and
Survey.8,11,12,13,14,15,16 possible inhalation pneumonia. Can be secondary to hiatal hernia
in this breed. Reported at a frequency of 4.0% in the CSPCA Health
Cobolamin Deficiency: Affected Shar Pei present with signs of Through Education Health Survey.8
chronic small intestinal disease, gastrointestinal protein loss, and
possibly exocrine pancreatic insufficiency. Shar Pei have a 55.6x Cataracts: Capsular and anterior cortex cataracts predominate
odds ratio versus other breeds. A region of chromosome 13 has in the breed, though posterior and nuclear cataracts also occur.
been identified that cosegregates with cobalamin deficiency in the Identified in 3.77% of Shar Peis CERF examined by veterinary
Chinese Shar Pei, but the actual gene and mechanism causing the ophthalmologists between 2000-2005. CERF does not recommend
disease has not been identified. Undetermined mode of inheritance. breeding any Shar Pei with a cataract. Reported at a frequency of
Test with serum cobalamin and B12 levels. Treat with cobalamin 3.0% in the CSPCA Health Through Education Health Survey.6,8
supplementation. Affected dogs should not be bred.17,18
Chronic Superficial Keratitis (Pannus): Chronic corneal
Persistent Pupillary Membranes: Strands of fetal remnant inflammatory process that can cause vision problems due to
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The corneal pigmentation. Treatment with topical ocular lubricants and
later three forms can impair vision, and dogs affected with these anti-inflammatory medication. Identified in 2.83% of Shar Peis CERF
forms should not be bred. Identified in 6.60% of Shar Pei CERF examined by veterinary ophthalmologists between 2000-2005.6
examined by veterinary ophthalmologists between 2000-2005, with
3.77% iris to iris, 1.89% iris to cornea, and 1.89% iris to lens. Dorn Corneal Dystrophy: The epithelial/stromal form occurs in the breed,
reports a 7.47x odds ratio versus other breeds.6,19 causing a bilateral, white to gray, non-inflammatory corneal opacity.
Identified in 2.83% of Shar Peis CERF examined by veterinary
Aggression: Inter-dog aggression is reported at 15.0%, and ophthalmologists between 2000-2005.6
aggression toward people reported at 6.4% in the CSPCA Health
Through Education Health Survey.8 Mast Cell Tumors: An increased incidence of mast cell tumors
is seen in Shar Peis. In one study, 2.2% of all mast cell tumors
Primary Seborrhea: Abnormality of epidermal differentiation, submitted for pathology occurred in Shar Peis, despite the breed
keratinization and cornification, where the epithelial turnover rate accounting for only 0.7% of all pathology submissions. In addition,
increases to as short as 3-4 days. Characterized by a greasy, flakey, thin 28% of the mast cell tumors occurred in Shar Peis under 2 years of
haircoat. Dorn reports a 54.36x odds ratio versus other breeds.20 age. Reported at a frequency of 3.5% in the CSPCA Health Through
Education Health Survey.8,26
Bacterial Skin Infection: Reported at a frequency of 5.0% in the
CSPCA Health Through Education Health Survey.8 Ectropion: Ectropion, a rolling out of the eyelids, can cause frequent
conjunctivitis, and ocular discharge. It is reported in 1.89% of
Hypothyroidism: Inherited autoimmune thyroiditis. 4.5% positive Shar Peis CERF examined by veterinary ophthalmologists between
for thyroid auto-antibodies based on testing at Michigan State 2000-2005.6
University. (Ave. for all breeds is 7.5%.) Reported at a frequency of
10.6% in the CSPCA Health Through Education Health Survey.8,21,22 Retinal Dysplasia: Focal folds and geographic retinal dysplasia are
seen in the breed. Dogs with the geographic form should not be
Renal Amyloidosis (RA): Breed-specific syndrome seen in young bred. Reported in 1.89% of Shar Pei CERF examined by veterinary
Chinese Shar Pei dogs causing renal failure. May be preceded ophthalmologists between 2000-2005.6
148
Gastric Dilatation-Volvulus (bloat, GDV): Polygenically inherited,
life-threatening twisting of the stomach within the abdomen.
Miscellaneous
• Breed name synonyms: Shar-pei, Chinese Fighting Dog
Requires immediate treatment. Reported at a frequency of 1.3% in • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
the CSPCA Health Through Education Health Survey.8,27 ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 47 (2,583 dogs registered)
Esophageal Hiatal Hernia: Congenital disorder seen at an
• Internet resources: Chinese Shar-Pei Club of America Inc.:
increased frequency in the breed. Clinical signs are regurgitation,
www.cspca.com
vomiting, and hypersalivation. Diagnose with survey or barium
Shar-Pei Club of Great Britain: www.sharpei-clubofgb.co.uk
radiographs showing displacement of the esophagogastric
Chinese Shar-pei Club of Canada: www.peiclub.com
junction and stomach into the thoracic cavity. Affected dogs can
also develop secondary megaesophagus, gastroesophageal reflux,
esophageal hypomotility, or aspiration pneumonia. Treatment is References
with surgery.28,29,30 1. Ordeix L, Fondevila D, Ferrer L, et. al.: Quantitative study of “flame
follicles” in skin sections of Shar-pei dogs. Vet Dermatol. 2002
Primary Immunodeficiency: Primary immunodeficiency syndromes Oct;13(5):261-5.
are described in the breed; including IgA deficiency, and combined 2. Battison A: Apparent pseudohyperkalemia in a Chinese Shar Pei dog. Vet
Clin Pathol. 2007 Mar;36(1):89-93.
IgM, IgA, and IgG deficiency. Clinical signs include frequent
3. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
recurrent infections (respiratory and skin), and malignancy.31,32,33
4. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Pemphigus Foliaceus: The breed has an increased risk (7.9x odds
Sep-Oct;38(5):467-77.
ratio) of developing pemphigus foliaceus. Clinical signs include 5. Lazarus JA, Pickett JP, Champagne ES: Primary lens luxation in the
crusting lesions to the dorsal part of the muzzle and head, Chinese Shar Pei: clinical and hereditary characteristics. Vet Ophthalmol.
progressing to the body. Diagnosis is with biopsy.34 1998;1(2-3):101-107.
6. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Lingual Melanoma: Malignant melanoma of the tongue occurs at College of Veterinary Ophthalmologists. ACVO, 2007.
increased frequency in Shar Peis compared to other breeds.35 7. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing lens
luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
Brachycephalic Syndrome, Brachygnathism, Cleft Lip/Palate, 8. Chinese Shar Pei Club of America Health Through Education Committee:
Factor XII Deficiency, Fold Dermatitis, Keratoconjunctivitis Health Survey Results. 2007.
Sicca, Osteochondritis Dessicans - Shoulder, Prognathism, 9. Rivas AL, Tintle L, Kimball ES, et. al.: A canine febrile disorder associated
Progressive Retinal Atrophy, Prolapsed Gland of Nictitans, with elevated interleukin-6. Clin Immunol Immunopathol. 1992
Seborrhea, and Subaortic Stenosis are reported.36 Jul;64(1):36-45.
10. May C, Hammill J, Bennett D: Chinese shar pei fever syndrome: a
preliminary report. Vet Rec. 1992 Dec 19-26;131(25-26):586-7.
Isolated Case Studies 11. von Bomhard D, Kraft W: Idiopathic mucinosis cutis in Chinese
Neutrophilic Vasculitis: Three young Shar-Pei dogs presented Shar pei dogs: epidemiology, clinical features, histopathologic findings
with fever, malaise, and widespread cutaneous lesions consisting and treatment. Tierarztl Prax Ausg K Klientiere Heimtiere. 1998
skin discolouration, edema, and pus-filled bullae that progressed to May;26(3):189-96.
ulceration, necrosis, and granulation. Immune-mediated vasculitis 12. Lopez A, Spracklin D, McConkey S, et. al.: Cutaneous mucinosis and
was diagnosed, and treatment was with steroids. Two of the three mastocytosis in a shar-pei. Can Vet J. 1999 Dec;40(12):881-3.
recovered.37 13. Welle M, Grimm S, Suter M, et. al.: Mast cell density and subtypes in the
skin of Shar Pei dogs with cutaneous mucinosis. Zentralbl Veterinarmed A.
Gastrointestinal Epitheliotropic Lymphoma: Three Shar Pei 1999 Jul;46(5):309-16.
14. Zanna G, Fondevila D, Bardagí M, et. al.: Cutaneous mucinosis in shar-pei
dogs between the ages of 4-8 years were diagnosed with T-cell
dogs is due to hyaluronic acid deposition and is associated with high levels
lymphoma of the gastrointerstinal system. Clinical signs were
of hyaluronic acid in serum. Vet Dermatol. 2008 Oct;19(5):314-8.
diarrhea, progressive anorexia, weight loss, and vomiting.38 15. Zanna G, Docampo MJ, Fondevila D, et. al.: Hereditary cutaneous
mucinosis in shar pei dogs is associated with increased hyaluronan
Ciliary Dysfunction: A litter of Shar Pei pups was studied with synthase-2 mRNA transcription by cultured dermal fibroblasts. Vet
recurrent repiratory infections without immunodeficiency. Absent Dermatol. 2009 Oct;20(5-6):377-82.
ciliary function was identified in one of the pups.39 16. Akey JM, Ruhe AL, Akey DT, et. al.: Tracking footprints of artificial
selection in the dog genome. Proc Natl Acad Sci U S A. 2010 Jan
Genetic Tests 19;107(3):1160-5.
17. Grützner N, Bishop MA, Suchodolski JS, et. al.: Association Study
Tests of Genotype: Direct test for coat and nose color is available
of Cobalamin Deficiency in the Chinese Shar Pei. J Hered. 2010
from Healthgene and VetGen.
Mar-Apr;101(2):211-7.
18. Bishop MA, Xenoulis PG, Suchodolski JS, et. al.: Prevalence of Cobalamin
Tests of Phenotype: CHIC Certification: Required tests are; CERF
Deficiency in Chinese Shar Peis
eye examination, hip and elbow radiographs, patella examination, 19. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
and thyroid profile including autoantibodies. (See CHIC website: veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
www.caninehealthinfo.org) 2000.
20. Hall JA: Congenital and Hereditary Defects in Skin Disease.2005
Recommended cardiac evaluation. Proceedings, Western Veterinary Conference 2005.
149
21. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
22. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
23. DiBartola SP, Tarr MJ, Webb DM, et. al.: Familial renal amyloidosis in
Chinese Shar Pei dogs. J Am Vet Med Assoc. 1990 Aug 15;197(4):483-7.
24. Rivas AL, Tintle L, Meyers-Wallen V, et. al.: Inheritance of renal
amyloidosis in Chinese Shar-pei dogs. J Hered. 1993 Nov-Dec;84(6):438-42.
25. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
in pure-bred dogs in North America. Vet Ophthalmol. 2004
Mar-Apr;7(2):97-111.
26. Miller DM: The occurrence of mast cell tumors in young Shar-Peis. J Vet
Diagn Invest. 1995 Jul;7(3):360-3.
27. Glickman LT, Glickman NW, Schellenberg DB, et. al.: Incidence of and
breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet
Med Assoc. 2000 Jan 1;216(1):40-5.
28. Rahal SC, Mamprim MJ, Muniz LM, et. al.: Type-4 esophageal
hiatal hernia in a Chinese Shar-pei dog. Vet Radiol Ultrasound. 2003
Nov-Dec;44(6):646-7.
29. Callan MB, Washabau RJ, Saunders HM, et. al.: Congenital esophageal
hiatal hernia in the Chinese shar-pei dog. J Vet Intern Med. 1993
Jul-Aug;7(4):210-5.
30. Guiot LP, Lansdowne JL, Rouppert P, et. al.: Hiatal hernia in the dog:
a clinical report of four Chinese shar peis. J Am Anim Hosp Assoc. 2008
Nov-Dec;44(6):335-41.
31. Moroff SD, Hurvitz AI, Peterson ME, et. al.: IgA deficiency in shar-pei
dogs. Vet Immunol Immunopathol. 1986 Nov;13(3):181-8.
32. Rivas AL, Tintle L, Argentieri D, et. al.: A primary immunodefi-
ciency syndrome in Shar-Pei dogs. Clin Immunol Immunopathol. 1995
Mar;74(3):243-51.
33. Miller WH Jr, Wellington JR, Scott DW: Dermatologic disorders of
Chinese Shar Peis: 58 cases (1981-1989). J Am Vet Med Assoc. 1992 Apr
1;200(7):986-90.
34. Kuhl KA, Shofer FS, Goldschmidt MH: Comparative histopathology of
pemphigus foliaceus and superficial folliculitis in the dog. Vet Pathol. 1994
Jan;31(1):19-27.
35. Dennis MM, Ehrhart N, Duncan CG, et. al.: Frequency of and risk factors
associated with lingual lesions in dogs: 1,196 cases (1995-2004). J Am Vet
Med Assoc. 2006 May 15;228(10):1533-7.
36. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 210. AAHA Press, 1999.
37. Malik R, Foster SF, Martin P, et. al.: Acute febrile neutrophilic vasculitis of
the skin of young Shar-Pei dogs. Aust Vet J. 2002 Apr;80(4):200-6.
38. Steinberg H, Dubielzig RR, Thomson J, et. al.: Primary gastrointestinal
lymphosarcoma with epitheliotropism in three Shar-pei and one boxer dog.
Vet Pathol. 1995 Jul;32(4):423-6.
39. Dhein CR, Prieur DJ, Riggs MW, et. al.: Suspected ciliary dysfunction
in Chinese Shar Pei pups with pneumonia. Am J Vet Res. 1990
Mar;51(3):439-46
40. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 543-546.
150
Chinook
dark, slightly pendulous lips. Scissors bite. Ears are wide set, with
thick leather and a good cover of fur, and variably set. From drop
to prick or helicopter ears are accepted, though both ears should
match in setting. Neck is moderately arched. Overall conformation
is slightly longer than tall. Ribs well sprung, topline is level though
with a curve slightly upwards through the loin. Thorax is deep.
Abdomen well tucked up. Feet are oval and toes well knuckled up.
Pads are thick and darkly pigmented, and plenty of fur is present
around the foot and between toes. Limbs straight, with good bone
and well muscled. Dewclaws on the forelimb may be removed, rear
dewclaws if present are always removed. Front feet are slightly
The Breed History deviated outward. Gait is characteristically a long fluid trot.
A single dog named Chinook gave rise to this Northern type breed
in Wonalancet, New Hampshire. He was born in 1917, the offspring
of one of the Peary expedition dog’s daughters. Chinook went to
Recognized Behavior Issues and Traits
Breed attributes reported include: Very calm, really friendly, not
the South Pole on the Byrd expedition of 1927. In 1991, the UKC
aggressive—though a reserved attitude to strangers or strange
recognized the Chinook as a breed. Breed origins are not documented,
places is not discouraged. As a team dog, their aggressive
though Spitz-type and Mastiff-types are thought to have been
tendencies to other dogs are not well developed. Shyness/
included. A very close brush with extinction occurred in the 1970’s,
fearfulness is a problem in the breed, with 11% of Chinooks
but a few dedicated breeders gathered the 12 breeding dogs together
reported in the 2003 COA Chinook health survey.1
in a few homes and by 1990, their numbers had increased to 140,
and in ’96, 450. A crossbreeding program has been instituted to help
increase the gene pool of the dogs. Outcrosses are very selective, with Normal Breed Variations
4 generation pedigree analysis to check for any disorders—only clear None reported
dogs are used. Offspring are then crossed with purebred Chinooks and
in the fourth generation are considered for registration to register if Drug Sensitivities
all health checks and performance meet the breed standard. None reported
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: none
• Registries: UKC, AKC Misc. class, CKC
• Breed resources: Chinook Club of America (AKC):
www.chinookclubofamerica.org
Chinook Owners Association (UKC): www.chinook.org
Chinook Health Fund:
http://chinookhealthfund.homestead.com/home.html
152
Chow Chow
chows. Lip margins, and all oral cavity membranes are black and
the tongue is blue-black. The neck is full, well muscled and arched,
the topline is straight and level, and ribs are well sprung. Limbs
are straight, dewclaws may be removed, and feet are compact and
sit on well-knuckled toes. A broad pelvis is evident. The tail is well
feathered. The long rough coated dogs possess a well-developed
ruff, especially in males (sometimes referred to as lion-like). The
tapered tail is set high and carried over the back and covered with a
profusion of hair. The normal gait is stilted due to the conformation
of the rear limbs (straight through both tarsus and stifle).
155
24. Buchanan JW: Causes and prevalence of cardiovascular diseases. In Kirk
RW, Bonagura JD, eds: Current veterinary therapy XI, Philadelphia, 1992,
WB Saunders.
25. Schrope DP, Kelch WJ: Signalment, clinical signs, and prognostic
indicators associated with high-grade second- or third-degree
atrioventricular block in dogs: 124 cases (January 1, 1997-December 31,
1997). J Am Vet Med Assoc. 2006 Jun 1;228(11):1710-7.
26. Batchelor DJ, Noble PJ, Cripps PJ, et. al.: Breed associations for
canine exocrine pancreatic insufficiency. J Vet Intern Med. 2007
Mar-Apr;21(2):207-14.
27. Brown CA, Crowell WA, Brown SA, et. al.: Suspected familial renal
disease in chow chows. J Am Vet Med Assoc. 1990 Apr 15;196(8):1279-84.
28. Vianna ML, Tobias KM: Atresia ani in the dog: a retrospective study. J
Am Anim Hosp Assoc. 2005 Sep-Oct;41(5):317-22.
29. Vandevelde M, Braund KG, Walker TL, et. al.: Dysmyelination of the
central nervous system in the Chow-Chow dog. Acta Neuropathol (Berl).
1978 Jun 30;42(3):211-5.
30. Vandevelde M, Braund KG, Luttgen PJ, et. al.: Dysmyelination in
Chow Chow dogs: further studies in older dogs. Acta Neuropathol (Berl).
1981;55(2):81-7.
31. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 210-211. AAHA Press, 1999.
32. Hoover JP, Henry GA, Panciera RJ: Bronchial cartilage dysplasia with
multifocal lobar bullous emphysema and lung torsions in a pup. J Am Vet
Med Assoc. 1992 Aug 15;201(4):599-602.
33. Maddux JM, Edwards DF, Barnhill MA, et. al.: Neutrophil function in
dogs with congenital ciliary dyskinesia. Vet Pathol. 1991 Sep;28(5):347-53.
34. Edwards DF, Kennedy JR, Toal RL, et. al.: Kartagener’s syndrome in
a chow chow dog with normal ciliary ultrastructure. Vet Pathol. 1989
Jul;26(4):338-40.
35. Booth MJ: Atypical dermoid sinus in a chow chow dog. J S Afr Vet
Assoc. 1998 Sep;69(3):102-4.
36. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 547-552.
156
Clumber Spaniel
removed. In North America, tails are docked. They move with an
easy, rolling gait and are designed to move through thick cover. The
topline is level and back is long, legs are straight, feet large but not
splayed.
Retinal Dysplasia: Retinal folds, geographic, and generalized retinal Recommend patella examination, thyroid profile including
dysplasia with detachment are recognized in the breed. Reported autoantibodies and cardiac evaluation.
in 7.02% of Clumber Spaniels CERF examined by veterinary
ophthalmologists between 2000-2005.7 Miscellaneous
• Breed name synonyms: Clumber
Distichiasis: Abnormally placed eyelashes that irritate the cornea • Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain),
and conjunctiva. Can cause secondary corneal ulceration. Identified ANKC (Australian National Kennel Club), NKC (National Kennel Club)
in 6.40% of Clumber Spaniels CERF examined by veterinary • AKC rank (year 2008): 177 (280 dogs registered)
ophthalmologists between 2000-2005.7 • Internet resources: Clumber Spaniel Club of America:
www.clumbers.org
Cataracts: Posterior cortex intermediate and anterior cortex
Clumber Spaniel Club of Canada: http://clumbercanada.webs.com/
punctate cataracts predominate in the breed. Onset 6-18 months of
The Clumber Spaniel Club (UK): www.clumberspanielclub.co.uk
age. Unknown mode of inheritance. Reported in 5.32% of Clumber
Clumber Spaniel Health Foundation: www.clumberhealth.org
Spaniels examined at veterinary teaching hospitals. Identified
in 4.31% of Clumber Spaniels CERF examined by veterinary
ophthalmologists between 2000-2005. Reported at a frequency References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
of 5.2% (mostly punctate) in the Clumber Spaniel Club of America
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
Health Survey 2001/2002. CERF does not recommend breeding any 2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Clumber Spaniel with a cataract.3,7,8 3. Froman, R: Clumber Spaniel Club of America Health Survey 2001/2002.
4. Jarvinen AK, Sankari S: Lactic acidosis in a Clumber spaniel. Acta Vet
Hypothyroidism: Inherited autoimmune thyroiditis. 4.5% positive for Scand. 1996;37(1):119-21.
thyroid auto-antibodies based on testing at Michigan State University. 5. Shelton GD, Engvall E: Muscular dystrophies and other inherited
(Ave. for all breeds is 7.5%). Reported at a frequency of 13.9% in the myopathies. Vet Clin North Am Small Anim Pract 2002: 32 (1):103-124.
Clumber Spaniel Club of America Health Survey 2001/2002.3,9,10 6. Cameron JM, Maj MC, Levandovskiy V, et. al.: Identification of a canine
model of pyruvate dehydrogenase phosphatase 1 deficiency. Mol Genet
Anasarca (Lethal Congenital Edema): Puppies are born dead and Metab. 2007 Jan;90(1):15-23.
edematous. Can also be associated with cleft palate. Reported at a 7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
frequency of 4.4% in the Clumber Spaniel Club of America Health College of Veterinary Ophthalmologists. ACVO, 2007.
Survey 2001/2002.3 8. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
Cryptorchidism (Retained Testicles): Can be unilateral or bilateral. 9. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
This is a sex-limited disorder with an unknown mode of inheritance. Population and Animal Health, Michigan State University. April, 2007.
10. Nachreiner RF, Refsal KR, Graham PA, et, al.:Prevalence of serum thyroid
Reported at a frequency of 3.5% in the Clumber Spaniel Club of
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
America Health Survey 2001/2002.3 Am Vet Med Assoc 2002 Feb 15;220(4): 466-71.
11. The Genetic Connection: A Guide to Health Problems in Purebred Dogs.
Inflammatory/Irritable Bowel Disease (IBD): Presents with L Ackerman. p.211, AAHA Press, 1999.
chronic vomiting, diarrhea, and/or weight loss. Affected dogs can 12. The Complete Dog Book, 20th Ed. The American Kennel Club.Howell Book
usually be controlled with diet and/or medications. Reported at a House, NY 2006. P. 79-82.
158
Cocker Spaniel
Recognized Behavior Issues and Traits
These dogs are gentle social dogs that are playful and affectionate
with family members, and very loyal. They are considered of
medium trainability, and are generally good with children. Early
socialization and training is very important for these dogs.
Those poorly socialized and of timid personality may be snappy,
and some lines are known to have temperament changes such
as fearful-dominant personalities. These lines may also be
dominant-aggressive. For the most part this breed has been
carefully selected for gentle, friendly personality. They need plenty
The Breed History of exercise and play time.
The Cocker Spaniel is the smallest member of the sporting division, They require regular ear hygiene and lots of coat care, with average
and resulted from the selection of small dogs from the land spaniel shedding. They have an average to high barking tendency.
group. Breed status was given to this dog in 1892 (England Kennel
Club). After import to the USA around 1880, the American type
became distinct from the English cocker type, being shorter, heavier Normal Physiologic Variations
coated and having a rounder skull, and now are two quite distinct None reported
breeds; American and English Cocker Spaniel. The American cocker
is often just termed Cocker Spaniel. The feature role of a cocker Drug Sensitivities
type dog in the cartoon “Lady and the Tramp” by Disney resulted in None reported
a large sudden surge of the popularity of this breed.
Inherited Diseases
Breeding for Function Patella Luxation: Polygenically inherited laxity of patellar
This dog was bred to be a hunting dog, and though considered a ligaments, causing luxation, lameness, and later degenerative joint
land spaniel, will work in water readily. The name cocker is thought disease. Treat surgically if causing clinical signs. OFA reports 18.0%
to derive from “woodcock”, game that they were particularly suited affected.1
for. Today, they commonly serve as a valued home companion,
enjoy agility competitions, and still maintain status as one of the Hip Dysplasia: Polygenically inherited trait causing degenerative
most popular AKC breeds. joint disease and hip arthritis. OFA reports 6.5% affected.1
159
Bronchiectasis: Clinical signs of chronic cough with excessive Comprehensive Breed Health Survey. Dorn reports a 2.06x odds
airway mucous. Diagnosis with radiographs. Reported at a ratio for conjunctivitis versus other breeds.9,10
frequency of 15.9% and an odds ratio of 4.15x versus other breeds.
Treatment is with bronchodilators and possibly corticosteroids.11 Epilepsy: Inherited seizures. Can be generalized or partial seizures.
Reported at a frequency of 3.6% in the 2005 Cocker Spaniel
Hypothyroidism: Inherited autoimmune thyroiditis. 15.7% positive Comprehensive Breed Health Survey.10
for thyroid auto-antibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5%). Reported at a frequency Keratoconjunctivitis Sicca (KCS), Chronic Superficial
of 3.8% in the 2005 Cocker Spaniel Comprehensive Breed Health Keratitis (Pannus), Dry Eye: These ocular conditions can cause
Survey.10,12,13 conjunctivitis, corneal ulcerations, and vision problems due to
corneal pigmentation. Age of onset 2-5 years. Treatment with
Behavioral Disorders: The 2005 Cocker Spaniel Comprehensive topical ocular lubricants and anti-inflammatory medication. Pannus
Breed Health Survey reports 10.5% of Cocker Spaniels with was identified in 0.77% of Cocker Spaniels CERF examined by
behavioral disorders. These include submissive urination (4.7%), veterinary ophthalmologists between 2000-2005. KCS is reported
separation anxiety (4.4%), and fearfulness towards; people (3.9%), at a frequency of 3.4% in the 2005 Cocker Spaniel Comprehensive
noise (3.9%), children (2.5%), and their environment (2.5%).10 Breed Health Survey. CERF does not recommend breeding any
Cocker Spaniel with KCS.2,10
Retinal Dysplasia: Focal retinal dysplasia and retinal folds are
recognized in the breed. Severe cases can progress to retinal Aggression: The breed is one identified with a tendency toward
detachment. Reported in 10.04% of Cocker Spaniels CERF examined severe dominance aggression. This may be most extreme in intact
by veterinary ophthalmologists between 2000-2005.2 males, though neutered males and females can also be affected.
Reported at a frequency of 3.3% in the 2005 Cocker Spaniel
Chronic Otitis with Ossification of the External Ear Canal: Comprehensive Breed Health Survey.10,22
Cocker Spaniels are prone to chronic ear infections, and to
dystrophic ossification and closing down of the external ear canal. Umbilical Hernia: Reported at a frequency of 2.9% in the 2005
Dorn reports a 1.45x odds ratio versus other breeds. A Greek Cocker Spaniel Comprehensive Breed Health Survey.10
study reported a 8.99x odds ratio versus other breeds. Chronic ear
infections were reported at a frequency of 9.0% in the 2005 Cocker Deafness: In the Cocker Spaniel, this can be congenital, or
Spaniel Comprehensive Breed Health Survey.9,10,14,15 secondary to severe, chronic otitis. Can be bilateral or unilateral.
Diagnose with BAER testing. Reported at a frequency of 2.8% in the
Cataracts: Anterior and posterior cortex intermediate and punctate 2005 Cocker Spaniel Comprehensive Breed Health Survey.10
cataracts predominate in the breed. Onset of cataracts may
occur at less than 2 years, with rapid progression to maturity and Corneal Dystrophy: The breed can develop a posterior
associated with significant lens-induced inflammation. Reported polymorphous dystrophy that does not lead to corneal edema.
at a frequency of 8.77% in one study. Identified in 6.96% of Cocker Identified in 2.47% of Cocker Spaniels CERF examined by veterinary
Spaniels CERF examined by veterinary ophthalmologists between ophthalmologists between 2000-2005.2,23
2000-2005. Reported at a frequency of 5.9% in the 2005 Cocker
Spaniel Comprehensive Breed Health Survey. Dorn reports a 2.04x Ectropion: Ectropion, a rolling out of the eyelids, can cause
odds ratio versus other breeds. One study showed a 2.6x odds frequent conjunctivitis, and ocular discharge. Identified in 1.52%
ratio versus other breeds. CERF does not recommend breeding any of Cocker Spaniels CERF examined by veterinary ophthalmologists
Cocker Spaniel with a cataract. 2,9,10,16,17 between 2000-2005.2
Glaucoma: Ocular condition causing increased pressure within Immune-Mediated Hemolytic Anemia (IMHA) and Idiopathic
the eyeball, and secondary blindness due to damage to the retina. Thrombocytopenia Purpura (ITP): Autoimmune destruction of
Diagnose with tonometry and gonioscopy. One study shows blood cells. Cocker Spaniels have a 12.2x odds ratio for IMHA versus
5.52% Cocker Spaniels affected; the highest frequency of primary other breeds. Females are more frequently affected than males.
glaucoma versus other breeds. A female preponderance occurs Unknown mode of inheritance. IMHA is reported at a frequency of
in the breed. Secondary glaucoma can also occur after cataract 1.0%, and ITP at 0.7% in the 2005 Cocker Spaniel Comprehensive
formation in the breed. One report found an odds ratio of 3.7x for Breed Health Survey.10,24,25
secondary glaucoma in Cocker Spaniels. Dorn reports a 5.73x odds
Idiopathic Seborrhea: Primary inherited skin disorder presenting
ratio for glaucoma versus other breeds. CERF does not recommend
with greasy skin and haircoat. Unknown mode of inheritance. The
breeding any Cocker Spaniel with glaucoma.2,9,18,19,20,21
condition responds to treatment with etretinate. Dorn reports a
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis, 3.19x odds ratio versus other breeds.9,26,27
otitis, and pyotraumatic dermatitis. Reported at a frequency of 5.1%
Dilated Cardiomyopathy: The breed can develop a taurine
in the 2005 Cocker Spaniel Comprehensive Breed Health Survey.10
responsive dilated cardiomyopathy. Affected dogs present in
Prolapsed Gland of the Nictitans (Cherry Eye): This condition is heart failure, and have very low plasma taurine levels. Most
secondary to chronic conjunctivitis, usually of an allergic nature. affected dogs show a significant (clinical and ECHO) response to
Reported at a frequency of 4.4% in the 2005 Cocker Spaniel taurine supplementation and can usually be weaned off heart
medications.28,29
160
Vitamin A responsive Dermatosis: Inherited skin disorder lactic, pyruvic and acetoacetic acids, increased urinary excretion of
presenting with seborrhea and keratinization. Differentiated from carnitine esters, and increased plasma alanine, consistent with a
idiopathic seborrhea by skin biopsy and responsiveness to Vitamin A block in oxidative metabolism.47
supplementation.30
Progressive Ataxia with Seizures: Case history of a young male
Second and Third Degree Heart Block: Cocker Spaniels are a Cocker Spaniel with progressive neurological disease evident by
breed listed as predisposed to high-grade second- or third-degree 3 months of age, and progressing to uncontrollable seizures by
AVB. The breed is also at risk for sick sinus syndrome. Heavier, 15 months. Significant lesions were found only in the brain. They
older, and sexually intact female dogs were overrepresented in the consisted of hypoplasia of the cerebellum and the presence of large
study group. Weakness, lethargy, exercise intolerance, and syncope pale proteinacious inclusions in the perikaryon of neurons in the
were the most common clinical signs. Pacemaker implantation is neocortex and in macrophages.48
recommended.31,32
Congenital Myotonia: A 16-week-old, male Cocker Spaniel
Plasmacytoma/Plasma Cell Tumor: Cocker Spaniels were found to suffered from pelvic-limb “bunny hopping” as well as rigidity,
have a 10.0x greater risk of developing plasma cell tumors of the spasticity, and ataxia in all limbs. Electrophysiology, and muscle
tongue than other breeds. Other published case reports document histopathological and histochemical evaluations led to a diagnosis
plasmacytoma of the penis, anus and 3rd eyelid. This is a benign of congenital myotonia.49
tumor, and treatment is with surgery.33,34,35,36
Focal Myasthenia Gravis: A 10-month-old dog presented with
Ceroid-Lipofuscinosis: Rare, fatal degenerative neurological megaesophagus, aspiration pneumonia, no appendicular muscle
disease. Affected Cocker Spaniels have presented between 18 weakness, but facial muscle weakness. The condition responded
months and 6 years of age with variable signs of progressive hind to anticholinesterase, and serum antibodies against acetylcholine
limb paresis, incoordination, behavior changes, seizures, and/or receptors were documented.50
blindness. Unknown mode of inheritance.37,38
Cerebellar Vermian Hypoplasia: An eight-week-old female
Incomplete Ossification of the Humeral Condyle: Cocker Spaniels Cocker Spaniel was presented with ataxia, dysmetria and intention
have an increased incidence of incomplete ossification of the tremor. Cerebellar hypoplasia with vermal defect was identified on
humeral condyle, and associated humeral condylar fractures or necropsy, comparable to Dandy-Walker syndrome.51
degenerative joint disease. There is a male preponderance. A recessive
mode of inheritance was suggested based on pedigree analysis.39 Phosphofructokinase Deficiency (PFK): A 3-year-old female
American Cocker Spaniel with chronic hemolytic crises was
Episcleritis: Cocker Spaniels are over-represented with a diagnosis identified with the same mutation found in the autosomal recessive
of diffuse or nodular episcleritis. Affected dogs can show unilateral disorder of the English springer spaniel.52
or bilateral inflammation and congestion of the scleral vessels
with corneal edema and stromal infiltrate of CD3 T-lymphocytes. Dimelia: A Cocker Spaniel was examined with two left forelimb
In one study, 6 of 19 cases were Cocker Spaniels. Treatment is with paws, both originating from the carpus, with symmetrical
immunosuppressive medications.40,41 duplication of metacarpal bones and phalanges. In addition, the left
radial head was subluxated and asynchronous growth of the left
Abnormal Platelet Function: Moderate to severe bleeding due to radius and ulna was noted.53
platelet ADP deficiency was identified in 3 families of dogs. Platelet
counts, plasma coagulant function and von Willebrand factor are Black hair Follicular Dysplasia, Brachygnathism, Chronic
normal, but there is prolonged bleeding time, prolonged platelet Inflammatory Hepatic Disease, Cleft Lip/Palate, Cryptorchidism,
aggregation time in response to ADP and collagen.42 Cyclic Hematopoiesis, Ectodermal Defect, Factor IX Deficiency,
Factor X Deficiency, Hypotrichosis, IgA Deficiency, Intervertebral
Oral Malignant Melanoma: Malignant cancer usually involving the Disc Disease, Malignant Hyperthermia, Microphthalmia,
gingiva. Can be pigmented or non-pigmented. One study identified Narcolepsy, Optic Nerve Coloboma and Hypoplasia, Pelger-Huet
a 1.65x relative risk versus other breeds.43 Anomaly, Portosystemic Shunt, Prognathism, Pulmonic Stenosis,
Renal Dysplasia, Sebaceous Adenitis, Vascular ring Anomaly and
Isolated Case Studies von Willebrand’s Disease are reported.54
Nasal Dermoid Sinus Cysts: A few cases have been reported
in Cocker Spaniels. Affected dogs present with a subcutaneous Genetic Tests
mass or draining tract over the midline bridge of the nose. Tests of Genotype: Direct test for prcd-PRA is available from
Surgical removal is curative. In another case study, an intracranial Optigen.
epidermoid cyst caused syringomyelia.44,45,46
Direct test for Phosphofructokinase deficiency is available from
Lipid Storage Myopathy: A six-year-old male Cocker Spaniel HealthGene, Optigen, PennGen, and VetGen (very rarely seen in the
presented with a three-week history of generalized weakness breed).
and muscle pain. Muscle biopsies revealed numerous large lipid
droplets within type 1 fibres and to a lesser degree within type 2 Direct tests for coat colors (black, brown and buff/red) are available
fibres. Biochemical testing showed elevated urinary excretion of from HealthGene and VetGen.
161
Tests of Phenotype: CHIC Certification: Required testing includes 18. Sapienza JS, van der Woerdt A: Combined transscleral diode laser
hip radiographs, and CERF eye examination. (See CHIC website; cyclophotocoagulation and Ahmed gonioimplantation in dogs with
www.caninehealthinfo.org). primary glaucoma: 51 cases (1996-2004). Vet Ophthalmol. 2005
Mar-Apr;8(2):121-7.
Additional Recommended tests include patella evaluation, thyroid 19. Gelatt KN, MacKay EO: Secondary glaucomas in the dog in North
profile including autoantibodies, elbow radiographs, and cardiac America. Vet Ophthalmol. 2004 Jul-Aug;7(4):245-59.
20. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas in
evaluation.
pure-bred dogs in North America. Vet Ophthalmol. 2004 Mar-Apr;7(2):97-
111.
Miscellaneous 21. Johnsen DA, Maggs DJ, Kass PH: Evaluation of risk factors for
• Breed name synonyms: Cocker, Cocking Spaniel, Cocker Spaniel. development of secondary glaucoma in dogs: 156 cases (1999-2004). J Am
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), Vet Med Assoc. 2006 Oct 15;229(8):1270-4.
ANKC (Australian National Kennel Club), NKC (National Kennel Club) 22. Stafford KJ: Opinions of veterinarians regarding aggression in different
• AKC rank (year 2008): 21 (9,481 dogs registered) breeds of dogs. N Z Vet J. 1996 Aug;44(4):138-41.
23. Cooley PL, Dice PF 2nd: Corneal dystrophy in the dog and cat. Vet Clin
• Internet resources: American Spaniel Club of America:
North Am Small Anim Pract. 1990 May;20(3):681-92.
www.asc-cockerspaniel.org 24. Miller SA, Hohenhaus AE, Hale AS: Case-control study of blood type,
American Cocker Spaniel Club of Canada: www.acscc.ca breed, sex, and bacteremia in dogs with immune-mediated hemolytic
American Cocker Spaniel Club of Great Britain: www.acscgb.com anemia. J Am Vet Med Assoc. 2004 Jan 15;224(2):232-5.
25. Balch A & Mackin A: Canine immune-mediated hemolytic anemia:
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163
Collie-Rough
and Smooth
Recognized Behavior Issues and Traits
Reported breed characteristics include that these dogs are
particularly good around children in general. This breed is loyal and
makes a good family watchdog—they are vigorous alarm barkers.
They have high intelligence and are easy to train. They can be aloof
with strangers, and are active outdoors, though less active than
border Collies on average. Sometimes, they will nip at children’s
heels in an attempt to herd them, but training can eliminate this
tendency. Regular grooming is necessary; they are considered high
shedders. Note that rough and smooth types may occur in the same
The Breed History litter of puppies.
The rough and smooth Collie can both trace their origins to
Scotland and England. In the early 19th century a taller, more Normal Physiologic Variations
refined dog had evolved. A favorite breed of Queen Victoria, and Merle Coat Color: Caused by a dominant mutation in the SILV
also a star as “Lassie” on television, this breed has maintained gene. Breeding two merle dogs together should be avoided, as
popularity for many years. The name may have arisen from the homozygous dogs can be born with multiple defects, including
name of the sheep they often guarded in Scotland called the Colley blindness, deafness, and heart anomalies.1
sheep. Others propose the name is Gaelic for “useful”.
Drug Sensitivities
Breeding for Function MDR1 Mutation (Ivermectin/Drug Toxicity): Autosomal
These, the quintessential herding dog were strictly working dogs recessive disorder in the MDR1 gene allows high CNS drug levels
until about 200 years ago. They have now taken their place as a of ivermectin, doramectin, loperamide, vincristine, moxidectin, and
competition dog, but also are a valued companion. They have also other drugs. Causes neurological signs, including tremors, seizures,
excelled as rescue and guide dogs. and coma. A genetic test is available for the mutated gene, showing
35.4% of Collies are affected, and 42.0% are carriers. In Germany,
Physical Characteristics 33.0% test homozygous affected, and 43.1% test as carriers.2,3,4
Height at Withers: female 22-24” (56-61 cm), male 24-26”
(61-66 cm) Inherited Diseases
Collie Eye Anomaly/Choroidal Hypoplasia/Coloboma (CEA/CH):
Weight: females 50-65 lb (23-29.5 kg) , males 60-75lb (27-34 kg). Autosomal recessive disorder of eye development that can lead to
retinal detachment and blindness. Reported in 67.77% of Collies
Coat: Rough Collie standard: The thick double haircoat runs CERF examined by veterinary ophthalmologists between 2000-2005.
over the body except on head and legs; the outer layer is harsh CERF does not recommend breeding affected dogs. Reported at a
and straight, the inner layer is soft and wooly. Around the neck is frequency of 24.1% in the Collie Health Foundation Online Health
a pronounced mane of very thick hair that is more developed in Survey. In switzerland, 8.9% smooth and 36.9% rough collies were
males. Recognized colors include tri-color, blue merle, white and affected. Dorn reports a 31.46x odds ratio versus other breeds. A
sable and white. Note that the “white” dog has a predominance of genetic test is available.5,6,7,8,9,10
white with markings of sable, blue merle or tri-color.
Smooth: A thick undercoat and a short (1”), dense flat coat are the Hip Dysplasia: Polygenically inherited trait causing degenerative
standard. joint disease and hip arthritis. OFA reports 2.8% affected. Reported
at a frequency of 3.2% in the Collie Health Foundation Online
Longevity: 14-16 years. Health Survey.7,11
Points of Conformation: This breed of dog has a very bright Elbow Dysplasia: Polygenically inherited trait causing elbow
demeanor and their alert “Collie expression” is one of the points arthritis. OFA reports 1.0% affected.11
of judging. The dog presents a balanced appearance with straight
limbs, deep chest, and a smallish head (dolichocephalic skull) with a Grey Collie Cyclic Neutropenia: Collies that are homozygous for
slight stop and a tapering but blunted muzzle. The eyes are medium the dilute (d locus) gene are Grey Collies. Grey Collies can have an
sized, almond-shaped and match coat color except in the merle. The autosomal recessive disorder where circulating neutrophil numbers
ears are normally tipped at the top quarter. Topline is level. Their drop every 12 days due to a bone marrow abnormality in blood cell
feet are small, but the toes are well arched. The tail reaches to the production. Affected dogs are prone to serious infection during
tarsal joint or lower. episodes of neutropenia, and usually die from chronic infectious
insults to the organs. A genetic test is available.12,13
164
Progressive Retinal Atrophy (PRA, rcd-2): An autosomal Dermatomyositis: Inherited disorder causing patches of scaling,
recessive, early onset rod, cone dysplasia form of PRA can occur crusting and alopecia over the muzzle, periorbital skin and
in the breed with an onset of 6 weeks of age, and progressing to distal limbs, and an associated myositis especially affecting the
blindness by 1 year. A genetic test is available.8,14,15 masticatory muscles. Onset between 3-6 months of age. Mode
of inheritance is unknown, though some researchers suspect
von Willebrand’s disease (vWD): Type II vWD in the Collie is a autosomal dominant with incomplete penetrance. Reported at a
serious, sometimes fatal, autosomal recessive bleeding disorder. frequency of 1.5% in the Collie Health Foundation Online Health
Cryoprecipitate is more effective, with fewer side effects, than fresh Survey.7,20,21
frozen plasma in controlling bleeding episodes. A genetic test is
available. Distichiasis: Abnormally placed eyelashes that irritate the cornea
and conjunctiva. Can cause secondary corneal ulceration. Identified
Patella Luxation: Polygenically inherited laxity of patellar in 1.39% of Collies CERF examined by veterinary ophthalmologists
ligaments, causing luxation, lameness, and later degenerative joint between 2000-2005.8
disease. Treat surgically if causing clinical signs. Too few Collies
have been screened by OFA to determine an accurate frequency.11 Cataracts: Nuclear cataracts predominate in the breed. Identified
in 1.03% of Collies CERF examined by veterinary ophthalmologists
Disease Predispositions between 2000-2005. CERF does not recommend breeding any Collie
Persistent Pupillary Membranes: Strands of fetal remnant with a cataract.8
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
Autoimmune Hemolytic Anemia (AIHA): Collies have an
The later three forms can impair vision, and dogs affected with
increased risk of developing AIHA versus other breeds. Females are
these forms should not be bred. Identified in 16.31% of Collies CERF
more frequently affected than males. Clinical features included pale
examined by veterinary ophthalmologists between 2000-2005. Dorn
mucous membranes, weakness, lethargy and collapse. Treatment
reports a 4.53x odds ratio versus other breeds.5,8
with prednisone is successful in most cases.22
Retinal Dysplasia: Focal retinal dysplasia and retinal folds are
Pemphigus Foliaceus: The breed has an increased risk (3.9x odds
recognized in the breed. Severe cases can progress to retinal
ratio) of developing pemphigus foliaceus. Clinical signs include
detachment. Reported in 7.58% of Collies CERF examined by
crusting lesions to the dorsal part of the muzzle and head,
veterinary ophthalmologists between 2000-2005.8
progressing to the body. Diagnosis is with biopsy.23
Demodicosis, Generalized: Overgrowth of demodex mites in
Chronic Pancreatitis: Often subclinical inflammation of the
the skin causing hair loss and dermatitis. An immune deficiency
pancreas that can cause intermittent discomfort and gastrointes-
underlies the condition. Reported at a frequency of 6.3% in the
tinal upsets, and can possibly lead to pancreatic insufficiency or
Collie Health Foundation Online Health Survey.7
diabetes mellitus. Collies have a 2.0x relative risk versus other
Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting breeds.24
of the stomach within the abdomen. Requires immediate veterinary
Corneal Dystrophy: The breed can have an epithelial/stromal form
attention. Glickman found a 2.1x risk of developing GDV per year of
of corneal dystrophy. Age of onset 2-5 years. Identified in 0.56%
life in Collies. Reported at a frequency of 5.3% in the Collie Health
of Collies CERF examined by veterinary ophthalmologists between
Foundation Online Health Survey.7,16
2000-2005.8,25
Hypothyroidism: Inherited autoimmune thyroiditis. 4.5% positive
Vesicular Cutaneous Lupus Erythematosus (Nasal Solar
for thyroid auto-antibodies based on testing at Michigan State
Dermatitis): Adult onset vesicular form of lupus that causes
University. (Ave. for all breeds is 7.5%) Reported at a frequency of
annular, polycyclic and serpiginous ulcerations distributed over
5.1% in the Collie Health Foundation Online Health Survey.7,17,18
sparsely haired areas of the body. These especially occur during
Idiopathic Epilepsy: Inherited seizures. Can be generalized or partial the summer months due to ultraviolet exposure. Treatment is with
seizures. Collies have an increased incidence versus other breeds. immunosuppressive drugs and sunscreen.26
Control with anti-seizure medication. Unknown mode of inheritance.
Pancreatic Acinar Atrophy (Exocrine pancreatic insufficiency):
Seizures were reported at a frequency of 5.1%, and epilepsy at 1.6%
Collies are a breed at risk for immune-mediated pancreatic acinar
in the Collie Health Foundation Online Health Survey.7,19
atrophy. Clinical signs are poor weight gain, and steatorrhea.
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis Treatment is with enzyme supplementation. Breeding studies
and pyotraumatic dermatitis. Reported at a frequency of 4.3% in suggest an autosomal recessive mode of inheritance in German
the Collie Health Foundation Online Health Survey.7 shepherd dogs, another breed found at risk.27,28,29
165
Gastric Carcinoma: The Collie breed appears to have a higher
incidence of gastric carcinoma compared to other breeds. The most
Genetic Tests
Tests of Genotype: Direct tests for CEA/CH and rcd2 (PRA) are
frequent clinical features are vomiting, polydipsia and weight loss, available from Optigen.
with endoscopic findings of a large deep ulcer with thickened,
irregular rims and walls.33 Direct test for MDR1 is available from Washington State Univ.
http://www.vetmed.wsu.edu/depts-VCPL/
Perineal Hernia: Older male Collies have a predisposition to
developing perineal hernias. Treatment is surgical.34 Direct test for the cyclic neutropenia is available from HealthGene
and VetGen.
Nasal Adenocarcinoma: Collies have an increased risk versus other
breeds of developing nasal adenocarcinoma. Clinical signs include Direct test for coat colors sable and tricolor (a locus) is available
chronic nasal infection, discharge, and epistaxis.35 from HealthGene.
Diabetes Mellitus (Sugar Diabetes): Treat with insulin injections, Direct test for von Willebrand’s disease is available from VetGen.
diet, and glucose monitoring. A British study reported Collies with
an increased incidence versus other breeds; however an American Direct test for a DM susceptability gene is available from the OFA.
study found Collies to have a decreased risk. Unknown mode of
inheritance.36,37 CHIC Certification: Required testing includes genetic tests for rcd2
and MDR1. (See CHIC website; www.caninehealthinfo.org).
Colorectal Polyp: The Collie breed is over-represented with
diagnoses of colorectal polyps versus other breeds. Clinical signs Tests of Phenotype: Recommended tests: hip and elbow
include dyschezia, periodic intermittent diarrhea and melena, and radiographs, thyroid profile including autoantibodies, patella
rectal prolapse of the polyp. Treatment is with surgery. Some polyps evaluation, CERF eye examination, and cardiac evaluation.
can be malignant.38
167
Curly
Coated Retriever
moderate in length, and not throaty. The topline is level, with
a slight slope downward at the croup. The thorax is deep and
moderately sprung ribs stay full towards the rear of the rib cage.
The abdomen is moderately tucked up. The tail is straight, thick,
tapering and reaches to the tarsus. Limbs are straight boned,
and the feet are round with well-knuckled toes. Metacarpals and
metatarsals are short. The dewclaws on the forelimb are often
removed, and the ones on the hind limbs are usually removed. The
dog moves with a long stride, with agility, speed and smoothness.
Weight: 70-80 lb (32-36 kg). Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. OFA reports 0.5% affected.1
Coat: The distinctive curly dense coat is made up of an outer coat
with discrete short tight curls, though straight shorter hair is found Patella Luxation: Polygenically inherited laxity of patellar
on the face, feet and the pinna hair covering is intermediate in curl. ligaments, causing luxation, lameness, and later degenerative
Accepted coat colors are black and liver. Very small white patches joint disease. Treat surgically if causing clinical signs. Too few
are allowed. Black is dominant, liver is recessive in inheritance. Curly-coated Retrievers have been screened by OFA to determine an
Rare yellows occur but are not an accepted breed color. Has low accurate frequency.1
grooming needs except during shedding times; the coat does not
need trimming. Some breeders rarely or never brush these dogs but Glycogenosis Type IIIa (Glycogen Storage Disease, GSD): An
just periodically bathe them. autosomal recessive inherited metabolic disorder that causes liver
and skeletal muscle disease due to deficiency of the glycogen
Longevity: 10-13 years debranching enzyme (GDE) and tissue storage of abnormally
structured glycogen. Clinical signs include episodic exercise
Points of Conformation: High head carriage, a distinct, tightly intolerance, collapse, and lethargy. This disorder was discovered
curled water-resistant coat, slightly longer than tall conformation in an extended family of Curly-coated Retrievers (CCR), with
characterize the Curly-coated Retriever. They possess moderate representative cases from USA, Canada, and New Zealand. A genetic
muscling and bone. The wedge-shaped head is more narrow, test is available and shows 0.5% affected and 8.7% carrier.2
refined, with the muzzle tapering more than with the other
retrievers. The stop is shallow, and the almond shaped eyes are Exercise Induced Collapse (EIC, Dynamin 1 Mutation): An
black, brown or amber. The large nose is black or brown. The small autosomal recessive disorder of muscle weakness, incoordination
ears are folded and close lying, with heavy leather. The neck is and life threatening collapse accompanied by hyperthermia after
168
just five to fifteen minutes of intense exercise or excitement. After hemolytic hyperbilirubinemia, hyperhistaminemia, renal and hepatic
10 to 30 minutes of rest, most dogs return to normal. Limited injuries. Mast cells were distributed systemically, but predominantly
genetic testing reveals over 10% carrier Curly Coated Retrievers. A in the diaphragm and liver with a large mass among the serosa of
direct genetic test is available.3 ileum, cecum and colon.10
Distichiasis: Abnormally placed eyelashes that irritate the cornea Direct test for presence of black and liver coat colors, and black and
and conjunctiva. Can cause secondary corneal ulceration. Identified brown nose is available from HealthGene and VetGen.
in 7.64% of Curly Coated Retrievers CERF examined by veterinary
ophthalmologists between 2000-2005.6 Tests of Phenotype: CHIC Certification: Required testing includes
hip radiographs, congenital cardiac evaluation by a cadiologist,
Persistent Pupillary Membranes: Strands of fetal remnant and CERF eye examination. Optional recommended tests are; elbow
connecting; iris to iris, cornea, lens, or involving sheets of tissue. radiographs, and direct GSD IIIa test. (See CHIC website; www.
The later three forms can impair vision, and dogs affected with caninehealthinfo.org).
these forms should not be bred. Identified in 3.82% of Curly Coated
Retrievers CERF examined by veterinary ophthalmologists between Recommend thyroid profile, including autoantibodies, and patella
2000-2005.6 evaluation.
Punctate Keratitis: Focal circular rings usually affecting the central Congenital Myasthenia Gravis: Disorder of exercise induced
subepithelial and/or anterior portion of the cornea. There often is an muscle weakness identified in immature miniature dachshunds.
associated dry eye with corneal erosions. The mode of inheritance is Clinical signs resolve spontaneously by 6 months of age.47
unknown. CERF does not recommend breeding any affected dogs.10,38
Nasopharyngeal Dysgenesis/stenosis: Congenital disorder
Optic Nerve Coloboma: A congenital cavity in the optic nerve characterized by expiratory cheek puffing, upper respiratory
which, if large, may cause blindness or vision impairment. Identified dyspnea, macroglossia, and dysphagia. Treatment is with surgery.
in 2.38% of smooth miniature Dachshunds CERF examined by Unknown mode of inheritance.48
veterinary ophthalmologists between 2000-2005. CERF does not
recommend breeding affected dogs.10 Sterile Panniculitis: Rare, dermatological disease of subcutaneous
fat inflammation characterized by deep cutaneous nodules that
Microphthalmia: A congenital defect characterized by small globes often ulcerate and drain pus or oil. Treat with immunosuppressive
of the eye. Often associated with merle. Identified in 2.38% of medications. Miniature Dachshunds represent 51.2% of all cases.
smooth miniature, 2.33% of wirehaired miniature, and 1.66% of Unknown mode of inheritance.49
longhaired miniature Dachshunds CERF examined by veterinary
ophthalmologists between 2000-2005. CERF does not recommend Acanthosis Nigricans, Brachygnathism, Bullous Pemphigoid,
breeding affected dogs.10 Calcinosis Circumscripta, Cleft Lip/Palate, Cryptorchidism,
Cutaneous Asthenia, Demodicosis, Dermoid, Entropion,
172
Glaucoma, Heterochromia Iridis, Juvenile Cellulitis,
Keratoconjunctivitis Sicca, Micropapilla, Portosystemic
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174
Dalmatian
moderate, skull is flat, muzzle blocky, and the nose is black or brown
to match the coat. The lips are close and dry. The neck is fairly long,
not throaty, and is slightly arched. The topline smoothly descends
towards the rear. The thorax is deep, ribs are well sprung, and the
abdomen has a moderate tuck up. The curved tail tapers at the tip
and reaches the tarsus at rest. Limbs are straight boned, dewclaws
may be removed. Feet are very compact with very tough thick pads.
Strong nails match the coat color or are white, and the toes are
very well arched up.
Elbow Dysplasia: Polygenically inherited trait causing elbow Behavioral Problems: Dalmatians are over-represented in
arthritis. OFA reports 0.4% affected.7 veterinary behavioral consultations versus other breeds in all
categories, including aggression, anxiety, house soiling, and
Patella Luxation: Polygenically inherited laxity of patellar phobias.17
ligaments, causing luxation, lameness, and later degenerative joint
disease. Treat surgically if causing clinical signs. Too few Dalmatians Glaucoma: Primary, narrow angle glaucoma occurs in the breed.
have been screened by OFA to determine an accurate frequency.7 Can cause blindness due to retinal damage, or secondary lens
luxation. Screen with gonioscopy and tonometry. Reported
Disease Predispositions increased incidence in Dalmatians versus other breeds. CERF does
Urate Urolithiasis: All Dalmatians are affected with hyperurico- not recommend breeding any Dalmatian with glaucoma.15,18
suria, and urate crystals are uniformly formed in the breed. Reports
Cataracts: Intermediate cataracts predominate in the breed.
show that 34% of male Dalmatians go on to form urate stones.
Reported in 1.69% of Dalmatians CERF examined by veterinary
Male Dalmatians have a 14.0x odds ratio for forming urate stones
ophthalmologists between 2000-2005. CERF does not recommend
versus female Dalmatians. The heritability of urate bladder stone
breeding any Dalmatian with a cataract.15
formation is reported to be 0.87. Dorn reports a 9.03x odds ratio
versus other breeds. Treatment is with surgical removal, and Iris Coloboma: Developmental defect of the iris. Identified in
prevention with medications. Reported at a frequency of 3.0% in 1.52% of Dalmatians CERF-examined by veterinary ophthalmolo-
the 2002 Dalmatian Club of America Health Survey.1,3,8,9,10 gists between 2000-2005. CERF does not recommend breeding any
Dalmatian with a coloboma.15
Hypothyroidism: Inherited autoimmune thyroiditis. 16.3% positive
for thyroid autoantibodies based on testing at Michigan State Persistent Pupillary Membranes: Strands of fetal remnant
University. (Ave. for all breeds is 7.5%) Reported at a frequency of connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
3.0% in the 2002 Dalmatian Club of America Health Survey.10,11,12 later three forms can impair vision, and dogs affected with these
forms should not be bred. Identified in 1.18% of Dalmatians CERF
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis
examined by veterinary ophthalmologists between 2000-2005.15
and pyotraumatic dermatitis. Dalmatians have a significantly
increased risk for atopy versus other breeds. Reported at a Iris Sphincter Dysplasia (ISD): Abnormality of persistently dilated
frequency of 9.0% in the 2002 Dalmatian Club of America Health pupils seen in the breed. The majority of affected dogs are liver
Survey.10,13 spotted, but black spotted dogs with this disorder have also been
identified. Slit lamp examination of the eyes by an ophthalmologist
Dalmatian Bronzing Syndrome (Xanthomatosis): Skin condition
reveals dysplasia (abnormal development) or atrophy (degeneration)
in dalmatians characterized by a patchy haircoat and bronze hue
of the muscles responsible for pupillary contraction. This iris
with folliculitis. This appears to be related to the excessive uric
sphincter dysplasia has been noted in puppies as young as 13 weeks
acid excretion that occurs in the Dalmatian. Not all Dalmatians are
of age as well as in adults.15,19
affected, even though all have elevated uric acid excretion.14
Cervical Spondylomyelopathy (Wobbler Syndrome): Presents
Distichiasis: Abnormally placed eyelashes that irritate the cornea
with neck pain, UMN spasticity and ataxia. Imaging studies suggest
and conjunctiva. Can cause secondary corneal ulceration. Identified
that the primary lesion is spinal cord compression at C5-6 or
in 2.37% of Dalmatians CERF-examined by veterinary ophthalmolo-
C6-7. MRI is superior to myelography in determining site, severity,
gists between 2000-2005.15
and nature of the spinal cord compression. Seen at an increased
Corneal Dystrophy: The breed can have an epithelial/stromal form incidence in the breed. Undetermined mode of inheritance.20
of corneal dystrophy. Age of onset 2-5 years. Identified in 2.37%
Copper-Associated Liver Disease: Copper toxicosis is a
of Dalmatians CERF-examined by veterinary ophthalmologists
documented disorder in Dalmatians. Affected dogs present with
between 2000-2005.15
gastrointestinal clinical signs, including anorexia and vomiting.
Idiopathic Epilepsy: Inherited seizures. The breed is reported All animals have increased ALT and ALP without cholestasis. The
with both generalized and partial-onset seizures. 18.2% start as mean hepatic copper concentration for nine Dalmatians was 3,197
generalized seizures, and 36.4% begin as partial seizures (with the microg/g dry weight liver (normal, < 450 microg/g) in one report.
rest mixed) at a mean age of 3.2 years. 91% of affected Dalmatians The findings indicate a primary metabolic defect in hepatic copper
progress to generalized seizures. Dorn reports a 4.05x odds ratio metabolism.21,22
versus other breeds. Reported at a frequency of 2.0% in the 2002
Actinic Keratosis: Affected dogs present with alopecia, erythema,
Dalmatian Club of America Health Survey. Control with anti-seizure
comedones, scales, excoriation, pustules, epidermal collarettes,
176
crusts and scars, with pathologic development of epidermal Spinal Dysraphism (Syringomyelia, Myelodysplasia): Spinal cord
hyperplasia, parakeratosis, and orthokeratosis. Lesions occur disorder identified in a Dalmatian at 8 weeks of age. Presented as a
secondary to prolonged UV/sunlight exposure, and may be a bunny hopping gait with loss of reciprocal hind limb movement.35
precursor to squamous cell carcinoma. Seen at an increased
frequency in the breed.23 Genetic Tests
Tests of Genotype: Direct tests for black and liver (brown) colors,
Laryngeal Paralysis-Polyneuropathy: Rare disorder in young
and black or brown nose are available from HealthGene and VetGen.
Dalmatians presenting with laryngeal paralysis and megaesophagus.
Neurogenic atrophy is present in intrinsic laryngeal and Direct test for hyperuricosuria is available from UC-Davis VGL and
appendicular skeletal muscles. Pathology reveals a diffuse, the Animal Health Trust.
generalized polyneuropathy, dominated by axonal degeneration.
Unknown mode of inheritance.24,25 Tests of Phenotype: CHIC Certification: Required testing includes
hip radiographs and BAER hearing test. Elective tests include CERF
Neuronal Ceroid-Lipofuscinosis (NCL): Rare, fatal inherited eye examination and thyroid profile including autoantibodies. (See
degenerative neurological disease. Affected Dalmatians present CHIC website; www.caninehealthinfo.org).
between 6-12 months of age, and die between 1.5 to 8 years of
age. They present with variable signs of blindness, tremor, ataxia, Additional recommended tests include patella evaluation, elbow
and seizures. Also reported as leucodystrophy in earlier reports. radiographs, and cardiac evaluation.
Unknown mode of inheritance. CERF does not recommend breeding
any Dalmatian with NCL.15,26,27
Miscellaneous
Brachygnathism, Calcium Oxalate Urolithiasis, Ciliary • Breed name synonyms: Coach Dog, Fire Dog, Fire House Dog,
Dyskinesia, Dermoid, Diabetes Mellitus, Entropion, IgA Carriage Dog
Deficiency, Microphthalmia, Muscular Dystrophy, Pannus, • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
Prognathism, Progressive Retinal Atrophy, Sebaceous Adenitis, ANKC (Australian National Kennel Club), NKC (National Kennel Club)
Spina Bifida, Uveal Hypopigmentation, and Wry Mouth are • AKC rank (year 2008): 76 (983 dogs registered)
reported.28 • Internet resources: The Dalmation Club of America:
www.thedca.org
The Dalmatian Club of Canada: www.dalmatianclubofcanada.ca
Isolated Case Studies British Dalmatian Club: www.britishdalmatianclub.org.uk
Dilated Cardiomyopathy (DCM): Identified in eight male Dalmatian Club of America Foundation (DCAF): www.dcaf.org
Dalmatians fed low protein diets (for prevention of urate uroliths.)
All dogs had left-sided heart failure with severe left ventricular
dilatation. Mean age of onset was 6.8 years, with a median survival References
1. Bannasch D, Safra N, Young A, et. al.: Mutations in the SLC2A9 gene
of 10 months. Taurine levels were normal in the affected dogs.29
cause hyperuricosuria and hyperuricemia in the dog. PLoS Genet. 2008
Nov;4(11):e1000246.
Alport Syndrome: Autosomal dominant Alport Syndrome was
2. Blais MC, Berman L, Oakley DA, et. al.: Canine Dal blood type: A
identified in a family of Dalmatians in Australia. Affected dogs
red cell antigen lacking in some Dalmatians. J Vet Intern Med. 2007
presented with hematuria, renal failure and deafness at a mean age Mar-Apr;21(2):281-6.
of 18 months.30 3. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Hypertrophic Cardiomyopathy: This heart disease has been 2000.
reported in the Dalmatian, possibly associated with mitral valve 4. Cargill EJ, Famula TR, Strain GM, et. al.: Heritability and
dysplasia.31 segregation analysis of deafness in U.S. Dalmatians. Genetics. 2004
Mar;166(3):1385-93.
Acute Respiratory Distress Syndrome (ARDS): Reported in 11 5. Strain GM: Deafness prevalence and pigmentation and gender
young Dalmatians from four litters. After trauma, tachypnea and associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
noisy respiration progressed to strenuous and rapid respirations, 6. Stritzel S, Wöhlke A, & Distl O: A role of the microphthalmia-
cyanosis, vomiting, and death. Affected dogs had multiple associated transcription factor in congenital sensorineural deafness
foci of marked atypical hyperplasia and squamous metaplasia and eye pigmentation in Dalmatian dogs. J Anim Breed Genet. 2009
of the bronchiolar epithelium, patchy ongoing fibrosis with Feb;126(1):59-62.
7. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
myofibroblastic metaplasia, smooth muscle hyperplasia and
8. Albasan H, Lulich JP, Osborne CA, et. al.: Evaluation of the association
occasional honeycombing of alveolar walls, and hyperplasia of
between sex and risk of forming urate uroliths in Dalmatians. J Am Vet Med
atypical type II pneumocytes. Some affected dogs had renal aplasia Assoc. 2005 Aug 15;227(4):565-9.
and hydrocephalus.32,33 9. Bannasch DL, Ling GV, Bea J, et. al.: Inheritance of urinary calculi in the
Dalmatian. J Vet Intern Med. 2004 Jul-Aug;18(4):483-7.
Cerebrospinal Hypomyelinogenesis: Identified in a newborn 10. Dalmatian Club of America Foundation: The Dalmatian Club of America
Dalmatian with generalized body tremors, which interfered with the Health Survey. 2002.
pup’s ability to suckle, walk, and maintain sternal recumbency. The 11. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
pup was euthanatized at eight weeks of age.34 Population and Animal Health, Michigan State University. April, 2007.
12. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
177
serum thyroid hormone autoantibodies in dogs with clinical signs of 36. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71. Book House, NY 2006. p. 553-557.
13. Schick RO, Fadok VA: Responses of atopic dogs to regional allergens:
268 cases (1981-1984). J Am Vet Med Assoc. 1986 Dec 1;189(11):1493-6.
14. Ackerman L: Pattern Approach to Dermatologic Diagnosis. 2002.
Proceedings, Tufts Animal Expo 2002.
15. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
16. Licht BG, Licht MH, Harper KM, et. al.: Clinical presentations of naturally
occurring canine seizures: similarities to human seizures. Epilepsy Behav.
2002 Oct;3(5):460-470.
17. Bamberger M & Houpt KA: Signalment factors, comorbidity, and trends
in behavior diagnoses in dogs: 1,644 cases (1991-2001). J Am Vet Med
Assoc. 2006 Nov 15;229(10):1591-601.
18. Slater MR, Erb HN: Effects of risk factors and prophylactic treatment
on primary glaucoma in the dog.J Am Vet Med Assoc. 1986 May
1;188(9):1028-30.
19. The Dalmatian Club of America Inc. www.thedca.org/eyes.html Last
accessed July 1, 2010.
20. da Costa RC & Parent J: Magnetic Resonance Imaging Findings in 60
Dogs with Cervical Spondylomyelopathy. Proceedings, 2009 ACVIM Forum.
2009.
21. Webb CB, Twedt DC, Meyer DJ: Copper-associated liver disease in
Dalmatians: a review of 10 dogs (1998-2001). J Vet Intern Med. 2002
Nov-Dec;16(6):665-8.
22. Vannevel JY: Liver disease in young dalmatians. Can Vet J. 1996
Jun;37(6):329.
23. Costa SS, Munhoz TD, Calazans SG, et. al.: Clinical and Epidemiological
Evaluation of Actinic Keratosis in Seven Dogs. Proceedings, 2009 WSAVA
World Congress. 2009.
24. Braund KG, Shores A, Cochrane S, et. al.: Laryngeal paralysis-
polyneuropathy complex in young Dalmatians. Am J Vet Res. 1994
Apr;55(4):534-42.
25. Braund KG, Steinberg HS, Shores A, et. al.: Laryngeal paralysis in
immature and mature dogs as one sign of a more diffuse polyneuropathy. J
Am Vet Med Assoc. 1989 Jun 15;194(12):1735-40.
26. Goebel HH, Bilzer T, Dahme E, et. al.: Morphological studies in canine
(Dalmatian) neuronal ceroid-lipofuscinosis. Am J Med Genet Suppl.
1988;5:127-39.
27. Bjerkas I: Hereditary “cavitating” leucodystrophy in Dalmation dogs.
Light and electron microscopic studies. Acta Neuropathol (Berl). 1977 Oct
10;40(2):163-9.
28. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 214. AAHA Press, 1999.
29. Freeman LM, Michel KE, Brown DJ, et. al.: Idiopathic dilated
cardiomyopathy in Dalmatians: nine cases (1990-1995). J Am Vet Med
Assoc. 1996 Nov 1;209(9):1592-6.
30. Hood JC, Huxtable C, Naito I, et. al.: A novel model of autosomal
dominant Alport syndrome in Dalmatian dogs. Nephrol Dial Transplant.
2002 Dec;17(12):2094-8.
31. De Majo M, Britti D, Masucci M, et. al.: Hypertrophic obstructive
cardiomyopathy associated to mitral valve dysplasia in the Dalmatian dog:
two cases. Vet Res Commun. 2003 Jan;27 Suppl 1:391-3.
32. Jarvinen AK, Saario E, Andresen E, et. al.: Lung injury leading to
respiratory distress syndrome in young Dalmatian dogs. J Vet Intern Med.
1995 May-Jun;9(3):162-8.
33. Syrjä P, Saari S, Rajamäki M, et. al.: Pulmonary histopathology in
dalmatians with familial acute respiratory distress syndrome (ARDS). J
Comp Pathol. 2009 Nov;141(4):254-9.
34. Greene CE, Vandevelde M, Hoff EJ: Congenital cerebrospinal
hypomyelinogenesis in a pup. J Am Vet Med Assoc. 1977 Sep
15;171(6):534-6.
35. Neufeld JL, Little PB: Spinal dysraphism in a Dalmatian dog. Can Vet J.
1974 Nov;15(11):335-6.
178
Dandie
Dinmont Terrier
of their strong chase instinct, they should not be left off-leash
unless they are contained in an enclosure. The bark is loud for their
size, and they make good alarm bark defenders. They need human
contact, and may become one-man dogs. Their overall activity levels
are somewhat lower than other terrier breeds.
Genetic Tests
Tests of Genotype: Direct test for mustard and pepper coat color is
available from Health Gene.
Miscellaneous
• Breed name synonyms: Dandie
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club)
• AKC rank: (year 2008): 146 (77 dogs registered)
• Internet resources: Dandie Dinmont Terrier Club of America:
http://clubs.akc.org/ddtca
Dandie Dinmont Terrier Club of Canada:
www.dandiedinmont.org
The Dandie Dinmont Terrier Club (UK): http://ddtc.co.uk/
180
Doberman Pinscher
Recognized Behavior Issues and Traits
This is reported to be a very loyal dog and the Doberman is a
natural protector. High intelligence, fearlessness, high activity and
alertness, and stamina in service characterize this breed. Dobes are
easy to train using positive reinforcement, and starting at a very
early age, it is important to include proper socialization to people
and other pets. If not properly trained, aggression may develop.
This can also happen if Dobes are kenneled or left alone excessively.
They need lots of contact with people and frequent exercise and
stimulation. They are average shedders and generally need only
The Breed History minimal grooming. This breed is over-represented in flank sucking
behavior, a compulsive disorder.1
This breed originated in Germany and was recognized in 1900.
In the USA, the parent club was formed in 1921. The Doberman
originates from a number of breeds including the Rottweiler, Normal Physiologic Variations
German pinscher, and Black and Tan terrier. The name of the breed Dilute coat color (d locus) is due to the homozygous recessive
originates with a German man, Louis Dobermann who was credited expression of a mutation in the melanophilin gene (MLPH). This can
for early breed development. predispose to color dilution alopecia. A genetic test is available.2
Weight: females 66-75 lb (30- 34 kg), males 66-80 lb (30-36.5 kg). Inherited Diseases
von Willebrand’s Disease Type 1 (vWD): Autosomal recessive
Coat: Breed colors include black, red, fawn and blue with legs, genetic disorder causing a mild bleeding syndrome. A genetic test is
throat and face (muzzle and eye) marked with rusty pigmentation. available from VetGen that reports 25% affected, and 49% carrier in
White spots on chest of less than a half-inch square are allowed. the breed. Dorn reports a 806.44x odds ratio versus other breeds.5,6
Smooth short and dense hair coat lies close to the skin and is
glossy. Black is dominant over red, and non-dilution is dominant Dilated Cardiomyopathy (DCM): An autosomal dominant with
over dilution. Albinos may be born, but it is a disqualification. incomplete penetrance form of heart disease characterized by
syncope, dilated cardiomyopathy, sudden death, ventricular
Longevity: 13 years. tachycardia, and heart failure. Ventricular arrhythmia precedes
heart dilation, and may be involved in the cause of DCM in the
Points of Conformation: Medium sized, powerful, agile, and breed. Diagnose with 24 hour holter ECG and echocardiogram
muscular athletic dog, the Dobermans’ way of moving and (ECHO). Pimobendan significantly improves the congestive heart
carriage is proud and springy. The head is long and wedged with failure associated with DCM in Doberman Pinschers. A European
almond-shaped brown eyes. In coats other than black, iris pigment study found 50.7% of Dobermans over 8 years of age with an
may be lighter to match coat, but the darker spectrum of coloration ECHO or holter diagnosis of DCM. A study of cardiac troponin (cTnl)
is preferred. The medium length and size ears are usually cropped levels showed that levels greater than 0.22 ng/ml could with high
and carried in a pricked position in North America. They have a sensitivity and specificity identify dogs that will eventually develop
slight stop, and flat cheeks taper to a black nose in black dogs and a DCM prior to any abnormal ECHO or holter changes. An autosomal
brown-tan-gray coloration is associated with the other coat colors dominant mutation in a mitochondrial protein gene has been
(red-fawn-blue respectively). A well arched neck that widens at the identified. A genetic test for this gene is available.11,12,13,14,15,16
base, a straight topline, deep-chested with well-sprung ribs, and
a tail usually docked short characterize this breed. They possess Hip Dysplasia: Polygenically inherited trait causing degenerative
straight limbs and feet well knuckled and compact. Dewclaws may joint disease and hip arthritis. OFA reports 6.2% affected.7
be removed.
181
Elbow Dysplasia: Polygenically inherited trait causing elbow disorder has an underlying immunodeficiency in its pathogenesis.
arthritis. OFA reports 1.0% affected.7 Dorn reports a 3.57x odds ratio versus other breeds.5,27
Patella Luxation: Polygenically inherited laxity of patellar Hormonal Urinary Incontinence: Studies show a breed prevalence
ligaments, causing luxation, lameness, and later degenerative joint for urinary incontinence in spayed female Doberman pinschers.28
disease. Treat surgically if causing clinical signs. Too few Doberman
Pinschers have been screened by OFA to determine an accurate Persistent Hyperplastic Tunica Vasculosa Lentis and Primary
frequency.7 Vitreous (PHTVL/PHPV): Congenital disorder presenting in the
breed with variable lesions from spots on the posterior lens to
Narcolepsy: Rare, autosomal recessive disorder causing sudden posterior lenticonus, and posterior polar subcapsular cataracts.
collapse and a sleep-like state elicited by excitement. Clinical Reported at a frequency of 6.7% in the Netherlands, and lower
episodes begin at four weeks of age, with maximal symptoms by frequencies in the US. CERF does not recommend breeding any
10-32 weeks of age. A genetic test is available.8 Doberman Pinscher with PHTVL/PHPV. Inheritance suspected to be
autosomal dominant with incomplete penetrance.20,29
Congenital Blindness: A rare autosomal recessive disorder occurs
in the breed, presenting with microphthalmia, corneal opacification, Persistent Pupillary Membranes: Strands of fetal remnant
absence of the anterior chamber, aphakia, retinal detachment, connecting; iris to iris, cornea, lens, or involving sheets of tissue.
and dysplasia, and partial depigmentation of the retinal pigment The later three forms can impair vision, and dogs affected with
epithelial cells.9,10 these forms should not be bred. Identified in 3.05% of Doberman
pinschers CERF-examined by veterinary ophthalmologists between
Disease Predispositions 2000-2005.20
Hypothyroidism: Inherited autoimmune thyroiditis. 8.4% positive
Chronic Active Hepatitis (Copper Toxicosis): The disease is
for thyroid auto-antibodies based on testing at Michigan State
predominantly seen in female dogs, usually 4 - 7 years of age.
University. (Ave. for all breeds is 7.5%). May be associated with
Clinical signs include polyuria/polydipsia, weight loss, anorexia,
a DLA class II allele. Dorn reports a 2.51x odds ratio versus other
icterus, and ascites. Affected dogs have increased liver enzymes,
breeds.5,17,18,19
bile acids, and hepatic copper concentrations. Pathology shows
Cataracts: Capsular and posterior suture punctate cataracts micronodular cirrhosis, fibrosis, necrosis and lymphocyte and
predominate in the breed. Identified in 4.46% of Doberman plasma cell infiltration of the portal triads. The disease is strongly
Pinschers CERF examined by veterinary ophthalmologists between linked to a homozygous DLA-MHC haplotype, indicating an immune
2000-2005. CERF does not recommend breeding any Doberman basis.30,31,32,33
Pinscher with a cataract.20
Retinal Dysplasia: Retinal folds are recognized in the breed. Can
Cervical Vertebral Instability (Wobbler Syndrome): Presents lead to retinal detachment and blindness. Reported in 2.25% of
with UMN spasticity and ataxia. Imaging studies suggest that the Doberman pinschers CERF-examined by veterinary ophthalmolo-
primary lesion is foramenal stenosis and intervertebral instability gists between 2000-2005.20
at C6-7. MRI is superior to myelography in determining site,
Distichiasis: Abnormally placed eyelashes that irritate the cornea
severity, and nature of the spinal cord compression. Dorn reports
and conjunctiva. Can cause secondary corneal ulceration. Identified
a 94.93x odds ratio versus other breeds. Undetermined mode of
in 1.44% of Doberman pinschers CERF-examined by veterinary
inheritance.5,21,22
ophthalmologists between 2000-2005.20
Acral Lick Dermatitis (Lick Granuloma) and Flank Sucking:
Follicular dysplasia: Condition causing hair loss in young adult
Behavioral disorders causing skin lesions frequently seen in the
Doberman Pinschers. Most often seen as Color Dilution Alopecia
Doberman pinscher breed. These may have an obsessive-compulsive
in some blue or fawn (dilute)-colored Doberman pinschers, but can
component.1,23
also be seen in non-dilute red or black and tan dogs. Starts as a
Prostatic Disease: Doberman pinschers are the most frequently gradual onset of dry, dull and poor hair coat quality. Progresses to
affected breed with prostatic disease. Intact males have the highest poor hair regrowth, follicular papules and comedomes. Hair loss
risk for bacterial prostatitis, prostate cancer, benign prostatic and comedome formation are usually most severe on the trunk. A
hyperplasia, and prostatic cysts. Mean age of onset is 8.9 years. genetic test is available for the dilute gene.2,34,35
Short CAG-1 repeats in the AR-gene are associated with increased
Dancing Doberman Disease (Peripheral Neuropathy): Slowly
risk for prostate cancer.24,25
progressive breed-related disorder that develops between six
Gastric Dilatation-Volvulus (Bloat, GDV): Polygenically inherited, months and seven years of age. Affected dogs have a tendency to
life-threatening twisting of the stomach within the abdomen. flex and straighten one and then both hind limbs while standing.
Requires immediate veterinary attention. Doberman pinschers with The gait remains normal while walking, but may eventually develop
the deepest thorax relative to width have the greatest risk for GDV.26 weakness in the hind legs, and be reluctant to stand. Unknown
mode of inheritance.36
Demodicosis (Generalized): Doberman pinschers are shown
to have a hereditary predisposition for demodectic mange. This Synovial Myxoma Tumors: Doberman pinschers are
overrepresented with synovial myxoma tumors, which offer a much
182
better prognosis (without metastasis) than other synovial cell Direct test for narcolepsy is available from Optigen and HealthGene.
tumors. The most common sites are stifle and digits.37,38
Direct tests for coat color (black/brown and dilute) are available
Congenital Deafness and Vestibular Disease: Rare congenital from HealthGene and VetGen.
disorder reported in the Doberman pinscher. Affected dogs show
early signs of head tilt, lack of coordination, and circling, and Tests of Phenotype: CHIC Certification: Required testing includes
become deaf by 3 weeks of age. An autosomal recessive inheritance hip radiographs, CERF eye examination, thyroid profile including
is proposed.39 autoantibodies, genetic test for vWD, cardiac evaluation (ECHO
and holter), and working dog evaluation (from DPCA). (See CHIC
Juvenile Renal Disease: The disease presents in young Doberman website; www.caninehealthinfo.org).
pinschers as anorexia, weight loss, vomiting, lethargy, polydipsia,
polyuria, and dehydration. Laboratory findings are azotemia, Recommend elbow radiographs and patella evaluation.
hyperphosphatemia, lymphopenia, non-regenerative anemia,
hypercholesterolemia, and proteinuria.40,41 Miscellaneous
• Breed name synonyms: Dobe, Doberman, Dobie, Dobermann,
Atherosclerosis: Doberman pinschers have a higher prevalence Thuringer Pinscher, Plizeilich Soldatenhund.
versus other breeds. Most common clinical signs are lethargy, • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
anorexia, weakness, dyspnea, collapse, and vomiting. Hypercholes- ANKC (Australian National Kennel Club), NKC (National Kennel Club)
terolemia, lipidemia, and hypothyroidism are common in affected • AKC rank (year 2008): 18 (10,547 dogs registered)
dogs. Myocardial fibrosis, infarction, and thickened arteries with • Internet resources: Doberman Pinscher Club of America:
narrow lumens are found on necropsy.42 www.DPCA.org
Doberman Pinscher Club of Canada: www.dpcc.ca
Atrial septal defect, Brachygnathism, Bullous Pemphigoid,
The Doberman Club (UK): www.thedobermannclub.co.uk
Chromosomal Intersex, Ciliary Dyskenesis, Diabetes Mellitus,
United Doberman Club: www.uniteddobermanclub.com
Familial Benign Pemphigus, Fanconi Syndrome, Hemivertebra,
Histiocytosis, Hypertrophic Osteodystrophy, Icthyosis,
Lupoid Onychopathy, Malignant Hyperthermia, Mucinosis, References
Osteochondritis Dessicans-Stifle, Oligodontia, Panosteitis, 1. Moon-Fanelli AA, Dodman NH & Cottam N: Blanket and flank sucking in
Pemphigus Foliaceous, Prognathism, Progressive Retinal Doberman Pinschers. J Am Vet Med Assoc. 2007 Sep 15;231(6):907-12.
Atrophy, Renal Agenesis, Seasonal Flank Alopecia, Sebaceous 2. Philipp U, Hamann H, Mecklenburg L, et. al.: Polymorphisms within the
Adenitis, Supernumerary Teeth, Vitiligo, Wry Mouth, and Zinc canine MLPH gene are associated with dilute coat color in dogs. BMC
Genet. 2005 Jun 16;6:34.
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3. Cribb AE, Spielberg SP: An in vitro investigation of predisposition
to sulphonamide idiosyncratic toxicity in dogs. Vet Res Commun.
Isolated Case Studies 1990;14(3):241-52.
Chronic Rhinitis and Pneumonia: Eight related Doberman 4. Giger U, Werner LL, Millichamp NJ, et. al.: Sulfadiazine-induced allergy in
pinschers were identified with chronic rhinitis and pneumonia. A six Doberman pinschers. J Am Vet Med Assoc. 1985 Mar 1;186(5):479-84.
defect in the bactericidal ability of neutrophils was identified.44 5. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Congenital Peripheral Vestibular Disease: Individual Doberman 2000.
pinschers from repeat breedings had unilateral or bilateral congenital 6. Brooks MB, Erb HN, Foureman PA, et. al.: von Willebrand disease
phenotype and von Willebrand factor marker genotype in Doberman
peripheral vestibular disease. Clinical pathology was normal. Marked
Pinschers. Am J Vet Res. 2001 Mar;62(3):364-9.
lymphocytic labyrinthitis was discovered microscopically. The 7. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
occurrence in separate litters suggests an inherited disorder.45 8. Hungs M, Fan J, Lin L, et. al.: Identification and functional analysis of
mutations in the hypocretin (orexin) genes of narcoleptic canines. Genome
Situs Inversus and Diaphragmatic Hernia: A 4 year old female Res. 2001 Apr;11(4):531-9.
Doberman Pinscher developed dyspnea during sedation. A 9. Bergsjo T, Arnesen K, Heim P, et. al.: Congenital blindness with ocular
diaphragmatic hernia was diagnosed, and situs inversus of both developmental anomalies, including retinal dysplasia, in Doberman Pinscher
the thorasic and abdominal viscera was discovered during surgical dogs. J Am Vet Med Assoc. 1984 Jun 1;184(11):1383-6.
repair.46 10. Peiffer RL Jr, Fischer CA: Microphthalmia, retinal dysplasia, and anterior
segment dysgenesis in a litter of Doberman Pinschers. J Am Vet Med Assoc.
Proximal Femoral Focal Deficiency (PFFD): A 3 month old 1983 Oct 15;183(8):875-8.
Doberman Pinscher was identified with a unilateral dysgenesis of 11. Calvert CA, Wall M: Results of ambulatory electrocardiography in overtly
the femoral head and neck.47 healthy Doberman Pinschers with equivocal echocardiographic evidence of
dilated cardiomyopathy. J Am Vet Med Assoc. 2001 Sep 15;219(6):782-4.
12. Calvert CA, Jacobs GJ, Smith DD, et. al.: Association between results
Genetic Tests of ambulatory electrocardiography and development of cardiomyopathy
Tests of Genotype: Direct test for vWD is available from VetGen. during long-term follow-up of Doberman pinschers. J Am Vet Med Assoc.
2000 Jan 1;216(1):34-9.
Direct test for DCM is available from North Carolina State University 13. Meurs KM, Fox PR, Norgard M, et. al.: A prospective genetic evaluation
- Meurs Lab. of familial dilated cardiomyopathy in the Doberman pinscher. J Vet Intern
Med. 2007 Sep-Oct;21(5):1016-20.
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14. O’Grady MR, Minors SL, O’Sullivan ML, et. al.: Effect of Pimobendan on Cases. Vet Pathol. 2010 Sep;47(5):931-6.
Case Fatality Rate in Doberman Pinschers with Congestive Heart Failure 39. Wilkes MK, Palmer AC: Congenital deafness and vestibular deficit in the
Caused by Dilated Cardiomyopathy. J Vet Intern Med. 2008 Jun 4. doberman. J. of Small Animal Practice. 1992;33: 218-224.
15. Wess G, Schulze A, Butz V, et. al.: Prevalence of Dilated Cardiomyopathy 40. Picut CA, Lewis RM: Juvenile renal disease in the Doberman Pinscher:
in Doberman Pinschers in Various Age Groups. J Vet Intern Med. 2010 ultrastructural changes of the glomerular basement membrane. J Comp
May-Jun;24(3):533-8.24. Lai CL, L’Eplattenier H, van den Ham R, et. al.: Pathol. 1987 Sep;97(5):587-96.
Androgen receptor CAG repeat polymorphisms in canine prostate cancer. J 41. Chew DJ, DiBartola SP, Boyce JT, et. al.: Juvenile renal disease in
Vet Intern Med. 2008 Nov-Dec;22(6):1380-4. Doberman Pinscher dogs. J Am Vet Med Assoc. 1983 Mar 1;182(5):481-5.
16. Wess G, Simak J, Mahling M, et. al.: Cardiac Troponin I in Doberman 42. Liu SK, Tilley LP, Tappe JP, et. al.: Clinical and pathologic findings in dogs
Pinschers with Cardiomyopathy. J Vet Intern Med. 2010 Jul-Aug;24(4):843-9. with atherosclerosis: 21 cases (1970-1983). J Am Vet Med Assoc. 1986 Jul
17. Kennedy LJ, Quarmby S, Happ GM, et. al.: Association of canine 15;189(2):227-32.
hypothyroidism with a common major histocompatibility complex DLA 43. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
class II allele. Tissue Antigens. 2006 Jul;68(1):82-6. Ackerman. p 214-15 AAHA Press, 1999.
18. Nachreiner R & Refsal K: Personal communication, Diagnostic Center 44. Breitschwerdt EB, Brown TT, De Buysscher EV, et. al.: Rhinitis,
for Population and Animal Health, Michigan State University. April, 2007. pneumonia, and defective neutrophil function in the Doberman pinscher.
19. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of Am J Vet Res. 1987 Jul;48(7):1054-62.
serum thyroid hormone autoantibodies in dogs with clinical signs of 45. Forbes S, Cook JR Jr: Congenital peripheral vestibular disease attributed
hypothyroidism. J Am Vet Med Assoc. 2002 Feb 15;220(4):466-71. to lymphocytic labyrinthitis in two related litters of Doberman pinscher
20. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American pups. J Am Vet Med Assoc. 1991 Feb 1;198(3):447-9.
College of Veterinary Ophthalmologists. ACVO, 2007 46. Witsberger TH, Dismukes DI, Kelmer EY, et. al.: Situs inversus totalis in
21. da Costa RC, Parent J, Dobson H, et. al.: Comparison of magnetic a dog with a chronic diaphragmatic hernia. J Am Anim Hosp Assoc. 2009
resonance imaging and myelography in 18 Doberman pinscher dogs Sep-Oct;45(5):245-8.
with cervical spondylomyelopathy. Vet Radiol Ultrasound. 2006 47. Salavati M: Proximal femoral focal deficiency (PFFD) in a young
Oct-Nov;47(6):523-31. Doberman pinscher. J Small Anim Pract. 2008 Sep;49(9):486.
22. Mason TA: Cervical vertebral instability (wobbler syndrome) in the dog. 48. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Vet Rec. 1979 Feb 17;104(7):142-5. Book House, NY 2006. p. 258-261.
23. Virga V: Behavioral Dermatology: Psychogenic Alopecia, ALD and
Related Syndromes. Proceedings, 2004 Northeast Veterinary Conference.
2004.
24. Krawiec DR, Heflin D: Study of prostatic disease in dogs: 177 cases
(1981-1986). J Am Vet Med Assoc. 1992 Apr 15;200(8):1119-22.
25. Lai CL, L’Eplattenier H, van den Ham R, et. al.: Androgen receptor CAG
repeat polymorphisms in canine prostate cancer. J Vet Intern Med. 2008
Nov-Dec;22(6):1380-4.
26. Glickman LT, Glickman NW, Perez CM, et. al.: Analysis of risk factors
for gastric dilatation and dilatation-volvulus in dogs. J Am Vet Med Assoc.
1994 May 1;204(9):1465-71.
27. Wilkie BN, Markham RJ, Hazlett C: Deficient cutaneous response
to PHA-P in healthy puppies from a kennel with a high prevalence of
demodicosis. Can J Comp Med. 1979 Oct;43(4):415-9.
28. Arnold S: Urinary incontinence in castrated bitches. Part 1:
Significance, clinical aspects and etiopathogenesis. Schweiz Arch Tierheilkd.
1997;139(6):271-6.
29. Stades FC, Boeve MH, van den Brom WE, et. al.: The incidence of
PHTVL/PHPV in Doberman and the results of breeding rules. Vet Q. 1991
Jan;13(1):24-9.
30. Johnson GF, Zawie DA, Gilbertson SR, et. al.: Chronic active hepatitis in
Doberman pinschers. J Am Vet Med Assoc. 1982 Jun 15;180(12):1438-42.
31. Mandigers PJ, van den Ingh TS, Spee B, et. al.: Chronic hepatitis in
Doberman pinschers. A review. Vet Q. 2004 Sep;26(3):98-106.
32. Crawford MA, Schall WD, Jensen RK, et. al.: Chronic active
hepatitis in 26 Doberman pinschers. J Am Vet Med Assoc. 1985 Dec
15;187(12):1343-50.
33. Dyggve H, Kennedy LJ, Meri S, et. al.: Linkage of Doberman Hepatitis to
the Canine Major Histocompatibility Complex. Proceedings, 19th ECVIM-CA
Congress, 2009.
34. Miller WH Jr.: Follicular dysplasia in adult black and red Doberman
pinschers. Vet Dermatol 1990;1:181–187.
35. Moura E & Cirio SM: Follicular dysplasia of the adult doberman
pinscher. J Am Anim Hosp Assoc. 2010 Mar-Apr;46(2):143-7.
36. Olby N: Spinal Cord Disease, Neuropathies, and Behavioral Problems.
Proceedings, 2004 Western Veterinary Conference. 2004.
37. Craig LE, Julian ME, Ferracone JD: The diagnosis and prognosis of
synovial tumors in dogs: 35 cases. Vet Pathol. 2002 Jan;39(1):66-73.
38. Craig LE, Krimer PM, Cooley AJ, et. al.: Canine Synovial Myxoma: 39
184
Dogue de Bordeaux
between the upper and lower incisors. The lower jaw curves
upwards. The skin is supple, ample and loose. The tail preferably
reaches the hock but not below. the Dogue is well up on his toes
despite his weight. The gait is supple and close to the ground, with
great reach and drive.
Points of Conformation: The length of the body, measured from Disease Predispositions
the point of the shoulder to the point of the buttock, is greater than Aortic Stenosis (AS): Narrowing of the outflow tract of the
the height at the withers, in the proportion of 11/10. The depth of heart, causing a murmer and possible later heart disease. 72% of
the chest is more than half the height at the withers. The head is Dogues de Bordeaux have an aortic murmur, with 17% having
large, rather short, and trapezium shaped when viewed from above echocardiographic aortic outflow velocity consistent with aortic
and in front. The eyes are oval and set wide apart. The ear is small stenosis. Undetermined mode of inheritance. An Isreali cohort had
in proportion to the skull and of a slightly darker color than the concurrent tricuspid valve dysplasia.2,6
coat. The cheeks are prominent due to the very strong development
of the muscles. The bite is undershot so that there is no contact
185
Ectropion: Rolling out of eyelids, often with a medial canthal lymphoid tissue. A possible B-cell congenital immune deficiency
pocket. Can cause secondary conjunctivitis. Can be secondary was suspected.12
to Ectropion is reported in 16.67% of Dogues de Bordeaux CERF
examined by veterinary ophthalmologists between 2000-2005.4 Lymphocytic Insulitis/Juvenile Diabetes Mellitus: A 3-mo-old
Dogue de Bordeaux presented with persistent hyperglycemia and
Distichiasis: Abnormally placed eyelashes that irritate the cornea insulinopenia. Histological analysis of the pancreas T-cell infiltration
and conjunctiva. Can cause secondary corneal ulceration. Reported of the islets of Langerhans, demonstrating an immune mediated
in 6.67% of Dogues de Bordeaux CERF examined by veterinary juvenile diabetes.13
ophthalmologists between 2000-2005.5
Congenital Valvular Pulmonic Stenosis, Tricuspid Valve Dysplasia,
Persistent Pupillary Membranes: Strands of fetal remnant and Chronic Atrial Fibrillation: A 4-year-old male Dogue de
connecting; iris to iris, cornea, lens, or involving sheets of tissue. Bordeaux dog with congenital valvular pulmonic stenosis, tricuspid
The later three forms can impair vision, and dogs affected with valve dysplasia, and chronic atrial fibrillation had its ventricular heart
these forms should not be bred. Identified in 6.67% of Dogues de rate controlled with a novel vagal stimulation system.14
Bordeaux CERF examined by veterinary ophthalmologists between
2000-2005.5 Thoracic Stenosis: Two immature Dogues de Bordeaux presented
for treatment of paraparesis. Thoracic stenosis was found at T4-6,
Cranial Cruciate Ligament (ACL) Rupture: Traumatic tearing of the with lateral compression of the thoracic spinal cord caused by
ACL in the stifle, causing lameness and secondary arthritis. Treat with over-sized pedicles. Dorsal laminectomy and partial pediculectomy
surgery. Reported at an increased incidence versus other breeds.7 stabilized their condition.15
186
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
9. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
10. Segalini V, Hericher T, Grellet A, et. al.: Thyroid function and infertility
in the dog: a survey in five breeds. Reprod Domest Anim. 2009 Jul;44 Suppl
2:211-3.
11. Paradis M: Footpad hyperkeratosis in a family of Dogue de Bordeaux.
Veterinary Dermatology 1992;3:75-78.
12. Lobetti RG: Suspected primary immune deficiency in a Donge de
Bordeaux dog. J S Afr Vet Assoc. 2002 Sep;73(3):133-4.
13. Jouvion G, Abadie J, Bach JM, et. al.: Lymphocytic insulitis in a juvenile
dog with diabetes mellitus. Endocr Pathol. 2006 Fall;17(3):283-90.
14. Ohad DG, Sinai Y, Zaretsky A, et. al.: Ventricular rate control using
a novel vagus nerve stimulating system in a dog with chronic atrial
fibrillation. J Vet Cardiol. 2008 Dec;10(2):147-54.
15. Talbot CE, Pratt J, & Jeffery ND: Imaging Findings and Surgical
Treatment of Thoracic Stenosis in Two Dogues de Bordeaux. Proceedings,
2008 British Small Animal Veterinary Congress. 2008.
16. AKC Breed Website: www.akc.org/breeds/dogue_de_bordeaux/ Last
accessed July 1, 2010.
187
English
Cocker Spaniel
Recognized Behavior Issues and Traits
This dog is reported to be: a high energy pet with staying power
suited for hunting, and has moderate grooming needs. They are
average shedders. They need to be socialized early and training
should begin early also. They do well in town or country with
regular exercise. They are good alarm barkers. They get along very
well with calm children. There is some variability in temperament
between different lines of dogs. (See Aggression/Shyness below)
Inherited Epilepsy: Grand-mal seizures. Control with Congenital Vestibular Disease: Reported in a litter of English
anticonvulsant medication. Reported at a frequency of 1.92% in the cocker spaniel puppies, marked by loss of balance and ataxia
189
initially. Subsequent compensation left only one individual with 12. English Cocker Spaniel Club of America, Slater MS: 2002 ECS Health
“permanent” head tilt.25 Survey Report. 2004.
13. Engelhardt A, Stock KF, Hamann H, et. al.: A retrospective study
on the prevalence of primary cataracts in two pedigrees from the
Genetic Tests German population of English Cocker Spaniels. Vet Ophthalmol. 2008
Tests of Genotype: Direct tests for HN and prcd-PRA are available Jul-Aug;11(4):215-21.
from Optigen. (Both tests are recommended for breeding dogs.) 14. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
Direct tests for black, liver and red colors, and black and brown nose 15. Podberscek AL, Serpell JA: Aggressive behaviour in English cocker
are available from HealthGene and VetGen. spaniels and the personality of their owners. Vet Rec 1997: 141[3]:73-6.
16. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
Tests of Phenotype: CHIC Certification: Required tests include hip in pure-bred dogs in North America. Vet Ophthalmol. 2004
radiographs, genetic test for prcd-PRA, patella evaluation, and two Mar-Apr;7(2):97-111.
of the following: thyroid profile including autoantibodies, genetic 17. Dietz HH: Retinal dysplasia in dogs--a review. Nord Vet Med. 1985
test for FN, BAER hearing test, or CERF eye examination. (See CHIC Jan-Feb;37(1):1-9.
website; www.caninehealthinfo.org). 18. Sanchez RF, Innocent G, Mould J, et. al.: Canine keratoconjunctivitis
sicca: disease trends in a review of 229 cases. J Small Anim Pract. 2007
Recommend cardiac evaluation by a cardiologist and elbow Apr;48(4):211-7.
19. Staaden RV: Cardiomyopathy of English cocker spaniels. J Am Vet Med
radiographs.
Assoc. 1981 Jun 15;178(12):1289-92.
20. Watson PJ: Chronic Hepatitis in Dogs. Proceedings, 2009 British Small
Miscellaneous Animal Veterinary Congress. 2009.
• Breed name synonyms: Cocker, Woodcock spaniel, Cocker 21. McLellan GJ, Cappello R, Mayhew IG, et. al.: Clinical and pathological
Spaniel observations in English cocker spaniels with primary metabolic vitamin
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), E deficiency and retinal pigment epithelial dystrophy. Vet Rec. 2003 Sep
ANKC (Australian National Kennel Club), NKC (National Kennel Club) 6;153(10):287-92.
22. Davidson MG: Congenital cataracts in English cocker spaniels. Vet Rec.
• AKC rank (year 2008): 70 (1,247 dogs registered)
1988 Jun 4;122(23):568.
• Internet resources: English Cocker Spaniel Club of America:
23. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
www.ecsca.org Ackerman. p. 212, AAHA Press, 1999.
English Cocker Spaniel Club of Canada: www.ecscc.ca 24. Lautzenhiser SJ, Bjorling DE: Urinary incontinence in a dog with an
The Cocker Spaniel Club (UK): www.thecockerspanielclub.co.uk ectopic ureterocele. J Am Anim Hosp Assoc. 2002 Jan-Feb;38(1):29-32.
25. Bedford PG: Congenital vestibular disease in the English cocker spaniel.
References Vet Rec. 1979 Dec 8;105(23):530-1.
26. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
1. Gooding JP, Robinson WF, Mews GC: Echocardiographic characterization
of dilatation cardiomyopathy in the English cocker spaniel. Am J Vet Res. Book House, NY 2006. p 89-92.
1986 Sep;47(9):1978-83.
2. Gooding JP, Robinson WF, Mews GC: Echocardiographic assessment of
left ventricular dimensions in clinically normal English cocker spaniels. Am J
Vet Res. 1986 Feb;47(2):296-300.
3. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
5. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
6. Lees GE, Helman RG, Kashtan CE, et. al.: A model of autosomal
recessive Alport syndrome in English cocker spaniel dogs. Kidney Int. 1998
Sep;54(3):706-19.
7. Davidson AG, Bell RJ, Lees GE, et. al.: Genetic cause of autosomal
recessive hereditary nephropathy in the English Cocker Spaniel. J Vet Intern
Med. 2007 May-Jun;21(3):394-401.
8. Engelhardt A, Stock KF, Hamann H, et. al.: Analysis of systematic
and genetic effects on the prevalence of primary cataract, persistent
pupillary membrane and distichiasis in the two color variants of English
Cocker Spaniels in Germany. Berl Munch Tierarztl Wochenschr. 2007
Nov-Dec;120(11-12):490-8.
9. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
10. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
11. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
190
English Foxhound
Needs mental stimulation and human contact if housed solo. Gets
along well with other dogs. Moderate barking tendency; also may
howl. Has a moderate shedding tendency. Still kept primarily for
hunting rather than as a house pet.
Points of Conformation: The dog is square and moderate in all Deafness: Congenital deafness can be unilateral or bilateral.
proportions. The head is of a size to match the dog, with large nose, Diagnosed by BAER testing.7
the ears are set low and pendulous with moderate leather, and
often the tips are rounded (the distal segment is trimmed off). The Renal Amyloidosis: Multiple reported cases of kidney failure in
neck is long and not throaty, with slight arch. The thorax is deep related English Foxhounds. Affected dogs have an acute onset of
and the rib cage does not taper up caudally but extends well back. kidney dysfunction, and die within one week. Histological findings
Feet are round and toes are well knuckled up. Topline is level, and in the kidneys show the presence of both glomerular and interstitial
the tail is carried gaily when alert. It tapers at the tip with a fringe amyloid.8
of hair (slight brush). Very straight legs, and a low ground-covering
Ocular Disorders: Not enough English Foxhounds have had CERF
gait characterize the breed.
eye examinations to determine accurate frequencies for ocular
disorders.9
Recognized Behavior Issues and Traits
Reported breed attributes include: Likes to be in a pack, good if Brachygnathism, Hound Ataxia, Prognathism, and Thrombopathia
raised in a household and good with children if socialized early. are reported.10
High activity, high exercise needs, and thus not well placed in
apartments. Low grooming needs, let loose in a fenced area only or
may run off after scents.
191
Isolated Case Studies
None reported.
Genetic Tests
Tests of Genotype: Direct test for coat color alleles is available
from VetGen.
Miscellaneous
• Breed name synonyms: Foxhound
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 157 (17 dogs registered)
• Internet resources: English Foxhound Club of America (AKC):
13007 Brandywine Rd.
Brandywine, MD 20613
Masters of Foxhounds Association of America:
www.mfha.com
References
1. Bowles CA, Alsaker RD, Wolfle TL: Studies of the Pelger-Huet anomaly in
foxhounds. Am J Pathol. 1979 Jul;96(1):237-47.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Swenson CL, Silverman J, Stromberg PC, et. al.: Visceral leishmaniasis in
an English foxhound from an Ohio research colony. J Am Vet Med Assoc.
1988 Nov 1;193(9):1089-92.
6. Grosjean NL, Vrable RA, Murphy AJ, et. al.: Seroprevalence of antibodies
against Leishmania spp among dogs in the United States. J Am Vet Med
Assoc. 2003 Mar 1;222(5):603-6.
7. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32
8. Mason NJ, Day MJ: Renal amyloidosis in related English foxhounds. J
Small Anim Pract. 1996 Jun;37(6):255-60..
9. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007
10. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. P 218. AAHA Press, 1999.
11. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 173-176.
192
English Setter
Recognized Behavior Issues and Traits
Reports of this breed note that they possess an affectionate, docile
disposition. They are high activity dogs though, and need regular
exercise, and are thus not well placed for city living. They are
generally quiet in the house, and are quite placid. Training should
start early and they often have a streak of independence. They are
alarm barkers.
The coat just needs regular brushing; they are average shedders.
They are good with children, and crave close contact with their
families. If left alone for extended periods, they may engage in
The Breed History boredom vices such as digging and chewing. Their prominent flews
As the name implies, they are of English origin, and were renowned result in some drooling.
bird dogs that first came into the record in the late 1800s. Springer
spaniel, Water spaniel and Spanish pointer breeds may have all
contributed to this breed’s development. The term setter relates Normal Physiologic Variations
to the crouching posture (set) the dog originally took when they English Setters may be more prone to developing eccentrocytes
located the bird. - RBCs that appear in a peripheral blood smear to have their
hemoglobin shifted to one side of the cell.1
Breeding for Function
Bred as a bird-hunting dog, to set and retrieve, this dog has Drug Sensitivities
established himself as a top field trial performer. They are also None reported
prized as companion dogs. The modern field dog has a bit stockier
and smaller constitution and less of a coat than the show or Inherited Diseases
companion type. They do well in agility competitions. Hip Dysplasia: Polygenically inherited trait causing degenerative
joint disease and hip arthritis. OFA reports 16.5% affected. Dorn
Physical Characteristics reports a 1.49x odds ratio versus other breeds.2,3
Height at Withers: female 24” (61 cm), male 25” (63.5 cm)
Elbow Dysplasia: Polygenically inherited trait causing elbow arthritis.
Weight: females 60-65 lb (27-29.5 kg), males 65-80 lb (29.5-36.5 kg) Reported 3.7x odds ratio for ununited anconeal process form of
elbow dysplasia versus other breeds. OFA reports 15.1% affected.2,4
Coat: The flat long and straight to slightly wavy silky coat with
feathers may be tri-color, lemon or liver belton, blue (black) or orange Patella Luxation: Polygenically inherited laxity of patellar ligaments,
(tan) belton. Belton markings are a white background with flecking causing luxation, lameness, and later degenerative joint disease. Treat
(speckles) or roan of these colors admixed. Flecking is preferred. surgically if causing clinical signs. Too few English Setters have been
screened by OFA to determine an accurate frequency.2
Longevity: 11-12 years.
Neuronal Ceroid-Lipofuscinosis: Rare, fatal autosomal recessive
Points of Conformation: Due to their origins as gundogs for inherited degenerative neurological disease. Affected English setters
vigorous hunting, this athletic, graceful dog is bred for function. present between 6-12 months of age, and die between 20-27
They have mesocephalic skulls, with a well-defined stop and long months of age. They present with variable signs of progressive hind
square muzzle. The occiput is prominent, nose is black or dark limb paresis, incoordination, behavior changes, seizures, and/or
brown, pendulous flews are present, and eyes are dark brown and blindness. A genetic test is available.5,6
round. Moderate-length ears are of thin leather, pendulous and
set low. A long arched fine neck and level topline (can also slightly Disease Predispositions
slope to the rear) are typical. Their deep chest is not broad, and Hypothyroidism: Inherited autoimmune thyroiditis. 31.4% positive
a moderate loin tuck is present. Tapering, the tail finishes at the for thyroid auto-antibodies based on testing at Michigan State
tarsus joint, and is carried horizontally. Forelegs are strong and University. (Ave. for all breeds is 7.5%) Dorn reports a 1.26x odds
straight, the feet are compact and toes are well arched. Dewclaws ratio versus other breeds.3,7,8
are often removed. The gait appears effortless, characterized by
long, low strides with straight movement. Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis
and pyotraumatic dermatitis. English setters have a significantly
increased risk for atopy versus other breeds. Dorn reports a 1.91x
odds ratio versus other breeds.3,9
193
Deafness: Congenital deafness can be unilateral or bilateral. Tests of Phenotype: CHIC Certification: Required tests are; hip
Diagnosed by BAER testing. Strain reports total (uni or bilateral) and elbow radiographs, and BAER testing for deafness. Optional
deafness frequency of 12.4% based on BAER testing. 10.3% of all recommended thyroid profile including autoantibodies. (See CHIC
English setters test unilaterally deaf, and 2.1% test bilaterally deaf. website: www.caninehealthinfo.org)
The ESAA maintains a BAER test registry: www.esaa.com/health/
Baersearch.asp.10 Recommend CERF eye examination, patella evaluation, and cardiac
evaluation.
Distichiasis: Abnormally placed eyelashes that irritate the
cornea and conjunctiva. Can cause secondary corneal ulceration. Miscellaneous
Identified in 7.24% of English setters CERF-examined by veterinary • Breed name synonyms: Llewellin (historical but the term
ophthalmologists between 2000-2005.11 Llewellin Setter is sometimes used today for the field variety),
Laverack (historical type), Setting Spaniel (historical)
Mammary Cancer: Dorn reports a 36.54x odds ratio for mammary
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain),
gland cancer versus other breeds.3
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
Osteochondritis Dissecans (OCD), Shoulder: Abnormality of • AKC rank (year 2008): 86 (752 registered)
cartilage development causing lameness. Severe cases may require • Internet resources: English Setter Association of America:
surgery. English setters have a greater than 5x risk of developing www.esaa.com
shoulder OCD than other breeds. Males are affected more than English Setter Association of England:
females. Another study reported a 10.1x odds ratio versus other www.englishsetterassociation.co.uk
breeds. Unknown mode of inheritance.4,12 English Setter Club of Canada:
www.englishsetterclubofcanada.com
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The References
later three forms can impair vision, and dogs affected with these 1. Caldin M, Carli E, Furlanello T, et. al.: A retrospective study of 60 cases of
forms should not be bred. Identified in 1.81% of English Setters CERF eccentrocytosis in the dog. Vet Clin Pathol. 2005 Sep;34(3):224-31.
examined by veterinary ophthalmologists between 2000-2005.11 2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
Cataracts: Anterior or posterior intermediate and punctate veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
cataracts occur in the breed. Identified in 2.71% of English 2000.
setters CERF-examined by veterinary ophthalmologists between 4. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
2000-2005. CERF does not recommend breeding any English Setter developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
with a cataract.11
5. Katz ML, Khan S, Awano T, et. al.: A mutation in the CLN8 gene in English
Setter dogs with neuronal ceroid-lipofuscinosis. Biochem Biophys Res
Symmetrical Lupoid Onychodystrophy (SLO): Disorder causing
Commun. 2005 Feb 11;327(2):541-7.
loss of toenails. Onset between 2-8 years of age affecting 1-2 nails, 6. Koppang N: The English setter with ceroid-lipofuscinosis: a suitable model
then progressing to all toenails within 2-9 weeks. Requires lifelong for the juvenile type of ceroid-lipofuscinosis in humans. Am J Med Genet
treatment with oral fatty acid supplementation +/- prednisone. Suppl. 1988;5:117-25.
Kindreds of affected English setters have been identified, but a 7. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
mode of inheritance is not known.13 Population and Animal Health, Michigan State University. April, 2007.
8. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
Brachygnathism, Central PRA, Cutaneous Asthenia, Ectropion, hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Factor VIII Deficiency, Familial Benign Pemphigus, GM2 Vet Med Assoc. 2002 Feb 15;220(4):466-71.
gangliosidosis, Keratoconjunctivitis Sicca, Malassezia 9. Schick RO, Fadok VA: Responses of atopic dogs to regional allergens: 268
Dermatitis, Methemoglobin Reductase Deficiency, Prognathism, cases (1981-1984). J Am Vet Med Assoc. 1986 Dec 1;189(11):1493-6.
von Willebrands Disease, and Wry Mouth are reported.14 10. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
11. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Isolated Case Studies College of Veterinary Ophthalmologists. ACVO, 2007.
Exocrine Pancreatic Insufficiency: Reported in a family of 12. Slater MR, Scarlett JM, Kaderly RE, Bonnett BN: Breed, gender and
English setters with juvenile onset chronic inadequate digestion, age as risk factors for canine osteochondritis dissecans. Veterinary and
voluminous foul smelling feces, weight loss with increased appetite, Comparative Orthopaedics and Traumatology 1991; 4:100-106.
occasional vomiting, and abdominal pain.15 13. Ziener ML, Bettenay SV & Mueller RS: Symmetrical onychomadesis in
Norwegian Gordon and English setters. Vet Dermatol. 2008 Apr;19(2):88-94.
14. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Genetic Tests Ackerman. p.216 AAHA Press, 1999.
Tests of Genotype: Direct test for NCL is available from the 15. Boari A, Williams DA, Famiglibergamini P: Observations on Exocrine
University of Missouri. Pancreatic Insufficiency in a Family of English Setter Dogs. Journal of Small
Animal Practice 1994; 35: 247-250.
Direct tests for black or black tricolor, liver or liver tricolor 16. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
and lemon colors, and black or brown nose are available from House, NY 2006. p. 63-66.
HealthGene and VetGen.
194
English
Springer Spaniel
and trained early and are classed as high-energy dogs. They are
solid alarm barkers. They require daily grooming and periodic
trimming and clipping, and attention to ear cleanliness is important.
Bradyarrhythmia: English Springer Spaniels were over represented Direct tests for black or liver colors, and black or brown nose are
in a UK study of dogs with slow heart rates requiring pacemaker available from HealthGene and VetGen.
implantation. English Springer Spaniels presented at a younger
age, with a median survival time of 30 months. Diagnoses included Tests of Phenotype: Recommended tests include hip and elbow
persistent atrial standstill, AV block, and sick sinus syndrome.28 radiographs, CERF eye examination, patella evaluation, thyroid
profile including autoantibodies, and cardiac evaluation.
Pyothorax: Production and filling of pus in the chest cavity. English
Springer Spaniels comprised 6 of 15 reported cases of pyothorax in Miscellaneous
one study. Treatment is with long-term antibiotics.29 • Breed name synonyms: Field spaniel (historical), Springer,
Springer spaniel
Myasthenia Gravis: A rare, congenital form of myasthenia gravis
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
occurs in English Springer Spaniels. Clinical signs are evident from
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
six to eight weeks of age, and include exercise induced weakness
• AKC rank (year 2008): 27 (6,690 dogs registered)
without megaesophagus. Raised antibody levels to acetylcholine
• Internet resources: English Springer Spaniel Field Trial
receptor do not occur.30
Association Inc. (parent club in the US): www.essfta.org
Congenital Hypomyelinization (Shaking Pups): Rare The English Springer Spaniel Club of Great Britain:
developmental disorder of lack of myelin in the spinal cord, www.englishspringer.org
brainstem and cerebral hemispheres. Affected dogs are reduced size English Springer Spaniel Club of Canada:
and show gross generalized tremor, particularly when aroused, at www.geocities.com/essccanada/
about 10-12 days of age. Possible X-linked recessive inheritance.31,32
References
Ciliary Dyskinesia: Inherited abnormal anatomy and function of 1. Reisner IR, Houpt KA, Shofer FS: National survey of owner-directed
cilia. Causes chronic secondary rhinitis and bronchopneumonia aggression in English Springer Spaniels. J Am Vet Med Assoc. 2005 Nov
due to abnormal respiratory ciliary clearance, and infertility due to 15;227(10):1594-603.
abnormal sperm motility. Breeding studies suggest an autosomal 2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
recessive mode of inheritance.33,34 3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
Cerebellar abiotrophy, Cutaneous Asthenia, Deafness, 4. Whiteley HE, Young S: The external limiting membrane in developing
Diabetes Mellitus, Ectropion, Entropion, Factor XI Deficiency, normal and dysplastic canine retina. Tissue Cell. 1986;18(2):231-9.
5. O’Toole D, Young S, Severin GA, et. al.: Retinal dysplasia of English
Microphthalmia, Narcolepsy, Patent Ductus Arteriosus,
springer spaniel dogs: light microscopy of the postnatal lesions. Vet Pathol.
Protein-Losing Enteropathy, Ventricular Septal Defect, von 1983 May;20(3):298-311.
Willebrand’s Disease, and Wooly Syndrome are reported.35 6. Miyadera K, Kato K, Aguirre-Hernández J, et. al.: Phenotypic variation and
genotype-phenotype discordance in canine cone-rod dystrophy with an
Isolated Case Studies RPGRIP1 mutation. Mol Vis. 2009 Nov 11;15:2287-305.
Dyserythropoiesis, Polymyopathy, and Cardiomegaly: Three 7. Giger U, Reilly MP, Asakura T, et. al.: Autosomal recessive inherited
related English Springer Spaniels were identified with regurgitation phosphofructokinase deficiency in English springer spaniel dogs. Anim
Genet. 1986;17(1):15-23.
from an early age, slowly progressive temporal muscle atrophy with
8. Skelly BJ, Sargan DR, Winchester BG, et. al.: Genomic screening
partial trismus, and mild generalized skeletal muscle atrophy. All for fucosidosis in English Springer Spaniels. Am J Vet Res. 1999
dogs exhibited moderate dyserythropoietic anemia, polymyopathy Jun;60(6):726-9.
with megaesophagus, and varying degrees of cardiomegaly.36 9. Smith MO, Wenger DA, Hill SL, et. al.: Fucosidosis in a family of
American-bred English Springer Spaniels. J Am Vet Med Assoc. 1996 Dec
Suspected Mitochondrial Myopathy: A three-year-old, male 15;209(12):2088-90.
English Springer Spaniel presented with a three-month history of 10. Alroy J, Orgad U, DeGasperi R, et. al.: Canine GM1-gangliosidosis. A
weakness, incoordination and marked muscle atrophy. Electromyo- clinical, morphologic, histochemical, and biochemical comparison of two
graphy, nerve-conduction velocity, and muscule biopsy studies were different models. Am J Pathol. 1992 Mar;140(3):675-89.
consistent with a mitochondrial myopathy.37 11. Bamberger M, Houpt KA: Signalment factors, comorbidity, and trends in
behavior diagnoses in dogs: 1,644 cases (1991-2001). J Am Vet Med Assoc.
2006 Nov 15;229(10):1591-601.
Genetic Tests 12. Bjerkas E, Ekesten B, Farstad W: Pectinate ligament dysplasia and
Tests of Genotype: Direct test for Phosphofructokinase (PFK) narrowing of the iridocorneal angle associated with glaucoma in the
deficiency is available from HealthGene, Optigen, PennGen, VetGen, English Springer Spaniel. Vet Ophthalmol. 2002 Mar;5(1):49-54.
and the Animal Health Trust. 13. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
Direct test for PRA risk factor is available from the University of hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
Missouri and the Animal Health Trust. 14. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
197
15. Gelatt KN, MacKay EO: Secondary glaucomas in the dog in North
America. Vet Ophthalmol. 2004 Jul-Aug;7(4):245-59.
16. Kuhl KA, Shofer FS, Goldschmidt MH: Comparative histopathology of
pemphigus foliaceus and superficial folliculitis in the dog. Vet Pathol. 1994
Jan;31(1):19-27.
17. Patterson EE, Armstrong PJ, O’Brien DP, et. al.: Clinical description and
mode of inheritance of idiopathic epilepsy in English springer spaniels. J
Am Vet Med Assoc. 2005 Jan 1;226(1):54-8.
18. Dorn CR: Canine breed-specific risks of frequently diagnosed
diseases at veterinary teaching hospitals. Monograph. AKC Canine Health
Foundation. 2000.
19. Scott DW, Miller WH: Primary seborrhoea in English springer spaniels:
a retrospective study of 14 cases. J Small Anim Pract. 1996 Apr;37(4):173-8.
20. Hawkins EC, Basseches J, Berry CR, et. al.: Demographic, clinical, and
radiographic features of bronchiectasis in dogs: 316 cases (1988-2000). J
Am Vet Med Assoc. 2003 Dec 1;223(11):1628-35.
21. Mason KV, Halliwell RE, McDougal BJ: Characterization of lichenoid-
psoriasiform dermatosis of springer spaniels. J Am Vet Med Assoc. 1986 Oct
15;189(8):897-901.
22. Rivera P, Melin M, Biagi T, et. al.: Mammary tumor development
in dogs is associated with BRCA1 and BRCA2. Cancer Res. 2009 Nov
15;69(22):8770-4.
23. Hernblad Tevell E, Bergvall K, & Egenvall A: Sebaceous adenitis in
Swedish dogs, a retrospective study of 104 cases. Acta Vet Scand. 2008 May
25;50:11.
24. Macklin, A: Immune-Mediated Hemolytic Anemia: Pathophysiology &
Diagnosis. Proceedings, 2009 Western Veterinary Conference. 2009.
25. McAlees TJ: Immune-mediated haemolytic anaemia in 110 dogs in
Victoria, Australia. Aust Vet J. 2010 Jan;88(1-2):25-8.
26. Watson PJ, Scase TJ, Roulois AJA, et. al.: Prevalence and Breed
Distribution of Hepatic Lesions at Post Mortem in a First Opinion Dog
Population and Their Association with Pancreatic Disease. Proceedings,
2009 British Small Animal Veterinary Congress. 2009.
27. Bexfield NH, Scase TJ, Warman SM, et. al.: Chronic Hepatitis in the
English Springer Spaniel. Proceedings, 17th ECVIM-CA Congress. 2007.
28. Fonfara S, Loureiro JF, Swift S, et. al.: English springer spaniels with
significant bradyarrhythmias--presentation, troponin I and follow-up after
pacemaker implantation. J Small Anim Pract. 2010 Mar;51(3):155-61.
29. Johnson MS, Martin MW: Successful medical treatment of 15 dogs with
pyothorax. J Small Anim Pract. 2007 Jan;48(1):12-6.
30. Oda K, Lambert EH, Lennon VA, et. al.: Congenital canine myasthenia
gravis: I. Deficient junctional acetylcholine receptors. Muscle Nerve. 1984
Nov-Dec;7(9):705-16.
31. Inuzuka T, Duncan ID, Quarles RH: Myelin proteins in the CNS of
‘shaking pups’. Brain Res. 1986 Jun;392(1-2):43-50.
32. Griffiths IR, Duncan ID, McCulloch M, et. al.: Shaking pups: a disorder
of central myelination in the Spaniel dog. Part 1. Clinical, genetic and
light-microscopical observations. J Neurol Sci. 1981 Jun;50(3):423-33.
33. Maddux JM, Edwards DF, Barnhill MA, et. al.: Neutrophil function in
dogs with congenital ciliary dyskinesia. Vet Pathol. 1991 Sep;28(5):347-53.
34. Edwards DF, Kennedy JR, Patton CS, et. al.: Familial immotile-cilia
syndrome in English springer spaniel dogs. Am J Med Genet. 1989
Jul;33(3):290-8.
35. The Genetic Connection: A Guide to Health Problems in Purebred Dogs.
L Ackerman. p. 212, AAHA Press, 1999.
36. Holland CT, Canfield PJ, Watson AD, et. al.: Dyserythropoiesis,
polymyopathy, and cardiac disease in three related English springer
spaniels. J Vet Intern Med. 1991 May-Jun;5(3):151-9.
37. Tauro A, Talbot CE, Pratt JN, et. al.: Suspected mitochondrial myopathy
in a springer spaniel. Vet Rec. 2008 Sep 27;163(13):396-7.
38. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p 93-98.
198
English Toy Spaniel
but are not faulted. They have a lively gait that is straight with a
good length of stride.
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: King Charles Spaniel, Toy Spaniel, Prince
Charles, Blenheim.
• Registries: AKC, CKC, UKC, NKC (National Kennel Club)
• AKC rank (year 2008): 125 (235 dogs registered)
• Internet resources: English Toy Spaniel Club of America:
www.englishtoyspanielclubofamerica.org
King Charles Spaniel Club (UK):
www.king-charles-spaniel-club.co.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
200
Entlebucher
Mountain Dog
ground to withers. Tail is natural bob or cropped, with the tail set
in continuation of the gently sloping croup. Shoulders are laid
back. Upper arm length equal or slightly shorter than shoulder
blade. Angle of shoulder blade forming a right angle. Stilfe is well
angulated. Legs are short, sturdy, straight and parallel. Paws point
straight forward, slightly rounded and well-arched. The gait is
ground covering, free, and fluid with good reach and strong drive
from rear. As the speed of the gait increases, legs converge – the
rear more pronounced.
Genetic Tests
Tests of Genotype: Direct test for prcd-PRA is available from
Optigen.
Miscellaneous
• Breed name synonyms: Entlebucher Sennenhund, Entlebucher
Cattle Dog, Entelbuch Mountain Dog, Shepherd Dog from
Entlebuch, Dog of the Alpine Herdsman, Entles
• Registries: AKC, UKC, CKC, FCI, KCGB (Kennel Club of Great
Britain), NKC (National Kennel Club)
• AKC rank (none): AKC recognized in January, 2011. Entire stud
book entered.
202
Field Spaniel
muscular with a slight arch. The topline is level. The thorax is deep,
the rib cage stays deep caudally and ribs are well sprung. There
is little abdominal tuck up, and the low set tail is usually docked.
Limbs are straight boned, feet are webbed, large, and round with
thick pads. No dewclaws. These dogs are smooth moving with a
long low gait and high head carriage.
Genetic Tests
Tests of Genotype: Direct test for black liver colors, and black or
brown nose are available from HealthGene and VetGen.
Miscellaneous
• Breed name synonyms: none
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 140 (117 dogs registered)
• Internet resources: Field Spaniel Society of America:
http://fieldspaniels.org/
Field Spaniel Society (UK): www.fieldspanielsociety.co.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Field Spaniel Society of America: 2002-2003 Field Spaniel Health Survey.
2003.
3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
6. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
204
Finnish Spitz
and triangular, with a sharp point. Dark-rimmed eyes are almond
in shape, slanted and moderately wide set; darker colored eyes
preferred. There is a pronounced stop, the skull is broad and fairly
flat, and the narrow muzzle tapers. The nose and lips are black and
lips are tight. The topline is level, and the neck is muscular, not
throaty. The thorax is deep with well-sprung ribs, and the abdomen
only slightly tucked up. The tail is moderately high set, reaching the
tarsus in length, and curls over the topline to rest along the thigh,
with a well-developed plume. The limbs are straight boned with
moderate muscling and bone, the feet are round, compact, and toes
well arched. The dewclaws may be removed in front and in North
The Breed History America, are removed in back also.
This is the National Dog of Finland. Several thousand years ago in
Central Russia, Spitz-type progenitor dogs such as the Russian Laika
likely served as the primary gene pool. Due to outcrossing, by the
Recognized Behavior Issues and Traits
Reported breed characteristics include: Excellent with children, loyal,
year 1880 The Finnish Spitz dogs were nearly extinct. The final breed
friendly, courageous, lively with an independent streak, even strong
standard was drawn up in 1897 (final American standard, 1976).
willed. The Finnish Spitz likes cold environments. A well-developed
The first specimens arrived in England in 1927, and were exported
tendency to bark exists due to their history as barking hunting dogs.
to the USA in 1959. AKC accepted the Finnish Spitz for registry in
This type of dog makes a good watchdog. Good with children and
the late 1980s.
other pets, though inter-male dog aggression can be exhibited. High
intelligence is characteristic; Finnish Spitz dogs are easily bored,
Breeding for Function and thus obedience training requires patience. Grooming needs are
Originally, the breed was a treeing dog (wild turkey, squirrels and moderate, except during the heavy shedding season, and they have
martins), though now especially in North America he is primarily moderate to high exercise needs.
a companion dog. In Finland, barking contests are held; this breed
possesses other types of vocalizations as well.
Normal Physiologic Variations
Pointing with his head, and tracking using sight, sound, and scent None reported
are breed characteristics. In Finland, any champion must prove
himself in the field as well as the show ring. King barkers are those Drug Sensitivities
dogs that have a distinctive yodel that is judged to be optimal for None reported
hunting performance.
Inherited Diseases
Physical Characteristics Hip Dysplasia: Polygenically inherited trait causing degenerative
Height at Withers: female 15.5-18” (39.5-45.5 cm), male 17.5-20” joint disease and hip arthritis. OFA reports 6.1% affected.1
(44.5-51 cm)
Patella Luxation: Polygenically inherited laxity of patellar ligaments,
Weight: 31-35 lb (14-16 kg) causing luxation, lameness, and later degenerative joint disease.
Treat surgically if causing clinical signs. OFA reports 2.9% affected.1
Coat: The double coat is dense, outer coat is short (1-2” or 2.5-5
cm) and stands off; it is a very harsh and straight outer coat. The Elbow Dysplasia: Polygenically inherited trait causing elbow
undercoat is lighter in color than the outer coat. Coat color is a arthritis. Too few Finnish Spitz have been screened by OFA to
red-gold color with a spectrum of a dark, light or in-between shade; determine an accurate frequency.1
coat and ruff is less well developed in the female. Only a few white
markings are allowed; tips of toes and chest marks are allowed.
Puppies are allowed to have more than what meets the breed
Disease Predispositions
Hypothyroidism: Inherited autoimmune thyroiditis. Too few Finnish
standard in dark hairs but they generally fade as the dog matures. Spitz have been tested for thyroid autoantibodies at Michigan State
University to determine an accurate breed frequency. (Ave. for all
Longevity: 12-15 years
breeds is 7.5%).2,3
Points of Conformation: A classic foxy “spitz” type is required,
Cataracts: Anterior and capsular punctate cataracts predominate
with the classic pointed muzzle, erect ears and alert expression.
in the breed. Identified in 4.35% of Finnish Spitz CERF examined by
This dog is also characterized by a square conformation, high
veterinary ophthalmologists between 2000-2005. CERF does not
head carriage and quick gait. The small ears are alertly pricked
recommend breeding any Finnish Spitz with a cataract.4
205
Diabetes Mellitus: Sugar diabetes. Caused by a lack of insulin 3. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
production by the pancreas. Control by insulin injections, diet, and Population and Animal Health, Michigan State University. April, 2007.
glucose monitoring. Dorn reports an 8.07x odds ratio in Finnish 4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Spitz versus other breeds. Unknown mode of inheritance.5,6 College of Veterinary Ophthalmologists. ACVO, 2007.
5. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
Idiopathic Epilepsy (Inherited Seizures): Focal and generalized veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
seizures occur in the breed. Control with anticonvulsant medication.
6. Marmor M, Willeberg P, Glickman LT, et. al.: Epizootiologic patterns of
Dorn reports a 7.08x odds ratio in Finnish Spitz versus other breeds. diabetes mellitus in dogs. Am J Vet Res 1982: 43:465-70.
Quantitative EEG analysis can be a useful diagnostic tool in this 7. Jeserevics J, Viitmaa R, Cizinauskas S, et. al.: Electroencepha-
breed. Unknown mode of inheritance.5,7 lography findings in healthy and Finnish Spitz dogs with epilepsy:
visual and background quantitative analysis. J Vet Intern Med. 2007
Immune-Mediated Hemolytic Anemia: Auto-immune disorder Nov-Dec;21(6):1299-306.
where the body produces antibodies against its own red blood cells. 8. Miller SA, Hohenhaus AE, Hale AS: Case-control study of blood type,
Treated with immunosuppressive drugs. There is generally a female breed, sex, and bacteremia in dogs with immune-mediated hemolytic
preponderance with this disorder. One study found a significantly anemia. J Am Vet Med Assoc. 2004 Jan 15;224(2):232-5.
higher risk in Finnish Spitz versus other breeds. Unknown mode of 9. Rosychuk RAW: Canine Alopecias: What’s New? Proceedings, 2008
inheritance.8 Western Veterinary Conference. 2008.
10. Breton K: Death & Derm: Deadly Dermatologic Diseases. Proceedings,
Alopecia-X (black skin disease, BSD, coat funk): Progressive, 2004 ACVIM Forum. 2004.
symmetrical, non-pruritic, truncal hair loss usually beginning in 11. Kuhl KA, Shofer FS, Goldschmidt MH: Comparative histopathology of
early adulthood. ACTH, LDDS, and thyroid panel results are normal. pemphigus foliaceus and superficial folliculitis in the dog. Vet Pathol. 1994
Jan;31(1):19-27.
Oral trilostane reverses the condition in some cases. The disorder
12. Vianna ML, Tobias KM: Atresia ani in the dog: a retrospective study. J
appears to be familial.9 Am Anim Hosp Assoc. 2005 Sep-Oct;41(5):317-22.
13. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Pemphigus Foliaceous: Immune mediated skin disease Ackerman. p. 217. AAHA Press, 1999.
characterized by crusty eruptions and pustules on the nasal plane, 14. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
around the eyes and on the footpad. Mean age of onset is 4 years. Book House, NY 2006. p. 558-562.
Diagnosis by biopsy. The Finnish Spitz has a breed predisposition.
Unknown mode of inheritance.10,11
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: Finsk Spets, Suomenpystykorva, Finky,
Finkie, Finnish Barking Birddog (historical).
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club).
• AKC rank (year 2008): 153 (47 dogs registered)
• Internet resources: Finnish Spitz Club of America:
www.finnishspitzclub.org
The Finnish Spitz Club (Finland): www.spj.fi
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
206
Flat-Coated Retriever
bend to the tail is present, but not curled. Limbs are straight boned,
moderate in length and front dewclaws may be removed (rear
dewclaws are absent), feet are oval to round and toes well arched
with thick pads.
Coat: The thick to slightly wavy flat glossy double coat has well Elbow Dysplasia: Polygenically inherited trait causing elbow
developed feathering. Solid black or liver are accepted colors. Hairs arthritis. OFA reports 0.8% affected.1
are fine and the undercoat is dense.
Genetic Tests
Tests of Genotype: Direct tests for black, liver and yellow coat
colors and black and brown nose are available from HeathGene and
VetGen.
208
French Bulldog
Recognized Behavior Issues and Traits
Reported breed traits include: Intelligent, affectionate, alert, playful,
love human companionship, low barking tendency, low shedding
tendency, and low grooming needs. Good for city or country.
Considered a good dog for seniors. Needs daily hygiene of facial
wrinkles to prevent dermatitis. Tend to snore.
Points of Conformation: They possess a compact square Hemophilia B (Factor IX Deficiency): X-linked recessive
conformation with heavy bone and muscling. The broad-based coagulation disorder causing severe bleeding in this breed. In one
fine-leathered erect “bat” ears of the French Bulldog distinguish family, concurrent Hemophilia A was identified.4
it from the English Bulldog (the latter having rose ears). Another
distinguishing feature is the shape of the skull. In the French Bulldog Disease Predispositions
it is flat between the ears but domed over the eyes, producing Hemivertebra and Butterfly Vertebra: Misshapen or malformed
a strong-browed appearance. The head is large and square. The vertebra. May cause scoliosis, pain, or spinal cord compression if
muzzle is short, broad and blocky, and the stop is well defined such severe. In the majority of affected French Bulldogs, the thoracic
that between the eyes there is a distinct groove. Wrinkles are set on vertebrae are involved. Reported at a frequency of 35.1% in the
a very short nose. The nose is black except in lighter colored dogs. FBDCA Health Survey. Unknown mode of inheritance.5
The moderately deep-set dark eyes are set well apart and low in the
skull forward facing, are round and moderate in size and don’t show Brachycephalic Complex: The brachycephalic complex includes
the nictitans. The lower jaw is prognathic with very prominent black stenotic nares, elongated soft palate, everted laryngeal
flews. The neck is short, thick and arched, and covered with very saccules, laryngeal collapse, and occasionally hypoplastic
loose skin. The short back is arched (roach). The abdomen is tucked trachea. Can also cause bronchial collapse. Can cause difficulty
up and the thorax is deep and broad (barrel-shaped). The tail may be breathing, and collapse if severe, or stressed. The FBDCA Health
screwed or straight, is low set, short and tapers to a fine tip. Limbs Survey reports the following frequencies: stenotic nares (21.6%0,
are ideally straight boned, feet are compact, and toes well knuckled elongated soft palate (15.8%), and hypoplastic trachea (4.36%).5,6,7
up. The nails are stubby. Forelimbs are set wide apart. The gait is
somewhat rolling due to the broad thorax.
209
Allergic Dermatitis (Atopy): Inhalant or food allergy. Presents with therapy. Unknown mode of inheritance.12,13,14
pruritis and pyotraumatic dermatitis (hot spots). French Bulldogs
show an increased prevalence versus other breeds for both inhalant Pulmonic Stenosis (PS): Congenital cardiac disorder of restricted
and food allergy. Reported at a frequency of 28.0% in the FBDCA pulmonic outflow. Echocardiogram findings of restriction of right
Health Survey, with food allergy reported at 14.2%.5,8 ventricular outflow tract, pulmonic valve and/or main pulmonary
artery on transthoracic imaging from the right parasternal and
Distichiasis: Abnormally placed eyelashes that irritate the left cranial parasternal short-axis views. Reported at an increased
cornea and conjunctiva. Can cause secondary corneal ulceration. frequency in the breed.15
Identified in 6.96% of French Bulldogs CERF examined by veterinary
ophthalmologists between 2000-2005.3 Hiatal Hernia: French Bulldogs have a predisposition to
paraesophageal hiatal hernia.16,17
Intervertebral Disc Disease (IVDD): Acute spinal cord disease due
to prolapsed disk material. Clinical signs include back pain, scuffing Necrotizing Meningoencephalitis: A non-suppurative acute to
of paws, spinal ataxia, limb weakness, and paralysis. Reported at a chronic necrotizing meningoencephalitis is identified in French
frequency of 5.5% in the FBDCA Health Survey.5 Bulldogs, similar to that seen in the Pug, Maltese and Yorkshire
Terrier breeds. Affected dogs present with seizures, ataxia, blindness
Persistent Pupillary Membranes: Strands of fetal remnant and mentation changes from 1 to 10 years of age.18,19
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
The later three forms can impair vision, and dogs affected with Anasarca, Cleft Palate/Lip, Deafness, Fold Dermatitis, Spina
these forms should not be bred. Identified in 4.50% of French Bifida, and von Willebrand’s Disease are reported.20
Bulldogs CERF examined by veterinary ophthalmologists between
2000-2005.3 Isolated Case Studies
Ventricular Septal Defect (VSD): Case report of a 4-month-old
Cryptorchidism (Retained Testicles): Can be unilateral or bilateral. male French Bulldog with a left heart base grade 3/6 systolic
Reported at a frequency of 4.2% in the FBDCA Health Survey.5 murmur, and a right heart base grade 4/6 systolic murmur. Doppler
ultrasonography and cardiac catheterization revealed a supracristal
Demodicosis: Generalized demodicosis has an underlying
ventricular septal defect (VSD) with accompanying aortic
immunodeficiency in its pathogenesis. Reported at a frequency of
regurgitation.21
4.1% in the FBDCA Health Survey.5
Muscular Dystrophy: An 8 month old male French Bull dog was
Degenerative Myelopathy (DM): Affected dogs show an insidious
diagnosed with dystrophin deficient muscular dystrophy. Clinical
onset of upper motor neuron (UMN) paraparesis at an average age of
signs included; apathy, muscle weakness, dysphagia, regurgitation
11.4 years. The disease eventually progresses to severe tetraparesis.
and dyspnea.22
Affected dogs have normal results on myelography, MRI, and CSF
analysis. Necropsy confirms the condition. Unknown mode of Fibrinoid Leukodystrophy: A 1 and 1/2 year old French bulldog
inheritance. A direct genetic test for an autosomal recessive DM exhibited megaesophagus, general emaciation and weakness,
susceptibility gene is available. All affected dogs are homozygous and died due to aspiration pneumonia. Histopathology revealed
for the gene, however, only a small percentage of homozygous dogs discolored foci in the white matter of the cerebellum and brain
develop DM. The susceptibility allele occurs at a frequency of 23% stem, with Rothenthal fibers and hypertrophic astrocytes in the
in the breed. Clinical DM is reported at a frequency of 2.3% in the perivascular, subependymal and subpial area.23
FBDCA Health Survey.5,9
Oligodendroglioma: A 5-year-old, male French bulldog presented
Retinal Dysplasia: Retinal folds, geographic, and generalized retinal with bradycardia, dyspnea, and decerebrate rigidity was necropsied.
dysplasia with detachment are recognized in the breed. Can cause Macroscopic findings were restricted to a brain mass consisting of
retinal detachment and blindness. Reported in 2.05% of French diffuse proliferated neoplastic oligodendroglial cells characterized
Bulldogs CERF examined by veterinary ophthalmologists between by small, round, and hyperchromatic nuclei with clear cytoplasm
2000-2005.3 and the cells aggressively invaded into the adjacent parenchyma.
The mass was diagnosed as oligodendroglioma.24
Entropion: Rolling in of the eyelids, which can predispose to corneal
irritation and ulceration. Reported in 1.36% of French Bulldogs CERF XX Sex Reversal: A 3-month-old outwardly female French Bulldog
examined by veterinary ophthalmologists between 2000-2005.3 presented with an enlarged clitoris with an os clitoris, and inguinal
hernias containing testicles. A diagnosis of SRY-negative XX sex
Hypothyroidism: Inherited autoimmune thyroiditis. 1.1% positive
reversal was made based on the gonadal histology and cytogenetic
for thyroid autoantibodies based on testing at Michigan State
analysis.25
University. (Ave. for all breeds is 7.5%).10,11
Histiocytic Ulcerative Colitis: Several case studies are published. Genetic Tests
Affected dogs present with chronic large bowel diarrhea, Tests of Genotype: Direct test for juvenile cataract is available
tenesmus and hematochezia. Colonic biopsies are characterized by from the Animal Health Trust and VetGen.
infiltrations of PAS positive histiocytes in the lamina propria. There
may only be minimal improvement with nutritional and medical Direct test for the DM susceptability gene is available from OFA.
210
Direct tests for fawn, brindle(black) and liver coat colors, and black 18. Timmann D, Konar M, Howard J, et. al.: Necrotising encephalitis in a
or brown nose are available from HealthGene. French bulldog. J Small Anim Pract. 2007 Jun;48(6):339-42.
19. Spitzbarth I, Schenk HC, Tipold A, et. al.: Immunohistochemical
Tests of Phenotype: CHIC Certification: Required testing includes Characterization of Inflammatory and Glial Responses in a Case of
hip radiographs, CERF eye examination (recommended annually) Necrotizing Leucoencephalitis in a French Bulldog. J Comp Pathol. 2010
and patella evaluation. Recommended tests include thyroid profile Feb-Apr;142(2-3):235-41.
20. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
including autoantibodies, and congenital cardiac disease evaluation.
Ackerman. p. 207. AAHA Press, 1999.
(See CHIC website; www.caninehealthinfo.org).
21. Shimizu M, Tanaka R, Hirao H, et. al.: Percutaneous transcatheter coil
embolization of a ventricular septal defect in a dog. J Am Vet Med Assoc.
Recommend elbow radiographs.
2005 Jan 1;226(1):69-72, 52-3.
22. Gama Filho HAN, Oliveira CM, Dias CTS, et. al.: Muscular Dystrophy
Miscellaneous in a French Bulldog: First Case Report. Proceedings, 2009 WSAVA World
• Breed Name Synonyms: Frenchie, Boule Dogue Français Congress. 2009
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 23. Ito T, Uchida K, Nakamura M, et. al.: Fibrinoid Leukodystrophy
ANKC (Australian National Kennel Club), NKC (National Kennel Club) (Alexander’s Disease-Like Disorder) in a Young Adult French Bulldog. J Vet
Med Sci. 2010 Oct;72(10):1387-90.
• AKC rank (year 2008): 26 (6,963 dogs registered)
24. Park CH: Oligodendroglioma in a French bulldog. J Vet Sci. 2003
• Internet resources: French Bulldog Club of America:
Aug;4(2):195-7.
www.frenchbulldogclub.org 25. Campos M, Moreno-Manzano V, García-Roselló M, et. al.: SRY-Negative
French Bulldog Club of England: XX Sex Reversal in a French Bulldog. Reprod Domest Anim. 2011
www.frenchbulldogclubofengland.org.uk Feb;46(1):185-8.
French Bulldog Fanciers of Canada: 26. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
www.frenchbulldogfanciers.com Book House, NY 2006. p. 563-566.
References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
4. Slappendel RJ: Hemophilia A and hemophilia B in a family of French
bulldogs. Tijdschr Diergeneeskd. 1975 Oct 15;100(20):1075-88.
5. French Bull Dog Club of America: 2009 FBDCA Health Survey. 2009.
6. Monnet M: Brachycephalic Airway Syndrome. Proceedings, 2004 World
Small Animal Veterinary Association Congress. 2004.
7. De Lorenzi D, Bertoncello D, & Drigo M: Bronchial abnormalities found in
a consecutive series of 40 brachycephalic dogs. J Am Vet Med Assoc. 2009
Oct 1;235(7):835-40
8. Tarpataki N, Pápa K, Reiczigel J, et. al.: Prevalence and features of canine
atopic dermatitis in Hungary. Acta Vet Hung. 2006 Sep;54(3):353-66.
9. Coates JR, Zeng R, Awano T, et. al.: An SOD1 Mutation Associated with
Degenerative Myelopathy Occurs in Many Dog Breeds. Proceedings 2009
ACVIM Forum. 2009.
10. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
11. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum
thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc. 2002 Feb 15;220(4):466-71.
12. Tanaka H, Nakayama M, Takase K, et. al.: Histiocytic ulcerative colitis in a
French bulldog. J Vet Med Sci. 2003 Mar;65(3):431-3.
13. Van der Gaag I, Van Toorenburg JV, Voorhout G, et. al.: Histiocytic
ulcerative colitis in a French Bulldog. J Small Anim Pract. 1978
May;19(5):283-90.
14. Hall EJ: Breed-Specific Intestinal Disease. Proceedings, 2004 World
Small Animal Veterinary Association Congress. 2004.
15. Toschi Corneliani R, Locatelli C, Domenech O, et. al.: Retrospective Study
of Pulmonic Stenosis in 259 Dogs. Proceedings, 18th ECVIM-CA Congress.
2008.
16. Washabau RJ: Diagnosis and Management of Swallowing Disorders.
Proceedings, 2009 WSAVA World Congress. 2009.
17. Teunissen GH, Happe RP, Van Toorenburg J, et. al.: Esophageal hiatal
hernia. Case report of a dog and a cheetah. Tijdschr Diergeneeskd. 1978 Jul
15;103(14):742-9.
211
German Pinscher
dewclaws may be removed, round feet are small, well knuckled up
with dark nails and pads. The gait is fluid with good reach, and no
rolling.
Genetic Tests
Tests of Genotype: Direct test for von Willebrand’s Disease (vWD)
is available from VetGen.
Miscellaneous
• Breed name synonyms: Standard Pinscher, Historical SYN:
Smooth Haired Pinscher.
• Registries: AKC, CKC, FCI, KCGB (Kennel Club of Great Britain),
213
German Shepherd Dog
in size and length; not throaty. The thorax is deep and ribs well
sprung, and ribs stay deep far back in the rib cage, resulting in a
short loin. The topline is level, but slowly descending, with withers
higher than the rear, and the abdomen is moderately tucked up.
The tail extends to the tarsus, is low set, and gently curved. The
limbs are straight boned, the long bones oval in cross-section. All
dewclaws may be removed, but normally are left on in front and
removed behind. Feet are compact, toes moderately arched, pads
thick, and nails are tough and dark.
Patella Luxation: Polygenically inherited trait causing stifle Hypothyroidism: Inherited autoimmune thyroiditis. Reported at a
instability and arthritis. OFA reports 0.8% affected.3 frequency of 5.5% in the AGSDCF 2004 Health Survey. 6.4% positive
for thyroid autoantibodies based on testing at Michigan State
Hereditary Multifocal Renal Cystadenocarcinoma and Nodular University. (Ave. for all breeds is 7.5%).5,26,27
Dermatofibrosis: Rare, autosomal recessive kidney cancer
characterized by bilateral, multifocal tumors in the kidneys, uterine Panosteitis: Self-limiting disorder of intermittent lameness
leiomyomas and nodules in the skin consisting of dense collagen involving the diaphyseal and metaphyseal areas of the tubular long
fibers. Mean age of onset is 6.4 years, and mean age of death is 9.3 bones in young dogs prior to skeletal maturation. Reported 3.3x
years. A mutation has been identified in Norwegian and US families odds ratio versus other breeds. Reported at a frequency of 10.1% in
of German Shepherd dogs. A genetic test is available.13,14 the AGSDCF 2004 Health Survey.4,5
Hemophilia A: Rare, x-linked recessive bleeding disorder. Males Gastric Dilatation-Volvulus (Bloat, GDV)/Intestinal Volvulus/
are primarily affected. Affected dogs can show bleeding from Splenic Torsion: German Shepherds are at increased risk for
the mouth, subcutaneous and intramuscular haematomas and life-threatening twisting of the stomach, intestines, or spleen
lameness due to joint hematomas.15,16 within the abdomen. Requires immediate veterinary attention.
Gastic or intestinal volvulus was the cause of death of 15% of
von Willebrand’s disease (vWD): Rare, autosomal recessive mild German Shepherds in one teaching hospital study. GDV is reported
bleeding disorder documented in some German Shepherd families at a frequency of 8.5% in the AGSDCF 2004 Health Survey.5,28,29,30,31
in South Africa. No test for carriers is available.17
Stifle Osteochondritis Dessicans (OCD): Polygenically inherited
Hyperuricosuria (HUU)/Urate Bladder Stones: An autosomal cartilage defect. Causes stifle joint pain and lameness in young
recessive mutation in the SLC2A9 gene causes urate urolithiasis and growing dogs. Mild cases can resolve with rest, while more severe
can predispose male dogs to urinary obstruction. Estimated at a cases require surgery. Reported 17.5x odds ratio versus other breeds.4
carrier frequency of 2.60% in the breed. A genetic test is available.11
Perianal Fistula/Furunculosis: Inflammatory disorder creating
Mucopolysaccharidosis (MPSVII): Rare, autosomal recessive perianal ulceration and fistulas. Treat with anti-inflammatory
lysosomal storage disorder presenting with progressive juvenile medications and tacrolimus. Dorn reports a 14.31x odds ratio
inability to ambulate, skeletal deformities, corneal cloudiness, versus other breeds. Reported at a frequency of 5.3% with a male
cytoplasmic granules in the neutrophils and lymphocytes of blood preponderance in the AGSDCF 2004 Health Survey. Presence of a
and CSF and urinary glycosaminoglycans. A genetic test is available.18 specific allele in the major histocompatability complex produces an
odds ratio of 3.7x versus German Shepherds without the allele, and
Pituitary Dwarfism: Rare, autosomal recessive disorder of pituitary dogs homozygous for this allele have an earlier onset. A test for the
disfunction. Affected dogs present with growth retardation and susceptibility gene is available.5,6,32,33
stagnant development of the hair coat. The disorder is due to
a combined deficiency of GH, TSH, and prolactin together with Degenerative Myelopathy (DM): Affected dogs show an insidious
impaired release of gonadotropins. ACTH secretion is preserved. onset of upper motor neuron (UMN) paraparesis at an average
The combined pituitary hormone deficiency is associated with cyst age of 11.4 years. The disease eventually progresses to severe
formation and pituitary hypoplasia.19,20,21 tetraparesis. Affected dogs have normal results on myelography,
MRI, and CSF analysis. Necropsy confirms the condition. Unknown
Platelet Procoagulant Deficiency: Rare autosomal recessive mode of inheritance. A direct genetic test for an autosomal
bleeding disorder of platelet function that diminishes fibrin recessive DM susceptibility gene (SOD1 mutation) is available. OFA
clot formation. Affected dogs have increased residual serum reports 21% test homozygous, and 30% test heterozygous for the
prothrombin assays. The defective gene is linked to canine susceptibility gene. All affected dogs are homozygous for the gene,
chromosome 27.22 however, only a small percentage of homozygous dogs develop DM.
Some studies suggest an immune or inflammatory pathogenesis for
Disease Predispositions DM in German Shepherds. Reported at a frequency of 9.2% in the
Behavioral Abnormalities: German Shepherd dogs are AGSDCF 2004 Health Survey.3,5,34,35
overrepresented for aggression behavioral diagnoses in a veterinary
school behavior service population. These include interdog Corneal Dystrophy: Inherited disorder causing epithelial/stromal
aggression and aggression toward humans. The AGSDCF 2004 white to grey oval or ring shaped opacities in the corneas. Reported
215
in 4.88% of German Shepherd dogs CERF-examined by veterinary or entrapment of cauda equina nerve roots. Survey radiographs are
ophthalmologists between 2000-2005.36 not predictive for the development of DLS. Lumbosacral transitional
vertebra can predispose to DLS, and cause an earlier onset.
Hypertrophic Osteodystrophy (HOD): Immune-mediated disorder Treatment is by dorsal decompressive laminectomy.43,44,45,46,47,48
causing fever, and painful, swollen joints and bones in young dogs.
Occurs mostly within 3-14 days post-vaccination. Age of onset is Immune dysfunction/IgA deficiency: Several disorders seen in
8-16 weeks. Reported 9.6x odds ratio versus other breeds. Unknown the German Shepherd dog appear to be related to a deficiency
mode of inheritance.4 of IgA function. These include inflammatory bowel disease,
mucocutaneous pyoderma, systemic aspergillosis, and
Hemangiosarcoma: Malignant neoplasm most often presenting in leishmaniosis. See under specific disease headings.
the spleen, heart, or bone marrow. Splenic hemangiosarcoma most
often presents due to an acute bleed. Usually metastatic by the time Inflammatory Bowel Disease (IBD): German Shepherds are
of diagnosis. German Shepherds have a 4.7x odds ratio versus other overrepresented for cases of inflammatory bowel disease and
breeds.28,37 antibiotic responsive diarrhea. It is thought that an immune
dysfunction can be the cause, and some researchers propose
Cranial Cruciate Ligament (ACL) Rupture: Traumatic tearing of the an intestinal IgA abnormality. Chronic diarrhea is reported at a
ACL in the stifle, causing lameness and secondary arthritis. Treat with frequency of 4.2%, and IBD 3.7% in the AGSDCF 2004 Health
surgery. Affected German Shepherd dogs have a significantly greater Survey.5,49,50
tibial plateau angle (TPA) versus other breeds. TPA measurements
may be helpful to screen prospective breeding dogs.38,39 Aortic Stenosis (Subaortic Stenosis, SAS): Affected dogs present
with a left heart base murmur, aortic velocities greater than 1.5
Congential or Juvenile Cataract: German Shepherd dogs can m/second on Doppler echocardiography, aortic regurgitation, and
develop bilateral posterior cortical cataracts at 8-12 weeks of age mitral regurgitation. Can cause exercise intolerance, syncope,
that progress to involve the Y-sutures and nucleus. These juvenile and progress to heart failure. German Shepherds are reported at
cataracts are thought to be recessively inherited. A rare congenital an increased frequency versus other breeds. Unknown mode of
cataract has been observed in German Shepherd dogs and is inheritance–considered polygenic.51
thought to be dominantly inherited. Reported at a frequency of
3.4% in the AGSDCF 2004 Health Survey. Cataracts are reported Ventricular Arrhythmia/Sudden Cardiac Death: An inherited
in 4.97% of German Shepherd dogs CERF-examined by veterinary arrhythmia in young German Shepherd dogs can cause sudden
ophthalmologists between 2000-2005. CERF does not recommend death, usually between 22-26 weeks of age due to ventricular
breeding any German Shepherd dog with a cataract.5,36,40,41 tachycardia (VT). Affected dogs often have no clinical signs prior
to a fatal arrhythmia. 24-hour Holter monitoring can identify
Chronic Superficial Keratitis (Pannus): Chronic corneal ventricular premature contractions (VPCs), VPC couplets, and VT. The
inflammatory process that can cause vision problems due to disorder may be related to abnormalities in calcium cycling between
corneal pigmentation. Treatment with topical ocular lubricants and cells. The mode of inheritance is undetermined.52,53,54,55
anti-inflammatory medication. German Shepherds are at increased
risk. Identified in 3.16% of German Shepherd dogs CERF-examined Perineal Hernia: German Shepherds are the most frequent breed
by veterinary ophthalmologists between 2000-2005. CERF does not diagnosed with perineal hernia. Treat with surgery.56
recommend breeding any German Shepherd dog with pannus.36,42
Epilepsy (Inherited Seizures): Inherited seizures can be generalized
Persistent Pupillary Membranes: Strands of fetal remnant or partial seizures. A male preponderance is reported in the breed.
connecting; iris to iris, cornea, lens, or involving sheets of tissue. Control with anticonvulsant medications. Undetermined mode of
The later three forms can impair vision, and dogs affected with inheritance.57
these forms should not be bred. Identified in 1.99% of German
Shepherd dogs CERF-examined by veterinary ophthalmologists Aquired Megaesophagus: German Shepherds are overrepresented
between 2000-2005.36 in diagnoses of acquired megaesophagus. Causes include peripheral
neuropathy, laryngeal paralysis, acquired myasthenia gravis,
Retinal Dysplasia: Retinal folds, geographic, and generalized retinal esophagitis, and gastric dilatation. Hypothyroidism is not associated
dysplasia with detachment are recognized in the breed. Can lead with megaesophagus. Clinical signs include regurgitation, excess
to blindness. Reported in 1.99% of German Shepherd dogs CERF salivation, and aspiration pneumonia.58
examined by veterinary ophthalmologists between 2000-2005.36
Myesthenia Gravis: An immune-mediated disorder of circulating
Degenerative Lumbosacral Stenosis (DLS)/Cauda Equina anti-acetylcholine receptor antibodies cause generalized appendicular
Syndrome: Lumbosacral spinal cord compression due to DLS muscle weakness with or without megaesophagus, or selective
occurs most frequently in German Shepherd dogs (25.6% of cases). esophageal, facial and pharyngeal muscular weakness. German
Clinical signs of lumbar pain, pelvic limb lameness, urinary and Shepherds are reported with a 4.8x odds ratio versus other breeds.59,60
fecal incontinence and self mutilation occur at an average age of
5.4 years. The disorder can present with IV disc degeneration, sacral Systemic Lupus Erythomatosis (SLE)/Discoid Lupus
osteochondrosis, vertebral end plate sclerosis, facet joint tropism, Erythematosus (DLE): German Shepherds are overrepresented
ventral sacral subluxation, ligamentum flavum hypertrophy, and/ for these immune-mediated diseases. SLE primarily affects
male German Shepherds at approximately 5 years of age with
216
polyarthritis, and renal and mucocutaneous disorders. In DLE cases, Nerve Hypoplasia, Osteochondrodysplasia, Pelger-Huet Anomaly,
German Shepherds comprised 44.4% of all cases in one study, Pemphigus Erythematosus, Peripheral Vestibular Disease,
and also tend to have more multifocal lesions. Treatment is with Sebaceous Adenitis, Tricuspid Valve Dysplasia, Uveodermato-
immune-modulating drugs.61,62 logical Syndrome, Vitiligo, and Wry Mouth are reported.76
Leishmaniosis/Visceral Leishmaniosis: German Shepherd dogs are Direct test for Mucopolysaccharidosis (MPSVII) is available from
overrepresented in cases of leishmaniosis. Affected dogs can present PennGen.
with peripheral lymphadenopathy, splenomegaly, and anemia.
Direct test for Renal Cystadenocarcinoma Nodular Dermatofibrosis
Susceptability may be due to an IgA abnormality.71,72,73
is available from VetGen.
Familial Cutaneous Vasculopathy: Affected young puppies present Direct test for HUU is available from the UC-Davis VGL and the
with pyrexia, footpad swelling and depigmentation, crusting and Animal Health Trust.
ulceration of ear tips and tail tips, and focal depigmentation of the
nasal planum. Biopsies show multifocal nodular dermatitis with Direct test for coat length is available from the Animal Health Trust,
neutrophils and mononuclear inflammatory cells surround foci of and VetGen.
dermal collagenolysis, and degenerative and inflammatory vessel
lesions. The disease is thought to be a immune mediated disease Direct test for bicolor, solid black and sable colors are available from
against abnormal collagen. Breeding studies suggest an autosomal HealthGene and VetGen.
recessive mode of inheritance.74
Direct test for MDR1 (ivermectin sensitivity) gene in white German
Dilated Cardiomyopathy (DCM): A UK study identified 4 German Shepherds is available from Washington State Univ. http://www.
Shepherd dogs under 8 years of age in heart failure due to dilated vetmed.wsu.edu/depts-VCPL/test.aspx
cardiomyopathy. Other studies have not shown a breed prevalence.
In this study, increased expression of the SERCA1 gene in the Tests of Phenotype: CHIC Certification: Required testing includes
myocardium is thought to be an adaptive response.75 hip and elbow radiographs, and temperament test. Optional tests
include cardiac evaluation, thyroid profile including autoantibodies,
Acral lick Dermatitis, Base-Narrow Canines, Brachygnathism, CERF eye examination (annually until 6 years, then every other
Central PRA, Cerebellar Abiotrophy, Cervical Vertebral year), and DM susceptibility test. (See CHIC website; www.
Instability, Cleft Lip/Palate, Cutaneous Asthenia, Deafness, caninehealthinfo.org).
Demodicosis, Dermatomyositis, Dermoid, Ectodermal Dysplasia,
Factor IX Deficiency, Giant Axonal Neuropathy, Hyperparathy-
roidism, Lupoid Onchyopathy, Lymphedema, Masticatory
Myositis, Micropapilla, Mitral Valve Disease, Oligodontia, Optic
217
Miscellaneous 1997 Nov;38(11):498-505.
15. Stokol T,& Parry B: Efficacy of fresh-frozen plasma and cryoprecipitate
• Breed Name Synonyms: German Shepherd, Deutsche in dogs with von Willebrand’s disease or hemophilia A. J Vet Intern Med.
Schäferhund, German Shepard, German Shephard, Alsatian, 1998 Mar-Apr;12(2):84-92.
German Police Dog. 16. Parry BW, Howard MA, Mansell PD, et. al.: Haemophilia A in German
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great shepherd dogs. Aust Vet J. 1988 Sep;65(9):276-9.
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3. OFA Website breed statistics: www.offa.org Last accessed July,1 2010 26. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
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in distinguishing myasthenia gravis from other causes of canine
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219
German
Shorthaired Pointer
Recognized Behavior Issues and Traits
They make good companion dogs as well as hunting companions.
Because they are bred to work all day, a dog kept for a companion
requires a high level of exercise and mental stimulation to stay
healthy both physically and emotionally. They are intelligent and
active around the house, and need close human companionship.
Their grooming needs are low, and they are average shedders. They
are alarm barkers, aloof with strangers, and develop a strong bond
with their caregiver. These dogs can dig and jump out of a yard if
left unattended. They are not suitable for apartment life.
The Breed History
Many breeds have been crossed to produce this elegant Normal Physiologic Variations
hunting dog including the English foxhound, German bird dog, None reported
Schweisshunde, Spanish pointer, English pointer and perhaps
others. This breed was first exported to North America in the 1920s, Drug Sensitivities
and first entered into the AKC registry in 1930. None reported
Gastric Dilatation-Volvulus (Bloat, GDV): Polygenically inherited, Acral Mutilation Syndrome, Brachygnathism, Epidermosis
life-threatening twisting of the stomach within the abdomen. Bullosa, Factor IX Deficiency, Factor XII Deficiency, GM-2
221
Gangliosidosis, Hypoadrenocorticism, Lymphedema, Seasonal 4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Flank Alopecia, and Subaortic Stenosis are reported.21 College of Veterinary Ophthalmologists. ACVO, 2007.
5. Kramer JW, Venta PJ, Klein SR, et. al.: A von Willebrand’s factor genomic
nucleotide variant and polymerase chain reaction diagnostic test associated
Isolated Case Studies with inheritable type-2 von Willebrand’s disease in a line of german
Paroxysmal Dyskinesia: A male German Shorthaired Pointer Shorthaired Pointer dogs. Vet Pathol. 2004 May;41(3):221-8.
presented with an intermittent gait abnormality initially seen 6. Meyers-Wallen VN, Bowman L, Acland GM, et. al.: Sry-negative XX
at 1 year of age. With excitement, the dog developed kyphosis, sex reversal in the German Shorthaired Pointer dog. J Hered. 1995
and bilateral hip and stifle flexion with ambulation. The episodes Sep-Oct;86(5):369-74.
usually lasted up to 30 minutes. The condition was eliminated with 7. Sommer MM, Meyers-Wallen VN: XX true hermaphroditism in a dog. J
anticonvulsant medication, and returned when the medication was Am Vet Med Assoc. 1991 Feb 1;198(3):435-8.
stopped.22 8. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Hemophilia A: Factor VIII deficiency, was diagnosed in a Vet Med Assoc 2002 Feb 15;220(4):466-71.
male German Shorthaired Pointer as a result of testing for a 9. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
coagulopathy. This is an X-linked recessive genetic disorder.23 Population and Animal Health, Michigan State University. April, 2007.
10. Byrne MJ, Byrne GM: Inheritance of “overshot” malocclusion in German
Branchial Cyst: A 7 year-old spayed German Shorthaired Pointer Shorthaired Pointers. Vet Rec. 1992 Apr 25;130(17):375-6.
was determined to have a branchial cyst in the subcutaneous 11. Dorn CR: Canine breed-specific risks of frequently diagnosed
tissues of the cervical/facial area.24 diseases at veterinary teaching hospitals. Monograph. AKC Canine Health
Foundation. 2000.
Muscular Dystrophy: X-linked recessive muscular dystrophy was 12. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
identified in a family of German Shorthaired Pointers, due to a large developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
deletion in the dystrophin gene.25 Sep-Oct;38(5):467-77.
13. Bryden SL, White SD, Dunston SM: Clinical, Histopathological
and Immunological Characteristics of Exfoliative Cutaneous Lupus
Genetic Tests Erythematosus in 25 German Short-Haired Pointers. Vet Dermatol
Tests of Genotype: Direct test for cone degeneration (CD) is 2005:16[4]:239-252.
available from Optigen. 14. Mauldin EA, Morris DO, Brown DC, et. al.: Exfoliative cutaneous lupus
erythematosus in German shorthaired pointer dogs: disease development,
Direct tests for black, red/orange and brown colors, and black or progression and evaluation of three immunomodulatory drugs (ciclosporin,
brown nose are available from HealthGene and VetGen. hydroxychloroquine, and adalimumab) in a controlled environment. Vet
Dermatol. 2010 Apr 1. [Epub ahead of print]
Direct test for vWD is available from VetGen. 15. Shelton GD, Schule A, Kass PH: Risk factors for acquired myasthenia
gravis in dogs: 1,154 cases (1991-1995). J Am Vet Med Assoc. 1997 Dec
Tests of Phenotype: CHIC Certification: Cardiac Evaluation by 1;211(11):1428-31.
a specialist/cardiologist, hip radiographs, CERF eye evaluation 16. Dorn CR, Priester WA: Epidemiologic analysis of oral and pharyngeal
(each year until 6, then every 2 years), and direct genetic test for cancer in dogs, cats, horses, and cattle. J Am Vet Med Assoc. 1976 Dec
cone degeneration. Optional tests include elbow radiographs, and 1;169(11):1202-6.
thyroid profile including autoantibodies. (See CHIC website; www. 17. Kramer JW, Schiffer SP, Sande RD, et. al.: Characterization of heritable
caninehealthinfo.org). thoracic hemivertebra of the German Shorthaired Pointer. J Am Vet Med
Assoc. 1982 Oct 15;181(8):814-5.
Recommend patella evaluation. 18. Martin CL & Leach R: Everted membrane nictitans in German
Shorthaired Pointers. J Am Vet Med Assoc 1970; 157:1229.
Miscellaneous 19. Berger SL: Persistent hyperplastic tunica vasculosa lentis/persistent
hyperplastic primary vitreous in the German Shorthaired Pointer. Proc Am
• Breed name synonyms: GSP, Kurzhaar, Deutscher Kurzhaariger Coll Vet Ophthalmol 1995; 26:42.
Vorstehund, German Shorthair, German Pointer 20. Vianna ML, Tobias KM: Atresia ani in the dog: a retrospective study. J
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), Am Anim Hosp Assoc. 2005 Sep-Oct;41(5):317-22.
ANKC (Australian National Kennel Club), NKC (National Kennel Club) 21. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
• AKC rank (year 2008): 16 (11,110 dogs registered) Ackerman. p 219 AAHA Press, 1999.
• Internet resources: German Shorthaired Pointer of America 22. Harcourt-Brown T: Anticonvulsant responsive, episodic movement
Inc.: www.gspca.org disorder in a German Shorthaired Pointer. J Small Anim Pract. 2008 Jul 4.
German Shorthaired Pointer Club of Canada: 23. Joseph SA, Brooks MB, Coccari PJ, et. al.: Hemophilia A in a German
www.gspcanada.com Shorthaired Pointer: clinical presentations and diagnosis. J Am Anim Hosp
The German Shorthaired Pointer Club (UK): www.gsp.org.uk Assoc. 1996 Jan-Feb;32(1):25-8.
24. Clark DM, Kostolich M, Mosier D: Branchial cyst in a dog. J Am Vet Med
References Assoc. 1989 Jan 1;194(1):67-8.
25. Schatzberg S, Olby N, Steingold S, et. al.: A polymerase chain reaction
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
screening strategy for the promoter of the canine dystrophin gene. Am J
2. Slater MR: 2005 German Shorthaired Pointer Health Survey: Final Report.
Vet Res. 1999 Sep;60(9):1040-6.
Jan 29, 2007.
26. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
3. Sidjanin DJ, Lowe JK, McElwee JL, et. al.: Canine CNGB3 mutations
Book House, NY 2006. p 24-28.
establish cone degeneration as orthologous to the human achromatopsia
locus ACHM3. Hum Mol Genet. 2002 Aug 1;11(16):1823-33.
222
German
Wirehaired Pointer
long, eyes are brown, oval, and medium sized. Pendulous ears are
moderate in size and rounded, hanging closely alongside the head.
The nose is brown, the muzzle is square and the stop moderate.
The slightly arched neck is moderately long and clean, the topline
gradually descends towards the rear. The thorax is deep and ribs
well sprung. Abdominal tuck up is obvious. The high set tail is
carried above the topline when alert. The tail if docked is shortened
to about 2/5 of the native length. Limbs are straight boned and
they are slightly longer than tall. Dewclaws are generally removed.
Round feet have webbed toes and possess heavy nails and pads,
with well knuckled up toes. The gait is smooth, and long strided.
The Breed History
In the 1800s, demand was high for all-purpose hunting dogs. In
Germany, the name “retrieving pointer”, or “Deutsch-Drahthaar”
Recognized Behavior Issues and Traits
Reported breed characteristics include: Stable temperament, active,
was applied to all such general purpose wirehaired dogs. The name high exercise needs, low grooming needs, aloof with strangers,
translates as German (Deutsch) Wire (draht) hair (haar). From this intelligent. They have a moderate shedding tendency, and love to
type of wirehaired dog, four subtypes were developed around 1870. please. They may become a one-man dog and are loyal to family.
In addition to the German Wirehaired pointer, these offshoots also Good with children if they are socialized early, and the children
included Pudelpointer, Stichelhaar and Griffon. Wirehaired pointers are calm. Will ably defend home or self if threatened. These dogs
were general purpose dogs with Poodle, Pointer, and French need mental stimulation or they may become destructive. Early
Wirehaired Pointing Griffon traits. The first breed standard dates obedience training is important. Typically they have a low tendency
to the year 1902. The first German Wirehaired Pointer dogs were to dig, keep leashed unless in a fenced enclosure. This type of dog is
exported to America in the 1920s. Initial AKC breed registration generally considered too active for apartment life.
occurred in 1959. The German Shorthaired pointer is not just a
short haired version of this breed; their origins differ significantly.
The Wirehaired Pointer has no direct hound descendents whereas
Normal Physiologic Variations
In a survey in Great Brittian, 47.8% of German Wirehaired pointer
the Shorthaired Pointer does.
litters were born via ceseran section.1
Weight: 45-70 lb (20-32 kg). Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Coat: Somewhat water repellent, the coat lies flat, with wiry, disease. Treat surgically if causing clinical signs. Too few German
straight hairs about 1.5-2” (4-5 cm) long, Well developed brows, Wirehaired Pointers have been screened by OFA to determine an
beard and moustache help to protect the face from underbrush. The accurate frequency.2
dense undercoat is shed during warmer months. Liver and white
spotted is the standard color for the breed, with liver roan, ticking von Willebrand’s disease (vWD): Type II vWD in the German
and roan in liver and white dogs, or solid liver being other accepted Wirehaired Pointer is a serious, sometimes fatal, autosomal
colorations. The face, (though not necessarily muzzle) and ears are recessive bleeding disorder. Cryoprecipitate is more effective, with
liver, sometimes with a white blaze. fewer side effects, than fresh frozen plasma in controlling bleeding
episodes. A genetic test is available.4,5
Longevity: 12-14 years
Hemophilia B (Factor IX Deficiency): Mild, X-linked recessive
Points of Conformation: The German Wirehaired pointer is bleeding disorder documented in this breed. A genetic test is
medium sized, with sturdy constitution, the head is moderately available.6
223
Disease Predispositions Miscellaneous
Hypothyroidism: Inherited autoimmune thyroiditis. 18.6% positive • Breed name synonyms: Deutscher Drahthaariger Vorstehhund,
for thyroid auto-antibodies based on testing at Michigan State Drahthaar, German Pointer (Wirehaired).
University. (Ave. for all breeds is 7.5%). One of the ten highest • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
breeds in frequency of the disorder.7,8 ANKC (Australian National Kennel Club), NKC (National Kennel Club).
• AKC rank (year 2008): 72 (1,213 dogs registered)
Humeral Osteochondritis Dissecans (OCD): Polygenically inherited • Internet resources: German Wirehaired Pointer Club of
cartilage defect of the humeral head. Causes shoulder joint pain America: http://www.gwpca.com/
and lameness in young growing dogs. Mild cases can resolve with Verein Deutsch-Drahthaar Group Canada: www.vdd-canada.ca
rest, while more severe cases require surgery. There is a 2.24:1 male German Wirehaired Pointer Club (UK): www.gwpclub.co.uk
to female ratio. 75% of all cases are unilateral. Reported 38.8x odds
ratio versus other breeds. Reported at a frequency of 1.36% in the
German Wirehaired Pointer.3,9
References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
Cataracts: Cataracts occur in the breed. Onset 6-18 months of age. 2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Unknown mode of inheritance. Too few German Wirehaired Pointers 3. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
have been CERF eye examined to determine an accurate frequency developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
in the breed. CERF does not recommend breeding any German Sep-Oct;38(5):467-77.
Wirehaired Pointer with a cataract.10 4. Kramer JW, Venta PJ, Klein SR, et. al.: A von Willebrand’s factor genomic
nucleotide variant and polymerase chain reaction diagnostic test associated
Atrioventricular (Heart) Block: German Wirehaired Pointers are with inheritable type-2 von Willebrand’s disease in a line of german
found to be at increased risk of high-grade second- or third-degree shorthaired pointer dogs. Vet Pathol. 2004 May;41(3):221-8.
atrioventricular block versus other breeds. Treatment is with a 5. Brooks M, Raymond S, Catalfamo J: Severe, recessive von Willebrand’s
pacemaker.11 disease in German Wirehaired Pointers. J Am Vet Med Assoc. 1996 Sep
1;209(5):926-9.
Brachygnathism, Entropion, Osteochondritis Dessicans- 6. Brooks MB, Gu W, Barnas JL, et. al.: A Line 1 insertion in the Factor IX
Shoulder, Prognathism, and Retinal Dysplasia are reported.12 gene segregates with mild hemophilia B in dogs. Mamm Genome. 2003
Nov;14(11):788-95.
7. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
Isolated Case Studies hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Day Blindness: A 5 month old German Wirehaired Pointer Vet Med Assoc 2002 Feb 15;220(4):466-71.
presented with day blindness (achromatopsia), consistent with cone 8. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
degeneration seen in German Shorthaired Pointers.13 Population and Animal Health, Michigan State University. April, 2007.
9. Rudd RG, Whitehair JG, Margolis JH: Results of management of
Diffuse Bronchiolo-alveolar Carcinoma: An eight-year-old osteochondritis dissecans of the humeral head in dogs : 44 cases [1982 to
female German Wirehaired Pointer was presented with signs of 1987]. J Am Anim Hosp Assoc 1990: 26[2]:173-178.
respiratory distress. Radiography indicated the presence of a diffuse 10. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
interstitial lung disease. A primary lung cancer with an unusually College of Veterinary Ophthalmologists. ACVO, 2007.
11. Schrope DP & Kelch WJ: Signalment, clinical signs, and prognostic
diffuse distribution of miliary/micronodular lesions was found at
indicators associated with high-grade second- or third-degree
postmortem examination. Histological diagnosis was bronchiolo- atrioventricular block in dogs: 124 cases (January 1, 1997-December 31,
alveolar carcinoma.14 1997). J Am Vet Med Assoc. 2006 Jun 1;228(11):1710-7.
12. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Genetic Tests Ackerman. p. 219-20. AAHA Press, 1999.
Tests of Genotype: Direct test for Hemophilia B is available from 13. McElroy RP: Day blindness in a German wirehaired pointer. Vet Rec.
Cornell Animal Health Diagnostic Center (607.253.3900). 2006 Feb 4;158(5):175.
14. Bertazzolo W, Zuliani D, Pogliani E, et. al.: Diffuse bronchiolo-alveolar
Direct test for vWD is available from VetGen. carcinoma in a dog. J Small Anim Pract. 2002 Jun;43(6):265-8.
15. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Direct test for black, red/orange and brown colors, and black or Book House, NY 2006. p. 29-32.
brown nose is available from HealthGene and VetGen.
224
Giant Schnauzer
towards the rear quarters. Limbs are straight boned. The tail is
carried high when active, and usually docked to be 1.5-3.0” (3.5-7.5
cm). Feet are compact and the toes well arched. Black nails and
thick pads are standard. Dewclaws are usually removed from
forelimbs; if present on hind limbs, they are removed. The gait is
strong, straight, low, and has a spring to the stride.
References
1. Kidd LB, Salavaggione OE, Szumlanski CL, et. al.: Thiopurine methyltrans-
ferase activity in red blood cells of dogs. J Vet Intern Med. 2004
Mar-Apr;18(2):214-8.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Fyfe JC, Giger U, Hall CA, et. al.: Inherited selective intestinal cobalamin
malabsorption and cobalamin deficiency in dogs. Pediatr Res. 1991
Jan;29(1):24-31.
4. Greco DS, Feldman EC, Peterson ME, et. al.: Congenital hypothyroid
dwarfism in a family of giant schnauzers. J Vet Intern Med. 1991
Mar-Apr;5(2):57-65.
5. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
6. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc. 2002 Feb 15;220(4):466-71.
7. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
8. Ferm K, Björnerfeldt S, Karlsson A, et. al.: Prevalence of diagnostic
characteristics indicating canine autoimmune lymphocytic thyroiditis
in giant schnauzer and hovawart dogs. J Small Anim Pract. 2009
Apr;50(4):176-9.
9. Wilbe M, Sundberg K, Hansen IR, et. al.: Increased genetic risk or
protection for canine autoimmune lymphocytic thyroiditis in Giant
Schnauzers depends on DLA class II genotype. Tissue Antigens. 2010
Jun;75(6):712-9.
10. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
11. Patterson E: Clinical Characteristics and Inheritance of Idiopathic
Epilepsy. Proceedings, 2007 Tufts’ Canine and Feline Breeding and Genetics
Conference. 2007.
12. Arnold S: Urinary incontinence in castrated bitches. Part 1:
Significance, clinical aspects and etiopathogenesis. Schweiz Arch Tierheilkd.
1997;139(6):271-6.
13. Blendinger C, Blendinger K, Bostedt H: Urinary incontinence in spayed
bitches. 1. Pathogenesis, incidence and disposition. Tierarztl Prax. 1995
Jun;23(3):291-9.
14. Glickman LT, Glickman NW, Perez CM, et. al.: Analysis of risk factors
for gastric dilatation and dilatation-volvulus in dogs. J Am Vet Med Assoc.
1994 May 1;204(9):1465-71.
15. Paradis M, Scott DW, Breton L: Squamous cell carcinoma of the nail bed
in three related giant schnauzers. Vet Rec. 1989 Sep 16;125(12):322-4.
16. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 236-37. AAHA Press, 1999.
17. Vargo CL, Taylor SM & Haines DM: Immune mediated neutropenia
and thrombocytopenia in 3 giant schnauzers. Can Vet J. 2007
Nov;48(11):1159-63.
18. Torres SM, Brien TO, Scott DW: Dermal arteritis of the nasal philtrum
in a Giant Schnauzer and three Saint Bernard dogs. Vet Dermatol. 2002
Oct;13(5):275-81.
227
Glen of
Imaal Terrier
Game for a fight with other dogs, but can live fine with other pets
if socialized early to them. A little less active than other terrier
breeds. Strong chase instinct—need to be loose only in a secured
fence enclosure—the fence needs to be designed to counteract
their excellent digging skills. They have a low bark tendency. Work
silently. Not considered the best of swimmers. Good with older
children—can be a bit strong and active for youngsters.
Points of Conformation: Head is large, skull broad, eyes are round Disease Predispositions
and wide set. Rose or half prick ears are small and set back and high Hypothyroidism: Inherited autoimmune thyroiditis. 7.1% positive
on the skull. A scissors bite or level bite is accepted. Muzzle tapering for thyroid auto-antibodies based on testing at Michigan State
to the black nose, and stop is pronounced. The neck is thick, and University. (Ave. for all breeds is 7.5%).4,5
topline is unique to the breed, with a gentle curve up to the lumbar
area. Limbs are short, and have some bowing—the compact front Allergic Skin Disease: Inhalant or food allergies. Causes pruritis and
feet turn slightly out while the rear feet are straight. The thorax pyotraumatic dermatitis (hot spots). Reported to occur in the breed.
is deep and full but not barrel shaped. Hindquarters are heavily
muscled. Generally the tail is docked to 1/2 length, and is carried Distichiasis: Abnormally placed eyelashes that irritate the cornea
high while active. The gait is smooth, flowing and covers a lot of and conjunctiva. Can cause secondary corneal ulceration. Identified
ground with each stride. Is longer than tall in overall proportions. in 4.13% of Glen of Imaal Terriers CERF examined by veterinary
ophthalmologists between 2000-2005.2
Recognized Behavior Issues and Traits Cataracts: Anterior and equatorial cortex cataracts predominate
Breed attributes reported include: Courageous, stoic, hardy, in the breed. Identified in 3.31% of Glen of Imaal Terriers CERF
stubborn, independent, spirited when working, but tame at home. examined by veterinary ophthalmologists between 2000-2005.
228
CERF does not recommend breeding any Glen of Imaal Terrier with
a cataract.2
Genetic Tests
Tests of Genotype: Direct test for crd3 is available from Optigen.
Miscellaneous
• Breed name synonyms: none
• Registries: AKC, UKC, ANKC (Australian National Kennel Club),
NKC (National Kennel Club), KCGB, FCI
• AKC rank (year 2008): 156 (32 dogs registered)
• Breed resources: Glen of Imaal Club of America: www.glens.org
The Glen of Imaal Terrier Association (UK): www.goita.co.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007
3. Goldstein O, Mezey JG, Boyko AR, et. al.: An ADAM9 mutation in canine
cone-rod dystrophy 3 establishes homology with human cone-rod
dystrophy 9. Mol Vis. 2010 Aug 11;16:1549-69.
4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc. 2002 Feb 15;220(4):466-71.
5. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
6. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 220. AAHA Press, 1999.
7. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 378-381.
229
Golden Retriever
Limbs are straight boned, and the dewclaws are usually left on
forelimbs. The feet are round shaped, well knuckled, and compact.
Patella Luxation: Polygenically inherited laxity of patellar Hypothyroidism: Inherited autoimmune thyroiditis. 13.2% positive
ligaments, causing luxation, lameness, and later degenerative joint for thyroid autoantibodies based on testing at Michigan State
disease. Treat surgically if causing clinical signs. OFA reports 2.7% University. (Ave. for all breeds is 7.5%). Dorn reports a 1.86x odds
affected.2 ratio versus other breeds. Reported at a frequency of 23.75% in the
1998 GRCA National Health Survey.3,16,17,18
Progressive Retinal Atrophy (prcd-PRA): Autosomal recessive
progressive rod cone degeneration (prcd) form. Age of onset is Distichiasis: Abnormally placed eyelashes that irritate the cornea
between 3-8 years of age, eventually causing blindness. Optigen and conjunctiva. Can cause secondary corneal ulceration. Identified
testing reports 1% affected, and 26% carriers in Golden Retrievers. in 9.70% of Golden Retrievers CERF examined by veterinary
Another autosomal recessive form of PRA (GR-PRA1) also occurs ophthalmologists between 2000-2005. Dorn reports a 1.97x odds
in the breed, with an average age of onset of 7 years. Genetic ratio versus other breeds. Reported at a frequency of 4.78% in the
testing shows gene frequencies of 5% (UK), 6% (Sweden) 2% 1998 GRCA National Health Survey.3,5,16
(France), and < 0.5% (US).5,6
Cataracts: Posterior cortical cataracts predominate in the breed,
Hemophilia A (Factor VIII Deficiency): X-linked recessive disorder usually between 9 months to 3 years of age. The breed also can
causing excessive bleeding after trauma or surgery. Affected Golden develop Y-suture cataracts. Identified in 5.61% of Golden Retrievers
Retrievers are identified in the US and Canada.7 CERF examined by veterinary ophthalmologists between 2000-2005.
Reported at a frequency of 12.74% in the 1998 GRCA National
Spectrin Deficiency: Rare, autosomal dominant disorder of Health Survey. CERF does not recommend breeding any Golden
erythrocyte osmotic fragility and spherocytosis. Can preclude Retriever with a cataract.3,15,19,20
hemolytic anemia in the breed. Identified in 17% of Dutch Golden
Retrievers.8 Epilepsy (Inherited Seizures): Generalized seizures are usually
seen in Golden Retrievers with an onset of 1 to 3 years of age. Treat
von Willebrand’s Disease: Autosomal recessive disorder of mild with anticonvulsant medications. Unknown mode of inheritance.
bleeding, usually associated with surgery, trauma, estrus, or Seizures are reported at a frequency of 8.93% in the 1998 GRCA
parturition. Reported at a frequency of 18% in a Dutch population National Health Survey.3,21
of Golden Retrievers, though a similar high frequency is not evident
in the US population.9 Hemangiosarcoma: Malignant cancer of red blood cells, usually
involving the spleen, liver, heart, or bone marrow. Molecular genetic
Ichthyosis/Primary Cornification Defect: An autosomal studies increased expassion of vascular endothelial growth factor
recessive inherited, nonpruritic skin disease affecting young reception (VEGFR1) in the breed. Reported at a frequency of 7.34%
Golden Retrievers of either sex and characterized by symmetrical, in the 1998 GRCA National Health Survey.3,22
predominantly ventro-lateral scaling and hyperpigmentation
of the trunk. Pathology reveals moderate to severe laminated Lymphoma/Lymphosarcoma: Malignant cancer of lymphoid tissue.
or compact orthokeratotic epidermal hyperkeratosis without Both B-cell and T-cell (mycosis fungoides) occur in the breed.
significant involvement of the stratum granulosum. A genetic test is Reported at a frequency of 5.06% in the 1998 GRCA National
available.10,11,12 Health Survey.3,23
Sensorimotor Axonopathy: Rare, maternally (mitochondria) Iris Cysts: Fluid filled sacs arising from the posterior surface of
inherited disorder causing a slowly progressive course of ataxia and the iris, to which they may remain attached or break free and
dysmetria with an insidious onset between 2 and 8 months of age. float into the anterior chamber. Usually occur in mature dogs.
Necropsy reveals a central and peripheral sensorimotor axonopathy, Can occasionally block the iridocorneal angle causing uveitis and
with the proprioceptive pathways being most severely affected. glaucoma. Identified in 4.33% of Golden Retrievers CERF examined
Caused by a mutation in the mitochondrial tRNA (tyr) gene.13,14 by veterinary ophthalmologists between 2000-2005.5
Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting Spontaneous Chronic Corneal Epithelial Defects (SCCED):
of the stomach within the abdomen. Requires immediate veterinary Golden Retrievers are reported as a breed with an increased
attention. Reported at a frequency of 2.98% in the 1998 GRCA prevalence of spontaneous corneal epithelial defects. Research
National Health Survey.3 indicates a role of substance P.37
Panosteitis: Affected dogs show intermittent lameness involving Oral Malignant Melanoma: Malignant cancer usually involving the
the diaphyseal and metaphyseal areas of the tubular long bones gingiva. Can be pigmented or non-pigmented. One study identified
prior to skeletal maturation. Reported at a frequency of 2.42% in a 1.84x relative risk versus other breeds.38
the 1998 GRCA National Health Survey.3
Idiopathic Horner’s Syndrome: Horner’s syndrome consists of
Osteochondritis Dessicans (OCD): Defect in cartilage maturation unilateral miosis, ptosis, enophthalmos, and prolapsed nictitans.
in young dogs, causing joint lesions and lameness. Treatment Male Golden Retrievers are overrepresented in canine cases. Most
with rest, or surgery in severe cases. Severe cases can result in cases resolve over time.39
later arthritis and degenerative joint disease. Reported 12.6x odds
ratio for shoulder OCD, and 3.9x odds ratio for stifle OCD versus Juvenile Renal Dysplasia: Affected Golden Retrievers under 3 years
other breeds. Reported at a frequency of 2.42% in the 1998 GRCA of age initially present with polydipsia/polyuria and isosthenuria.
National Health Survey.3,4 With progressive renal failure, vomiting, anorexia, and weight
loss develop. Histopathological findings include cystic glomerular
Osteosarcoma: Malignant bone cancer, usually affecting the atrophy, periglomerular fibrosis, fetal glomeruli, collecting tubule
appendicular skeleton. Cytogenetic studies show recurrent epithelial hyperplasia, and primitive mesenchymal connective tissue.
breed-related mutation. Reported at a frequency of 2.28% in the Unknown mode of inheritance.40,41
1998 GRCA National Health Survey.3,27
Megaesophagus: Golden Retrievers are overrepresented in
Persistent Pupillary Membranes: Strands of fetal remnant diagnoses of acquired megaesophagus. Causes include peripheral
connecting; iris to iris, cornea, lens, or involving sheets of tissue. neuropathy, laryngeal paralysis, acquired myasthenia gravis,
The later three forms can impair vision, and dogs affected with esophagitis, and gastric dilatation. Hypothyroidism is not
these forms should not be bred. Identified in 2.19% of Golden associated with megaesophagus in the breed. Clinical signs include
Retrievers CERF examined by veterinary ophthalmologists between regurgitation, excess salivation, and aspiration pneumonia.42
2000-2005.5
Myesthenia Gravis: An immune-mediated disorder of circulating
Cranial Cruciate Ligament (ACL) Rupture: Traumatic tearing anti-acetylcholine receptor antibodies cause generalized
of the ACL in the stifle, causing lameness and secondary arthritis. appendicular muscle weakness with or without megaesophagus,
Treat with surgery. Reported at an increased incidence versus or selective esophageal, facial and pharyngeal muscular weakness.
other breeds. Reported at a frequency of 2.08% in the 1998 GRCA Golden Retrievers are reported with a 2.2x odds ratio versus other
National Health Survey.3,28 breeds.43,44
Uveitis: Inflammation of the uveal tract of the eye. Can progress to Cricopharyngeal Dysfunction/Achalasia: Congenital abnormality
cataracts, glaucoma, or blindness. Can be idiopathic, or secondary of the upper esophageal sphincter due to stricture, or abnormal
to neoplasia (lymphoma), infection, or iris cysts. Golden Retrievers function. Diagnose with video fluoroscopy. Reported as a
are the most commonly reported breed with the disorder.29,30,31 breed-related disorder, with a major autosomal recessive gene
controlling its expression, and a heritability of 0.61.45
Glaucoma: Increased intra-ocular pressure, that can lead to blindmess
from retinal death or detachment, uveitis, and corneal lesions. Can Idiopathic Pericardial Effusion: Golden Retrievers are
be primary or secondary. Golden Retrievers represent 5% of reported overrepresented with this diagnosis, which is not due to tumor,
cases of glaucoma. Of these, 52% are associated with iris cysts.31,32 trauma, or infection. Prognosis is good with pericardectomy.46
Retinal Dysplasia: Focal retinal dysplasia and retinal folds are Intracranial Meningioma: One study found that Golden Retrievers
recognized in the breed. Identified in 1.36% of Golden Retrievers are overrepresented compared to other breeds for intracranial
CERF-examined by veterinary ophthalmologists between meningiomas. These are the most common brain tumor in dogs, and
2000-2005. Suggested autosomal recessive inheritance.5,33 can be benign, or malignant.47,48
232
Choroid Plexus Brain Tumor: Golden Retrievers are
overrepresented in reported cases of choroid plexus carcinoma and
Genetic Tests
Tests of Genotype: Direct test for prcd-PRA is available from
choroid plexus papilloma. The breed has a 3.7x relative risk versus Optigen. (Recommended for breeding dogs.)
other breeds.49
Direct test for GR-PRA1 is available from thje Animal Health Trust
Lingual Fibrosarcoma: Golden Retrievers have a 3.64x odds ratio and Optigen.
versus other breeds of developing this cancer of the tongue.50
Direct test for Ichthyosis is available from Antagene.
Limbal Melanoma: Benign eye mass, usually originating from the
dorsal limbus. Golden Retrievers have a 5.8x odds ratio of limbal Tests of Phenotype: CHIC Certification: Required testing includes
melanomas versus other breeds.51 hip and elbow radiographs, CERF eye examination (annually until 8
years), and cardiac evaluation by a cardiologist. (See CHIC website;
Leukemia: A UK study showed that Golden Retrievers were www.caninehealthinfo.org).
overrepresented versus other breeds with diagnoses of acute and
chronic lymphoid leukaemia (ALL and CLL), and acute and chronic Recommend thyroid profile including autoantibodies, and patella
myeloid leukaemia (AML and CML).52 evaluation.
Thyroid Cancer: Golden Retrievers have a 2.2 odds ratio versus
other breeds of developing thyroid cancer. Affected dogs are usually Miscellaneous
between 10-15 years of age with a thyroid mass, and a diagnosis of • Breed name synonyms: Yellow Retriever, Russian Retriever,
carcinoma, or less frequently adenocarcinoma.53 Golden, Golden Flat-coat (historical).
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
Acral lick Dermatitis, Anasarca, Central Progressive Retinal ANKC (Australian National Kennel Club), NKC (National Kennel Club).
Atrophy, Cerebellar Abiotrophy, Cervical Vertebral Instability, • AKC rank (year 2008): 4 (34,485 dogs registered)
Degenerative Myelopathy, Entropion, Hypoadrenocorticism, • Internet resources: Golden Retriever Club of America:
Juvenile Cellulitis, Micropapilla, Nodular Dermatofibrosis, www.grca.org
Oligodontia, Optic Nerve Hypoplasia, Proliferative Episcleritis, Golden Retriever Club of Canada: www.grcc.net
Seasonal Flank Alopecia, Sebaceous Adenitis, Silica Urolithiasis, The Golden Retriever Club (UK):
Supernumerary Teeth, and Tetralogy of Fallot are reported.54 www.thegoldenretrieverclub.co.uk
233
genetic data of ichthyosis in the golden retriever: a prospective study. J 37. Murphy CJ, Marfurt CF, McDermott A, et. al.: Spontaneous chronic
Small Anim Pract. 2009 May;50(5):227-35. corneal epithelial defects (SCCED) in dogs: clinical features, innervation,
13. Jäderlund KH, Orvind E, Johnsson E, et. al.: A neurologic syndrome in and effect of topical SP, with or without IGF-1. Invest Ophthalmol Vis Sci.
Golden Retrievers presenting as a sensory ataxic neuropathy. J Vet Intern 2001 Sep;42(10):2252-61.
Med. 2007 Nov-Dec;21(6):1307-15. 38. Ramos-Vara JA, Beissenherz ME, Miller MA, et. al.: Retrospective
14. Baranowska I, Jäderlund KH, Nennesmo I, et. al.: Sensory ataxic study of 338 canine oral melanomas with clinical, histologic,
neuropathy in golden retriever dogs is caused by a deletion in the and immunohistochemical review of 129 cases. Vet Pathol. 2000
mitochondrial tRNATyr gene. PLoS Genet. 2009 May;5(5):e1000499. Nov;37(6):597-608.
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Jul;65(7):1014-20. 40. de Morais HS, DiBartola SP & Chew DJ: Juvenile renal disease in
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veterinary teaching hospitals. Monograph. AKC Canine Health Foundation. 15;209(4):792-7.
2000. 41. Kerlin RL & Van Winkle TJ: Renal dysplasia in golden retrievers. Vet
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for Population and Animal Health, Michigan State University. April, 2007. in distinguishing myasthenia gravis from other causes of canine
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21. Lengweiler C & Jaggy A: Clinical, epidemiologic and therapeutic aspects 45. Davidson AP, Pollard RE, Bannasch DL, et. al.: Inheritance of
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22. Tamburini BA, Trapp S, Phang TL, et. al.: Gene expression profiles of 46. Aronsohn MG & Carpenter JL: Surgical treatment of idiopathic
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27. Thomas R, Wang HJ, Tsai PC, et. al.: Influence of genetic background on 51. Donaldson D, Sansom J, Scase T, et. al.: Canine limbal melanoma: 30
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28. Morris E & Lipowitz AJ: Comparison of tibial plateau angles in dogs with 52. Adam F, Villiers E, Watson S, et. al.: Clinical pathological and
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Feb 1;218(3):363-6. confirmed canine leukaemia. Vet Comp Oncol. 2009 Sep;7(3):181-95.
29. Massa KL, Gilger BC, Miller TL, et. al.: Causes of uveitis in dogs: 102 53. Wucherer KL & Wilke V: Thyroid cancer in dogs: an update based on 638
cases (1989-2000). Vet Ophthalmol. 2002 Jun;5(2):93-8. cases (1995-2005). J Am Anim Hosp Assoc. 2010 Jul-Aug;46(4):249-54.
30. Sapienza JS, Simó FJ & Prades-Sapienza A: Golden Retriever uveitis: 75 54. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
cases (1994-1999). Vet Ophthalmol. 2000;3(4):241-246. Ackerman. p. 220. AAHA Press, 1999.
31. Esson D, Armour M, Mundy P, et. al.: The histopathological and 55. Bélanger MC, Ouellet M, Queney G, et. al.: Taurine-deficient dilated
immunohistochemical characteristics of pigmentary and cystic glaucoma in cardiomyopathy in a family of golden retrievers. J Am Anim Hosp Assoc.
the Golden Retriever. Vet Ophthalmol. 2009 Nov-Dec;12(6):361-8. 2005 Sep-Oct;41(5):284-91.
32. Deehr AJ & Dubielzig RR: A histopathological study of iridociliary cysts 56. Morrison WB, Wilsman NJ, Fox LE, et. al.: Primary ciliary dyskinesia in
and glaucoma in Golden Retrievers. Vet Ophthalmol. 1998;1(2-3):153-158. the dog. J Vet Intern Med. 1987 Apr-Jun;1(2):67-74
33. Long SE & Crispin SM: Inheritance of multifocal retinal dysplasia in the 57. Afzelius BA, Carlsten J & Karlsson S: Clinical, pathologic, and ultrastruc-
golden retriever in the UK. Vet Rec. 1999 Dec 11;145(24):702-4. tural features of situs inversus and immotile-cilia syndrome in a dog. J Am
34. Naranjo C, Dubielzig RR, & Friedrichs KR: Canine ocular histiocytic Vet Med Assoc. 1984 Mar 1;184(5):560-3.
sarcoma. Vet Ophthalmol. 2007 May-Jun;10(3):179-85. 58. Reichler IM, Hoerauf A, Guscetti F, et. al.: Primary ciliary dyskinesia with
35. Moore PF, Affolter VK, Vernau W, et. al.: Canine hemophagocytic situs inversus totalis, hydrocephalus internus and cardiac malformations in
histiocytic sarcoma: a proliferative disorder of CD11d+ macrophages. Vet a dog. J Small Anim Pract. 2001 Jul;42(7):345-8.
Pathol. 2006 Sep;43(5):632-45. 59. Matsuki N, Yamato O, Kusuda M, et. al.: Magnetic resonance imaging of
36. Schultz RM, Puchalski SM, Kent M, et. al.: Skeletal lesions of GM2-gangliosidosis in a golden retriever. Can Vet J. 2005 Mar;46(3):275-8.
histiocytic sarcoma in nineteen dogs. Vet Radiol Ultrasound. 2007 60. Braund KG, Mehta JR, Toivio-Kinnucan M, et. al.: Congenital
Nov-Dec;48(6):539-43. hypomyelinating polyneuropathy in two golden retriever littermates. Vet
Pathol. 1989 May;26(3):202-8.
234
61. da Costa RC, Parent JM, Poma R, et. al.: Multisystem axonopathy
and neuronopathy in Golden Retriever dogs. J Vet Intern Med. 2009
Jul-Aug;23(4):935-9.
62. Sharp NJ, Kornegay JN, Van Camp SD, et. al.: An error in dystrophin mRNA
processing in golden retriever muscular dystrophy, an animal homologue of
Duchenne muscular dystrophy. Genomics. 1992 May;13(1):115-21.
63. Kornegay JN, Tuler SM, Miller DM, et. al.: Muscular dystrophy in a litter of
golden retriever dogs. Muscle Nerve. 1988 Oct;11(10):1056-64.
64. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 47-51.
235
Gordon Setter
They have compact feet with arched toes and straight strong limbs.
Their gait is characterized by long easy strides, and it is normal to
see the tail flag while going. Legs arc in a straight flowing motion.
Ectropion: Rolling out of eyelids, often with a medial canthal Genetic Tests
pocket. Can also cause secondary conjunctivitis, which Dorn finds Tests of Genotype: Direct test for black, liver, and red coat color is
has a 2.49x odds ratio in Gordon Setters versus other breeds. available from VetGen.
Ectropion is reported in 1.2% of Gordon Setters CERF examined by
veterinary ophthalmologists between 2000-2005.5,10 Direct test for rcd4 PRA is available from the Animal Health Trust
Retinal Dysplasia: Retinal folds, geographic, and generalized retinal Tests of Phenotype: CHIC Certification: Required testing includes
dysplasia with detachment are recognized in the breed. Can lead to hip radiographs, elbow radiographs, and CERF eye examination. (See
blindness. Reported in 1.6% of Gordon Setters CERF examined by CHIC website; www.caninehealthinfo.org).
veterinary ophthalmologists between 2000-2005.5
Recommend thyroid profile including autoantibodies, patella
Juvenile Renal Disease: Progressive renal dysfunction in young evaluation, and heart examination.
Gordon Setters. Typically presents with increased drinking and
urination, weight loss or unthriftiness, consistently dilute urine,
and elevated kidney blood tests. Affected dogs do not leak urinary
protein until late in the disease. Onset from weeks of age to over a
237
Miscellaneous 20. Salmeri KR, Bellah JR, Ackerman N, et. al.: Unilateral congenital
aneurysm of the jugular, linguofacial, and maxillary veins in a dog. J Am Vet
• Breed name synonyms: Gordon, Black and Tan (historical) Med Assoc. 1991 Feb 15;198(4):651-4.
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), 21. Coons FH, George JW, Appel GO: Reticuloendotheliosis in a dog. Cornell
ANKC (Australian National Kennel Club), NKC (National Kennel Club) Vet. 1976 Apr;66(2):249-57.
• AKC rank (year 2008): 92 (636 dogs registered) 22. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
• Internet resources: Gordon Setter Club of America Inc. Book House, NY 2006. p 67-71.
www.gsca.org
British Gordon Setter Club: www.britishgordonsetterclub.org.uk
Gordon Setter Club of Canada: www.gordensetterclubcanada.com
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Genevois JP, Remy D, Viguier E, et. al.: Prevalence of hip dysplasia
according to official radiographic screening, among 31 breeds of dogs in
France. Vet Comp Orthop Traumatol. 2008;21(1):21-4.
3. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
4. de Lahunta A, Fenner WR, Indrieri RJ, et. al.: Hereditary cerebellar
cortical abiotrophy in the Gordon Setter. J Am Vet Med Assoc. 1980 Sep
15;177(6):538-41.
5. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
6. Bell JS: Health Update on Progressive Retinal Atrophy and Juvenile Renal
Dysplasia in the Gordon Setter. Gordon Setter News. Oct 2003.
7. Steinberg HS, Troncoso JC, Cork LC, et. al.: Clinical features of inherited
cerebellar degeneration in Gordon setters. J Am Vet Med Assoc. 1981 Nov
1;179(9):886-90.
8. Yaeger MJ, Majercik K, Carter M: An autosomal recessive, lethal,
neurologic disease of Gordon Setter puppies. J Vet Diagn Invest. 2000
Nov;12(6):570-3.
9. Gorgi AA, O’Brien DP, Shelton GD, et. al.: Inborn Error of Metabolism
In Gordon Setter Puppies: Organic Acid Profile and Candidate Gene
Sequencing.Proceedings, 2008 ACVIM Forum. 2008.
10. Dorn CR: Canine breed-specific risks of frequently diagnosed
diseases at veterinary teaching hospitals. Monograph. AKC Canine Health
Foundation. 2000.
11. Slater MR: 2004 GSCA Gordon Setter Health Survey: Final Report.
December 17, 2004.
12. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
13. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc. 2002 Feb 15;220(4):466-71.
14. Glickman LT, Glickman NW, Perez CM, et. al.: Analysis of risk factors for
gastric dilatation and dilatation-volvulus in dogs. J Am Vet Med Assoc. 1994
May 1;204(9):1465-7
15. Ramos-Vara JA, Beissenherz ME, Miller MA, et. al.: Retrospective
study of 338 canine oral melanomas with clinical, histologic, and
immunohistochemical review of 129 cases. Vet Pathol. 2000 Nov;37(6):597-
608.
16. Ovrebo Bohnhorst J, Hanssen I, Moen T: Antinuclear antibodies (ANA)
in Gordon setters with symmetrical lupoid onychodystrophy and black hair
follicular dysplasia. Acta Vet Scand. 2001;42(3):323-9.
17. Ziener ML, Bettenay SV & Mueller RS: Symmetrical onychomadesis
in Norwegian Gordon and English setters. Vet Dermatol. 2008
Apr;19(2):88-94.
18. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p 220-21, AAHA Press, 1999.
19. Naughton GK, Mahaffey M, Bystryn JC, et. al.: Antibodies to surface
antigens of pigmented cells in animals with vitiligo. Proc Soc Exp Biol Med.
1986 Mar;181(3):423-6.
238
Great Dane
pronounced stop. The nose is ridged but not split. The conformation
is well balanced; the build is heavier in males, both in bone and
musculature. The gait is a straight, low, elastic long and powerful
ground-covering stride. The almond-shaped eyes are usually darkly
pigmented, medium-sized and deep-set and the palpebral margins
do not evert. Ears are medium sized, high-set and the leather is
moderately thick. The folded ears rest close to the cheeks. Ears are
sometimes cropped to stay pricked in North America. The nose is
large and pigmented black or close to black except in harlequins
where a spotted nose is allowed. The neck is long and free of
dewlaps, arched, and the topline is short and level. The thorax is
The Breed History very deep and broad, and ribs are well sprung. Abdomen tuck up is
The name “Great Dane” originates in the French language; the pronounced. The tail is set high, is thick at the base, then tapers to
meaning is “Big Danish”. Proudly termed “King of Dogs”, “Gentle reach to the tarsus; is carried level during movement and low when
Giant” or “Apollo of Dogs” by breed fanciers, this was actually a at rest. Limbs are long and straight boned, feet are compact and
breed originating in Germany, so it is unclear how it became named well knuckled, and dewclaw removal is optional.
“Dane”. The Tibetan Mastiff is thought to be a direct ancestor of the
Great Dane. Also linked to breed development is the Alaunt from
Asian Russia, the English Mastiff and the Irish Wolfhound. Other
Recognized Behavior Issues and Traits
Reported breed characteristics include: Courageous in the hunt, but
reports place Greyhound in the mix later in the breed development,
friendly and gentle in the home—even playful. Good with children,
a step that may have greatly refined the mastiff type. Distinct Great
easy to groom, clean but needs lots of space to exercise in a fenced
Dane lineage can be traced back about 400 years. In a meeting
area. Not suitable for an apartment or small homes. Fairly good
that took place about 1880, a resolution was passed to name this
trainability, some are aggressive with other dogs unless they know
breed “Deutsche Dogge” which translates roughly as “German
them, early obedience training is important, they possess average
Mastiff,” and at that time, it was decreed that the breed name Great
activity levels, and have moderate to high exercise needs. This is
Dane should not be applied to this breed, but in spite of this, the
a late maturing breed. Some Great Danes can be shy and people
name persists today in English-speaking countries. The first breed
aggressive.
standard was adopted in 1891.
Coat: The very short, thick and glossy coat is accepted in the
following colors: Fawn (yellow-gold with black mask), brindle
(yellow-gold base with well defined black stripes and usually black
masked), blue (steel blue), black, and harlequin (white base with
medium-sized irregular patches of black over the haircoat).
AO, aorta; LA, left atrium; LV, left ventricle; FS, fractional shortening; Panosteitis: Self-limiting disease of young, large breed dogs involving
EF, ejection fraction; LVET, left ventricular ejection time; Vcf, the diaphyseal and metaphyseal areas of the tubular long bones.
velocity of circumferential; EPSS, E-point to septal separation; VS, Affected dogs show intermittent lameness. Reported at a frequency
ventricular septum; VS%∆, change in VS thickness between diastole of 5% in the Great Dane Club Of America National Health Survey.7
and systole; LVW, left ventricular wall; HR, heart rate; N, number of
animals. Ectropion: Rolling out of eyelids, often with a medial canthal pocket.
Can cause secondary conjunctivitis. Reported in 4.87% of Great Danes
CERF-examined by veterinary ophthalmologists between 2000-2005.
Drug Sensitivities Reported at a frequency of 4% in the Great Dane Club Of America
None reported National Health Survey.7,15
Inherited Diseases Distichiasis: Abnormally placed eyelashes that irritate the cornea and
Hip Dysplasia: Polygenically inherited trait causing degenerative conjunctiva. Can cause secondary corneal ulceration. Identified in
joint disease and hip arthritis. OFA reports 12.0% affected.5 4.50% of Great Danes CERF-examined by veterinary ophthalmologists
between 2000-2005.15
Dilated Cardiomyopathy (DCM): Affected dogs have reduced
shortening fraction (FS) in the presence of clinical and radiographic Eury/Macroblepharon: An exceptionally large palpebral fissure. With
signs of left-sided or biventricular heart failure. Atrial fibrillation laxity, may lead to lower lid ectropion and upper lid entropion. Either
is the most common arrhythmia. Some affected Great Danes may of these conditions may lead to severe ocular irritation. Identified in
be asymptomatic, with ECHO or Doppler necessary to make the 4.50% of Great Danes CERF-examined by veterinary ophthalmologists
diagnosis. Molecular genetic studies show changes in calstabin and between 2000-2005.15
triad in gene expression. Pedigree analysis suggests that DCM in the
breed involves a major X-linked recessive gene, although polygenic Demodicosis (Generalized): Dorn reports a 1.79x odds ratio for
inheritance cannot be ruled out. Reported at a frequency of 5% in developing demodectic mange versus other breeds. This disorder has
the Great Dane Club Of America National Health Survey.6,7,8,9 an underlying immunodeficiency in its pathogenesis. Reported at a
frequency of 4% in the Great Dane Club Of America National Health
Elbow Dysplasia: Polygenically inherited trait causing elbow Survey.7,10
arthritis. OFA reports 3.8% affected.5
Osteosarcoma (OSA): Great Danes are a breed with a predisposition
Patella Luxation: Polygenically inherited laxity of patellar ligaments, (5x Odds Ratio) for developing malignant osteosarcoma versus other
causing luxation, lameness, and later degenerative joint disease. breeds. One study showed a prevalence of 4.4%, and an Odds Ratio
Treat surgically if causing clinical signs. OFA reports 1.4% affected.5 of 12.0x versus other breeds. Forelimb OSA was more frequent than
hindlimb OSA in Great Danes. Reported at a frequency of 3% in the
Great Dane Club Of America National Health Survey.7,16,17
240
Entropion: Rolling in of eyelids, often causing corneal irritation Hypoadrenocorticism (Addison’s Disease): Immune mediated
or ulceration. Entropion is reported in 2.31% of Great Danes destruction of the adrenal gland. Typical presentation of lethargy,
CERF-examined by veterinary ophthalmologists between 2000-2005. poor appetite, vomiting, weakness, and dehydration occurring from
Reported at a frequency of 3% in the Great Dane Club Of America 4 months to several years of age. Treatment with DOCA injections or
National Health Survey.7,15 oral fludrocortisone. Great Danes are at significantly higher risk versus
other breeds. Unknown mode of inheritance. Reported at a frequency
Cervical Vertebral Instability (Wobbler Syndrome): Vertebral of 0.3% in the Great Dane Club Of America National Health Survey.7,26
disorder causing spinal cord compression and ataxia. Radiographic
examinations suggest that the primary lesion is foramenal stenosis Mitral Valvular Malformation: Great Danes are overrepresented.
and intervertebral instability at C6-7. Reported at a frequency of 2% Affected dogs have mitral regurgitation, which can progress to
in the Great Dane Club Of America National Health Survey.7,18,19 congestive heart disease. Average age of recognition is 7.3 months.
Abnormalities include changes to the annulus, leaflets, chordae
Osteochondritis Dissecans (OCD): Abnormality of cartilage tendineae, and papillary muscles. Reported at a frequency of 0.1% in
development causing lameness in the shoulder, elbow, hock or stifle. the Great Dane Club Of America National Health Survey.7,27
Severe cases may require surgery. Dorn reports a 22.26x odds ratio
versus other breeds. Reported 87.0x odds ratio for elbow OCD, 32.8x Splenic Torsion: Great Danes are found to be at increased risk for
odds ratio for shoulder OCD, and 309.4x odds ratio for stifle OCD splenic torsion versus other breeds. Treatment is immediate surgery.28
versus other breeds. Reported at a frequency of 2% in the Great Dane
Club Of America National Health Survey.7,10,20,21 Inherited Myopathy: A hereditary, non-inflammatory myopathy
occurs in Great Danes of both sexes before one year of age. Clinical
Hypertrophic Osteodystrophy (HOD): Immune-mediated disorder signs are exercise intolerance, muscle wasting, and an exercise-in-
causing fever, and painful, swollen joints and bones in young Great duced tremor. Serum creatinine kinase levels are elevated. Affected
Danes. Occurs mostly within 3-14 days post-vaccination. Age of onset muscles show slow oxydatine fiber phenotype disrupted sarcomeric
is 8-16 weeks. Unknown mode of inheritance. Reported 189.8x odds architecture and accumulation of mitochondrial organelles. Most
ratio versus other breeds. Reported at a frequency of 2% in the Great dogs are affected severely, though some may survive into adulthood.
Dane Club Of America National Health Survey.7,21,22 All have had fawn or brindle coat coloration. An autosomal recessive
inheritance is suspected.29,30
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. Megaesophagus: Great Danes are overrepresented in diagnoses of
The later three forms can impair vision, and dogs affected with primary megaesophagus. Onset can be at weaning, or in adulthood.
these forms should not be bred. Identified in 1.52% of Great Danes Clinical signs include regurgitation, excess salivation, and aspiration
CERF-examined by veterinary ophthalmologists between 2000-2005. pneumonia.31
Dorn reports a 3.59x odds ratio versus other breeds.10,15
Epidermolysis Bullosa Acquisita (Bullous Pemphigus): Eruptive
Diskospondylitis: Great Danes have a 7.3x odds ratio for developing autoimmune skin disorder characterized by vesicles that rapidly
vertebral infection versus mixed breed dogs. Treatment is with progress to ulcers, typically in the oral cavity, pads and medial pinnae.
long-term antibiotics.23 Seen in young to adolescent Great Danes. Variable response to steroids
and immunosuppressive therapy.32,33
Eversion of the Cartilage of the Third Eyelid: A scroll-like curling
of the cartilage of the third eyelid, usually everting the margin. Acral lick Dermatitis, Brachygnathism, Color Dilution Alopecia,
May cause mild ocular irritation. Identified in 1.22% of Great Danes Cystinuria, Hemeralopia, Lymphedema, Oligodontia, Prognathism,
CERF-examined by veterinary ophthalmologists between 2000-2005.15 Progressive Retinal Atrophy, Retinal Dysplasia, Spinal Muscular
Atrophy, Subaortic stenosis, Tricuspid Valve Dysplasia, Uveal
Iris Ciliary Body Cysts: Pigmented cysts arise from pigmented Hypopigmentation, Vascular Ring Anomaly, von Willebrand’s
epithelial cells of the ciliary body. Ciliary body cysts, may predispose Disease, Wry Mouth, and Zinc-Responsive Dermatosis are
to glaucoma. Review of hospital admissions shows a 37.01 odds reported.34
ratio for ciliary body cysts in Great Danes. Identified in 1.03% of
Great Danes CERF-examined by veterinary ophthalmologists between
2000-2005.15,25
Isolated Case Studies
Cecocolic Volvulus: Two male Great Danes were diagnosed with
Primary Glaucoma (Goniodysgenesis): Goniodysgenesis has a volvulus of the cecum and large intestines. Clinical signs included
heritability of 0.52 in Great Danes, and this is positively correlated peracute to acute onset of vomiting, mild abdominal distention and
to the high incidence of glaucoma in the breed. Reported at a pain, lack of feces, and tenesmus. Diagnosis by radiography.35
frequency of 0.3% in the Great Dane Club Of America National Health
Primary Orthostatic Tremors: Two unrelated two year old
Survey. CERF does not recommend breeding any Great Dane with
Great Danes were identified with orthostatic tremors that only
glaucoma.7,15,24
occurred when standing at rest. The tremors were controlled with
Secondary Glaucoma (with Ciliary Body Cysts): Occurs with cysts phenobarbitol.36
in the anterior and posterior chamber. Review of hospital admissions
Recurrent Limb Edema: Great Danes have been identified with
shows a 2.23x odds ratio for glaucoma and 37.01x odds ratio for
multiple episodes of cool, pitting edema limited to one or more limbs.
ciliary body cysts in Great Danes.25
241
Episodes lasted for several days, and the time between episodes varied serum thyroid hormone autoantibodies in dogs with clinical signs of
from 2 weeks to 1 year. No etiology is identified, and the edema was hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
unresponsive to treatment.37 14. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
15. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Myasthenia Gravis: A case report identified three Great Dane
College of Veterinary Ophthalmologists. ACVO, 2007.
littermates all developing myasthenia gravis between 2-3 years of 16. Misdorp W, Hart AA: Some prognostic and epidemiologic factors in
age. Acetylcholine receptor auto-antibody titres were positive.38 canine osteosarcoma. J Natl Cancer Inst. 1979 Mar;62(3):537-45.
17. Rosenberger JA, Pablo NV, & Crawford PC: Prevalence of and intrinsic
Genetic Tests risk factors for appendicular osteosarcoma in dogs: 179 cases (1996-2005).
J Am Vet Med Assoc. 2007 Oct 1;231(7):1076-80.
Tests of Genotype: Direct tests for coat color (including mask and 18. Mason TA: Cervical vertebral instability (wobbler syndrome) in the dog.
dilute) are available from HealthGene and VetGen. Vet Rec. 1979 Feb 17;104(7):142-5.
19. Drost WT, Lehenbauer TW, Reeves J: Mensuration of cervical vertebral
Tests of Phenotype: CHIC Certification: Required testing includes ratios in Doberman pinschers and Great Danes. Vet Radiol Ultrasound. 2002
hip radiographs, CERF eye examination, thyroid profile including Mar-Apr;43(2):124-31.
autoantibodies and cardiac evaluation. (See CHIC website; www. 20. Slater MR, Scarlett JM, Kaderly RE, Bonnett BN: Breed, gender and
caninehealthinfo.org). age as risk factors for canine osteochondritis dissecans. Veterinary and
Comparative Orthopaedics and Traumatology 1991; 4:100-106.
Recommend elbow radiographs and patella evaluation. 21. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
Miscellaneous 22. Miller C: Hypertrophic osteodystrophy in a Great Dane puppy. Can Vet J.
• Breed name synonyms: Dane, Deutsche Dogge, German Mastiff, 2001 Jan;42(1):63-6.
Dogue Allemand (historical). 23. Burkert BA, Kerwin SC, Hosgood GL, et. al.: Signalment and clinical
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), features of diskospondylitis in dogs: 513 cases (1980-2001). J Am Vet Med
Assoc. 2005 Jul 15;227(2):268-75.
ANKC (Australian National Kennel Club), NKC (National Kennel Club). 24. Wood JL, Lakhani KH, Mason IK, et. al.: Relationship of the degree of
• AKC rank (year 2008): 22 (8,994 dogs registered) goniodysgenesis and other ocular measurements to glaucoma in Great
• Internet resources: Great Dane Club of America: www.gdca.org Danes. Am J Vet Res. 2001 Sep;62(9):1493-9
The Great Dane Club (UK): www.thegreatdaneclub.com 25. Spiess BM, Bolliger JO, Guscetti F, et. al.: Multiple ciliary body cysts
The Great Dane Club of Canada: www.gdcc.ca and secondary glaucoma in the Great Dane: a report of nine cases. Vet
Ophthalmol. 1998;1(1):41-45.
26. Peterson ME, Kintzer PP, Kass PH: Pretreatment clinical and laboratory
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diseases at veterinary teaching hospitals. Monograph. AKC Canine Health in Great Danes. J Vet Intern Med. 2005 Jul-Aug;19(4):606-9.
Foundation. 2000. 37. Webb JA, Abrams-Ogg A, Hall JA, et. al.: A Syndrome of Recurrent Limb
11. Ward MP, Patronek GJ, Glickman LT: Benefits of prophylactic gastropexy Edema in Great Danes. Proceedings, 18th ECVIM-CA Congress, 2008.
for dogs at risk of gastric dilatation-volvulus. Prev Vet Med. 2003 Sep 38. Kent M, Glass EN, Acierno M, et. al.: Adult onset acquired myasthenia
12;60(4):319-29. gravis in three Great Dane littermates. J Small Anim Pract. 2008
12. Glickman LT, Glickman NW, Schellenberg DB, et. al.: Incidence of and Dec;49(12):647-50.
breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet 39. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Med Assoc. 2000 Jan 1;216(1):40-5. Book House, NY 2006. p. 271-275.
13. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
242
Great Pyrenees
gait is powerful, smooth and covers lots of ground. Their muscling
and bone is medium in substance. The skull is wedge-shaped, and
almond-shaped eyes are medium in size and pigmented dark brown.
Palpebral margins are darkly pigmented. Ears are V-shaped with
rounded tips, and small-to-medium sized, set at eye level and rest
close to the head. They have a slightly tapering muzzle, no stop,
and the nose and lips are pigmented black. The Great Pyrenees has
a minimal dewlap, a strong medium length neck, topline is level,
thorax is deep and broad, and ribs well sprung. Some abdominal
tuck up is present. The bones of the tail reach the tarsus, the heavily
plumed tapering tail is carried both over the back and low. Legs
The Breed History are straight boned; the single dewclaw (front) and double dewclaw
Originally from Siberia or Central Asia, it is thought that this behind are not removed. Round feet are large and pads are thick.
breed entered Europe at least 1000 years BC. The ancient Asiatic
mastiff-type is believed to be the primary ancestor. Common
lineage may trace to Kuvasz, Kuvac, or Turkish Karabash dogs. As
Recognized Behavior Issues and Traits
Reported breed traits include: Devoted, intelligent, guarding family
an aside, it is reported that this breed, and/or the Pyrenean Mastiff,
and home as they would a sheep flock; quite territorial. Loyal and
when crossed with black English Retrievers may have given rise
fearless, they are sometimes independent, even strong willed, but
to the Newfoundland breed. The first formal breed standard was
known to be gentle and patient with human family members. Need
drawn up in 1927. Great Pyrenees were first registered with AKC in
to begin socialization and obedience training early. Slow to mature.
1933. The Pyrenean Mastiff is a much larger breed, though it likely
Needs open space, has moderate exercise needs but tends to be
arose from similar ancestors. At one point, the Great Pyrenean dog
quiet around the home. Need to keep in a fenced enclosure if off
was close to extinction. They are named after the mountain range
leash. High barking tendency exists in some dogs.
in which much of the breed development took place.
243
ratio versus other breeds. Reported at a frequency of 2.88% in the other breeds. Dorn reports an 8.95x odds ratio for OCD versus other
2004 GPCA Health Survey. OFA reports 1.2% affected.2,6,7,8 breeds.7,8
Glanzmann’s Thrombasthenia (GT): This defect causes frequent Distichiasis: Abnormally placed eyelashes that irritate the
epistaxis, and gingival bleeding during teething in young dogs. cornea and conjunctiva. Can cause secondary corneal ulceration.
Caused by a defect in intrinsic platelet function involving Identified in 1.98% of Great Pyrenees CERF examined by veterinary
glycoprotein complex IIb-IIIa. Affected dogs have normal platelet ophthalmologists between 2000-2005.5
numbers, and normal coagulation panels. Simple autosomal
recessive mode of inheritance. A genetic test is available.9,10 Hypoadrenocorticism (Addison’s Disease): Immune mediated
destruction of the adrenal gland. Typical presentation of lethargy,
Chondrodysplasia: Disproportionate dwarfism caused by a simple poor appetite, vomiting, weakness, and dehydration can occur from
autosomal recessive gene. Causes short limbs and short trunk. 4 months to several years of age. Treatment with DOCA injections
Radiographically, there is metaphyseal flaring of all long bones and or oral fludrocortisone. Reported at a frequency of 1.7% in the
costochondral junctions of the ribs. Vertebral bodies are poorly 2004 GPCA Health Survey.6
ossified, with thin, concave end plates. Affected dogs can also be
deaf. This condition occurs at a low frequency. There is ongoing Entropion: Entropion, a rolling in of the eyelids, can cause corneal
research at UC-Davis to identify the defective gene.11 irritation and ulceration. Identified in 1.49% of Great Pyrenees CERF
examined by veterinary ophthalmologists between 2000-2005.5
Disease Predispositions Corneal Dystrophy: The epithelial/stromal form occurs in the
Otitis Externa: 71.6% of Great Pyrenees have reported an ear breed, causing a bilateral, white to gray, non-inflammatory corneal
infection in the 2004 GPCA Health Survey.6 opacity. Identified in 1.24% of Great Pyrenees CERF examined by
veterinary ophthalmologists between 2000-2005.5
Panosteitis: Self-limiting disease of young, large breed dogs
involving the diaphyseal and metaphyseal areas of the tubular Gastric Dilation/Volvulus (Bloat): Life-threatening twisting of
long bones. Affected dogs show intermittent lameness. Treat with the stomach within the abdomen. Requires immediate veterinary
rest. Reported 5.3x odds ratio versus other breeds. Reported at a attention. Reported at a frequency of 1.0% in the 2004 GPCA
frequency of 39.7% in the 2004 GPCA Health Survey.6,8 Health Survey.6
Persistent Pupillary Membranes: Strands of fetal remnant Deafness: Unilateral or bilateral congenital deafness is reported by
connecting; iris to iris, cornea, lens, or involving sheets of tissue. Strain. Diagnosed by BAER testing. OFA reports a high frequency,
The later three forms can impair vision, and dogs affected with but too few Great Pyrenees have been tested for statistical
these forms should not be bred. Identified in 27.48% of Great accuracy.2,14
Pyrenees CERF examined by veterinary ophthalmologists between
2000-2005.5 Laryngeal Paralysis-polyneuropathy Complex: Affected Great
Pyrenees dogs present at less than 6 months of age with laryngeal
Arthritis: 11.6% of Geat Pyrenees reported arthritis between 4-12.5
paralysis and megaesophagus. Pathology reveals distal axonal
years of age in the 2004 GPCA Health Survey.6
degeneration. Prognosis is poor. An autosomal recessive mode of
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis inheritance is suspected.15
and pyotraumatic dermatitis (hot spots). Reported at a frequency of
8.7% in the 2004 GPCA Health Survey.6 Isolated Case Studies
Hemophilia A: Reported in a male puppy who developed facial
Hypothyroidism: Inherited autoimmune thyroiditis. 6.5% positive and shoulder hematomas and gingival bleeding. Coagulation
for thyroid auto-antibodies based on testing at Michigan State studies revealed normal bleeding and prothrombin times, prolonged
University. (Ave. for all breeds is 7.5%). Reported at a frequency of clotting and activated partial prothrombin times and decreased
6.0% in the 2004 GPCA Health Survey.6,12,13 factor VIII activity. The dam and a female littermate also had
decreased factor VIII activity and were probably carriers of the
Cataracts: Anterior, posterior, and equatorial intermediate cataracts disease.16
predominate in the breed. Identified in 5.69% of Great Pyrenees
CERF examined by veterinary ophthalmologists between 2000-2005. Factor XI Deficiency: Autosomal recessive bleeding disorder
CERF does not recommend breeding any Great Pyrenees with a reported to occur in the breed.17
cataract.5
Congenital Preputial and Penile Deformity: Report of surgical
Osteosarcoma: Malignant long bone cancer. Reported at a correction in a puppy, presenting with dysuria and prepuce edema.
frequency of 4.1% in the 2004 GPCA Health Survey.6 The dog had a stenotic preputial orifice, and an inability to extend
the penis from the prepuce.18
Osteochondrosis (OCD) of the Shoulder: Inherited cartilage
defect of the shoulder joint. Causes lameness in young growing Left Ventricular Outflow Tract-Right Atrial Communication
dogs. Male prevalence. Mild cases may heal on own with rest. (Gerbode Type Defect): Identified in a 6 year old male with
Severe cases require surgery. Reported 42.7x odds ratio versus associated with bacterial endocarditis. Vegetative mural endocardial
244
lesions were observed grossly, and gram-negative coccobacilli 7. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
that were consistent with Bordetella avium-like organisms were veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
observed histopathologically. LV-RA shunt (Gerbode defect) is a rare 2000.
cardiac defect in humans that can be either congenital or, more 8. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
rarely, secondary to septic endocarditis.19
Sep-Oct;38(5):467-77.
9. Boudreaux MK, Lipscomb DL: Clinical, biochemical, and molecular aspects
Craniomandibular Osteopathy: Reported two dogs with
of Glanzmann’s thrombasthenia in humans and dogs. Vet Pathol. 2001
mandibular swelling, pain, fever and, in dog 1, lameness.
May;38(3):249-60.
Radiographs demonstrated extensive, active new bone formation on 10. Lipscomb DL, Bourne C, Boudreaux MK: Two genetic defects in alphaIIb
the ventral aspect of the mandibular bodies of both dogs.20 are associated with type I Glanzmann’s thrombasthenia in a Great Pyrenees
dog: a 14-base insertion in exon 13 and a splicing defect of intron 13. Vet
Cor Triatriatum Dexter: A Young Great Pyrenees with poor growth Pathol 37[6]:581-8 2000 Nov.
and ascites was identified with a septum dividing the right atrium 11. Bingel SA, Sande RD: Chondrodysplasia in five Great Pyrenees. J Am Vet
into two separate chambers. Surgical correction was successful.21 Med Assoc. 1994 Sep 15;205(6):845-8.
12. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
Brachygnathism, Prognathism, Cervical Vertebral Instability, serum thyroid hormone autoantibodies in dogs with clinical signs of
Optic Nerve Hypoplasia, Tricuspid Valve Dysplasia, and von hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
Willebrand’s Disease are reported.22 13. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
14. Strain GM: Deafness prevalence and pigmentation and gender
Genetic Tests associations in dog breeds at risk. Vet J 2004; Jan;167(1):23-32.
Tests of Genotype: Direct test for Glannzmann’s thrombasthenia 15. Gabriel A, Poncelet L, Van Ham L, et. al.: Laryngeal paralysis-polyneu-
(GT) is available from the Auburn Univ-Boudreaux Lab. ropathy complex in young related Pyrenean mountain dogs. J Small Anim
Pract. 2006 Mar;47(3):144-9.
Direct test for Multifocal Retinopathy is available from Optigen. 16. Golden JG, Banknieder AR, Bruestle ME: Hemophilia in a Great Pyrenees.
Mod Vet Pract. 1980 Aug;61(8):671-4
Tests of Phenotype: CHIC Certification: Hip radiographs, patella 17. Fogh JM, Fogh IT: Inherited coagulation disorders. Vet Clin North Am
evaluation, and one of the following: thyroid profile including Small Anim Pract. 1988 Jan;18(1):231-43.
autoantibodies, CERF eye examination, cardiac examination, 18. Olsen, Dennis & Salwei, Rochelle: Surgical Correction of a Congenital
radiographs for elbow dysplasia or shoulder osteochondrosis (OCD), Preputial and Penile Deformity in a Dog. J Am Anim Hosp Assoc
and brainstem audio-evoked response (BAER) test for deafness. (See 37[2]:187-192 Mar-Apr’01
19. Ramirez GA, Espinosa de los Monteros A, Rodriguez F, Weisbrode
CHIC website; www.caninehealthinfo.org).
SE, Jaber JR, Herraez P: Left ventricular outflow tract-right atrial
communication (Gerbode type defect) associated with bacterial
Miscellaneous endocarditis in a dog. Vet Pathol. 2003 Sep;40(5):579-82.
• Breed name synonyms: Pyrenean Mountain Dog, Le Chien des 20. Franch J, Cesari JR, Font J: Craniomandibular osteopathy in two
Pyrénées, Le Grande Chien des Montagnes, Pyr, historical names: Pyrenean mountain dogs. Vet Rec. 1998 Apr 25;142(17):455-9.
Pyrenean bearhound, Pyrenean wolf dog. 21. Mitten RW, Edwards GA & Rishniw M: Diagnosis and management of
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), cor triatriatum dexter in a Pyrenean mountain dog and an Akita Inu. Aust
Vet J. 2001 Mar;79(3):177-80.
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
22. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
• AKC rank (year 2008): 62 (1,444 registered)
Ackerman. p. 221. AAHA Press, 1999.
• Internet resources: Great Pyrenees Club of America: 23. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
http://clubs.akc.org/gpca/ Book House, NY 2006. p. 276-280.
The Pyrenean Mountain Dog Club of Great Britain:
www.pmdc.org.uk
Great Pyrenees Club of Canada: http://pyrcanada.com
Great Pyrenees Club of America’s Health Information Center:
www.gpcahealth.org
References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Grahn BH, Cullen CL: Retinopathy of Great Pyrenees dogs: fluorescein
angiography, light microscopy and transmitting and scanning electron
microscopy. Vet Ophthalmol. 2001 Sep;4(3):191-9.
4. B.H. Grahn; H. Philibert; C.L. Cullen; D.M. Houston; H.A. Semple; S.M.
Schmutz: Multifocal Retinopathy of Great Pyrenees Dogs. Vet Comp
Ophthalmol 1[4]:211-221 Dec’98
5. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
6. GPCA Health Committee: 2004 GPCA Health Survey Report. Feb. 2006.
245
(Greater) Swiss
Mountain Dog
without throatiness. The topline is level, and the thorax is deep
with well-sprung ribs. The tail reaches the tarsus and is carried low
at rest, though during exercise it is elevated to topline. Legs are
straight boned, feet are round and the toes are well arched. Rear
dewclaws are generally removed. Gait should reflect power and be
ground covering, and for their size this breed is very agile.
Coat: Double coated, the inner coat is thick and short, the outer
Inherited Diseases
Hip Dysplasia: Polygenically inherited trait causing degenerative
coat is dense and hard (< 2” long). Coat color is a tri-color; a base joint disease and hip arthritis. OFA reports 19.1% affected.1
of black with rust and white markings. Symmetrical rust markings
of brows, cheek and chest, on the four legs and tail, with white Elbow Dysplasia: Polygenically inherited trait causing elbow
highlights of muzzle and blaze are standard. On the chest, a cross, arthritis. OFA reports 11.3% affected.1
and the tail tip and feet white markings are also important; also on
the neck a collar marking is permitted. Patella Luxation: Polygenically inherited laxity of patellar ligaments,
causing luxation, lameness, and later degenerative joint disease.
Longevity: 7-9 years Treat surgically if causing clinical signs. OFA reports 0.5% affected.1
Points of Conformation: Being a powerful draft dog, the
constitution is that of a heavily muscled and boned dog. The Disease Predispositions
skull is broad and flat, and the muzzle is blunt, and there are only Distichiasis: Abnormally placed eyelashes that irritate the cornea
minor flews. The medium-sized ears are triangular with rounded and conjunctiva. Can cause secondary corneal ulceration. Identified
tips, and are high-set and folded so that the ears lay close to the in 31.82% of Greater Swiss Mountain Dogs CERF examined by
head. Eyes are dark brown with a gentle expression, and they are veterinary ophthalmologists between 2000-2005.2
medium in size, with closely fitting black palpebral margins. The
Urinary Incontinence: Greater Swiss Mountain Dogs have
nose is also black. The neck is moderate in length and muscularity,
increased risk to develop urinary incontinence. Treat with DES (for
246
females) or phenylpropanolamine. Reported at a frequency of 11.0%
in the 2000-2001 GSMDCA Health Survey, with a frequency of
Genetic Tests
Tests of Genotype: none
20.0% in females.3
Tests of Phenotype: CHIC Certification: Required testing includes
Humeral Osteochondritis Dissecans: Polygenically inherited hip and elbow radiographs, and CERF eye examination. Optional
cartilage defect of the humeral head. Causes shoulder joint pain recommended tests include shoulder radiographs, and anecdotal
and lameness in young growing dogs. Mild cases can resolve data on epilepsy, splenic torsion, and gastric torsion. (See CHIC
with rest, while more severe cases require surgery. Reported at website; www.caninehealthinfo.org).
a frequency of 5.4% in the 2000-2001 GSMDCA Health Survey.
Diagnosed in 15.3% of Greater Swiss Mountain Dogs who had Recommend thyroid profile including autoantibodies, patella
shoulder radiographs taken. Unknown mode of inheritance.3 evaluation and cardiac evaluation.
Umbilical Hernia: Congenital opening in the body wall from where
the umbilical cord was attached. Reported at a frequency of 9.6% Miscellaneous
in the 2000-2001 GSMDCA Health Survey. Unknown mode of • Breed name synonyms: Swissy, Grosser Schweizer Sennenhund,
inheritance.3 Swiss Mountain Dog, Great Swiss Cattle Dog, Great Swiss
Mountain Dog, Greater Swiss Mountain dog.
Cataracts: Anterior cortex punctate and posterior cortex • Registries: AKC, CKC, NKC (National Kennel Club), FCI.
intermediate cataracts predominate in the breed. Identified in 8.12% • AKC rank (year 2008): 89 (715 dogs registered)
of Greater Swiss Mountain Dogs CERF examined by veterinary • Internet resources: Greater Swiss Mountain Dog Club of
ophthalmologists between 2000-2005. CERF does not recommend America: www.gsmdca.org
breeding any Greater Swiss Mountain Dog with a cataract.2 Great Swiss Mountain Dog Club of Great Britain:
www.gsmd.org.uk
Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting
of the stomach within the abdomen. Requires immediate veterinary
attention. Reported at a frequency of 5.3% in the 2000-2001
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
GSMDCA Health Survey. Unknown mode of inheritance.3 2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
Inherited Epilepsy: Grand-mal seizures. Control with 3. Greater Swiss Mountain Dog Club of America: 2000 & 2001 GSMDCA
anticonvulsant medication. Reported at a frequency of 4.6% in the Breed Health Survey. 2002.
2000-2001 GSMDCA Health Survey. Unknown mode of inheritance.3 4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Persistent Pupillary Membranes: Strands of fetal remnant Vet Med Assoc 2002 Feb 15;220(4):466-71.
connecting; iris to iris, cornea, lens, or involving sheets of tissue. 5. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
The later three forms can impair vision, and dogs affected with Population and Animal Health, Michigan State University. April, 2007.
these forms should not be bred. Identified in 3.97% of Greater 6. Thomas WB: Movement Disorders in Small Animals: Shaking, Head
Swiss Mountain Dogs CERF examined by veterinary ophthalmolo- Bobbing, Fly Biting, and Dancing Dobermans. Proceedings, 2002 Tufts
Animal Expo. 2002.
gists between 2000-2005.2
7. Flückiger M, Damur-Djuric N, Steffen F: Lumbosacral Transitional
Vertebra In the Dog: Prevalence in Different Breeds and in Dogs Suffering
Hypothyroidism: Inherited autoimmune thyroiditis. 3.7% positive
From Cauda Equine Compression Syndrome. Proceedings, 2004 World Small
for thyroid autoantibodies based on testing at Michigan State
Animal Veterinary Association Congress. 2004.
University. (Ave. for all breeds is 7.5%).4,5 8. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 222. AAHA Press, 1999.
Fly-biting Seizures/Partial Seizures: Seen at an increased 9. Heimann M, Beco L, Petein M, et. al.: Canine hyperplastic intraepidermal
frequency in the breed. Control with anticonvulsant medication. pustular and suprabasal acantholytic dermatosis with features of human
Reported at a frequency of 1.3% in the 2000-2001 GSMDCA Health pemphigus vegetans. Vet Pathol. 2007 Jul;44(4):550-5.
Survey. Unknown mode of inheritance.3,6 10. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 281-283.
Lumbosacral Transitional Vertebra (LTV): The breed has a
significantly greater incidence of LTV than other breeds. This can lead
to pain and neurological impairment from cauda equina syndrome.7
Conformation Points: This muscular, highly athletic dog has a long, Normal Systemic Blood Pressure Values are about 20 mmHg
flat, medium weight skull with a slight stop (dolichocephalic skull), higher than other breeds. Normal range for hematocrit varies with
dark eyes, small fine partially upright ears, a long muscular neck, geographic location, but is generally between 50-65%. This range is
very deep chest and well-sprung rib cage, with moderately arched higher than for many breeds.5
loins and a thin waist. They have fine-boned long limbs, with small
Up to 26% of all Greyhounds with normal blood clotting
compact feet well knuckled up, and carry their long tapering thin
parameters can show excessive bleeding after injury or surgical
tail low.
procedures. This is due to weaker clot strength (kinetics) and
increased fibrinolysis in the breed.6
Recognized Behavior Issues and Traits
The greyhound is known to be a very affectionate dog; gentle, but Thyroid Values: Greyhounds, as with all sight hounds, have lower
somewhat cautious around strangers. In the home environment, normal ranges for T4 and T3 concentrations compared to other
it requires a low to average amount of exercise only, but outdoors breeds. The following are average values:7
enjoys a good free run. It has a strong chase instinct, and this T4: 13.9 +/- 6.3 nmol/L
should be kept in mind when around other (smaller) pets and fT4: 11.6 +/- 6.5 pmol/L
248
cTSH: 0.20 +/- 0.21 ng/ml Thigh Alopecia: As Greyhounds age, they are prone to symmetrical
T4 after TSH admin: 36.4 +/- 10 nmol/L alopecia over their thigh areas. Reported at 20% in a pathological
fT4 after TSH admin: 16.7 +/- 7.2 pmol/L study of Greyhounds. Reported at a frequency of 16.3% in a
web-based Greyhound health survey.12,18
Greyhounds have higher normal creatinine levels than
non-Greyhounds, with a mean of 1.6 mg/dL (range 1.2-1.9 mg/dL).8 Endocardiosis (Mitral Valvular Disease): A pathological study of
deceased Greyhounds found that 10.4% had signs of endocardiosis
Drug Sensitivities or mitral valvular thickening. No correlation to clinical signs or
Anesthesia: Sight hounds require particular attention during heart disease were available. Heart murmers were reported at a
anesthesia. Their lean body conformation with high surface-area- frequency of 5.3% in a web-based Greyhound health survey.12,18,19
to-volume ratio predisposes them to hypothermia during
Vitreous Degeneration: Liquefaction of the vitreous gel which
anesthesia. Impaired biotransformation of drugs by the liver
may predispose to retinal detachment. Reported at a frequency of
results in prolonged recovery from barbiturate and thiobarbiturate
31% in a survey of retired racing Greyhounds. Identified in 3.42%
intravenous anesthetics.9
of Greyhounds CERF-examined by veterinary ophthalmologists
Deficient hydroxylation of propofol by hepatic cytochrome between 2000-2005. CERF does not recommend breeding any
P-450 isoforms may contribute to slow clearance of propofol by Greyhound with the condition.16,17
greyhounds.10
Chronic Glomerulonephritis: Chronic kidney diease was identified
microscopically on necropsy of 6.9% of Greyhounds in one study,
Inherited Diseases however it was found in 64% of those over 7.5 years of age. No
Hip Dysplasia: Polygenically inherited trait causing degenerative correlation to clinical disease or azotemia was investigated. Dorn
joint disease and hip arthritis. OFA reports 2.1% affected. Reported reports a 5.42x odds ratio for kidney disease versus other breeds.15,18
at a frequency of 0.6% in a web-based Greyhound health survey.11,12
Osteosarcoma: Malignant bone cancer, usually affecting the limbs.
Elbow Dysplasia: Polygenically inherited trait causing elbow Reported at a frequency of 5.9% in a web-based Greyhound health
arthritis. Too few Greyhounds have been evaluated by OFA to survey. The proximal humerus was the most frequent location,
determine an accurate frequency.11 with the distal radius, proximal tibia, distal tibia, distal femur, and
proximal femur the other locations reported. Another study showed
Patella Luxation: Polygenically inherited trait causing stifle a frequency of 6.2% with an average age of 9.9 years.12,20
instability and arthritis. Too few Greyhounds have been evaluated
by OFA to determine an accurate frequency.11 Digital Keratoma (Corns): Greyhounds have a predilection
to forming footpad corns, which are painful, hard keratin
Polyneuropathy: A rare, autosomal recessive polyneuropathy accumulations in the deep dermis and epidermis. There is a male
presenting with progressive weakness and gait abnormalities predilection with over 90% affecting digits 3 or 4 in the thoracic
between 3 and 9 months of age is identified in conformation limbs. Remove when identified. Reported at a frequency of 5.9% in
Greyhounds. Pathology reveals mild to marked reduction in nerve a web-based Greyhound health survey.12,21,22
fiber density, axonal swelling, and secondary muscle atrophy. The
disease is caused by a mutation in the NDRG1 gene. Limited testing Allergic Dermatitis: Inhalant or food allergies. Presents with
did not reveal the mutation in racing Greyhound lines. A direct pruritis and pyotraumatic dermatitis (hot spots). Inhalant allergy
genetic test is available.13 was reported at 1.4% and food allergy at 5.5% in a web-based
Greyhound health survey.12
Disease Predispositions
Supernumerary Teeth: One study found a 36.4% incidence of Cardiac Arrhythmias: In racing Greyhounds, maximal sprinting
supernumerary teeth; most often maxillary first premolars.14 increases the incidence of cardiac arrhythmias during the early
recovery period: mainly sinus tachycardia, ventricular extrasystoles,
Periodontal Disease: Dorn reports a 8.95x odds ratio for developing ventricular tachycardia, and electrical alternans.23
periodontal disease versus other breeds.15
Progressive Retinal Atrophy (PRA)/Retinal Degeneration:
Osteoarthritis: Degenerative joint disease accompanied by pain Undetermined mode of inheritance. PRA in the greyhound may
and lameness. Treat with anti-inflammatory drugs. Reported at a begin as early as 12 months of age, and affected dogs may progress
frequency of 17.5% in a web-based Greyhound health survey.12 to complete blindness at a relatively young age. Nyctalopia (night
blindness) is not an initial finding in affected Greyhounds. Reported
Cataracts: Posterior cortex imtermediate and anterior cortex at a frequency of 4% in a survey of retired racing Greyhounds. CERF
punctate cataracts predominate in the breed. Reported at a does not recommend breeding any Greyhound with PRA.16,17,24
frequency of 17% in a survey of retired racing Greyhounds.
Identified in 5.43% of Greyhounds CERF-examined by veterinary Chronic Superficial Keratitis (Pannus): A chronic corneal
ophthalmologists between 2000-2005. CERF Does not recommend inflammatory process that can cause vision problems due to
breeding any Greyhound with a cataract.16,17 corneal pigmentation. Treatment with topical ocular lubricants and
anti-inflammatory medication. One study found Greyhounds to be
a breed at increased risk. Reported at a frequency of 4% in a survey
249
of retired racing Greyhounds. Identified in 4.11% of Greyhounds Primary Lens Luxation: Often progresses to secondary glaucoma.
CERF-examined by veterinary ophthalmologists between Identified in 1.37% of Greyhounds CERF examined by veterinary
2000-2005. CERF does not recommend breeding any Greyhound ophthalmologists between 2000-2005. CERF does not recommend
with pannus.16,17,25 breeding any Greyhound with lens luxation.16
Sesamoid Disease: Greyhounds (especially racing Greyhounds) can Cranial Cruciate Ligament (ACL) Rupture: Traumatic tearing
develop acute to chronic forelimb lameness due to fragmentation of the ACL in the stifle, causing lameness and secondary arthritis.
of the 2nd and 7th metacarpophalangeal sesamoid bones, with Treat with surgery. Reported at a frequency of 1.1% in a web-based
secondary degenerative joint disease. One study showed that a Greyhound health survey.12
reduction in number of vascular foramina is correlated to increased
risk for the disease.26 Lymphoma/Lymphosarcoma: Malignant cancer of lymphoid tissue.
Can be B-cell or T-cell (mycosis fungoides) disease. Reported at a
Central Tarsal Bone Fracture: Racing Greyhounds can develop frequency of 1.1% in a web-based Greyhound health survey.12
factures of the central tarsal bone secondary to accumulation and
coalescence of branching arrays of fatigue microcracks. This may Hemangiosarcoma: A malignant cancer of red blood cells, usually
occur more frequently in the right hind limb; the outside limb involving the spleen, liver, heart, or bone marrow. Greyhounds are
when racing.27,28,29 found to be at increased risk of developing visceral and non-visceral
hemangiosarcomas and hemangiomas versus other breeds.
Otitis Externa (Chronic Ear Infections): Can also be secondary to Reported at a frequency of 1.1% in a web-based Greyhound health
allergic skin disease. Bacterial, yeast, or mixed infection. Reported at survey.12,36
a frequency of 2.5% in a web-based Greyhound health survey.12
Cutaneous and Renal Glomerular Vasculopathy (CRGV)
Inflammatory Bowel Disease (IBD): An immune mediated disorder (Alabama Rot): A vascular disease of unknown etiology affecting
presenting as gastrointestinal inflammation and irritation. It can the skin and kidneys of racing Greyhounds. Affected dogs can
present with vomiting, diarrhea, or weight loss. Affected dogs can present with symptoms of cutaneous ulcers of the extremities,
usually be controlled with diet and/or medications. Reported at a thrombocytopenia, and in advanced cases acute renal insufficiency.
frequency of 2.4% in a web-based Greyhound health survey.12 There is no evidence of infectious or immune-complex disease
in the pathogenesis. Prognosis for recovery is poor if azotemia is
Idiopathic Epilepsy (Inherited Seizures): Can be generalized or present.37,38,39
partial seizures. Control with anti-seizure medication. Reported at a
frequency of 2.4% in a web-based Greyhound health survey.12 Juvenile Endocrine and Exocrine Pancreatic Atrophy: Several
cases of Greyhounds with compound failure of the endocrine and
Lumbosacral Stenosis/Cauda Equina Syndrome: Narrowing of the exocrine pancreas have been identified. Cases range from 4 weeks
bony canal at the end of the spinal cord, can cause pain, ataxia, and to 18 months of age, with a median of 12 weeks. Clinical signs are
progressive neurological impairment. Reported at a frequency of typical for both endocrine and exocrine diseases. Pathology reveals
2.0% in a web-based Greyhound health survey.12 acinar cell apoptosis, zymogen granule loss, cytoplasmic clearing
or vacuolar change, lobular atrophy, islet loss, and lymphocytic or
Intervertebral Disc Disease (IVDD): Spinal cord disease due to lymphoplasmacytic pancreatitis.40
prolapsed disk material. Clinical signs include back pain, scuffing
of paws, spinal ataxia, limb weakness, and paralysis. Reported at a Greyhound Meningoencephalitis: Rare, non-suppurative
frequency of 2.0% in a web-based Greyhound health survey.12 meningoencephalitis primarily affecting young greyhounds
between 4-18 months of age. Affected dogs develop either acute or
Symmetrical Lupoid Onychodystrophy (SLO): Disorder causing insidious neurological signs including head tilting, circling, ataxia,
loss of toenails. Onset between 2-8 years of age affecting 1-2 nails, recumbency and blindness. Pathological changes include cerebral
then progressing to all toenails within 2-9 weeks. Requires lifelong cortex perivascular cuffing and gliosis. Gene expression studies
treatment with oral fatty acid supplementation +/- prednisone. identify an autoimmune pathogenesis. There is no treatment.41,42,43
Reported at a frequency of 1.8% in a web-based Greyhound health
survey.12 Malignant Hyperthermia: Exercise and anesthesia induced
malignant hyperthermia is reported in isolated Greyhound
Hypothyroidism: Inherited autoimmune thyroiditis. 1.7% positive cases.44,45,46,47
for thyroid autoantibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5). Reported at a frequency of Renal Arteriosclerosis: Endothelial damage to the renal arteries
11% in a web-based Greyhound health survey.12,30,31,32 due to hemodynamic forces of sheer stress and pressure pulse
velocity is identified in young, race-trained Greyhounds. Correlation
Babesiosis: Greyhounds comprise a significant percentage of dogs to later kidney disease is not determined.48
seropositive for Babesia canis vogeli. Reported at a frequency
of 2.6% in a web-based Greyhound health survey. Greyhounds Brachygnathism, Cryptorchidism, Factor VIII Deficiency, Gastric
presenting with immune-mediated hemolytic anemia or Dilation/Volvulus, Megaesophagus, Optic Nerve Hypoplasia,
thrombocytopenia should be screened for babesiosis.12,33,34,35 Osteochondritis Dessicans of the stifle and shoulder, Spina
Bifida, and von Willebrand’s disease are reported.49
250
Isolated Case Studies 7. Gaughan KR, Bruyette DS: Thyroid function testing in Greyhounds. Am J
Vet Res 2001;62:1130–1133.
Acute B cell Lymphoblastic Leukaemia: A 12 week old Greyhound 8. Feeman WE 3rd, Couto CG, & Gray TL: Serum creatinine concentrations in
with lethargy, inappetence, shifting lameness, pyrexia and retired racing Greyhounds. Vet Clin Pathol. 2003;32(1):40-2.
hepatosplenomegaly had anaemia, thrombocytopenla, neutropenia 9. Court MH: Anesthesia of the sighthound. Clin Tech Small Anim Pract
and large numbers of atypical mononuclear leucocytes. The pup 1999 Feb;14(1):38-43.
died 4 days after presentation.50 10. Court MH, Hay-Kraus BL, Hill DW, Kind AJ, Greenblatt DJ. Propofol
hydroxylation by dog liver microsomes: assay development and dog breed
Persistent Right Aortic Arch (PRAA): Repeat matings between differences. Drug Metab Dispos 1999 Nov;27(11):1293-9
two Greyhounds produced puppies with regurgitation and 11. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
secondary megaesophagus due to PRAA. Surgery is curative. 12. Lord LK, Yaissle JE, Marin L, et. al.: Results of a web-based
Greyhounds are not a breed reported with an increased incidence of health survey of retired racing Greyhounds. J Vet Intern Med. 2007
this inherited congenital disorder.51 Nov-Dec;21(6):1243-50.
13. Drögemüller C, Becker D, Kessler B, et. al.: A deletion in the N-myc
Avulsion of the Tibial Tubercle: Isolated cases are reported. In downstream regulated gene 1 (NDRG1) gene in Greyhounds with
one report, six of seven Greyhound pups aged 5-1/2 months old polyneuropathy. PLoS One. 2010 Jun 22;5(6):e11258.
14. Dole RS, Spurgeon TL. Frequency of supernumerary teeth in a
avulsed their tibial tubercle. Avulsion was bilateral in four of the
dolichocephalic canine breed, the greyhound. Am J Vet Res 1998
dogs. Osteochondrosis of the cranioproximal tibial physis was Jan;59(1):16-7
identified pathologically.52,53 15. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Genetic Tests 2000.
Tests of Genotype: Direct test for polyneuropathy is available from 16. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Optigen. College of Veterinary Ophthalmologists. ACVO, 2007.
17. Lynch GL: Ophthalmic examination findings in a group of retired racing
Direct test for black mask is available from HealthGene and VetGen. Greyhounds. Vet Ophthalmol. 2007 Nov-Dec;10(6):363-7.
18. Schoning P & Cowan LA: Gross and microscopic lesions of 230 Kansas
Tests of Phenotype: CHIC Certification: Cardiac evaluation greyhounds. J Vet Diagn Invest. 1993 Jul;5(3):392-7.
by a cardiologist, and blood sample donation to the CHIC DNA 19. Schoning PR: Endocardiosis and other heart disease in greyhounds.
Zentralbl Veterinarmed A. 1995 Apr;42(2):99-104.
repository. (See CHIC website: www.caninehealthinfo.com)
20. Rosenberger JA, Pablo NV, Crawford PC, et. al.: Prevalence of and
intrinsic risk factors for appendicular osteosarcoma in dogs: 179 cases
Recommend hip and elbow radiographs, CERF eye examination,
(1996-2005). J Am Vet Med Assoc. 2007 Oct 1;231(7):1076-80.
patella evaluation, and thyroid profile including autoantibodies. 21. Guilliard MJ, Segboer I & Shearer DH: Corns in dogs; signalment,
possible aetiology and response to surgical treatment. J Small Anim Pract.
Miscellaneous 2010 Mar;51(3):162-8.
• Breed Name Synonyms: none 22. Balara JM, McCarthy RJ, Kiupel M, et. al.: Clinical, histologic, and
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), immunohistochemical characterization of wart-like lesions on the paw
ANKC (Australian National Kennel Club), NKC (National Kennel Club) pads of dogs: 24 cases (2000-2007). J Am Vet Med Assoc. 2009 Jun
15;234(12):1555-8.
• AKC Rank (Year 2008): 129 (183 dogs registered)
23. Ponce Vazquez J, Pascual Gomez F, Alvarez Badillo A, Dolz Luna JF,
• Internet resources: Greyhound Club of America: Rodriguez Rodriguez LP. Cardiac arrhythmias induced by short-time
www.greyhoundclubofamerica.org maximal dynamic exercise (sprint): a study in greyhounds. Rev Esp Cardiol
National Greyhound Association (Racing Association, the sole 1998 Jul;51(7):559-65
registry for racing greyhounds): www.ngagreyhounds.com 24. Slatter DH, Blogg JR, & Constable IJ: Retinal degeneration in
Greyhound Rescue Adoption Service directory of Adoption Greyhounds. Aust Vet J. 1980 Mar;56(3):106-15.
Agencies: www.greyhound.org 25. Chavkin MJ, Roberts SM, Salman MD, et. al.: Risk factors for
development of chronic superficial keratitis in dogs. J Am Vet Med Assoc.
References 1994 May 15;204(10):1630-4.
26. Daniel A, Read RA & Cake MA: Vascular foramina of the metacarpopha-
1. Page A, Edmunds G, & Atwell RB: Echocardiographic values in the
langeal sesamoid bones of Greyhounds and their relationship to sesamoid
greyhound. Aust Vet J. 1993 Oct;70(10):361-4.
disease. Am J Vet Res. 2008 Jun;69(6):716-21.
2. Snyder PS, Sato T, Atkins CE. A comparison of echocardiographic indices
27. Tomlin JL, Lawes TJ, Blunn GW, et. al.: Fractographic examination of
of the nonracing, healthy greyhound to reference values for other breeds.
racing greyhound central (navicular) tarsal bone failure surfaces using
Vet Radiol Ultrasound 1995;36:387-392
scanning electron microscopy. Calcif Tissue Int. 2000 Sep;67(3):260-6.
3. Marin LM, Brown J, McBrien C, et. al.: Vertebral heart size in retired
28. Johnson KA, Muir P, Nicoll RG, et. al.: Asymmetric adaptive modeling of
racing Greyhounds. Vet Radiol Ultrasound. 2007 Jul-Aug;48(4):332-4.
central tarsal bones in racing greyhounds. Bone. 2000 Aug;27(2):257-63.
4. Fabrizio F, Baumwart R, Iazbik MC, et. al.: Left basilar systolic murmur in
29. Boudrieau RJ, Dee JF, & Dee LG: Central tarsal bone fractures in the
retired racing greyhounds. J Vet Intern Med. 2006 Jan-Feb;20(1):78-82.
racing Greyhound: a review of 114 cases. J Am Vet Med Assoc. 1984 Jun
5. Steiss JE, Brewer WG, Welles E, Wright JC: Hematologic and serum
15;184(12):1486-91.
biochemical reference values in retired Greyhounds. Compend Cont Educ
30. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
2000;22:243–248.
serum thyroid hormone autoantibodies in dogs with clinical signs of
6. Vilar P, Couto CG, Westendorf N, et. al.: Thromboelastographic tracings
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
in retired racing greyhounds and in non-greyhound dogs. J Vet Intern Med.
31. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
2008 Mar-Apr;22(2):374-9.
for Population and Animal Health, Michigan State University. April, 2007.
251
32. Sist MD, Refsal KR & Nachreiner RF: A Laboratory Survey of
Autoimmune Thyroiditis and Hypothyroidism in Selected Sight Hound
Breeds. Proceedings of the 2009 Tufts’ Canine and Feline Breeding and
Genetics Conference. 2009.
33. Taboada J, Harvey JW, Levy MG, Breitschwerdt EB. Seroprevalence
of babesiosis in Greyhounds in Florida. J Am Vet Med Assoc 1992 Jan
1;200(1):47-50
34. Birkenheuer AJ, Correa MT, Levy MG, et. al.: Geographic distribution of
babesiosis among dogs in the United States and association with dog bites:
150 cases (2000-2003). J Am Vet Med Assoc. 2005 Sep 15;227(6):942-7.
35. Breitschwerdt EB, Malone JB, MacWilliams P, et. al.: Babesiosis in the
Greyhound. J Am Vet Med Assoc. 1983 May 1;182(9):978-82.
36. Schultheiss PC: A retrospective study of visceral and nonvisceral
hemangiosarcoma and hemangiomas in domestic animals. J Vet Diagn
Invest. 2004 Nov;16(6):522-6.
37. Hertzke DM, Cowan LA, Schoning P, et. al.: Glomerular ultrastructural
lesions of idiopathic cutaneous and renal glomerular vasculopathy of
greyhounds. Vet Pathol. 1995 Sep;32(5):451-9.
38. Cowan LA, Hertzke DM, Fenwick BW, et. al.: Clinical and clinicopatho-
logic abnormalities in greyhounds with cutaneous and renal glomerular
vasculopathy: 18 cases (1992-1994). J Am Vet Med Assoc. 1997 Mar
15;210(6):789-93.
39. Carpenter JL, Andelman NC, Moore FM, et. al.: Idiopathic cutaneous
and renal glomerular vasculopathy of greyhounds. Vet Pathol. 1988
Nov;25(6):401-7.
40. Brenner K, Harkin KR, Andrews GA, et. al.: Juvenile pancreatic
atrophy in Greyhounds: 12 cases (1995-2000). J Vet Intern Med. 2009
Jan-Feb;23(1):67-71.
41. Daly P, Drudy D, Chalmers WS, et. al.: Greyhound meningoencephalitis:
PCR-based detection methods highlight an absence of the most likely
primary inducing agents. Vet Microbiol. 2006 Dec 20;118(3-4):189-200.
42. Callanan JJ, Mooney CT, Mulcahy G, et. al.: A novel nonsuppurative
meningoencephalitis in young greyhounds in Ireland. Vet Pathol. 2002
Jan;39(1):56-65.
43. Greer KA, Daly P, Murphy KE, et. al.: Analysis of gene expression in brain
tissue from Greyhounds with meningoencephalitis. Am J Vet Res. 2010
May;71(5):547-54.
44. Kirmayer AH, Klide AM, & Purvance JE: Malignant hyperthermia in a
dog: case report and review of the syndrome. J Am Vet Med Assoc. 1984
Nov 1;185(9):978-82.
45. Dickinson PJ & Sullivan M: Exercise induced hyperthermia in a racing
greyhound. Vet Rec. 1994 Nov 19;135(21):508.
46. Leary SL, Anderson LC, Manning PJ, et. al.: Recurrent malignant
hyperthermia in a Greyhound. J Am Vet Med Assoc. 1983 Mar
1;182(5):521-2.
47. Bagshaw RJ, Cox RH & Knight DH: Malignant hyperthermia in a
Greyhound. J Am Vet Med Assoc. 1978 Jan 1;172(1):61-2.
48. Bjotvedt G, Hendricks GM, & Brandon TA: Hemodynamic basis of renal
arteriosclerosis in young greyhounds. Lab Anim Sci. 1988 Feb;38(1):62-7.
49. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 222, AAHA Press, 1999.
50. Adams J, Mellanby RJ, Villiers E, et. al.: Acute B cell lymphoblastic
leukaemia in a 12-week-old greyhound. J Small Anim Pract. 2004
Nov;45(11):553-7.
51. Gunby JM, Hardie RJ, & Bjorling DE: Investigation of the potential
heritability of persistent right aortic arch in Greyhounds. J Am Vet Med
Assoc. 2004 Apr 1;224(7):1120-2, 1111.
52. Skelly CM, McAllister H, & Donnelly WJ: Avulsion of the tibial tuberosity
in a litter of greyhound puppies. J Small Anim Pract. 1997 Oct;38(10):445-9.
53. Power JW: Avulsion of the tibial tuberosity in the greyhound. Aust Vet J.
1976 Nov;52(11):491-5.
54. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. pp 177-179.
252
Harrier
or heavy, feet are round, well knuckled up and pads are tough and
thick. Gait is low, forward and looks effortless.
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: none
• Registries: AKC, FCI, CKC, UKC, ARHA, SKC, AMHB (Association of
Masters of Harriers and Beagles)
• AKC rank (year 2008): 155 (35 dogs registered)
• Breed resources: Harrier Club of America:
www.harrierclubofamerica.com
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Bagley RS: Differential Diagnosis of Animals with Intracranial Disease,
Part 2: Diseases of the Brain Stem, Cranial Nerves, and Cerebellum.
Proceedings, Atlantic Coast Veterinary Conference 2002.
4. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 203. AAHA Press, 1999.
5. Hoppe A, Karlstam E: Renal dysplasia in boxers and Finnish harriers. J
Small Anim Pract. 2000 Sep;41(9):422-6.
6. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 180-183.
254
Havanese
Front and rear dewclaws may be removed, limbs are straight boned,
and the feet have well developed pads; toes are well arched up.
Genetic Tests
Tests of Genotype: Direct test for black/chocolate is available from
VetGen.
Recommended tests include blood ammonia and bile acids test for
PSS, elbow radiographs, thyroid profile including autoantibodies,
and cardiac evaluation.
Miscellaneous
• Breed name synonyms: Havana Silk Dog (historical), Spanish Silk
Dog (historical), Bichon Havanais.
• Registries: AKC, UKC, ANKC (Australian National Kennel Club),
NKC (National Kennel Club)
• AKC rank (year 2008): 36 (4,435 dogs registered)
• Internet resources: Havanese Club of America:
www.havanese.org
Havanese Fanciers of Canada: www.havanesefanciers.com
Havanese Club of Great Britain: www.havaneseclub.co.uk
256
Ibizan Hound
is well tucked up, and the thin, low-set tail reaches to the tarsus
and may be curved, ring or saber shaped. The tail is carried high
while in action. Limbs are straight and long, fine-boned, and the
hare-type feet have thick pads and white nails. Characteristically,
there is lots of interdigital hair. The gait is springy, fairly high, and
appears effortless. This breed has the ability to jump high and wide,
and is as fast as any sight hounds. The eyes are small, oblique and
amber to caramel in color. The ears may rest folded when the dog is
relaxed. Front dewclaws may be removed.
Genetic Tests
Tests of Genotype: none
258
Icelandic Sheepdog
triangular when seen from above or the side, with a defined stop.
Scissors bite. Eyes are medium size and almond shaped. Level back,
muscular and strong. Forelegs are straight, parallel and strong,
with single or double dewclaws. Hindlegs are also straight, with
double dewclaws being more desirable. The gait displays agility
and endurance with good driving action covering the ground
effortlessly.
Weight: 20-30 pounds (9-14 kg). Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. Too few Icelandic Sheepdogs have been screened by OFA
Coat: Double coat, thick and weatherproof. There are two types: to determine an accurate frequency.2
short–haired and long-haired. Short–haired: The outer coat
of medium length, fairly coarse, with a thick, soft undercoat. Patella Luxation: Polygenically inherited laxity of patellar
Long–haired: The outer coat is longer than the above, fairly coarse, ligaments, causing luxation, lameness, and later degenerative joint
with a thick, soft undercoat. In both lengths, the hair is shorter on disease. Treat surgically if causing clinical signs. Too few Icelandic
the face, top of the head, ears and front of the legs; and longer on Sheepdogs have been screened by OFA to determine an accurate
the neck, chest and back of the thighs. Several colors are permitted frequency.2
but a single color should always be predominant. The predominant
colors are: various shades of tan, ranging from cream to reddish Disease Predispositions
brown; chocolate brown, grey, and black. White always accompanies Persistent Pupillary Membranes: Strands of fetal remnant
the predominant color. The most common white markings, which connecting; iris to iris, cornea, lens, or involving sheets of tissue.
are often irregular, are a blaze or a part of the face, collar, chest, The later three forms can impair vision, and dogs affected with
socks of varying lengths and tip of tail. On tan and grey dogs, a these forms should not be bred. Identified in 5.02% of Icelandic
black mask, black tips to the outer hairs and even occasional black Sheepdogs CERF examined by veterinary ophthalmologists between
hairs often occur. Black (tri–color) dogs have a black coat, white 2000-2005.3
markings as mentioned above and traditional markings in any of
the various tan colors on the cheeks, over the eyes (eyebrows) and Entropion: A rolling in of the eyelids that can cause corneal
on the legs. irritation and ulceration. Entropion is reported in 1.83% of Icelandic
Sheepdogs CERF examined by veterinary ophthalmologists between
Longevity: Around 12 years. 2000-2005.3
Points of Conformation: The Icelandic Sheepdog is a Nordic Cataracts: Cortical and capsular cataracts predominate in the
herding Spitz, slightly under medium sized with prick ears and a breed. Reported in 1.37% of Icelandic Sheepdogs CERF examined
curled tail. Seen from the side the dog is rectangular. The head is
259
by veterinary ophthalmologists between 2000-2005. Reported as a hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
breed health issue on the ISAA website.3 Vet Med Assoc 2002 Feb 15;220(4):466-71.
6. AKC Breed Website: www.akc.org/breeds/icelandic_sheepdog Last
Retinal Dysplasia: Retinal folds, geographic, and generalized accessed July 1, 2010.
retinal dysplasia with detachment are recognized in the breed. Can
lead to blindness. Reported in 1.37% of Icelandic Sheepdogs CERF
examined by veterinary ophthalmologists between 2000-2005.3
Genetic Tests
Tests of Genotype: Direct tests for coat color are available from
VetGen.
Miscellaneous
• Breed name synonyms: Iceland Sheepdog, Islandsk Farehond,
Friaar Dog, Islenkur Fjárhundur, Icelandic Dog.
• Registries: AKC, CKC, FCI
• AKC rank (none): Recognized June, 2010. Entire stud book entered.
• Internet resources: Icelandic Sheepdog Association of America:
www.icelanddogs.com
Canadian Icelandic Sheepdog Club:
http://canadianicelandicsheepdogclub.blogspot.com
References
1. Oliehoek PA, Bijma P & van der Meijden A: History and structure of the
closed pedigreed population of Icelandic Sheepdogs. Genet Sel Evol. 2009
Aug 6;41:39.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
260
Irish Red and
White Setter
moderately long, very muscular, but not too thick. There is a level
topline. The body is strong and muscular with a deep chest and
well sprung ribs. The feet are close-knit with plenty of feathering
between toes. The gait is long striding, very lively, graceful and
efficient. The forelegs and hind legs move perpendicularly to the
ground with no crossing or weaving.
Coat: The base color is white with solid red patches (clear islands Progressive Retinal Atrophy (PRA, RCD-1): Autosomal recessive,
of red color). Flecking but not roaning is permitted around the face early onset rod, cone dysplasia form of PRA with an onset of
and feet and up the foreleg as far as the elbow and up the hind leg 25 days of age, and progressing to blindness by one year old.
as far as the hock. Feathering is present on the back of the fore and The mutation is the same as in Irish Setters, showing a common
hind legs, on the outer ear flap, on the flank extending onto the ancestral origin. A genetic test is available. The frequency of carriers
chest and throat forming a fringe, and on the tail. in the breed has not been established.5,6,7
Longevity: 11-15 years. von Willebrand’s Disease Type 1 (vWD): Autosomal recessive
genetic disorder causing a mild bleeding syndrome. A direct genetic
Points of Conformation: The length of the body from point of test is available from the Animal Health Trust. Reported at a low
shoulders to base of tail is not shorter than the height at the top frequency in the breed.
of the withers. Bone is moderate in proportion to size. The eyes
are round, and dark hazel or dark brown. The skull is broad in Patella Luxation: Polygenically inherited laxity of patellar
proportion to the body and domed without showing an occipital ligaments, causing luxation, lameness, and later degenerative joint
protuberance. The stop is distinct, but not exaggerated. The neck is disease. Treat surgically if causing clinical signs. Too few Irish Red
261
and White Setters have been screened by OFA to determine an Tests of Phenotype: CHIC certification: Required testing
accurate frequency.4 includes hip radiographs, CERF eye examination, thyroid profile
including autoantibodies, and genetic tests for Rcd-1 PRA and
Disease Predispositions Canine Leukocyte Adhesion Deficiency. (See CHIC Website: www.
Hypothyroidism: Inherited autoimmune thyroiditis. 12.5% positive caninehealthinfo.org)
for thyroid autoantibodies based on testing at Michigan State
Recommend elbow radiographs, patella evaluation, and cardiac
University. (Ave. for all breeds is 7.5%).8,9
examination.
Distichiasis: Abnormally placed eyelashes that irritate the cornea
and conjunctiva. Can cause secondary corneal ulceration. Identified Miscellaneous
in 7.79% of Irish Red and White Setters CERF examined by • Breed name synonyms: Red and White Irish Setter,
veterinary ophthalmologists between 2000-2005.10 Parti-Colored Setter.
• Registries: AKC, UKC, KCGB (Kennel Club of Great Britain), ANKC
Persistent Pupillary Membranes: Strands of fetal remnant (Australian National Kennel Club), NKC (National Kennel Club), FCI.
connecting; iris to iris, cornea, lens, or involving sheets of tissue. • AKC rank: Became an AKC recognized breed Jan. 2009.
The later three forms can impair vision, and dogs affected with Entire studbook registered.
these forms should not be bred. Identified in 3.90% of Irish Red • Internet resources: Irish Red and White Setter Association:
and White Setters CERF examined by veterinary ophthalmologists www.irishredwhitesetterassociation.com
between 2000-2005.10 Irish Red and White Setter Club of Great Britain:
www.irishredandwhitesetterclub.com
Gastric Dilatation-Volvulus (Bloat, GDV): Life-threatening Irish Red and White Setter Club of Canada:
twisting of the stomach within the abdomen. Requires immediate www.irishredandwhitesetterclub.ca
veterinary attention. Irish Red and White Setters are at increased
risk versus other breeds. Dogs with the deepest thorax relative to
width have the greatest risk for GDV.11 References
1. Foureman P, Whiteley M, & Giger U: Canine leukocyte adhesion
Cataracts: Anterior and posterior cortical cataracts predominate in deficiency: presence of the Cys36Ser beta-2 integrin mutation in an
affected US Irish Setter cross-breed dog and in US Irish Red and White
the breed. Identified in 2.60% of Irish Red and White Setters CERF
Setters. J Vet Intern Med. 2002 Sep-Oct;16(5):518-23.
examined by veterinary ophthalmologists between 2000-2005.10
2. Kijas JM, Bauer TR Jr, Gafvert S, et. Al.: A missense mutation in the
beta-2 integrin gene (ITGB2) causes canine leukocyte adhesion deficiency.
Chronic Superficial Keratitis (CSK)/Pannus: Corneal disease
Genomics. 1999 Oct 1;61(1):101-7.
that can cause vision problems due to pigmentation. Treatment 3. Debenham SL, Millington A, Kijast J, et. al.: Canine leucocyte adhesion
with topical ocular lubricants and anti-inflammatory medication. deficiency in Irish red and white setters. J Small Anim Pract. 2002
Identified in 2.60% of Irish Red and White Setters CERF examined Feb;43(2):74-5.
by veterinary ophthalmologists between 2000-2005.10 4. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
5. Schellenberg D, Yi Q, Glickman NW, et. al.: Influence of thoracic
Retinal Dysplasia: Focal retinal dysplasia and retinal folds are conformation and genetics on the risk of gastric dilatation-volvulus in Irish
recognized in the breed. Identified in 2.60% of Irish Red and White setters. J Am Anim Hosp Assoc. 1998 Jan-Feb;34(1):64-73.
Setters CERF examined by veterinary ophthalmologists between 8. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
2000-2005.10 hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
Iris Cysts: Fluid filled sacs arising from the posterior surface of 9. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
the iris, to which they may remain attached or break free and Population and Animal Health, Michigan State University. April, 2007.
float into the anterior chamber. Usually occur in mature dogs. 10. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
Can occasionally block the iridocorneal angle causing glaucoma.
11. AKC Breed Website: www.akc.org/breeds/irish_red_white_setter/ Last
Identified in 1.30% of Irish Red and White Setters CERF examined
accessed July 1, 2010.
by veterinary ophthalmologists between 2000-2005.10
Genetic Tests
Tests of Genotype: Direct test for Canine Leukocyte Adhesion
Deficiency is available from Optigen and the Animal Health Trust.
Direct test for Rcd-1 PRA is available from Optigen, and the Animal
Health Trust.
Direct test for vWD is available from the Animal Health Trust.
262
Irish Setter
moderate shedders and their grooming needs are average.
Drug Sensitivities
None reported
Inherited Diseases
Hip Dysplasia: Polygenically inherited trait causing degenerative
The Breed History joint disease and hip arthritis. OFA reports 12.1% affected. Reported
In the 18th century in Ireland, this breed most probably originated at a frequency of 7.3% in the 2003 ISCA National Health Survey.1,2
from a mix of Pointer, Spaniel, English setter, and Gordon setter
breeds. The early specimens of these scent dogs were red and white, Elbow Dysplasia: Polygenically inherited trait causing elbow
but in the 19th century, they were progressively selected for the solid arthritis. OFA reports 3.4% affected.1
red color. Disney’s “Big Red” helped to propel this breed’s popularity.
AKC registry began in 1878. Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative
joint disease. Treat surgically if causing clinical signs. Too few
Breeding for Function Irish Setters have been screened by OFA to determine an accurate
Bred to be a gun dog for both pointing and retrieving, they are now
frequency.1
most widely seen in conformation shows, obedience trials, and as a
household pet. Progressive Retinal Atrophy (PRA, RCD-1): Autosomal recessive,
early onset rod, cone dysplasia form of PRA with an onset of
Physical Characteristics 25 days of age, and progressing to blindness by one year old. A
Height at Withers: female 25” (63.5 cm), male 27” (69 cm) genetic test is available, revealing 7% carriers and 0.5% affected. A
late-onset, rcd-4 PRA also occurs in the breed with a average age
Weight: females 60lb (27 kg), males 70 (32 kg). of onset of 10 years. A genetic test available.3,4,5
Coat: The beautiful medium-length smooth, flat and glossy coat Canine Leukocyte Adhesion Deficiency (CLAD): An autosomal
has a rich mahogany or chestnut red color. Small white markings recessive, fatal immunodeficiency disease found in Irish setters.
are not faulted on feet or chest. Affected dogs present with severe recurrent infections, neutrophilia
and low body weight. A genetic test is available, showing 11%
Longevity: 11-15 years. testing as carriers in Germany, and 7.6% testing as carriers in
Australia. The frequency in the US population is not published.6,7,8,9
Points of Conformation: A long, lean appearance with good bone,
finely chiseled muzzle, dark to medium brown colored eyes, ears Hypochondroplastic Dwarfism: A rare, autosomal recessive form
almost reaching the nose, well-defined stop and prominent occiput of dwarfism has been identified in the breed.10
characterize these dogs. These dogs have prominent flews and the
nose is pigmented black or brown. Their topline is gently inclined Hereditary Quadriplegia and Amblyopia: A rare, congenital,
downward to the rear, and the tail should almost reach the tarsus, autosomal recessive disorder causing inability to stand, tremor,
and is carried curving or straight nearly level with the back. They are amblyopia with nystagmus, and seizures has been identified in the
very deep-chested. breed.11,12
Distichiasis: Abnormally placed eyelashes that irritate the cornea IgA Deficiency: Inherited disorder seen in Irish setters causing
and conjunctiva. Can cause secondary corneal ulceration. Identified recurrent bacterial pneumonia, diarrhea, poor weight gain, skin
in 5.83% of Irish setters CERF-examined by veterinary ophthalmolo- infections, allergies, and immune-mediated diseases.26
gists between 2000-2005.11
Laryngeal Paralysis: Irish setters are a breed at increased risk
Persistent Pupillary Membranes: Strands of fetal remnant to develop geriatric laryngeal paralysis secondary to axonal
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The degeneration of the recurrent laryngeal nerve. Clinical signs are
later three forms can impair vision, and dogs affected with these exercise intolerance, inspiratory stridor, inspiratory dyspnea,
forms should not be bred. Identified in 5.56% of Irish Setters CERF gagging, coughing and dysphonia.27
examined by veterinary ophthalmologists between 2000-2005.11
Megaesophagus: Irish setters are identified as a breed at increased
Idiopathic Epilepsy: Inherited seizures can be generalized or risk of developing acquired megaesophagus. Causes include
partial seizures. Control with anticonvulsant medications. Reported peripheral neuropathy, laryngeal paralysis, acquired myasthenia
at a frequency of 5.3% in the 2003 ISCA National Health Survey. gravis, esophagitis, and gastric dilatation. Hypothyroidism is
Unknown mode of inheritance.2 not associated with megaesophagus. Clinical signs include
regurgitation, excess salivation, and aspiration pneumonia.28
Hypertrophic Osteodystrophy (HOD): Immune-mediated disorder
causing fever, and painful, swollen joints and bones in young Irish Degenerative Myelopathy (DM): Affected dogs show an insidious
Setters. Occurs mostly within 3-14 days post-vaccination. Age of onset of upper motor neuron (UMN) paraparesis at an average age of
onset is 8-16 weeks. Reported 14.3x odds ratio versus other breeds. 11.4 years. The disease eventually progresses to severe tetraparesis.
Reported at a frequency of 5.0% in the 2003 ISCA National Health Affected dogs have normal results on myelography, MRI, and CSF
Survey. Unknown mode of inheritance.2,19,20 analysis. Necropsy confirms the condition. Unknown mode of
inheritance. A direct genetic test for an autosomal recessive DM
Urinary Incontinence: Spayed female Irish setters are over susceptibility gene is available. All affected dogs are homozygous
represented compared with other breeds for urinary incontinence. for the gene, however, only a small percentage of homozygous dogs
Reported at a frequency of 5.0% in the 2003 ISCA National Health develop DM. Clinical DM is reported at a prevalence of 0.68% in the
Survey.2,21,22 breed.29
Osteosarcoma: The Irish Setter is a breed with an increased Acral lick Dermatitis, Brachygnathism, Cervical Vertebral
frequency of malignant osteosarcoma, usually in the long bones Instability, Color Dilution Alopecia, Cutaneous Asthenia,
of the limbs. Reported at a frequency of 4.6% in the 2003 ISCA Ectropion, Factor VIII Deficiency, Lissencephaly, Lupoid
National Health Survey.2,23 Onychopathy, Narcolepsy, Optic Nerve Hypoplasia,
Osteochondrodysplasia, Perianal Fistula, Prognathism, Retained
Cataracts: Anterior, posterior, and capsular intermediate and Primary Teeth, Sebaceous Adenitis, Tricuspid Valve Dysplasia,
punctate cataracts predominate in the breed. Identified in 3.89% Vascular Ring Anomaly, and von Willebrand’s Disease are
of Irish setters CERF-examined by veterinary ophthalmologists reported.30
between 2000-2005. Reported at a frequency of 5.3% in the 2003
ISCA National Health Survey. CERF does not recommend breeding
any Irish Setter with a cataract.2,11 Isolated Case Studies
Patent Ductus Arteriosis (PDA): A right to left shunting PDA was
Entropion: Rolling in of the eyelid. Can cause corneal irritation. identified in a six-month-old, female Irish setter presented with a
Entropion is reported in 2.22% of Irish setters CERF-examined by two-month history of progressive hindlimb weakness and collapse
veterinary ophthalmologists between 2000-2005. Reported at a on exercise. Thoracic auscultation revealed a soft systolic murmur
frequency of 2.1% in the 2003 ISCA National Health Survey.2,11 and a split second heart sound.31
Gluten (Wheat) Sensitive Enteropathy: Irish setters can Aortic Bulb/Valve Mineralization: Six of 20 affected dogs were
demonstrate an inherited gluen sensitivity that produces poor Irish setters in one study. The mineralization was visible radiograph-
weight gain or weight loss, with or without diarrhea. Pathologically ically, but did not cause clinical signs.32
264
Globoid Cell Leukodystrophy (Krabbe disease): A rare, autosomal protein deficiency in Irish setter dogs. Vet Immunol Immunopathol. 1992
recessive lysosomal storage disease causing severe neurological May;32(3-4):261-80.
symptoms including seizures, hypotonia, blindness, and death in 10. Hanssen I, Falck G, Grammeltvedt AT, Haug E, Isaksen CV: Hypochondro-
young affected dogs was identified in a family of Irish setters. A plastic dwarfism in the Irish setter. J Small Anim Pract. 1998 Jan;39(1):10-4.
11. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
genetic test was developed for this cohort.33
College of Veterinary Ophthalmologists. ACVO, 2007.
12. Palmer AC, Payne JE, Wallace ME: Hereditary quadriplegia and
Genetic Tests amblyopia in the Irish Setter. J Small Anim Pract. 1973 Jun;14(6):343-52.
Tests of Genotype: Direct test for Canine Leukocyte Adhesion 13. Schick RO, Fadok VA: Responses of atopic dogs to regional allergens:
Deficiency is available from HealthGene, Optigen and the Animal 268 cases (1981-1984). J Am Vet Med Assoc. 1986 Dec 1;189(11):1493-6.
Health Trust. 14. Ward MP, Patronek GJ, Glickman LT: Benefits of prophylactic gastropexy
for dogs at risk of gastric dilatation-volvulus. Prev Vet Med. 2003 Sep
Direct test for Rcd-1 PRA is available from HealthGene, Optigen, 12;60(4):319-29.
15. Schellenberg D, Yi Q, Glickman NW, et. al.: Influence of thoracic
VetGen, and the Animal Health Trust.
conformation and genetics on the risk of gastric dilatation-volvulus in Irish
setters. J Am Anim Hosp Assoc. 1998 Jan-Feb;34(1):64-73.
Direct test for Rcd-4 PRA is available from the Animal Health Trust.
16. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Direct test for a DM susceptability gene is available from OFA.
2000.
17. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
Tests of Phenotype: CHIC Certification: Required testing includes serum thyroid hormone autoantibodies in dogs with clinical signs of
hip radiographs, CERF eye examination or genetic test for PRA, and hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
thyroid profile including autoantibodies. (See CHIC website; www. 18. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
caninehealthinfo.org). for Population and Animal Health, Michigan State University. April, 2007.
19. McLaughlin R: Developmental Orthopedic Diseases in Dogs. 2003.
Recommend elbow radiographs, patella evaluation, and cardiac Proceedings, Western Veterinary Conference 2003.
examination. 20. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Miscellaneous Sep-Oct;38(5):467-77.
21. Holt PE, Thrusfield MV: Association in bitches between breed, size,
• Breed name synonyms: Irishman, Irish Red Setter (historical), neutering and docking, and acquired urinary incontinence due to
Red Setter incompetence of the urethral sphincter mechanism. Vet Rec. 1993 Aug
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 21;133(8):177-80.
ANKC(Australian National Kennel Club), NKC (National Kennel Club) 22. Blendinger C, Blendinger K, Bostedt H: Urinary incontinence in spayed
• AKC rank (year 2008): 69 (1,291 dogs registered) bitches. 1. Pathogenesis, incidence and disposition. Tierarztl Prax. 1995
• Internet resources: Irish Setter Club of America: Jun;23(3):291-9.
www.irishsetterclub.org 23. Misdorp W, Hart AA: Some prognostic and epidemiologic factors in
Irish setter Club of Canada: www.irishsettercanada.org canine osteosarcoma. J Natl Cancer Inst. 1979 Mar;62(3):537-45.
Irish Setter Association, England: www.isae.co.uk 24. Polvi A, Garden OA, Houlston RS, Maki M, Batt RM, Partanen J: Genetic
susceptibility to gluten sensitive enteropathy in Irish setter dogs is not
National Red Setter Field Trial Club: www.nrsftc.com
linked to the major histocompatibility complex. Tissue Antigens. 1998
Dec;52(6):543-9.
References 25. Hall EJ, Batt RM: Dietary modulation of gluten sensitivity in a naturally
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010. occurring enteropathy of Irish setter dogs. Gut. 1992 Feb;33(2):198-205.
2. Irish Setter Club of America: 2003 ISCA National Health Survey. 2004. 26. Norris CR, Gershwin LJ: Evaluation of systemic and secretory IgA
3. Djajadiningrat-Laanen SC, Boeve MH, Stades FC, van Oost BA: Familial concentrations and immunohistochemical stains for IgA-containing B cells
non-rcd1 generalised retinal degeneration in Irish setters. J Small Anim in mucosal tissues of an Irish setter with selective IgA deficiency. J Am Anim
Pract. 2003 Mar;44(3):113-6. Hosp Assoc. 2003 May-Jun;39(3):247-50.
4. Suber ML, Pittler SJ, Qin N, Wright GC, Holcombe V, Lee RH, Craft CM, 27. Burbidge HM: A review of laryngeal paralysis in dogs. Br Vet J. 1995
Lolley RN, Baehr W, Hurwitz RL: Irish setter dogs affected with rod/cone Jan-Feb;151(1):71-82.
dysplasia contain a nonsense mutation in the rod cGMP phosphodiesterase 28. Gaynor AR, Shofer FS, Washabau RJ: Risk factors for acquired
beta-subunit gene. Proc Natl Acad Sci U S A. 1993 May 1;90(9):3968-72. megaesophagus in dogs. J Am Vet Med Assoc. 1997 Dec 1;211(11):1406-12.
5. Aguirre GD, Baldwin V, Weeks KM, Acland GM, Ray K: Frequency of the 29. Coates JR & Wade C: Update on the Genetic Basis of Canine
codon 807 mutation in the cGMP phosphodiesterase beta-subunit gene in Degenerative Myelopathy. Proceedings, 2008 ACVIM Forum. 2008.
Irish setters and other dog breeds with hereditary retinal degeneration. J 30. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Hered. 1999 Jan-Feb;90(1):143-7. Ackerman. p. 223, AAHA Press, 1999.
6. Jobling AI, Ryan J, Augusteyn RC: The frequency of the canine leukocyte 31. Ferasin L, Rizzo F, Darke PG: Original investigation of right-to-left
adhesion deficiency (CLAD) allele within the Irish Setter population of shunting patent ductus arteriosus in an Irish setter puppy. Vet J. 2007 Mar;
Australia. Aust Vet J. 2003 Dec;81(12):763-5. 173(2): 443-8.
7. Pfeiffer I, Brenig B: Frequency of the canine leucocyte adhesion 32. Douglass JP, Berry CR, Thrall DE, Malarkey DE, Spaulding KA:
deficiency (CLAD) mutation among Irish red setters in Germany. J Anim Radiographic features of aortic bulb/valve mineralization in 20 dogs. Vet
Breed Genet. 2005 Apr;122(2):140-2. Radiol Ultrasound. 2003 Jan-Feb;44(1):20-7.
8. Kijas JM, Bauer TR Jr, Gafvert S, et. Al.: A missense mutation in the 33. McGraw RA, Carmichael KP: Molecular basis of globoid cell
beta-2 integrin gene (ITGB2) causes canine leukocyte adhesion deficiency. leukodystrophy in Irish setters. Vet J. 2006 Mar;171(2):370-2.
Genomics. 1999 Oct 1;61(1):101-7. 34. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
9. Trowald-Wigh G, Hakansson L, Johannisson A, et. al.: Leucocyte adhesion Book House, NY 2006. p 72-75.
265
Irish Terrier
Recognized Behavior Issues and Traits
Reported breed traits include: Loyal, high intelligence, high-spirited,
fiery attitude, and always on guard. Adaptable, at home in city or
rural environments, and enjoys children. Hardy; tolerates both warm
and cold.
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: Irish Red Terrier
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 130 (182 dogs registered)
• Internet resources: Irish Terrier Club of America: www.itca.info/
U.K. Irish Terrier Association: www.irishterrierassociation.co.uk
The Irish Terrier Association of Canada:
www.dogbiz.com/itac/index.html
References
1. Binder H, Arnold S, Schelling C, et. al.: Palmoplantar hyperkeratosis in
Irish terriers: evidence of autosomal recessive inheritance. J Small Anim
Pract. 2000 Feb;41(2):52-5.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Schatzberg S, Olby N, Steingold S, et. al.: A polymerase chain reaction
screening strategy for the promoter of the canine dystrophin gene. Am J
Vet Res. 1999 Sep;60(9):1040-6.
4. Wentink GH, Meijer AE, van der Linde-Sipman JS, et. al.: Myopathy in an
irish terrier with a metabolic defect of the isolated mitochondria. Zentralbl
Veterinarmed A. 1974 Jan;21(1):62-74
5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
7. Lewis LD, Morris ML Jr: Canine urolithiasis: diagnosis and treatment. Mod
Vet Pract. 1984 May;65(5):375-8.
8. Allen LBA, Pratt A, Lulich J, et. al.: Canine Cystine Urolithiasis:
Investigation of Cases Identified in the United Kingdom. Proceedings, 2008
British Small Animal Veterinary Congress. 2008.
9. Glaze MB: Fundus Interpretation Made Real. Proceedings, 2004 Northeast
Veterinary Conference. 2004.
10. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
267
Irish Water Spaniel
Recognized Behavior Issues and Traits
Reported breed characteristics include: Loyal with family, some
dogs are so reserved as to be aggressive with strangers, and
intelligent. They have a strong willingness to please, high activity
and exercise needs, and high trainability. Grooming needs consist of
a weekly combing. They are a low to moderate shedder depending
on the season. This breed is not always good with other pets. Early
obedience training and socialization are recommended. This breed
is considered a good watchdog, but has a low barking tendency
otherwise. They are also considered an excellent swimmer.
The Breed History
The tallest of the spaniel breeds is also an ancient one, and original Normal Physiologic Variations
spaniel type fits the modern type of this breed. A member of the Some Irish Water Spaniel females can have irregular heat cycles.
water spaniel group that includes the extinct Tweed water spaniel,
these dogs are thought to have arisen from the South Country Drug Sensitivities
Water Spaniel and the North Country Water Spaniel. Written The Irish Water Spaniel breed club websites alert to possible
records begin in 1607. The first Irish Water Spaniels came to reactions to potentiated sulfonamide antibiotics.
America around the year 1873. and became an AKC breed in 1884.
Inherited Diseases
Breeding for Function Elbow Dysplasia: Polygenically inherited trait causing elbow
Their primary function was to perform as a high endurance arthritis. OFA reports 16.1% affected.1
waterfowl retriever. They were bred with a heavy oily coat to allow
them to retrieve in cold waters. They were less commonly used for Hip Dysplasia: Polygenically inherited trait causing degenerative
upland game hunting. joint disease and hip arthritis. OFA reports 12.0% affected.1
Coat: The tail, front of the neck and face are covered in very short Disease Predispositions
hair. The main haircoat is a longer crisp, dense, oily, and tightly curly Distichiasis: Abnormally placed eyelashes that irritate the cornea
overcoat. The undercoat is short and dense. The standard coat color and conjunctiva. Can cause secondary corneal ulceration. Identified
is liver. The liver haircoat has a purplish tinge referred to as puce liver. in 18.55% of Irish Water Spaniels CERF examined by veterinary
ophthalmologists between 2000-2005.2
Longevity: 12-14 years
Follicular Dysplasia (Hair Loss): Hair loss may be somewhat
Points of Conformation: The water-repelling curly coat, rat-tail, cyclical, and typically affects the trunk and spares the head and
beard and sideburns and the loose curly topknot that reaches the distal extremities. Hair loss in IWS can be influenced by dietary
eyes of this dog are distinctive breed characteristics. They possess factors and an abnormality of their sex hormone intermediates,
a strong square conformation, and the wedge-shaped head is especially an exaggerated response of 17-hydroxyprogesterone
well chiseled. The skull is domed, stop is moderate, and occipital (17-OHP) in ACTH-response tests. Unknown mode of inheritance,
protuberance is prominent. The muzzle is long and square, the although one study suggested a dominant mode of inheritance.
nose large and liver colored. Almond shaped eyes are medium sized Diagnosis by skin biopsy. Treatment with melatonin.3,4,5
and hazel in color. The very long pendulous ears are low set with
extensive curly feathering at the tips. The neck is arched, long and Cataracts: Anterior and posterior cortex intermediate cataracts
muscular. The topline is level, though it may be slightly higher in predominate in the breed. Age of onset averages 5 years of age.
the rear. The thorax is deep and the ribs are well sprung. The rib Unknown mode of inheritance. Identified in 5.43% of Irish Water
cage extends well back. Limbs are straight boned, feet large and Spaniels CERF examined by veterinary ophthalmologists between
spreading with webbed toes, and the low set tail is generally carried 2000-2005. CERF does not recommend breeding any Irish Water
level. The ground-covering gait is long, low, smooth, and seems Spaniel with a cataract.2
effortless.
268
Hypothyroidism: Inherited autoimmune thyroiditis. 2.5% positive Kingdom. Vet Dermatol 2000: 11[2]:107-122.
for thyroid autoantibodies based on testing at Michigan State 5. White SD: Update on Follicular Alopecias: “Pseudo-Endocrinopathies”.
University. (Ave. for all breeds is 7.5%).6,7 Proceedings, 2005 ACVIM Forum. 2005.
6. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
Persistent Pupillary Membranes: Strands of fetal remnant hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
connecting; iris to iris, cornea, lens, or involving sheets of tissue. Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
7. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
The later three forms can impair vision, and dogs affected with
Population and Animal Health, Michigan State University. April, 2007.
these forms should not be bred. Identified in 2.26% of Irish Water 8. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Spaniels CERF examined by veterinary ophthalmologists between Ackerman. p. 223. AAHA Press, 1999.
2000-2005.2 9. Bouchard H: Epitheliotropic lymphoma in a dog. Can Vet J. 2000
Aug;41(8):628-30.
Entropion: Rolling in of the eyelid. Can cause corneal irritation. 10. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Entropion is reported in 1.36% of Irish Water Spaniels CERF Book House, NY 2006. p. 102-105.
examined by veterinary ophthalmologists between 2000-2005.2
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: IWS, Water Spaniel, Shannon Spaniel
(historical), Rat-tail or Whip-tail Spaniels, Southern Irish Water
Spaniel (all historical)
• Registries: AKC, CKC, ANKC (Australian National Kennel Club),
NKC (National Kennel Club)
• AKC rank (year 2008): 144 (83 dogs registered)
• Internet resources: Irish Water Spaniel Club of America:
http://iwsca.webs.com
Irish Water Spaniel Association of Canada: www.iwsac.org
UK Irish Water Spaniel Association:
www.irishwaterspaniels.org.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Cerundolo R, Lloyd DH, Pidduck HG: Studies on the inheritance of hair
loss in the Irish water spaniel. Vet Rec. 1999 Nov 6;145(19):542-4.
4. Cerundolo R, Lloyd DH, McNeil PE, et. al.: An Analysis of Factors
Underlying Hypotrichosis and Alopecia in Irish Water Spaniels in the United
269
Irish Wolfhound
broad, and the abdomen well tucked up.
271
bile acids and blood ammonia tests are used for diagnosis, as
fasting samples are often normal. Diagnosed in 2.1% of Irish
Genetic Tests
Tests of Genotype: None.
Wolfhounds in the Netherlands. Appears to be complexly inherited
without sex influence.20,21,22,23 Tests of Phenotype: CHIC Certification: Elbow and hip
radiographs, CERF eye examination, and cardiac evaluation.
Everted Cartilage of the Third Eyelid: A scroll-like curling of Optional testing includes serum bile acid test. (See CHIC website;
the cartilage of the third eyelid, usually everting the margin. Can www.caninehealthinfo.org).
be unilateral or bilateral, and cause ocular irritation. Identified
in 1.24% of Irish Wolfhounds CERF-examined by veterinary Recommend thyroid profile including autoantibodies and patella
ophthalmologists between 2000-2005.15 evaluation.
Osteochondritis Dissecans (OCD): Polygenically inherited cartilage
defect of the humeral head or stifle. Causes joint pain and Miscellaneous
lameness in young growing dogs. Mild cases can resolve with rest, • Breed name synonyms: Greyhound of Ireland, Wolfdog of
while more severe cases require surgery. There is a 2.24:1 male to Ireland, Irish dogs, Big dogs of Ireland, Great Hound of Ireland (all
female ratio. 75% of all cases are unilateral. Dorn reports a 3.65x historical), wolfhound, IW, Cu Faoil.
odds ratio versus other breeds. Another study reports a 523.5x odds • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ratio for stifle OCD, and a 47.1x odds ratio for shoulder OCD versus ANKC (Australian National Kennel Club), NKC (National Kennel Club).
other breeds. Shoulder OCD is reported at a frequency of 1.2% in • AKC rank (year 2008): 81 (863 dogs registered)
the Irish Wolfhound.6,13,24 • Internet resources: Irish Wolfhound Club of America:
www.iwclubofamerica.org
Progressive Retinal Atrophy (PRA): Inherited degeneration of Irish Wolfhound Club of Canada:
the retinal leading to blindness. Onset is early with blindness www.irishwolfhoundclubofcanada.ca
developing in the young adult (2-3 years of age). Presumed Irish Wolfhound Club (UK): www.irishwolfhoundclub.org.uk
autosomal recessive mode of inheritance. CERF does not The Irish Wolfhound Foundation, Inc.: www.iwfoundation.org
recommend breeding any Irish Wolfhound with PRA.15 Irish Wolfhound Health Group: www.iwhealthgroup.co.uk
272
14. Casal ML, Munuve RM, Janis MA, et. al.: Epilepsy in Irish Wolfhounds. J
Vet Intern Med. 2006 Jan-Feb;20(1):131-5.
15. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
16. Urfer SR, Gaillard C, & Steiger A: Lifespan and disease predispositions in
the Irish Wolfhound: a review. Vet Q. 2007 Sep;29(3):102-11.
17. Glickman LT, Glickman NW, Schellenberg DB, et. al.: Incidence of and
breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet
Med Assoc. 2000 Jan 1;216(1):40-5.
18. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
19. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
20. Kerr MG, van Doorn T: Mass screening of Irish wolfhound puppies for
portosystemic shunts by the dynamic bile acid test. Vet Rec. 1999 Jun
19;144(25):693-6.
21. Meyer HP, Rothuizen J, Ubbink GJ, et. al.: Increasing incidence of
hereditary intrahepatic portosystemic shunts in Irish wolfhounds in The
Netherlands (1984 to 1992). Vet Rec. 1995 Jan 7;136(1):13-6.
22. Tobias KM, Rohrbach BW: Association of breed with the diagnosis of
congenital portosystemic shunts in dogs: 2,400 cases (1980-2002). J Am
Vet Med Assoc. 2003 Dec 1;223(11):1636-9.
23. van Steenbeek FG, Leegwater PA, van Sluijs FJ, et. al.: Evidence of
inheritance of intrahepatic portosystemic shunts in Irish Wolfhounds. J Vet
Intern Med. 2009 Jul-Aug;23(4):950-2.
24. Rudd RG, Whitehair JG, Margolis JH: Results of management of
osteochondritis dissecans of the humeral head in dogs : 44 cases (1982 to
1987). J Am Anim Hosp Assoc 1990: 26[2]:173-178.
25. Leisewitz AL, Spencer JA, Jacobson LS, et. al.: Suspected primary
immunodeficiency syndrome in three related Irish wolfhounds. J Small
Anim Pract. 1997 May;38(5):209-12.
26. Clercx C, Reichler I, Peeters D, et. al.: Rhinitis/Bronchopneumonia
syndrome in Irish Wolfhounds. J Vet Intern Med. 2003 Nov-Dec;17(6):843-9.
27. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 224. AAHA Press, 1999.
28. Junker K, van den Ingh TS, Bossard MM, et. al.: Fibrocartilaginous
embolism of the spinal cord (FCE) in juvenile Irish Wolfhounds. Vet Q. 2000
Jul;22(3):154-6.
29. Peeters D, Clercx C, Michiels L, et. al.: Juvenile nephropathy in a
boxer, a rottweiler, a collie and an Irish wolfhound. Aust Vet J. 2000
Mar;78(3):162-5.
30. Vaughan-Scott T, Goldin J, Nesbit JW: Spinal nephroblastoma in an Irish
wolfhound. J S Afr Vet Assoc. 1999 Mar;70(1):25-8.
31. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 188-191.
273
Italian Greyhound
Recognized Behavior Issues and Traits
Reported breed characteristics include: Very affectionate, slightly
aloof with strangers, adapts well to rural or urban environment,
needs regular exercise but quiet around the home. Playful, easy
going, sensitive, intelligent, good with other pets and children
(gentle ones); they are needy of human contact and do not do well
if left alone. An Italian Greyhound demands lots of attention; some
have a degree of stubbornness. Easily bored, has a short attention
span. For their size, they have a loud bark. Not tolerant of extreme
temperature, especially cold. Sweater coverage is needed in cold
weather. Overall, not as easy to housetrain as some other breeds.
The Breed History Not an outdoor dog but adaptable to both rural and urban living.
The Italian Greyhound breed origins are not clear, though their place The Italian Greyhound is noted for high energy levels, particularly as
of origin is thought to be in Greece and Turkey, dating to the birth puppies. In a pack, the dog may be assertive.
of Christ. In Italy in the 16th century, these dogs were portrayed
in artwork of the Renaissance.The English Kennel club listed them
in their first studbook, and in the AKC registry, they first appear in
Normal Physiologic Variations
Sight hounds have lower normal ranges for T4 and T3 concentrations
1886, but were rare (less than 50 registrants) until the 1950s. compared to other breeds.1
274
Cryptorchidism: Retained testicles. Can be bilateral or unilateral.
Reported at a frequency of 11.26% in the 1993 IGCA Health Survey.5
Genetic Tests
Tests of Genotype: Direct genetic test for black, brown and fawn is
available from HealthGene.
Demodicosis: Demodectic mange dermatitis has an underlying
Tests of Phenotype: CHIC Certification: Required testing includes
immunodeficiency in its pathogenesis. Primarily seen as a focal
hip radiograph, CERF eye examination (at 36 months and then
disease in young Italian Greyhounds. Reported at a frequency
annually to age 10), thyroid profile including autoantibodies (at 3
of 10.42% in the 1993 IGCA Health Survey. Unknown mode of
years of age), and patella examination. (See CHIC website; www.
inheritance.5
caninehealthinfo.org).
Leg Fractures: Seen at an increased frequency due to reduced bone
Recommend elbow radiographs and cardiac examination.
density in thin leg bones. Reported at a frequency of 9.81% in the
1993 IGCA Health Survey.5
Miscellaneous
Inherited Epilepsy: Generalized seizures. Control with • Breed name synonyms: Piccolo Levrieri Italiani.
anticonvulsant medication. Reported at a frequency of 6.55% in the • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
1993 IGCA Health Survey. Unknown mode of inheritance.5 ANKC (Australian National Kennel Club), NKC (National Kennel
Club).
Cataracts: Anterior or posterior intermediate and punctate • AKC rank (year 2008): 61 (1,450 dogs registered)
cataracts occur in the breed. Onset 2-3 years of age. Identified • Internet resources: Italian Greyhound Club of America:
in 5.86% of Italian Greyhounds CERF examined by veterinary www.italiangreyhound.org
ophthalmologists between 2000-2005. CERF does not recommend The Italian Greyhound Club of Canada: www.igcc.ca
breeding any Italian Greyhound with a cataract.4 The Italian Greyhound Club UK:
www.theitaliangreyhoundclub.co.uk
Hypothyroidism: Inherited autoimmune thyroiditis. 4.4% positive
for thyroid auto-antibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5%).6,7 References
1. Kintzer PP & Peterson ME: Progress in the Diagnosis and Treatment of
Color Dilution Alopecia: Hair loss seen in some blue or dilute Canine Hypothyroidism. 2007. Proceedings, ACVIM 2007.
2. Court MH: Anesthesia of the sighthound. Clin Tech Small Anim Pract
colored Italian Greyhounds. Reported at a frequency of 3.12% in
1999 Feb;14(1):38-43.
the 1993 IGCA Health Survey. Unknown mode of inheritance.5,8
3. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Deafness: Reported to occur in the breed. Congenital deafness can
College of Veterinary Ophthalmologists. ACVO, 2007.
be unilateral or bilateral. Diagnosed by BAER testing.9 5. Italian Greyhound Club of America, Slater M: 1993 Survey on Health
Problems in Italian Greyhounds. 1994.
Progressive Retinal Atrophy (PRA): PRA is reported to occur in 6. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
the breed. Causes retinal deterioration and progressive blindness. hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Identified in 1.89% of Italian Greyhounds CERF examined by Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
veterinary ophthalmologists between 2000-2005. Assumed 7. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
autosomal recessive inheritance.4 Population and Animal Health, Michigan State University. April, 2007.
8. Briggs OM et al. Color mutant alopecia in a blue Italian Greyhound. J
Primary Lens Luxation: Occurs at an increased frequency in the Amer Anim Hosp Assoc. 1986; 22: 611-14.
breed. Often progresses to secondary glaucoma and blindness. 9. Strain GM: Deafness prevalence and pigmentation and gender
Reported relative risk of 8.44x versus other breeds.10 associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
10. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing
Persistent Pupillary Membranes: Strands of fetal remnant lens luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The 11. Schultheiss PC: A retrospective study of visceral and nonvisceral
later three forms can impair vision, and dogs affected with these hemangiosarcoma and hemangiomas in domestic animals. J Vet Diagn
Invest. 2004 Nov;16(6):522-6.
forms should not be bred. Identified in 1.00% of Italian Greyhounds
12. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
CERF examined by veterinary ophthalmologists between 2000-2005.4
Ackerman. p. 222. AAHA Press, 1999.
13. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Hemangiosarcoma and Hemangioma: Italian Greyhounds
Book House, NY 2006. p. 474-476.
are at increased risk of developing visceral and nonvisceral
hemangiosarcoma and hemangiomas.11
275
Japanese Chin
in the breed. The small ears are triangular and hang beside the head
with copious feathering, and fine leather. The nose is upturned,
nostrils wide and it sits between the eyes. The bite is only slightly
off ideally. Neck is moderate in length, and muscling, topline is level,
and thorax is moderately deep and round. They have a high set tail.
The limbs are straight boned and dewclaw removal is optional. Feet
are feathered and hare shaped.
Weight: 4-7 lb (2-3 kg), though some are up to 11 lb (5 kg)—the Hip Dysplasia and Legg-Calve Perthes Disease: Polygenically
larger body size is not preferred. inherited traits causing degenerative hip joint disease and arthritis.
OFA reports 8.3% affected.1
Coat: The single layered soft, silky, thick (profuse) coat is straight.
Most dogs are black and white, others are black and white with tan Elbow Dysplasia: Polygenically inherited trait causing elbow
points; other markings may include white with red, lemon, sable arthritis. Too few Japanese Chin have been screened by OFA to
and brindle. Markings on the face should be symmetrical—a blaze determine an accurate frequency.1
is preferred, and other markings have a preferred distribution laid
out in the breed standard. Coat stands off, and ruff and trousers are GM2 Gangliosidosis: A rare, autosomal recessive glycogen storage
present though the head has short hair cover. disease causing neurological signs has been identified in young
Japanese Chin. The biochemical and histopathologic diagnosis is
Longevity: 12-14 years GM2 gangliosidosis, with an increase in total beta-hexosaminidase
activity measured in vitro. A genetic test is available.9
Points of Conformation: They possess a high head carriage,
square, solid and compact conformation. Movement is animated
and straight, and they are described as having an “Oriental”
Disease Predispositions
Cataracts: Anterior, posterior, and equatorial cortex intermediate
expression. They have dark large eyes, the nose is matched to coat and punctate cataracts predominate in the breed. Reported in
color, and the very heavily plumed tail is carried over the back and 4.89% of Japanese Chin presented to veterinary teaching hospitals.
may be curved to either side. The muzzle is short, eyes are front Identified in 12.27% of Japanese Chin CERF examined by veterinary
facing and widely set, the stop is pronounced, head is broad, and ophthalmologists between 2000-2005. CERF does not recommend
the skull rounded. Note that a bit of white showing in the medial breeding any Japanese Chin with a cataract.3,4
canthus and around the edge of the cornea is considered desirable
276
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
Isolated Case Studies
None reported
The later three forms can impair vision, and dogs affected with
these forms should not be bred. Identified in 11.19% of Japanese
Chin CERF examined by veterinary ophthalmologists between Genetic Tests
2000-2005.3 Tests of Genotype: Direct test for coat colors is available from
HealthGene and VetGen.
Hypothyroidism: Inherited autoimmune thyroiditis. 6.2% positive
for thyroid auto-antibodies based on testing at Michigan State Direct test for Gen2-gangliosidosis is available from the OFA.
University. (Ave. for all breeds is 7.5%).5,6
Tests of Phenotype: CHIC Certification: Required testing includes
Entropion: Rolling in of the eyelid. Can cause corneal irritation or CERF eye examination (minimum 3 years of age), patella examination
ulceration. Entropion is reported in 5.42% of Japanese Chin CERF (minimum 1 year), and cardiac evaluation (minimum 4 years by a
examined by veterinary ophthalmologists between 2000-2005.3 cardiologist). (See CHIC website; www.caninehealthinfo.org).
Distichiasis: Abnormally placed eyelashes that irritate the Recommended tests include hip and elbow radiographs, and thyroid
cornea and conjunctiva. Can cause secondary corneal ulceration. profile including autoantibodies.
Identified in 5.05% of Japanese Chin CERF examined by veterinary
ophthalmologists between 2000-2005.3 Miscellaneous
• Breed name synonyms: Japanese Spaniel, Chin.
Persistent Hyaloid Artery: Congenital defect resulting from • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
abnormalities in the development and regression of the hyaloid ANKC (Australian National Kennel Club), NKC (National Kennel Club).
artery. Identified in 3.25% of Japanese Chin CERF examined by • AKC rank (year 2008): 74 (1,066 dogs registered)
veterinary ophthalmologists between 2000-2005.3 • Internet resources: Japanese Chin Club of America:
http://www.japanesechinonline.org/
Exposure Keratopathy Syndrome/Pigmentary Keratitis: Corneal Japanese Chin Club UK: www.japanesechinclub.co.uk/
reactivity and drying from ocular exposure secondary to shallow Japanese Spaniel Club of Canada:
orbits, exophthalmos, and lagophthalmos. Identified in 2.53% of www.japanesespanielclubofcanada.com
Japanese Chin CERF examined by veterinary ophthalmologists
between 2000-2005.3
References
Persistent Hyperplastic Tunica Vasculosa Lentis and Primary 1. OFA Website breed statistics: www.offa.org Last accessed SJuly 1, 2010.
Vitreous (PHTVL/PHPV): Congenital disorder presenting in the 2. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
breed with variable lesions from spots on the posterior lens to
Sep-Oct;38(5):467-77.
posterior lenticonus, and posterior polar subcapsular cataracts.
3. Ocular Disorders Presumed To Be Inherited In Purebred Dogs. American
Identified in 2.53% of Japanese Chin CERF examined by veterinary College Of Veterinary Ophthalmologists. ACVO,2007.
ophthalmologists between 2000-2005.3 4. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
Lens Luxation/Subluxation: Can be primary, or secondary. 5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
Identified in 1.44% of Japanese Chin CERF examined by veterinary hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
ophthalmologists between 2000-2005.3 Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Mitral Valve Disease (MVD): Japanese Chin dogs are prone to Population and Animal Health, Michigan State University. April, 2007.
early age mitral regurgitation. This condition may eventually lead 7. Axlund TW: Canine Spinal Cord Disease: The Non-painful Diseases.
to congestive heart disease, cardiac arrhythmias and cardiac failure. Proceedings, 2004 Atlantic Coast Veterinary Conference. 2004.
Unknown mode of inheritance. (See JCCA website) 8. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 224. AAHA Press, 1999.
Atlantoaxial Subluxation: Subluxation of the atlantoaxial 9. Cummings JF, Wood PA, Walkley SU, et. al.: GM2 gangliosidosis in a
joint is seen at an increased frequency in the breed. It can occur Japanese spaniel. Acta Neuropathol (Berl). 1985;67(3-4):247-53.
subsequent to a variety of lesions of the dens or atlantoaxial 10. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 477-480.
ligaments. In each case, dorsal displacement of the axis results
in compression of the cervical spinal cord. Unknown mode of
inheritance.7
277
Keeshond
limbs are straight boned. Feet are rounded and compact with black
nails. The gait is strong, showing lots of drive.
Weight: 55-65 lb (25-29.5 kg) Primary Hyperparathyroidism: Autosomal dominant disorder with
age-dependant penetrance. Average age of onset is 11.2 years.
Coat: The hair forms a lion’s ruff and trousers particularly in the Affected dogs present with hypercalcemia, inappetence, polyuria,
male, and breed specific markings around the eyes are termed polydipsia, and vomiting. Caused by a parathyroid gland adenoma.
spectacles. These markings include dark lines extending out from Progresses to hypercalcemic kidney failure. Reported at a frequency
the eyes. The undercoat is dense and colored gray or cream. The ears of 1.87% in the KCA Health Survey 2000. A linked-marker genetic
are black or off-black, the tip of tail is black, and outer coat hairs test is available, reporting 4.1% affected.1,3,4,5,6,7
are straight and harsh. Black, gray and cream are melded together
in the coat, with the tips of the guard hairs colored black. The ruff Cono-Truncal Septal Defect: A group of genetically and
and trousers are lighter than the main coat color, as are the feet. embryologically related cardiac malformations, including
They go through a high shedding phase twice a year when they sub-clinical defects of the conal septum, conal ventricular septal
blow their coats otherwise they have moderate grooming needs. defects, tetralogy of Fallot, and persistent truncus arteriosus. Three
predisposing gene markers are identified, showing a polygenic
Longevity: 12-14 years mode of inheritance.8,9
Points of Conformation: These dogs are compact and squarely Disease Predispositions
built, with moderately muscled and boned conformation and a Hypothyroidism: Inherited autoimmune thyroiditis. 6.4% positive
profuse standoff coat, a fox face with high head carriage and a for thyroid auto-antibodies based on testing at Michigan State
heavily plumed tail that rests closely over the back. The eyes are University. (Ave. for all breeds is 7.5%).10,11
medium-brown in color, almond shaped and the palpebral margins
are pigmented black. Ears are small and erect, high set, and the skull Distichiasis: Abnormally placed eyelashes that irritate the cornea
is wedge shaped with a definite stop. Lips are black and tight, neck and conjunctiva. Can cause secondary corneal ulceration. Identified
is moderate in length, and the topline descends slightly towards the in 5.66% of Keeshonden CERF examined by veterinary ophthalmolo-
rear. The thorax is rounded, the abdomen has moderate tuck up, and gists between 2000-2005.12
278
Cataracts: Posterior suture punctate cataracts predominate in the Tests of Phenotype: CHIC Certification: Hip and elbow
breed. Age of onset 1-3 years. Identified in 5.27% of Keeshonden radiographs, CERF eye examination, and patella evaluation. (See
CERF examined by veterinary ophthalmologists between 2000-2005. CHIC website; www.caninehealthinfo.org).
CERF does not recommend breeding any Keeshond with a cataract.12
Recommend thyroid profile including autoantibodies and cardiac
Allergic Dermatitis (Atopy): Inhalant or food allergy. Presents examination.
with pruritis and pyotraumatic dermatitis (hot spots). Reported at a
frequency of 3.19% in the KCA Health Survey 2000.6 Miscellaneous
• Breed name synonyms: Keeshound, Wolfspitz (German), Chien
Inherited Epilepsy: Generalized or partial seizures. Control with
Loup (Fr.), Lupini (Italy), Dutch Barge Dog (historical-England),
anticonvulsant medication. Age of onset 6 months to 3 years. Dorn
Dutch Keeshond.
reports a 9.36x odds ratio versus other breeds. One study suggests
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
an autosomal recessive mode of inheritance. Seizures are reported
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
at a frequency of 2.88% in the KCA Health Survey 2000.6,13,14
• AKC rank (year 2008): 95 (630 dogs registered)
Alopecia-X (Coat Funk): Progressive, symmetrical, non-pruritic, • Internet resources: The Keeshond Club of America:
truncal hair loss usually beginning in early adulthood. ACTH www.keeshond.org
stimulation test, low-dose dexamethazone stimulation test, and The Keeshond Club UK: www.keeshondclub.org.uk
thyroid panel results are normal. Elevated blood concentrations of The Keeshond Club of Canada: www.keeshondcanada.com
17-hydroxyprogesterone (17-OHP) are seen post ACTH stimulation.
Partial hair regrowth is reported in Keeshonden treated with References
melatonin. Reported at a frequency of 2.41% in the KCA Health 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Survey 2000. Unknown mode of inheritance.6,15,16 2. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Juvenile Diabetes Mellitus: Caused by a lack of insulin production Sep-Oct;38(5):467-77.
by the pancreas. Controlled by insulin injections, diet, and glucose 3. Weir EC, Norrdin RW, Barthold SW, et. al.: Primary hyperparathyroidism
monitoring. Affected dogs also form glucose-related cataracts. in a dog: biochemical, bone histomorphometric, and pathologic findings. J
Am Vet Med Assoc. 1986 Dec 1;189(11):1471-4.
Age of onset 2-6 months. Breeding studies suggest an autosomal
4. Skelly B: Hyperparathyroidism in the keeshond dog. Vet Rec. 2004 May
recessive mode of inheritance. Reported at a frequency of 0.78% in 22;154(21):672.
the KCA Health Survey 2000.6,17,18 5. Gear RN, Neiger R, Skelly BJ, et. al.: Primary hyperparathyroidism in 29
dogs: diagnosis, treatment, outcome and associated renal failure. J Small
Bladder Stones: One study reports a 5.47x odds ratio of forming Anim Pract. 2005 Jan;46(1):10-6.
calcium oxalate stones versus other breeds. Dorn reports a 2.81x 6. Keeshond Club of America: KCA 2000 Health Survey.
odds ratio versus other breeds. Composition of calculi not reported. 7. Goldstein RE, Atwater DZ, Cazolli DM, et. al.: Inheritance, mode of
Reported at a frequency of 0.31% in the KCA Health Survey inheritance, and candidate genes for primary hyperparathyroidism in
2000.6,19,20 Keeshonden. J Vet Intern Med. 2007 Jan-Feb;21(1):199-203.
8. Patterson DF, Pyle RL, Van Mierop L, et. al.: Hereditary defects the
Spontaneous Chronic Corneal Epithelial Defects (SCCED): conotruncal septum in Keeshond dogs: pathologic and genetic studies. Am
Keeshonden are reported as a breed with an increased prevalence of J Cardiol. 1974 Aug;34(2):187-205.
spontaneous corneal epithelial defects. Research indicates a role of 9. Werner P, Raducha MG, Prociuk U, et. al.: The keeshond defect in cardiac
substance P.21 conotruncal development is oligogenic. Hum Genet. 2005 Apr;116(5):368-77
10. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
Central progressive Retinal Atrophy, Cutaneous Asthenia, Optic serum thyroid hormone autoantibodies in dogs with clinical signs of
Nerve Hypoplasia, Oligodontia, and von Willebrand’s Disease are hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
11. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
reported.22
Population and Animal Health, Michigan State University. April, 2007.
12. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Isolated Case Studies College of Veterinary Ophthalmologists. ACVO, 2007.
Renal Cortical Hypoplasia: Congenital kidney disease was reported 13. Hall SJ, Wallace ME: Canine epilepsy: a genetic counselling programme
in a litter of Keeshonds.23 for keeshonds. Vet Rec. 1996 Apr 13;138(15):358-60.
14. Wallace ME: Keeshonds: a genetic study of epilepsy and EEG readings. J
Malignant Fibrous Histiocytoma: Identified in a retrobulbar Small Anim Pract. 1975 Jan;16(1):1-10.
location in a 12-year-old castrated male Keeshond dog.24 15. Frank LA, Hnilica KA, Oliver JW: Adrenal steroid hormone concentrations
in dogs with hair cycle arrest (Alopecia X) before and during treatment with
melatonin and mitotane. Vet Dermatol. 2004 Oct;15(5):278-84.
Genetic Tests 16. Frank LA, Hnilica KA, Rohrbach BW, et. al.: Retrospective evaluation of
Tests of Genotype: Linked marker test is available for Primary sex hormones and steroid hormone intermediates in dogs with alopecia.
Hyperparathyroidism from the Goldstein lab at Cornell (www.vet. Vet Dermatol. 2003 Apr;14(2):91-7.
cornell.edu/labs/goldstein/). 17. Kramer JW, Klaassen JK, Baskin DG, et. al.: Inheritance of diabetes
mellitus in Keeshond dogs. Am J Vet Res. 1988 Mar;49(3):428-31.
18. Kramer JW, Nottingham S, Robinette J, et. al.: Inherited, early onset,
279
insulin-requiring diabetes mellitus of Keeshond dogs. Diabetes. 1980
Jul;29(7):558-65.
19. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
20. Lekcharoensuk C, Lulich JP, Osborne CA, et. al.: Patient and
environmental factors associated with calcium oxalate urolithiasis in dogs.
J Am Vet Med Assoc. 2000 Aug 15;217(4):515-9.
21. Murphy CJ, Marfurt CF, McDermott A, et. al.: Spontaneous chronic
corneal epithelial defects (SCCED) in dogs: clinical features, innervation,
and effect of topical SP, with or without IGF-1. Invest Ophthalmol Vis Sci.
2001 Sep;42(10):2252-61.
22. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 224-5. AAHA Press, 1999.
23. Klopfer U, Neumann F, Trainin R: Renal cortical hypoplasia in a
Keeshond litter. Vet Med Small Anim Clin. 1975 Sep;70(9):1081-3.
24. Lassaline ME, Gelatt KN, Brooks DE, et. al.: Orbitotomy for retrobulbar
malignant fibrous histiocytoma in a dog. Vet Ophthalmol. 2005
Jan-Feb;8(1):1-6.
25. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 567-571.
280
Kerry Blue Terrier
Recognized Behavior Issues and Traits
Reported breed attributes include: They are considered to be good
guard dogs. Kerry Blues get along with children well and tolerate
play. They commonly exhibit inter-male aggression. They require an
early introduction to and supervision with cats or other small pets.
They have a low barking tendency, are diggers, and need regular
exercise and stimulating games. Intelligent, but easily bored, they
have an independent streak and can be stubborn. They need close
human contact, and do not do well as kenneled dogs. The Kerry Blue
does not tolerate hot weather well.
Coat: The coat is dense and hairs are wavy and soft in texture. It von Willebrand’s Disease Type 1 (vWD): Autosomal recessive
takes about 1 1/2 years for the adult coat to mature. Puppies are genetic disorder causing a mild bleeding syndrome, usually after
often black and during early maturity, very dark gray and brownish trauma or surgery. A genetic test is available.2
hair may intermingle in the coat until they are gradually replaced
Progressive Neuronal Abiotrophy (PNA, Multiple System
by the correct final hair color of blue (this correct color varies from
Degeneration): Fatal, autosomal recessive cerebellar disorder, with
light gray-blue to deep slate gray). Extremities may keep a darker
an onset between 9 and 16 weeks of age. Progresses to incapacity
color. Black adults are not accepted.
by 4-8 months of age. Histopathology shows progressive loss
Longevity: 14+ years of cerebellar cortical Purkinje’s cells, with bilateral symmetric
degeneration of the olivary nuclei followed by degeneration of the
Points of Conformation: This breed is characterized by a sturdy substantia nigra and caudate nucleus. No genetic test is available.3,4
conformation with lots of muscle and bone, and small dark eyes
somewhat deep set, triangular ears that are small with moderately Factor XI Deficiency: Rare, autosomal recessive bleeding disorder
thick leather and folded forward. The ear fold is above the topline causing a tendency for mild posttraumatic or postoperative
of the skull. The skull is flat with a very minimal stop. The nose is bleeding. Clotting tests show a prolonged activated partial
black. The neck is moderately long and strong, not throaty. The thromboplastin and activated clotting times. Treat with fresh-frozen
topline is short and level, and there is a slight abdominal tuck. The plasma. A genetic test is available.5
tail is high set, and carried high. The thorax is deep and somewhat
narrow, metatarsals and metacarpals are short and sturdy. Feet are Disease Predispositions
compact, small, and with deep strong footpads with black toenails. Sebaceous Cysts: Benign follicular skin cysts. Reported at a
Rear dewclaws disqualify. Gait is smooth, true, elastic and ground frequency of 22.7% in the KBTF Health Survey 2004. Unknown
covering with good rear drive. mode of inheritance.6
281
Spiculosis (Hard Hairs, Spikes): Hard keratinized hairs produced Vitreous Degeneration: A liquefaction of the vitreous gel which
by abnormal hair follicles. Reported at a frequency of 6.7% in the may predispose to retinal detachment and/or glaucoma. Identified
KBTF Health Survey 2004. Unknown mode of inheritance.6,7 in 1.32% of Kerry Blue Terriers CERF examined by veterinary
ophthalmologists between 2000-2005.8
Cataracts: Anterior cortex punctate and posterior suture
intermediate cataracts predominate in the breed. Reported at Craniomandibular Osteopathy, Dermoid Sinus, Entropion, Patent
a frequency of 4.7% in the KBTF Health Survey 2004. Identified Ductus Arteriosus, Progressive Retinal Atrophy, and XX Sex
in 3.52% of Kerry Blue Terriers CERF examined by veterinary Reversal are reported.16
ophthalmologists between 2000-2005. CERF does not recommend
breeding any Kerry Blue Terrier with a cataract.6,8 Isolated Case Studies
Congenital Intestinal Atresia: Case report of a Kerry Blue Terrier
Keratoconjunctivitis Sicca (KCS, Dry Eye): Inadequate tear with an undeveloped intestinal tract.17
production causing drying of the cornea and conjunctiva. Reported
at a frequency of 3.4% in the KBTF Health Survey 2004.6
Genetic Tests
Premolar Hypodontia: Multiple missing premolar syndromes Tests of Genotype: Direct gene test for vWD is available from VetGen.
are reported in the breed. The absence of the second premolars
Direct test for an autosomal recessive DM susceptibility gene is
appears to be an autosomal recessive disorder, while missing fourth
available from OFA.
premolars appears to have a more complex, polygenic mode of
inheritance. Studies show that Kerry Blue Terriers with missing Direct gene test for Factor XI deficiency is available from PennGen.
teeth have smaller litter sizes (ave. 3.64 versus 5.72) suggesting a
pleiotrophic effect. Missing teeth are reported at a frequency of Tests of Phenotype: CHIC certification: Required testing
3.3% in the KBTF Health Survey 2004.6,9,10,11 includes hip radiographs and CERF eye examination. Optional
testing includes direct tests for von Willebrands disease, Factor XI
Food Allergy (Food Hypersensitivity/Food Intolerance): Presents deficiency, and the susceptibility gene for DM. (See CHIC Website:
with pruritis and pyotraumatic dermatitis (hot spots). Average age www.caninehealthinfo.org)
of onset of 1.7 years. Reported at a frequency of 3.3% in the KBTF
Health Survey 2004.6 Recommend thyroid profile including autoantibodies, elbow
radiographs, patella evaluation, and cardiac examination.
Hypothyroidism: Inherited autoimmune thyroiditis. 2.6% positive
for thyroid autoantibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5%).12,13 Miscellaneous
• Breed name synonyms: Kerry Blue, Irish Blue Terrier
Colitis/Chronic Large Bowel Diarrhea: Onset usually prior to 3 • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
years of age. Reported at a frequency of 2.7% in the KBTF Health ANKC (Australian National Kennel Club)
Survey 2004.6 • AKC rank (year 2008): 120 (274 dogs registered)
• Internet resources: United States Kerry Blue Terrier Club:
Degenerative Myelopathy (DM): Affected dogs show an insidious www.uskbtc.com
onset of upper motor neuron (UMN) paraparesis at an average The Kerry Blue Terrier Club of Canada: www.kbtcc.ca
age of 11.4 years. The disease eventually progresses to severe
tetraparesis with lower motor neuron signs. Affected dogs have References
normal results on myelography, MRI, and CSF analysis. Necropsy 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
confirms the condition. Unknown mode of inheritance. A direct 2. Wardrop KJ: Canine von Willebrand Disease. Proceedings, 2004 Western
genetic test for an autosomal recessive DM susceptibility gene is Veterinary Conference. 2004.
available. All affected dogs are homozygous for the gene, however, 3. O’brien DP, Johnson GS, Schnabel RD, et. al.: Genetic mapping of canine
only a small percentage of homozygous dogs develop DM. OFA multiple system degeneration and ectodermal dysplasia Loci. J Hered. 2005
Nov-Dec;96(7):727-34.
reports DM susceptibility gene frequencies of 44% carrier, and 12%
4. deLahunta A, Averill DR Jr: Hereditary cerebellar cortical and
homozygous “at-risk”. Clinical DM is reported at a frequency of extrapyramidal nuclear abiotrophy in Kerry Blue Terriers. J Am Vet Med
2.18% in the KBTC Health Survey 2004.1,6,14,15 Assoc. 1976 Jun 15;168(12):1119-24.
5. Knowler C, Giger U, Dodds WJ, et. al.: Factor XI deficiency in Kerry Blue
Persistent Pupillary Membranes: Strands of fetal remnant Terriers. J Am Vet Med Assoc. 1994 Dec 1;205(11):1557-61.
connecting; iris to iris, cornea, lens, or involving sheets of tissue. 6. Kerry Blue Terrier Foundation, Sell E: Health Survey 2004. 2004.
The later three forms can impair vision, and dogs affected with 7. McKeever PJ, Torres SMF, O’Brien TD: Spiculosis. J Am Anim Hosp Assoc
these forms should not be bred. Identified in 1.76% of Kerry Blue 1992: 28[3]:257-262.
Terriers CERF examined by veterinary ophthalmologists between 8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
2000-2005.8 College of Veterinary Ophthalmologists. ACVO, 2007.
9. Aksenovich TI, Zorkal’tsov IV, Aul’chenko IuS, et. al.: Inheritance of
hypodontia in Kerry Blue Terrier dogs. Genetika. 2004 May;40(5):658-66.
Distichiasis: Abnormally placed eyelashes that irritate the cornea
10. Zorkaltseva IV, Akberdin IR, Kulikova AV, et. al.: Changes in litter
and conjunctiva. Can cause secondary corneal ulceration. Identified size in Kerry blue terrier dogs with abnormal dentition. Genetika. 2006
in 1.32% of Kerry Blue Terriers CERF examined by veterinary Mar;42(3):427-9.
ophthalmologists between 2000-2005.8
282
11. Aksenovich TI, Kulikova AV, Kniazev SP, et. al.: Polymorphism of dental
formula and segregation of its variants in a pedigree of kerry blue terrier
dogs. Genetika. 2006 Mar;42(3):414-20.
12. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
13. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
14. Shelton GD, Johnson GC, Johnson GS, et. al.: Peripheral Nerve Pathology
in Canine Degenerative Myelopathy with Mutation in Superoxide Dismutase
1 Gene. Proceedings, 2009 ACVIM Forum. 2009.
15. Coates JR, Zeng R, Awano T, et. al.: An SOD1 Mutation Associated with
Degenerative Myelopathy Occurs in Many Dog Breeds. Proceedings 2009
ACVIM Forum. 2009.
16. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 225. AAHA Press, 1999.
17. Gough J: Congenital intestinal atresia in a Kerry blue terrier. Can Vet J.
1999 Nov;40(11):809.
18. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 387-390.
283
Komondor
Longevity: 12 years
284
Disease Predispositions 6. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 225. AAHA Press, 1999.
Cataracts: Anterior and equatorial cortex intermediate cataracts 7. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
predominate in the breed, with an onset of 2-3 years. Juvenile House, NY 2006. p. 284-287.
cataracts are also reported to occur. Cataracts are identified in
7.14% of Komondorok CERF examined by veterinary ophthalmolo-
gists between 2000-2005. CERF does not recommend breeding any
Komondor with a cataract.2
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: Hungarian Sheepdog.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club).
• AKC rank (year 2008): 151 (60 dogs registered)
• Internet resources: The Komondor Club of America Inc.:
http://clubs.akc.org/kca/
Komondor Club of Great Britain: www.komondor.co.uk/
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Matushek KJ & Cockshutt JR: Mesenteric and gastric volvulus in a dog. J
Am Vet Med Assoc. 1987 Aug 1;191(3):327-8.
285
Kuvasz
Recognized Behavior Issues and Traits
They are noted to be sensitive, devoted, protective, wary with
strangers, courageous, intelligent, and possessing a gentle
temperament when not guarding. They also go through seasonal
shedding, are slow to mature, need early socialization and
obedience training if adopted as a family dog with children and
other pets, are independent minded, and some are aggressive. These
dogs are not best for owners that have not handled dogs before.
They also need regular exercise and games, and lots of human
contact or they will develop boredom vices. They have average to
The Breed History high grooming needs.
The breed traces back perhaps five thousand years, and through
much of this time, this dog was a favorite of the ruling class. The Normal Physiologic Variations
breed name derives from the Turkish word kawasz, which translates None reported
as “armed guard of nobility”, or perhaps Arabic kawwasz, meaning
archer. Breed ancestors were larger, and likely came from Tibet. The Drug Sensitivities
Komondor is likely related to this breed, and less well documented None reported
are possible ties to the Maremma Sheepdog and Akbash dog.
Hungarian fanciers were responsible for much of the breed
evolution and standardization. AKC recognition occured in 1931.
Inherited Diseases
Hip Dysplasia: Polygenically inherited trait causing degenerative
joint disease and hip arthritis. Reported 10.2x odds ratio versus
Breeding for Function other breeds. OFA reports 18.4% affected.1,2
In early times, he was a valued guard dog. Later, once the nobility lost
exclusive ownership, they were adapted for herding tasks as guards Elbow Dysplasia: Polygenically inherited trait causing elbow
of the flock or herd. Now they are often kept for companionship. arthritis. OFA reports 6.7% affected.1
Coat: The thick double coat is always white. The outer coat is coarse Patella Luxation: Polygenically inherited laxity of patellar ligaments,
and straight to wavy, while the undercoat is fine and short. Coat causing luxation, lameness, and later degenerative joint disease.
length varies with the season. Skin is darkly pigmented. Treat surgically if causing clinical signs. OFA reports 0.8% affected.1
286
Humeral Osteochondritis Dissecans: Polygenically inherited
cartilage defect of the humeral head. Causes shoulder joint pain
Genetic Tests
Tests of Genotype: Direct test for prcd-PRA is available from
and lameness in young growing dogs. Mild cases can resolve with Optigen.
rest, while more severe cases require surgery. There is a 2.24:1 male
to female ratio. 75% of all cases are unilateral. Reported 29.1x odds Direct test for an autosomal recessive DM susceptibility gene is
ratio versus other breeds. Reported at a frequency of 2.96% in the available from OFA.
Kuvasz.2,6
Tests of Phenotype: CHIC Certification: Required testing
Corneal Dystrophy: The epithelial/stromal and endothelial forms includes hip and elbow radiographs, and thyroid profile
occur in the breed, causing a bilateral, white to gray, non-inflam- including autoantibodies. Optional recommended tests include
matory corneal opacity. Identified in 2.83% of Kuvaszok CERF patella examination, CERF eye examination, congenital cardiac
examined by veterinary ophthalmologists between 2000-2005. CERF evaluation, and genetic test for prcd PRA. (See CHIC website; www.
does not recommend breeding Kuvaszok with corneal dystrophy.3 caninehealthinfo.org).
Cataracts: Posterior cortical punctate cataracts predominate in the
breed. Identified in 2.33% of Kuvaszok CERF examined by veterinary Miscellaneous
ophthalmologists between 2000-2005. CERF does not recommend • Breed name synonyms: Hungarian Kuvasz, Kuvaszok (pl)
breeding any Kuvaszok with a cataract.3 • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
Hypertrophic Osteodystrophy (HOD): Puppies generally show • AKC rank (year 2008): 135 (145 dogs registered)
swollen, painful ends of long bones and may have a fever as well as • Internet resources: Kuvasz Club of America: www.kuvasz.com
loss of appetite. If these puppies are not diagnosed early permanent Kuvasz Club of Canada: www.kuvaszclubofcanada.org
damage may necessitate euthanasia. Research with Great Danes Kuvasz Fanciers of America Inc.:
(the breed showing a relatively high incidence of H.O.D.) shows http://hbalaw.com/KFA/index.htm
that a high energy, high protein diet or excess supplementation
may predispose puppies to H.O.D. Treatment consists of putting the References
affected animal onto a high quality but more moderate diet as well 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
as using analgesics to encourage the puppy to eat and stay mobile. 2. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
The typical age of onset 12-20 weeks. Seen at a low frequency in developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
the breed. (See KCA website) Sep-Oct;38(5):467-77.
3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Deafness: Congenital deafness occurs in the breed. Can be College of Veterinary Ophthalmologists. ACVO, 2007.
unilateral or bilateral. Diagnosed by BAER testing. Unknown mode 4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
of inheritance.7 hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
Degenerative Myelopathy (DM): Affected dogs show an insidious 5. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
onset of upper motor neuron (UMN) paraparesis at an average
6. Rudd RG, Whitehair JG, Margolis JH: Results of management of
age of 11.4 years. The disease eventually progresses to severe
osteochondritis dissecans of the humeral head in dogs : 44 cases [1982 to
tetraparesis with lower motor neuron signs. Affected dogs have 1987]. J Am Anim Hosp Assoc 1990: 26[2]:173-178.
normal results on myelography, MRI, and CSF analysis. Necropsy 7. Strain GM: Deafness prevalence and pigmentation and gender
confirms the condition. Unknown mode of inheritance. A direct associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
genetic test for an autosomal recessive DM susceptibility gene is 8. Kathmann I, Cizinauskas S, Doherr MG, et. al.: Daily controlled
available. All affected dogs are homozygous for the gene, however, physiotherapy increases survival time in dogs with suspected degenerative
only a small percentage of homozygous dogs develop DM. The gene myelopathy. J Vet Intern Med. 2006 Jul-Aug;20(4):927-32.
is present at a frequency of 22% in the breed.8,9 9. Coates JR, Zeng R, Awano T, et. al.: An SOD1 Mutation Associated with
Degenerative Myelopathy Occurs in Many Dog Breeds. Proceedings 2009
Allergic Inhalant Dermatitis, Cruciate Ligament Rupture, ACVIM Forum. 2009.
Dermatomyositis, Gastric Dilatation-Volvulus, Prognathism, and 10. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
von Willebrand’s Disease are reported.10 Ackerman. p. 225. AAHA Press, 1999.
11. Hazlett MJ, Smith-Maxie LL, de Lahunta A: A degenerative
encephalomyelopathy in 7 Kuvasz puppies. Can Vet J. 2005
Isolated Case Studies May;46(5):429-32.
Degenerative Encephalomyelopathy: Seven Kuvasz puppies 12. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
from 2 same-parentage litters developed weakness and ataxia. Book House, NY 2006. p. 288-292.
Six necropsied dogs had lesions in caudate nucleus, cerebellar
nuclei and folia, and spinal cord. Lesions seen were felt to be either
familial or due to the effects of an amprolium-induced thiamine
deficiency on the developing brains of these puppies.11
287
Labrador Retriever
Recognized Behavior Issues and Traits
These dogs are famous for their placid, loving temperament. They
enjoy play and need lots of human contact. Their loyalty and
intelligence make them a treasured companion dog. Good with
children and other pets, they are also easy to train but they need to
be trained from an early age. They require both mental challenge
and physical exercise for good health. If bored, they may resort
to chewing. They are average shedders that need only routine
grooming care. They gain weight easily.
Centro-Nuclear Myopathy (CNM): Autosomal recessive disorder Cranial Cruciate Ligament (ACL) Rupture: Traumatic tearing
of muscle weakness. Onset of progressive weight loss and loss of the ACL in the stifle, causing lameness and secondary arthritis.
of tendon reflexes by 2 months of age, and an awkward gait, Treat with surgery. Reported at an increased incidence versus
decreased exercise tolerance, and generalized muscle weakness other breeds. In one study, 23% of large breed dogs with the
between 2-5 months of age. Clinical signs stabilize in adult affected diagnosis were Labrador Retrievers. Dorn reports a 2.17x odds ratio
dogs. A genetic test is available.19,20 versus other breeds. There is no difference in tibial plateau angle
between affected and unaffected Labrador Retrievers with ACL
Tricuspid Valve (Right Atrioventricular) Dysplasia: Autosomal rupture.37,38,39,40
dominant disorder with incomplete penetrance. Congenital
malformation of the tricuspid valve leaflets, chordae tendineae, Osteochondritis Desicans (OCD): Inherited joint cartilage defect.
and/or right ventricular papillary muscles. Mild cases have no Causes joint pain and lameness in young growing dogs. Mild cases
clinical signs except tricuspid regurgitation on auscultation and can resolve with rest, while more severe cases require surgery.
echocardiography. Severely affected dogs show signs of ascites, Reported 45.9x odds ratio for hock OCD, 27.6x odds ratio for stifle
pleural effusion, exercise intolerance, syncope, weight loss, OCD and 13.1x odds ratio for shoulder OCD versus other breeds.7
arrythmia, and right sided heart failure. Labrador Retrievers have a
35x relative risk versus other breeds, with a heritability of 0.71. No Hypertrophic Osteodystrophy (HOD): Immune-mediated disorder
genetic test is available.21,22,23 causing fever, and painful, swollen joints and bones in young
Labrador Retrievers. Occurs mostly within 3-14 days post-vacci-
Cystinuria: Rare, autosomal recessive disease causing dysuria, nation. Age of onset is 8-16 weeks. Reported 5.9x odds ratio versus
stranguria, or obstruction due to cystine calculi, primarily in other breeds.7
affected males. Caused by a defect in cystine metabolism. Affected
females can have cystine crystals and calculi without clinical signs. Chronic Hepatitis/Copper Associated Hepatitis: A breed-related
A genetic test is available.24,25 hepatopathy occurs in Labrador Retrievers, characterized by
vomiting, polyuria/polydipsia, icterus, and abdominal pain and
Narcolepsy: Rare, autosomal recessive disorder causing sudden distention. Liver enzymes are elevated, and histopathology shows
collapse and a sleep-like state elicited by excitement. Clinical chronic inflammation, fibrosis, and copper accumulation. Feeding
episodes begin at four weeks of age, with maximal symptoms by low copper diets is helpful in controlling the disease. Incidence
10-32 weeks of age. A genetic test is available.26,27 is 1.2% in the breed, with a median age at diagnosis of 9.3 years.
Unknown mode of inheritance.41,42,43,44
Disease Predispositions Distichiasis: Abnormally placed eyelashes that irritate the cornea
Allergic Dermatitis: Inhalant or food allergies. Presents with pruritis
and conjunctiva. Can cause secondary corneal ulceration. Identified
and pyotraumatic dermatitis (hot spots). The breed has a significant
in 0.90% of Labrador Retrievers CERF examined by veterinary
frequency of allergies, with a computed heritability of 0.47.28
ophthalmologists between 2000-2005.9
Hypothyroidism: Inherited autoimmune thyroiditis. 5.7% positive
Corneal Dystrophy: Non-inflammatory epithelial/stromal corneal
for thyroid autoantibodies based on testing at Michigan State
opacity. Identified in 0.76% of Labrador Retrievers CERF examined
University. (Ave. for all breeds is 7.5).29,30
by veterinary ophthalmologists between 2000-2005.9
Persistent Pupillary Membranes: Strands of fetal remnant
Lymphoma/Lymphosarcoma: Malignant cancer of lymphoid tissue.
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
Both B-cell and T-cell (mycosis fungoides) occur in the breed.45
The later three forms can impair vision, and dogs affected with
these forms should not be bred. Identified in 3.41% of Labrador Entropion: A rolling in of the eyelids, can cause corneal irritation
Retrievers CERF examined by veterinary ophthalmologists between and ulceration. Correct with surgery. Reported at an increased
2000-2005.9 incidence versus other breeds. Identified in 0.44% of Labrador
Retrievers CERF examined by veterinary ophthalmologists between
Epilepsy (Inherited Seizures): Can be generalized or partial
2000-2005.9,46
seizures. Control with anticonvulsant medication. Occurs at
a frequency of 3.1% in Danish Labrador Retrievers with 24% Acquired Laryngeal Paralysis: Late-onset disorder of laryngeal
generalized, and 70% partial seizures. Proposed polygenic dysfunction secondary to axonal degeneration of the recurrent
inheritance with a major recessive gene of influence.31,32,33,34 laryngeal nerve. Affected dogs show exercise intolerance,
289
inspiratory stridor, inspiratory dyspnoea, gagging, coughing and Iridociliary Epithelial Tumors: These intraocular adenomas and
dysphonia. There is a male:female ratio of 1.56:1 and the average adenocarcinomas occur more frequently in the Labrador Retriever.
age of presentation is 9.9 years. Labrador Retrievers are identified as They rarely metastasize.65
the most frequently affected breed.47,48
Calcinosis Circumscripta: Calcinosis circumscripta is an
Diabetes Mellitus (Sugar Diabetes): Treat with insulin injections. uncommon syndrome of dystrophic, metastatic or iatrogenic
Age of onset between 5-12 years. Labrador Retrievers represent mineralization of calcium salts in soft tissues. Lesions usually occur
17.4% of all diagnosed cases.49 on the hind feet or tongue in 1-4 year old dogs. Nine percent of
canine cases occur in Labrador Retrievers.66
Immune-Mediated Hemolytic Anemia (IMHA): Autoimmune
destruction of red blood cells. Females are more frequently affected Ossification of the Infraspinatus Tendon-Bursa: Disorder
than males. Labrador Retrievers account for 8% of diagnosed cases. identified in 13 Labrador Retrievers with unilateral or bilateral
Unknown mode of inheritance.50,51 forelimb lameness between 2 to 10 years of age. Diagnose via
radiograph. Treat with rest, steroid injection, or surgery.67
Nasal Parakeratosis: Inherited disorder of nasal hyperkeratotic
lesions appearing between 6 and 12 months of age. Affected dogs Acral Lick Dermatitis, Central Axonopathy, Central PRA,
have mild to severe lesions of dry and rough keratin affecting Cervical Vertebral Instability, Cleft Lip/Palate, Degenerative
the dorsal aspect of the nasal planum. Fissures and erosions Myelopathy, Ectropion, Factor VIII Deficiency, Fanconi
can develop in severe cases. Proposed autosomal recessive Syndrome, Fibrinoid Leukodystrophy, Follicular Dysplasia,
inheritance.52,53 Gastric Dilatation w/Volvulus, Hypotrichosis, Juvenile Cellulitis,
Lymphedema, Malignant Hyperthermia, Megaesophagus,
Uveal Cysts: Labrador Retrievers have a higher frequency of uveal Microphthalmia, Micropapilla, Mucinosis, Myelodysplasia,
cysts than other breeds, with a mean age of cyst development of Myoclonus, Neuroaxonal Dystrophy, Optic Nerve Coloboma,
9.1 years.54 Optic Nerve Hypoplasia, Panosteitis, Seasonal Flank
Alopecia, Sebaceous Adenitis, Silica Urolithiasis, Spongiform
Secondary Glaucoma: Glaucoma causes increased pressure within Leukodystrophy, Supernumerary Teeth, Tetralogy of Fallot,
the eyeball and blindness due to damage to the retina. The breed is Vitamin A Responsive Dermatosis, Vitiligo, and von Willebrand’s
listed as predisposed to secondary glaucoma due to uveitis or lens Disease are reported.68
luxation. Screen with tonometry.55
Limbal Melanoma: Benign eye mass, usually originating from the Isolated Case Studies
dorsal limbus. Labrador Retrievers have a 3.0x odds ratio of limbal Hemophilia B (Factor IX deficiency): An affected male Labrador
melanomas versus other breeds.56 Retriever had clinically severe bleeding due to complete deletion of
the Factor IX gene. A genetic test was developed for this X-linked
Lingual Squamous Cell Carcinoma (SCC): Labrador Retrievers recessive gene.69
have a 2.41x odds ratio versus other breeds of developing this
tongue cancer. Females are overrepresented in one study.57 Cerebellar Abiotrophy: Several cases of juvenile cerebellar
degeneration have been diagnosed in Labrador Retrievers. Puppies
Atrioventricular (Heart) Block: Labrador Retrievers are found between 9 and 17 weeks of age developed rapidly progressive
to be at increased risk of high-grade second- or third-degree hypermetria, ataxia, and intension tremors resulting in euthanasia.70,71
atrioventricular block versus other breeds. Treatment is with a
pacemaker.58,59 X-linked Muscular Dystrophy: A dystrophin deficient muscular
dystrophy similar to human Duchenne’s muscular dystrophy was
Histiocytic Sarcoma/Histiocytosis: Malignant cancer of CD11d+ identified in a 3.5 month-old, male Labrador retriever. The dog
macrophages, producing masses in the spleen, liver, lung, bone presented with difficulty swallowing, poor body condition and a
marrow, +/or eye. Mean age of diagnosis of 8.61 +/- 2.43 years, protruding tongue.72
with a less than 6 month life expectancy. Labrador Retrievers are
overrepresented in diagnoses versus other breeds.60,61 Mytubular Myopathy: Three to four-month-old, male, Labrador
retrievers present with progressive weakness and muscle atrophy.
Ectopic Ureter: Congenital malformation where one or both Histology demonstrated central mitochondrial accumulations. A
ureters do not enter the body of the urinary bladder, often entering mutation in the MTM 1 gene causes this x-linked disease in the
the bladder neck or urethra causing incontinence. Labrador breed. Worldwide screening did not identify carriers outside of this
Retrievers are at increased risk versus other breeds. Unknown affected kindred in Canada.73,74
inheritance.62,63
Chondrodysplasia/Dwarfism: An apparently autosomal recessively
Digital Squamous Cell Carcinoma (SCC): Subungual (toe) inherited dwarfism without retinal lesions is identified in a kindred
squamous cell carcinoma occurs at increased frequency in black of Labrador Retrievers in the Netherlands. Candidate gene analysis
dogs. Treat with digital amputation. Labrador Retrievers account for was not successful in identifying a causative gene.75
23.8% of all cases.64
Neuronal Ceroid-Lipofuscinosis (NCL): An 8-year-old, neutered
male Labrador Retriever presented with an 11 month history of
290
progressive partial seizure activity (facial and ear twitching), and a 2 Jul-Aug;35(4):332-40.
week history of ataxia and dysphagia. Necropsy diagnosis confirmed 3. Phavaphutanon J, Mateescu RG, Tsai KL, et. al.: Evaluation of quantitative
NCL.76 trait loci for hip dysplasia in Labrador Retrievers. Am J Vet Res. 2009
Sep;70(9):1094-101.
Mucopolysaccharidosis Type II (MPSII): A 5-year-old male 4. Hou Y, Wang Y, Lust G, et. al.: Retrospective analysis for genetic
Labrador Retriever had progressive incoordination, visual improvement of hip joints of cohort labrador retrievers in the United
States: 1970-2007. PLoS One. 2010 Feb 24;5(2):e9410.
impairment, exercise intolerance, coarse facial features,
5. Engler J, Hamann H & Distl O: Estimation of population genetic
macrodactylia, unilateral corneal dystrophy, and generalized
parameters for radiographical findings of elbow dsyplasia in the Labrador
osteopenia. X-linked recessive MPSII was diagnosed.77 Retriever. Berl Munch Tierarztl Wochenschr. 2009 Sep-Oct;122(9-
10):378-85.
Sub-Follicular Panniculitis And Sebaceous Adenitis: A 6. Huck JL, Biery DN, Lawler DF, et. al.: A longitudinal study of the influence
6-year-old male black Labrador retriever presented with a 12 week of lifetime food restriction on development of osteoarthritis in the canine
course of nonpruritic multicentric, well-demarcated alopecia. elbow. Vet Surg. 2009 Feb;38(2):192-8.
Pathology revealed an inflammatory sebaceous adenitis and 7. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
sub-follicular panniculitis. Alopecia was permanent in these areas.78 developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
Genetic Tests 8. Gibbons SE, Macias C, Tonzing MA, et. al.: Patellar luxation in 70 large
breed dogs. J Small Anim Pract. 2006 Jan;47(1):3-9.
Tests of Genotype: Direct tests for prcd-PRA, and RD/OSD are 9. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
available from Optigen. College of Veterinary Ophthalmologists. ACVO, 2007.
10. Kommonen B, Kylmä T, Karhunen U, et. al.: Impaired retinal function
Direct test for exercise induced collapse (EIC) is available from the in young labrador retriever dogs heterozygous for late onset rod-cone
University of Minnesota Veterinary Diagnostic Lab. degeneration. Vision Res. 1997 Feb;37(3):365-70.
11. Morris Animal Foundation: Morris Animal Foundation Update: Genetic
Direct test for centronuclear myopathy (CNM) is available from the Tests Focus on Breed-Specific Vision Problems. Canine Pract 1999:24[4]:21.
Alfort Lab www.labradorcnm.com, and the Animal Health Trust. 12. Zangerl B, Goldstein O, Philp AR, et al.: Identical
mutation in a novel retinal gene causes progressive rod–cone
Direct test for cystinuria is available from PennGen. degeneration in dogs and retinitis pigmentosa in humans.
Genomics 2006; 88:551–563.
Direct test for Hemophilia B is available from HealthGene. 13. Taylor SM, Shmon CL, Adams VJ, et. al.: Evaluations of labrador
retrievers with exercise-induced collapse, including response to a
Direct test for Narcolepsy is available from Optigen and HealthGene. standardized strenuous exercise protocol. J Am Anim Hosp Assoc. 2009
Jan-Feb;45(1):3-13.
Direct tests for black, chocolate (brown), yellow, and diluted coat 14. Patterson EE, Minor KM, Tchernatynskaia AV, et. al.: A canine DNM1
colors and black and brown nose are available from HealthGene and mutation is highly associated with the syndrome of exercise-induced
VetGen. collapse. Nat Genet. 2008 Oct;40(10):1235-9.
15. Taylor SM, Shmon CL, Shelton GD, et. al.: Exercise-induced collapse
Tests of Phenotype: CHIC Certification: Required testing includes of Labrador retrievers: survey results and preliminary investigation of
hip and elbow radiographs, and CERF eye examination. Optional heritability. J Am Anim Hosp Assoc. 2008 Nov-Dec;44(6):295-301.
gene test for CNM (See CHIC website; www.caninehealthinfo.org). 16. Farnum CE, Jones K, Riis R, et. al.: Ocular-chondrodysplasia in labrador
retriever dogs: a morphometric and electron microscopical analysis. Calcif
Recommend thyroid profile including autoantibodies, patella Tissue Int. 1992 Jun;50(6):564-72.
evaluation, genetic test for EIC, and cardiac examination. 17. Carrig CB, Sponenberg DP, Schmidt GM, et. al.: Inheritance of associated
ocular and skeletal dysplasia in Labrador retrievers. J Am Vet Med Assoc.
1988 Nov 15;193(10):1269-72.
Miscellaneous 18. Goldstein O, Guyon R, Kukekova A, et. al.: COL9A2 and COL9A3
• Breed name synonyms: Lab, Labrador, Yellow Lab, Black Lab, mutations in canine autosomal recessive oculoskeletal dysplasia. Mamm
Chocolate Lab, St. John’s Retriever (historical) Genome. 2010 Aug;21(7-8):398-408.
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), 19. Pelé M, Tiret L, Kessler JL, et. al.: SINE exonic insertion in the PTPLA
ANKC (Australian National Kennel Club), NKC (National Kennel Club) gene leads to multiple splicing defects and segregates with the autosomal
• AKC rank (year 2008): 1 (100,736 dogs registered) recessive centronuclear myopathy in dogs. Hum Mol Genet. 2005 Jun
1;14(11):1417-27.
• Internet resources: The Labrador Retriever Club, Inc.:
20. Tiret L, Blot S, Kessler JL, et. al.: The cnm locus, a canine homologue of
www.thelabradorclub.com
human autosomal forms of centronuclear myopathy, maps to chromosome
Labrador Retriever Club of Canada: 2. Hum Genet. 2003 Sep;113(4):297-306.
www.labradorretrieverclub.ca 21. Chetboul V, Tran D, Carlos C, et. al.: Congenital malformations of the
The Labrador Retriever Club of Great Britain: tricuspid valve in domestic carnivores: a retrospective study of 50 cases.
www.thelabradorretrieverclub.com Schweiz Arch Tierheilkd. 2004 Jun;146(6):265-75.
22. Famula TR, Siemens LM, Davidson AP, et. al.: Evaluation of the genetic
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23. Andelfinger G, Wright KN, Lee HS, et. al.: Canine tricuspid valve
2. Morgan JP, Wind A, Davidson AP, et. al.: Bone dysplasias in the
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chromosome 9. J Med Genet. 2003 May;40(5):320-4.
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Res. 2008 Oct;69(10):1336-40. atrioventricular block in dogs: 124 cases (January 1, 1997-December 31,
37. Dorn CR: Canine breed-specific risks of frequently diagnosed 1997). J Am Vet Med Assoc. 2006 Jun 1;228(11):1710-7.
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38. Harasen G: Canine cranial cruciate ligament rupture in profile: 61. Moore PF, Affolter VK, Vernau W, et. al.: Canine hemophagocytic
2002-2007. Can Vet J. 2008 Feb;49(2):193-4. histiocytic sarcoma: a proliferative disorder of CD11d+ macrophages. Vet
39. Duval JM, Budsberg SC, Flo GL, et. al.: Breed, sex, and body weight as Pathol. 2006 Sep;43(5):632-45.
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Vet Med Assoc. 1999 Sep 15;215(6):811-4. ectopic ureter. Vet Radiol Ultrasound. 1998 May-Jun;39(3):218-23.
40. Reif U & Probst CW: Comparison of tibial plateau angles in normal 63. Holt PE & Moore AH: Canine ureteral ectopia: an analysis of 175 cases
and cranial cruciate deficient stifles of Labrador retrievers. Vet Surg. 2003 and comparison of surgical treatments. Vet Rec. 1995 Apr 8;136(14):345-9.
Jul-Aug;32(4):385-9. 64. O’Brien MG, Berg J & Engler SJ: Treatment by digital amputation of
41. Shih JL, Keating JH, Freeman LM, et. al.: Chronic hepatitis in Labrador subungual squamous cell carcinoma in dogs: 21 cases (1987-1988) J Am
Retrievers: clinical presentation and prognostic factors. J Vet Intern Med. Vet Med Assoc. 1992 Sep 1;201(5):759-61.
2007 Jan-Feb;21(1):33-9. 65. Dubielzig RR, Steinberg H, Garvin H, et. al.: Iridociliary epithelial
42. Hoffmann G, van den Ingh TS, Bode P, et. al.: Copper-associated tumors in 100 dogs and 17 cats: a morphological study. Vet Ophthalmol.
chronic hepatitis in Labrador Retrievers. J Vet Intern Med. 2006 1998;1(4):223-231.
Jul-Aug;20(4):856-61. 66. Tafti AK, Hanna P, Bourque AC: Calcinosis circumscripta in the dog: a
43. Smedley R, Mullaney T, Rumbeiha W, et. al.: Copper-associated hepatitis retrospective pathological study. J Vet Med A Physiol Pathol Clin Med. 2005
in Labrador Retrievers. Vet Pathol. 2009 May;46(3):484-90. Feb;52(1):13-7.
44. Hoffmann G, Jones PG, Biourge V, et. al.: Dietary management of 67. McKee WM, Macias C, May C, et. al.: Ossification of the infraspinatus
hepatic copper accumulation in Labrador Retrievers. J Vet Intern Med. 2009 tendon-bursa in 13 dogs. Vet Rec. 2007 Dec 22-29;161(25):846-52.
Sep-Oct;23(5):957-63 68. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
45. Wilkerson MJ, Dolce K, Koopman T, et. al.: Lineage differentiation of Ackerman. p 225-26, AAHA Press, 1999.
canine lymphoma/leukemias and aberrant expression of CD molecules. Vet 69. Brooks MB, Gu W & Ray K: Complete deletion of factor IX gene and
Immunol Immunopathol. 2005 Jul 15;106(3-4):179-96. inhibition of factor IX activity in a labrador retriever with hemophilia B. J
46. Read RA & Broun HC: Entropion correction in dogs and cats using a Am Vet Med Assoc. 1997 Dec 1;211(11):1418-21.
combination Hotz-Celsus and lateral eyelid wedge resection: results in 311 70. Bildfell RJ, Mitchell SK & de Lahunta A: Cerebellar cortical degeneration
eyes. Vet Ophthalmol. 2007 Jan-Feb;10(1):6-11. in a Labrador retriever. Can Vet J. 1995 Sep;36(9):570-2.
47. Snelling SR & Edwards GA: A retrospective study of unilateral 71. Perille AL, Baer K, Joseph RJ, et. al.: Postnatal cerebellar cortical
arytenoid lateralisation in the treatment of laryngeal paralysis in 100 dogs degeneration in Labrador Retriever puppies. Can Vet J. 1991
(1992-2000). Aust Vet J. 2003 Aug;81(8):464-8. Oct;32(10):619-621.
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72. Bergman RL, Inzana KD, Monroe WE, et. al.: Dystrophin-deficient
muscular dystrophy in a Labrador retriever. J Am Anim Hosp Assoc. 2002
May-Jun;38(3):255-61.
73. Cosford KL, Taylor SM, Thompson L, et. al.: A possible new inherited
myopathy in a young Labrador retriever. Can Vet J. 2008 Apr;49(4):393-7.
74. Shelton GD, Snead E, Böhm J, et. al.: A Missense Variant in the MTM1
Gene Associated with X-Linked Myotubular Myopathy in Labrador
Retrievers. Proceedings, 2009 ACVIM Forum. 2009.
75. Smit JJ, Temwitchitr J, Brocks BA, et. al.: Evaluation of candidate
genes as cause of chondrodysplasia in Labrador retrievers. Vet J. 2011
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76. Rossmeisl JH Jr, Duncan R, Fox J, et. al.: Neuronal ceroid-lipofuscinosis
in a Labrador Retriever. J Vet Diagn Invest. 2003 Sep;15(5):457-60.
77. Wilkerson MJ, Lewis DC, Marks SL, et. al.: Clinical and morphologic
features of mucopolysaccharidosis type II in a dog: naturally occurring
model of Hunter syndrome. Vet Pathol. 1998 May;35(3):230-3.
78. Varjonen K, Rest J & Bond R: Alopecia in a black Labrador retriever
associated with focal sub-follicular panniculitis and sebaceous adenitis. Vet
Dermatol. 2010 Mar 30. [Epub ahead of print]
79. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p 52-57.
293
Lakeland Terrier
slightly forward at the tip. It is commonly docked. The gait is long,
free and smooth.
Longevity: 13-14 years Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. Too few Lakeland Terriers have been screened by OFA to
Points of Conformation: Lakelands possess sturdy square determine an accurate frequency.1
conformation, moderate muscling and bone, and their expression
is alert. Smallish oval eyes are fairly wide set and colored to match Primary Lens Luxation (PLL): An autosomal recessive gene causes
the dog (hazel, brown, or dark brown), with dark palpebral margins. primary lens luxation. Homozygous affected dogs usually develop
Ears are triangular, small and the leather is thick. They fold forward, lens luxation between 4-8 years of age. Rarely, heterozygous
with the fold above the topline of the skull. The skull is fairly flat carriers can develop lens luxation, but at a later age. Lens luxation
and broad, muzzle is blocky, and there is a minimal stop. The nose can lead to secondary glaucoma and blindness. A genetic mutation
is black, but may be liver on liver colored dogs. The lips are dark, has been identified, and a genetic test is available.
neck is long and fine, not throaty, slightly arching, and there are
prominent shoulders. Limbs are straight boned and metacarpals Disease Predispositions
and metatarsals are short. Dewclaws are usually removed. The Persistent Pupillary Membranes: Strands of fetal remnant
feet are compact, toes well arched, and the pads thick and darkly connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
pigmented. The topline is level and the back is short, the thorax later three forms can impair vision, and dogs affected with these
is deep and narrow with ribs well sprung, and the abdomen is forms should not be bred. Identified in 9.38% of Lakeland Terriers
moderately tucked up. The high set tail is carried up and curves CERF examined by veterinary ophthalmologists between 2000-2005.2
294
Hypothyroidism: Inherited autoimmune thyroiditis. 7.7% positive 6. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
for thyroid auto-antibodies based on testing at Michigan State Ackerman. p. 226. AAHA Press, 1999.
University. (Ave. for all breeds is 7.5%).3,4 7. Rudorf H, Lane JG, Wotton PR: Everted laryngeal saccules:
ultrasonographic findings in a young Lakeland terrier. J Small Anim Pract.
Cataracts: Intermediate or punctate cataracts. Reported in 7.46% 1999 Jul;40(7):338-9.
of Lakeland Terriers presented to veterinary teaching hospitals. CERF 8. Ness MG: Osteochondroma causing progressive posterior paresis in a
lakeland terrier puppy. Vet Rec. 1993 Jun 12;132(24):608-9.
does not recommend breeding any Lakeland Terrier with a cataract.5
9. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 391-395.
Glaucoma: Primary, narrow angle glaucoma occurs in the breed.
Can cause secondary lens luxation. Screen with gonioscopy and
tonometry. Frequency and mode of inheritance in the breed has not
been determined.2
Genetic Tests
Tests of Genotype: Direct test for PLL is available from OFA and the
Animal Health Trust.
Miscellaneous
• Breed name synonyms: Lakeland, Patterdale Terrier (historical)
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 131 (176 dogs registered)
• Internet resources: The United States Lakeland Terrier Club:
www.uslakelandterrier.org
Lakeland Terrier Club (UK): http://lakelandterrierclub.org.uk/
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
295
Leonberger
tight arched toes. Dewclaws are usually present in the front, and
may be present in the back. The Leonberger has a ground–covering,
even and balanced gait. The stride is powerful, easy, free and elastic,
with good reach and strong drive giving the impression of effortless
power. In motion, the Leonberger maintains a level topline. As
the dog’s speed increases, the legs tend to converge toward the
centerline.
Coat: Leonbergers have a medium to long, water resistant, double Elbow Dysplasia: Polygenically inherited trait causing elbow
coat on the body and short fine hair on the muzzle and front of arthritis. OFA reports 4.8% affected.1
limbs. Mature males carry a mane. Coat colors are lion–yellow,
golden to red and red–brown, also sand colored (cream, pale yellow) Polyneuropathy/Inherited Motor And Sensory Neuropathy: It
and all combinations thereof, always with a black mask. A small, is believed that there are more than one causes of polyneuropathy
unobtrusive stripe or white patch on the chest and some white in the Leonberger breed. Polyneuropathy is a disorder of axonal
hairs on toes is tolerated. degeneration identified in the breed worldwide. Affected
Leonbergers present with exercise intolerance, laryngeal paralysis,
Longevity: 8-9 years. distal muscle atrophy and neuromuscular weakness. Affected
dogs between 1–3 years of age have a more severe form of the
Points of Conformation: Proportion of height at withers to length disease compared to older affected dogs that present between
of body is 9 to 10. Bone is medium to heavy and in proportion 8–9 years of age. The ratio of affected males to affected females is
to size of body with sufficient muscle to support frame. Head is approximately 2.5 to 1, and some research suggests that one form
rectangular with parallel lines. Stop is moderate. Eyes are dark of the disease can be x-linked. An autosomal recessive mutation
brown, medium size, oval to almond shaped. Ears are of medium (LPN1) has been identified that accounts for approximately
size, triangular, fleshy, hanging flat and close to the head. Nose is one-third of all cases of polyneuropathy in the breed. Dogs
large, black, with clearly outlined nostrils. Lips are tight, with no homozygous for this mutation will develop the severe form of the
drooling. Teeth are scissors to level. Withers are set above a firm disease by 3 years of age. It is possible that dogs heterozygous
level back that flows with a gently sloping croup into the tail. Chest (carrying one copy) for this mutation may develop the milder,
is broad, roomy, and deep, reaching at least to the level of the later-age form of the disease. A direct genetic test for this mutation
elbows. Fore and rear quarters are well muscled. Shoulders are well is available. The frequency of the disorder in the breed has not been
laid–back, 90 degrees to the foreleg. Hind end is well angulated. determined. Genetic mutations for other forms of the disease have
Legs are straight and powerful. Feet do not turn in or out, with not been identified.4,5,6
296
Patella Luxation: Polygenically inherited laxity of patellar frequency of 2.2% (3% of all dogs over 5 years of age) in the 2000
ligaments, causing luxation, lameness, and later degenerative LCA Health Survey. Unknown mode of inheritance.3
joint disease. Treat surgically if causing clinical signs. Too few
Leonbergers have been screened by OFA to determine an accurate Ectropion: Rolling out of eyelids, often with a medial canthal
frequency.1 pocket. Can cause secondary conjunctivitis. Can be secondary to
macroblepharon; an abnormally large eyelid opening. Ectropion is
reported in 1.60% and macroblepharon in 2.05% of Leonbergers
Disease Predispositions CERF examined by veterinary ophthalmologists between 2000-2005.7
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The Dilated Cardiomyopathy: Leonbergers are a predisposed breed
later three forms can impair vision, and dogs affected with these for this condition, resulting in heart failure. Undetermined mode
forms should not be bred. Identified in 16.21% of Leonbergers CERF of inheritance. Reported at a frequency of 0.75% (2.1% of all dogs
examined by veterinary ophthalmologists between 2000-2005.7 over 5 years of age) in the 2000 LCA Health Survey.3,13
Osteoarthritis: Leonbergers have an increased incidence of Hypoadrenocorticism (Addison’s disease): Immune mediated
arthritis. Reported at a frequency of 15% of all dogs over 5 years of destruction of the adrenal gland. Typical presentation of lethargy,
age in the 2000 LCA Health Survey.3 poor appetite, vomiting, weakness, and dehydration can occur from
4 months to several years of age. Treatment with DOCA injections
Hypothyroidism: Inherited autoimmune thyroiditis11.1% positive
or oral fludrocortisone. Some affected Leonbergers were diagnosed
for thyroid auto-antibodies based on testing at Michigan State
with concurrent hypothyroidism, suggesting a polyglandular
University. (Ave. for all breeds is 7.5%). Reported at a frequency of
syndrome. Reported at a frequency of 1% (2% of all dogs over 5
5.5% (9.3% of all dogs over 5 years of age) in the 2000 LCA Health
years of age) in the 2000 LCA Health Survey.3,12
Survey.3,8,9
Third Eyelid Eversion/Cartilage Anomaly: Developmental
Panosteitis: A self-limiting disease of young, large breed dogs
anomaly of the cartilage of the nictitating membrane. Eversion
involving the diaphyseal and metaphyseal areas of the tubular
causes conjunctival drying and inflammation. Identified in 1.14%
long bones, characterized by medullary fibrosis and both endosteal
of Leonbergers CERF examined by veterinary ophthalmologists
and subperiosteal new bone deposition. Affected dogs show
between 2000-2005.7
intermittent lameness. Treatment is with non-steroidal anti-inflam-
matory drugs and rest. Reported at a frequency of 11% in the 2000 Osteochondritis Dissecans (OCD): Abnormality of cartilage
LCA Health Survey.3 development causing lameness in the shoulder, elbow, hock or knee.
Severe cases may require surgery. Reported at a frequency of 1% in
Cataracts: Nuclear, posterior nuclear, or posterior polar cataracts
the 2000 LCA Health Survey.3
predominate in the breed. Identified in 5.94% of Leonbergers CERF
examined by veterinary ophthalmologists between 2000-2005. In Gastric Dilatation-Volvulus (bloat, GDV): Polygenically inherited,
a UK study, 24.6% of Leonbergers had cataracts, with the posterior life-threatening twisting of the stomach within the abdomen.
polar subcapsular form showing significant inheritance. Reported Requires immediate treatment. Reported as a breed health issue on
at a frequency of 2.7% (4.6% of all dogs over 5 years of age) in the the LCA website.
2000 LCA Health Survey. CERF does not recommend breeding any
Leonberger with a cataract.3,7,10 Perianal Fistula/Furunculosis: Inflammatory disorder creating
perianal ulceration and fistulas. Treat with anti-inflammatory
Osteosarcoma: Malignant bone cancer, usually affecting the limbs. A medications and tacrolimus. Reported as a breed health issue on
Swedish study showed an increased risk in the breed, with a median the LCA website.
age of onset of 7.2 years. Reported at a frequency of 3.2% (7.8% of
all dogs over 5 years of age) in the 2000 LCA Health Survey.3,11
Isolated Case Studies
Umbilical Hernia: Congenital umbilical hernias are reported at a Leukoencephalomyelopathy: Two unrelated 2 year old Leonbergers
frequency of 5.4% in the 2000 LCA Health Survey.3 (a male and a female) presenting with signs of progressive ataxia of
all 4 limbs, proprioceptive deficits, and thoracic limb hypermetria.
Entropion: Rolling in of eyelids, often causing corneal irritation were found to have a slowly progressive demyelinating
or ulceration. Entropion is reported in 4.34% of Leonbergers CERF leukoencephalomyelopathy. This disorder must be differentiated
examined by veterinary ophthalmologists between 2000-2005. from the polyneuropathies identified in the breed.14
Reported at a frequency of 3.2% in the 2000 LCA Health Survey.3,7
Miscellaneous
• Breed name synonyms: Leo
• Registries: AKC, UKC, CKC, FCI, KCGB (Kennel Club of Great
Britain), ANKC (Australian National Kennel Club), NKC (National
Kennel Club).
• AKC rank (None): AKC recognized in June, 2010. Entire stud
book entered.
• Internet resources: Leonberger Club of America:
www.leonbergerclubofamerica.com
Leonberger Club of Great Britain: http://leonbergerclub.org.uk
Leonberger Club of Canada:
www.leonbergerclubofcanada.com/temp/index.htm
LCA Health Committee website: www.leowatch.org
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Doskarova B, Kyllar M & Paral V: Morphometric assessment of the canine
hip joint using the acetabular angle of retrotorsion. Vet Comp Orthop
Traumatol. 2010, 23(5).
3. Zieher W & Leonberger Club of America Health Research and Education
Committee: Summary of the 2000 Health Survey Findings. Leowatch Vol. 2;
Spring, 2002.
4. Shelton GD, Podell M, Poncelet L, et. al.: Inherited polyneuropathy in
Leonberger dogs: a mixed or intermediate form of Charcot-Marie-Tooth
disease? Muscle Nerve. 2003 Apr;27(4):471-7.
5. Granger N: Canine inherited motor and sensory neuropathies: An
updated classification in 22 breeds and comparison to Charcot-Marie-
Tooth disease. Vet J. 2011 Jun;188(3):274-85.
6. Granger, N, Escriou, C, Thibaud, JL, et. al.: Polyneuropathy in Leonberger
dogs: an emerging pan-Europea polyneuropathy. Proceedings 2007 BSAVA
Congress. 2007:488–489.
7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
8. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
9. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
10. Heinrich CL, Lakhani KH, Featherstone HJ, et. al: Cataract in the UK
Leonberger population. Vet Ophthalmol. 2006 Sep-Oct;9(5):350-6.
11. Egenvall A, Nødtvedt A & von Euler H: Bone tumors in a population of
400 000 insured Swedish dogs up to 10 y of age: incidence and survival.
Can J Vet Res. 2007 Oct;71(4):292-9.
12. Smallwood LJ & Barsanti JA: Hypoadrenocorticism in a family of
leonbergers. J Am Anim Hosp Assoc. 1995 Jul-Aug;31(4):301-5.
13. Haggstrom J: Dilated Cardiomyopathy in Dogs: Diagnosis and
Treatment. Proceedings, 2008 World Small Animal Veterinary Association
World Congress. 2008.
14. Oevermann A, Bley T, Konar M, et. al.: A novel leukoencephalomyel-
opathy of Leonberger dogs. J Vet Intern Med. 2008 Mar-Apr;22(2):467-71.
15. AKC Breed Website: www.akc.org/breeds/leonberger Last accessed July
1, 2010.
298
Lhasa Apso
Recognized Behavior Issues and Traits
Reported breed characteristics include: They are dogs that generally
train easily, though some are a bit independent. They will respond to
gentle handling and are a trustworthy companion to their families
and are loyal. They enjoy plenty of close human contact. They are
wary of strangers and should be socialized when young to both
other pets and people.Some are aggressive; especially males. They
are good alarm barkers, and because of their historical function as
a watchdog they will respond to intruders. They are active dogs,
but require low exercise levels. High shedding, and high grooming
The Breed History requirements characterize Lhasas so some owners elect to have
them clipped once or twice per annum. They do well in town or
This breed originated in the mountains of Tibet, in the city of
country settings.
Lhasa where the harsh environment and high elevations led to the
selection of a very hardy dog type. They had been bred for their
heavy insulating coat to cope with the extremes of climate. They Normal Physiologic Variations
were so prized in Tibet that they were considered good luck and None reported
over a few thousand years, were only found in monasteries or in
the houses of nobles. They were also sent as gifts to China, where Drug Sensitivities
they contributed to the Shih Tzu and Pekingese breeds. They join None reported
the Tibetan Terrier and Tibetan Spaniel in the same group from this
region. This breed was first accepted into the AKC registry in 1935.
The first US imports came as gifts from the 13th Dalai Lama.
Inherited Diseases
Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Breeding for Function disease. Treat surgically if causing clinical signs. Reported 3.4x odds
They served as guard and alarm dogs for dwellings and monasteries, ratio versus other breeds. OFA reports 10.3% affected.1,2
and also for companionship.
Hip Dysplasia and Legg-Calve-Perthes Disease: Polygenically
Physical Characteristics inherited traits causing degenerative hip joint disease and arthritis.
Height at Withers: female 10 “ (25.4 cm), male 11” (28 cm) Reported 6.7x odds ratio for Legg-Calve-Perthes versus other
breeds. OFA reports 6.4% affected.1,2
Weight: females 13-15 lb (6-7 kg), males 13-18 lb (6-8 kg).
Renal Dysplasia: Autosomal dominant disorder with incomplete
Coat: Many colors are accepted, but the haircoat density is penetrance causing renal failure. Affected dogs can succumb to
significantly developed as protection against harsh conditions. The renal failure from birth to two years of age. Mildly affected dogs
beard is often dark, and hairs are often mixed color throughout can live with compensated renal insufficiency. Biopsy studies
the coat, and have a straight medium texture. The colors most suggest that a large portion of the breed is affected, although only
often seen are described as leonine (lion-like); honey, wheaten with a small percentage dies from the condition. A direct genetic test for
dark on the extremities. Parti-color, white, black, and slate are less a susceptibility gene is available. (Affected dogs all have one copy
commonly seen. of the gene, but most dogs with the gene will not develop kidney
failure.)3,4
Longevity: 14-15 years.
Progressive Retinal Atrophy (PRA): Autosomal recessive
Points of Conformation: The dog is built longer than high, and progressive degeneration of the retina leading to blindness. Age
the head, carried high, is well endowed with whiskers and beard of onset in the breed 2-8 years of age. There is no test for carriers.
hairs, the nose is black and the face profile is straight. Eyes should Identified in 1.06% of Lhasa Apsos CERF examined by veterinary
be dark brown in pigment, with keen bright expression, and the ophthalmologists between 2000-2005.5,6
ears are pendulous and well covered with long hair. The skull is
brachycephalic, and jaw is normally mildly prognathic. The tail Factor IX Deficiency (Hemophilia B): Rare X-linked inherited
should be carried well up, and sometimes a screw tip is noted at the bleeding disorder identified in the breed. A genetic test is available.7
terminus of the tail. The topline is straight with a slight slope, and
the back is short. The feet are compact and hair-covered as well for Elbow Dysplasia: Polygenically inherited trait causing elbow
warmth. arthritis. Too few Lhasa Apsos have been screened by OFA to
determine an accurate frequency.1
299
Disease Predispositions Retinal Dysplasia: Geographic retinal dysplasia occurs in
the breed. Can lead to blindness. Reported in 1.06% of Lhasa
Distichiasis: Abnormally placed eyelashes that irritate the cornea
and conjunctiva. Can cause secondary corneal ulceration. Identified Apsos CERF-examined by veterinary ophthalmologists between
in 3.72% of Lhasa Apsos CERF examined by veterinary ophthalmol- 2000-2005.5
ogists between 2000-2005.5
Persistent Pupillary Membranes: Strands of fetal remnant
Cataracts: Anterior or posterior cortex intermediate and punctate connecting; iris to iris, cornea, lens, or involving sheets of tissue.
cataracts predominate in the breed. In one large study, 4.61% of The later three forms can impair vision, and dogs affected with
Lhasa Apsos had cataracts. Identified in 3.27% of Lhasa Apsos CERF these forms should not be bred. Identified in 1.06% of Lhasa
examined by veterinary ophthalmologists between 2000-2005. CERF Apsos CERF-examined by veterinary ophthalmologists between
does not recommend breeding any Lhasa Apso with a cataract.5,8 2000-2005.5
Brachycephalic Complex: The brachycephalic complex includes Urinary Calculi: The breed is found to be at an increased risk of
Stenotic Nares, Elongated Soft Palate, Everted Laryngeal developing struvite and oxalate calculi. One study reported an odds
Saccules, Laryngeal Collapse, and occasionally Hypoplastic ratio of 10.95x for calcium oxalate stones versus other breeds.17,18
Trachea. Can cause respiratory distress, apnea, and hypoxia.9
Intervertebral Disc Disease (IVDD): Lhasa Apsos have an increased
Hypothyroidism: Inherited autoimmune thyroiditis. 3.2% positive risk of developing spinal cord disease due to prolapsed disk material.
for thyroid auto-antibodies based on testing at Michigan State Clinical signs include back pain, scuffing of paws, spinal ataxia, limb
University. (Ave. for all breeds is 7.5%).10,11 weakness, and paralysis. Requires immediate veterinary attention.19
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis Sebaceous Adenitis: Disorder of immune mediated sebaceous
and pyotraumatic dermatitis. Lhasa Apsos have a significantly gland destruction, presenting with hair loss, usually beginning
increased risk for atopy versus other breeds. Dorn reports a 1.19x with the dorsal midline and ears. Diagnosis by skin biopsy. Treat
odds ratio versus other breeds.12,13 with isotretinoin. An autosomal recessive mode of inheritance is
suspected.20,21
Exposure Keratopathy Syndrome/Pigmentary Keratopathy:
Corneal reactivity and drying from ocular exposure secondary to Portosystemic shunt (PSS, liver shunt): Congenital abnormal
shallow orbits, exophthalmos, and lagophthalmos. Identified in blood vessel connecting the portal and systemic circulation. Can be
2.66% of Lhasa Apsos CERF examined by veterinary ophthalmolo- intrahepatic or extrahepatic. Causes stunting, abnormal behavior,
gists between 2000-2005.5 possible seizures, and secondary ammonium urate urinary calculi.
Treatment of PSS includes partial ligation and/or medical and
Corneal Dystrophy: Lhasa Apsos can have an epithelial/stromal dietary control of symptoms. Tobias reports a 5.4x odds ratio versus
form of corneal dystrophy. Identified in 2.13% of Lhasa Apsos other breeds.22
CERF-examined by veterinary ophthalmologists between 2000-2005.5
Lissencephaly: A rare, inherited, congenital absence of cerebrocor-
Entropion: Rolling in of eyelids, often causing corneal irritation or tical convolutions. Clinical signs include behavioral, abnormalities,
ulceration. Reported in 1.60% of Lhasa Apsos CERF-examined by blindness, and seizures that occur during the first year of life.
veterinary ophthalmologists between 2000-2005.5 Diagnosis with MRI.23,24,25
Chronic Superficial Keratitis: This condition can cause conjunctivitis, Demodicosis, Ectodermal Defect, Epilepsy, Hydrocephalus,
corneal ulcerations, and vision problems due to corneal pigmentation. Hypotrichosis, Juvenile Cellulitis, Oligodontia, Pancreatitis,
Age of onset 2-5 years. Treatment with topical ocular lubricants and Seasonal Flank Alopecia, Vertebral Stenosis, and von
anti-inflammatory medication. Identified in 1.60% of Lhasa Apsos Willebrand’s Disease are reported.26
CERF-examined by veterinary ophthalmologists between 2000-2005.5
Isolated Case Studies
Keratoconjunctivitis Sicca (KCS, Dry Eye): Ocular condition Hydrocephalus, Syringomyelia, and Spinal Cord
causing lack of tear production and secondary conjunctivitis, Angiodysgenesis: A Lhasa Apso pup with weakness and ataxia was
corneal ulcerations, and vision problems. Age of onset 2-5 years. diagnosed with this combination of disorders.27
CERF does not recommend breeding any Lhasa Apso with KCS.5,14
Prolapsed Gland of the Nictitans (Cherry Eye): This condition Genetic Tests
occurs secondary to inflammation of the gland. Reported at an Tests of Genotype: Direct test for a renal dysplasia susceptibility
increased frequency in the breed.15 gene is available from Dogenes (www.dogenes.com).
Primary (Narrow Angle) Glaucoma: Ocular condition causing Direct test for Factor XI deficiency is available from HealthGene.
increased pressure within the eyeball, and secondary blindness due
Tests of Phenotype: Recommended tests are; CERF eye
to damage to the retina. Diagnose with tonometry and gonioscopy.
examination, hip and elbow radiographs, patella examination,
Diagnosed in 1.33% of Lhasa Apsos presented to veterinary
thyroid profile including autoantibodies, genetic test for renal
teaching hospitals.16
dysplasia susceptability, and cardiac examination.
300
Miscellaneous Vet Med Assoc. 2003 Dec 1;223(11):1636-9.
23. Zaki FA: Lissencephaly in Lhasa Apso dogs. J Am Vet Med Assoc. 1976
• Breed name synonyms: Abso Seng Kye (Engl: Bark Lion Sentinel Dec 1;169(11):1165, 1168.
Dog), Lhasa,Tibetan Apso, Lion Dog 24. Greene CE, Vandevelde M, Braund K: Lissencephaly in two Lhasa Apso
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), dogs. J Am Vet Med Assoc. 1976 Aug 15;169(4):405-10.
ANKC (Australian National Kennel Club), NKC (National Kennel Club) 25. Saito M, Sharp NJ, Kortz GD, et. al.: Magnetic resonance imaging
• AKC rank (year 2008): 56 (2,020 dogs registered) features of lissencephaly in 2 Lhasa Apsos. Vet Radiol Ultrasound. 2002
• Internet resources: American Lhasa Apso Club: Jul-Aug;43(4):331-7.
www.lhasaapso.org 26. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Lhasa Apso Canada: http://lhasa-apso-canada.com Ackerman. p 227, AAHA Press, 1999.
The Lhasa Apso Club (UK): www.lhasa-apso-club.org.uk 27. Schmahl W, Kaiser E: Hydrocephalus, syringomyelia, and spinal cord
angiodysgenesis in a Lhasa-apso dog. Vet Pathol. 1984 Mar;21(2):252-4.
28. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
References Book House, NY 2006. p. 572-574
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
3. Manderino DM, DeVries JG, Tamarkin J: Primary renal disease in a dog.
Mod Vet Pract. 1984 Aug;65(8):633-5.
4. O’Brien TD, Osborne CA, Yano BL, et. al.: Clinicopathologic manifestations
of progressive renal disease in Lhasa Apso and Shih Tzu dogs. J Am Vet Med
Assoc. 1982 Mar 15;180(6):658-64.
5. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
6. Bedford PGC: Retinopathies--Old and New. 2004. Proceedings, World
Small Animal Veterinary Association World Congress, 2004.
7. Mauser AE, Whitlark J, Whitney KM, et. al.: A deletion mutation causes
hemophilia B in Lhasa Apso dogs. Blood. 1996 Nov 1;88(9):3451-5.
8. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
9. Koch DA, Arnold S, Hubler M, et. al.: Brachycephalic Syndrome in Dogs.
Compend Contin Educ Pract Vet. January 2003;25(1):48-55.
10. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
11. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
12. Dorn CR: Canine breed-specific risks of frequently diagnosed
diseases at veterinary teaching hospitals. Monograph. AKC Canine Health
Foundation. 2000.
13. Schick RO, Fadok VA: Responses of atopic dogs to regional allergens:
268 cases (1981-1984). J Am Vet Med Assoc. 1986 Dec 1;189(11):1493-6.
14. Herrera D: Canine Keratoconjunctivitis Sicca. 2005. Proceedings, World
Small Animal Veterinary Association World Congress, 2005.
15. Herrera D: Surgery of the Eyelids. 2005. Proceedings, World Small
Animal Veterinary Association Congress, 2005.
16. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
in pure-bred dogs in North America. Vet Ophthalmol. 2004
Mar-Apr;7(2):97-111.
17. Houston DM & Moore AE: Canine and feline urolithiasis: examination of
over 50 000 urolith submissions to the Canadian veterinary urolith centre
from 1998 to 2008. Can Vet J. 2009 Dec;50(12):1263-8.
18. Lekcharoensuk C, Lulich JP, Osborne CA, et. al.: Patient and
environmental factors associated with calcium oxalate urolithiasis in dogs.
J Am Vet Med Assoc. 2000 Aug 15;217(4):515-9.
19. LeCouteur RA: Spinal Cord Diseases of Small Breed Dogs. 2006.
Proceedings, Western Veterinary Conference.
20. White S: Sebaceous Adenitis. 2001. Proceedings, World Small Animal
Veterinary Association World Congress, 2001
21. Hernblad Tevell E, Bergvall K, & Egenvall A: Sebaceous adenitis in
Swedish dogs, a retrospective study of 104 cases. Acta Vet Scand. 2008 May
25;50:11.
22. Tobias KM & Rohrbach BW: Association of breed with the diagnosis of
congenital portosystemic shunts in dogs: 2,400 cases (1980-2002). J Am
301
Löwchen
and other pets. Good alarm barkers. May dig or bark excessively if
bored. Possessing good trainability. Fine for apartment or city living.
Low to moderate exercise needs. The Lowchen has moderate to high
grooming needs but a low shedding tendency.
Drug Sensitivities
None reported
The Breed History
Records show that this European breed has been in existence Inherited Diseases
since the mid 15th century.1 The Lowchen belongs to the Bichon Patella Luxation: Polygenically inherited laxity of patellar
breed class. The nickname of “Little Lion Dog” can be traced back ligaments, causing luxation, lameness, and later degenerative joint
to the breed specific clip that results in a lion-like short coat over disease. Treat surgically if causing clinical signs. OFA reports 5.3%
the hindquarters and rear limbs down to the tarsus and the thick affected.1
natural mane hair which is left on. In the period between the end
of the Second World War and the 1960s, it was among the rarest of Hip Dysplasia and Legg-Calve Perthes Disease: Polygenically
breeds in the world, but has recently resurged in popularity. The AKC inherited traits causing degenerative hip joint disease and arthritis.
admitted them to the non-sporting group in 1999. OFA reports 3.3% affected.1
Physical Characteristics Progressive Retinal Atrophy (PRA): PRA in the Lowchen causes
Height at Withers: 12-14” (30.5-35.5 cm) progressive blindness, beginning with night blindness from 6
months to 2 years of age. Autosomal recessive mode of inheritance.
Weight: 8-18 lb (4-8 kg) There is no test for carriers.2
Coat: The long dense haircoat is straight to slightly wavy and fairly
soft in texture. There are no coat color limitations. Disease Predispositions
Persistent Pupillary Membranes: Strands of fetal remnant
Longevity: 13-14 years connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
later three forms can impair vision, and dogs affected with these
Points of Conformation: The Lowchen has a square conformation, forms should not be bred. Identified in 8.14% of Lowchen CERF
the skull is broad, the stop is moderate and muzzle is short and examined by veterinary ophthalmologists between 2000-2005.2
rounded. High head carriage during activity is characteristic.
Deep-set eyes are wide-set, face forward and are darkly colored. Distichiasis: Abnormally placed eyelashes that irritate the cornea
The mildly pendulous ears have plenty of feathering, the nose is and conjunctiva. Can cause secondary corneal ulceration. Identified
large and black or brown in pigmentation. The neck is moderate in in 4.46% of Lowchen CERF examined by veterinary ophthalmologists
length and muscling, is slightly arched, and the thorax is moderate between 2000-2005.2
in depth, ribs are well sprung, and the abdomen is slightly tucked
up. The tail is carried over the back unless at rest and is high set. Cataracts: Anterior or posterior cortex intermediate cataracts
The limbs are straight boned, metacarpals and metatarsals are predominate in the breed. Unknown mode of inheritance. Identified
short, dewclaws may be removed; especially the rear ones. The feet in 2.71% of Lowchen CERF examined by veterinary ophthalmolo-
are small, tight and compact, with the 3rd and 4th toe appearing gists between 2000-2005. CERF does not recommend breeding any
longer than the 1st and 5th; with well-developed pads; hind feet Lowchen with a cataract.2
are smaller than forefeet. The gait is a long, low stride.
Vitreous Degeneration: A liquefaction of the vitreous gel which
may predispose to retinal detachment and/or glaucoma. Reported in
Recognized Behavior Issues and Traits 1.74% of Lowchen dogs CERF examined by veterinary ophthalmolo-
Reported breed characteristics include: Lively, friendly, intelligent, gists between 2000-2005.2
strong-willed and may challenge other dogs or household members
for dominance. Generally, they are considered good with children
302
Hypothyroidism: Inherited autoimmune thyroiditis. Too few
Lowchen have been tested by Michigan State University for thyroid
autoantibodies to determine an accurate frequency. (Ave. for all
breeds is 7.5%).3,4
Genetic Test
Tests of Genotype: Direct tests for presence of black, brown
and red colors, and black and brown nose are available from
HealthGene.
Miscellaneous
• Breed name synonyms: Little Lion Dog, Petit Chien Lion.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
• AKC rank (year 2008): 137 (131 dogs registered)
• Internet resources: The Lowchen Club of America:
www.thelowchenclubofamerica.org
The Lowchen Club of Canada: www.lowchenclubofcanada.com
The Lowchen Club (UK): www.thelowchenclubuk.com
Lowchen World: http://lowchenworld.com
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 575-578.
303
Maltese
can be snappy. Some can be difficult to house train. The Maltese is
considered a low shedding, low allergy dog.
Drug Sensitivities
The Breed History None reported
Records of this breed in art can be found on the Isle of Malta
dated thousands of years ago. Roman, Greek and Egyptian records Inherited Diseases
trace the breed back to very early times. The AKC registered this Patella Luxation: Polygenically inherited laxity of patellar
Bichon-type breed in 1888. They are somewhat spaniel in type ligaments, causing luxation, lameness, and later degenerative joint
though they were sometimes called Maltese Terriers historically. disease. Treat surgically if causing clinical signs. Dorn reports a
1.92x odds ratio in Maltese versus other breeds. Another study
Breeding for Function reports a 6.5x odds ratio versus other breeds. OFA reports 5.0%
In early history, the Maltese dogs may have served for vermin affected.2,3,4
control. A companion dog exclusively for a very long time, Maltese
Hip Dysplasia and Legg-Calve-Perthes Disease: Polygenically
dogs were particularly sought after by women of high social
inherited traits causing degenerative hip joint disease and arthritis.
standing in the past.
Reported at a high frequency, but too few Maltese have been
screened by OFA to determine an accurate frequency.2
Physical Characteristics
Height at Withers: 10” (25 cm). Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. Too few Maltese have been evaluated by the OFA to
Weight: 4-6 lb (2-3 kg). determine an accurate frequency in the breed.2
Coat: The single haircoat hangs flat, is white, and the hairs are
long, straight and silky. The coat often reaches the floor or longer Disease Predispositions
at maturity and the topknot is usually tied up. The thick, luxurious Hypothyroidism: Inherited autoimmune thyroiditis. 16.5% positive
coat needs regular grooming. Due to the long white coat, this is for thyroid auto-antibodies based on testing at Michigan State
essentially an indoor dog and is suitable for apartment life. University. (Ave. for all breeds is 7.5%).5,6
Longevity: 14-15 years Cataracts: Anterior and posterior cortex intermediate cataracts
predominate in the breed. Identified in 7.23% of Maltese CERF
Points of Conformation: This is a toy dog with naturally high examined by veterinary ophthalmologists between 2000-2005.
head carriage, moderate stop, the skull slightly rounded, and the CERF does not recommend breeding any Maltese with a cataract.7
muzzle is tapered and of medium length; the nose is black. Eyes are
moderately set apart, dark, large, and palpebral margins are black. Persistent Pupillary Membranes: Strands of fetal remnant
Ears are well feathered and hanging from a low set position. Neck is connecting; iris to iris, cornea, lens, or involving sheets of tissue.
moderately short, body is square in conformation, the topline level, The later three forms can impair vision, and dogs affected with
thorax moderate in depth, and ribs are well sprung. The abdomen is these forms should not be bred. Identified in 7.23% of Maltese CERF
only slightly tucked up. Limbs are fine and straight boned, feet are examined by veterinary ophthalmologists between 2000-2005.7
small and round in shape, pads thick and black. The tail is high set
Retinal Dysplasia: Retinal folds and geographic dysplasia are
and sits over the back; is well plumed with hair. The gait is straight,
recognized in the breed. Can lead to blindness. Reported in 2.41%
energetic, quick and smoothly flowing.
of Maltese CERF-examined by veterinary ophthalmologists between
2000-2005.7
Recognized Behavior Issues and Traits
The reported breed characteristics include: Gentle nature, playful, Hydrocephalus: The breed is one with an increased frequency
intelligent, affectionate, and loves children. Exercise needs are low. of hydrocephalus. Diagnosis by radiography, MRI, or ultrasound
Activity levels are moderate. The Maltese is noted to be a vigorous (through an open fontanel). Dorn reports an 11.61x odds ratio in
alarm barker. Needs to have quiet, gentle children in the family or Maltese versus other breeds.3,8
304
Distichiasis: Abnormally placed eyelashes that irritate the cornea Testicular Tumors: A study in Taiwan suggests an increased
and conjunctiva. Can cause secondary corneal ulceration. Identified frequency of testicular tumors in intact males in the breed. This
in 1.20% of Maltese CERF-examined by veterinary ophthalmologists occurred with and without concurrent cryptorchidism.21
between 2000-2005.7
Splenic Masses: In an Australian study, Maltese were
Portosystemic Shunt (PSS, Liver Shunt): Abnormal blood vessels overrepresented versus other breeds for masses in the spleen.
connecting the systemic and portal blood flow. Vessels can be Histopathological diagnoses included benign and malignant
intrahepatic or extrahepatic. Hepatic microvascular dysplasia is masses.22
genetically related to PSS. Causes stunting, abnormal behavior and
possible seizures. Diagnose with paired fasted and feeding serum Atresia Ani (Imperforate Anus): An increased incidence of this
bile acid and/or ammonium levels, and abdominal ultrasound. congenital condition is reported in the breed, with a frequency of
Treatment of PSS includes partial ligation and/or medical and 0.069%, and an odds ratio of 13.39x. Treatment is surgery.23
dietary control of symptoms. 1.6% of Maltese presented to
veterinary teaching hospitals had PSS, with an odds ratio of 32x Brachygnathism, Cleft Lip/Plate, Mitral Valve Disease,
versus other breeds. Undetermined mode of inheritance.9,10 Oligodontia, Prognathism, Retained Primary Teeth, Sebaceous
Adentitis, Tracheal Collapse, and Wry Mouth are reported.24
Patent Ductus Arteriosus (PDA): Polygenically inherited
congenital heart disorder, where a fetal vessel remains open after
birth, causing a mixing of oxygenated and unoxygenated blood.
Isolated Case Studies
Exocrine Pancreatic Insufficiency: A 1.8-year-old female Maltese
Affected dogs are usually stunted, and have a loud heart murmur.
dog was presented because of a history of chronic diarrhea,
Diagnosis with Doppler ultrasound. Treat with surgery. Dorn reports
polyphagia, weight loss, and coprophagia. A definite diagnosis of
a 30.09x odds ratio in Maltese versus other breeds.3
exocrine pancreatic insufficiency was made based on low serum
Deafness: Congenital deafness can be unilateral of bilateral. trypsin-like immunoreactivity activity. The clinical signs disappeared
Diagnosed by BAER testing.11,12 after porcine pancreatic powder supplementation.25
Autoimmune Hemolytic Anemia (AIHA): Autoimmune Malonic Aciduria: A family of Maltese dogs with malonic aciduria
destruction of red blood cells. Clinical features include pale is reported. Affected dogs presented with episodes of seizures and
mucous membranes, weakness, lethargy and collapse. Treat with stupor with hypoglycemia, acidosis, and ketonuria. Urinary organic
immunosuppressive drugs. Reported 2.8x odds ratio versus other acid assays showed elevated malonic acid without elevation of
breeds in an Australian Study.13 methylmalonic acid. Treatment with frequent feedings of a low-fat
diet high in medium-chain triglycerides resulted in normalization of
Protein Losing Enteropathy (PLE, Lymphangiectasia): Presents clinical signs and a resolution of the malonic aciduria.26
with diarrhea, weight loss, and/or abdominal effusion due to
dilation of lymph vessels in the intestine. Inflammatory cell buildup Gallbladder Aplasia: Two cases of gallbladder aplasia are found
blocks normal absorption of nutrients. Can occur at any age, but in the literature. Affected dogs present with persistent mild
primarily affects middle-aged dogs. Maltese are a breed with hepatopathy and intermittent vomiting of bile. Absence of the
a predilection for the condition. Treatment consists of chronic gallbladder with malformation of the quadrate lobe of the liver,
anti-inflammatory medication and dietary restriction. Some dogs with histological evidence of bile duct proliferation and portal
with severe cases have a poor prognosis.14 fibrosis are found.27,28
Coat: The sleek short hair coat is black with mahogany markings; Elbow Dysplasia: Polygenically inherited trait causing elbow
distinct, not smudgy borders—well defined pattern. arthritis. Too few Manchester Terriers have been screened by OFA to
determine an accurate frequency.2
Longevity: 14-15 years.
Points of Conformation: These dogs have a long muzzle, flat Disease Predispositions
wedge-shaped skull, slight stop, and their bone structure is sleek Missing Teeth: Reported at a frequency of 18.37% in the Manchester
and athletic. Ears are naturally pricked up, and the dogs are a bit Terrier Health and Genetics Survey. Unknown mode of inheritance.1
longer than high. Almond-shaped slanting close-set dark eyes, and
a strong jaw ending in a black nose characterizes the face. Ears vary Hypothyroidism: Inherited autoimmune thyroiditis. 8.9% positive
only slightly with Standard ears being erect, cropped, or button. for thyroid auto-antibodies based on testing at Michigan State
Toys must have naturally erect ears only. The neck is slim, slightly University. (Ave. for all breeds is 7.5%).4,5
arched and moderately long, the topline has a slight arch, chest is
Anal Gland Disease: Anal sacculitis and anal gland infection.
narrow but deep, abdomen is mildly tucked, and a slightly curved
Dorn reports a 2.92x odds ratio in Manchester Terriers versus other
tail tapers to finish just short of the tarsal joint.
breeds. Reported at a frequency of 3.40% in the Manchester Terrier
Health and Genetics Survey.1,6
307
Cryptorchidism: Can be bilateral or unilateral. Reported at a Tests of Phenotype: CHIC Certification: Required testing includes
frequency of 3.21% in the Manchester Terrier Health and Genetics hip radiographs, thyroid profile including autoantibodies, and
Survey.1 genetic test for VWD. (See CHIC website: www.caninehealthinfo.org).
Demodicosis: Demodectic mange dermatitis has an underlying Recommend patella evaluation, elbow radiographs, CERF eye
immunodeficiency in its pathogenesis. Reported at a frequency examination, and cardiac examination.
of 2.53% in the Manchester Terrier Health and Genetics Survey.
Unknown mode of inheritance.1 Miscellaneous
• Breed name synonyms: Toy Manchester Terrier, Black and Tan
Seasonal Flank Alopecia: Bilateral, symmetrical hair loss affecting
Terrier (historical), Toy Black and Tan Terrier (historical), English
the flank, dorsum and tail. Dorn reports a 10.55x odds ratio in
Toy Terrier, Gentleman’s Terrier (historical)
Manchester Terriers versus other breeds. Reported at a frequency of
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain),
1.85% in the Manchester Terrier Health and Genetics Survey.1,6
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
Umbilical Hernia: Congenital opening in the body wall from • AKC rank (year 2008): 107 (404 dogs registered)
where the umbilical cord was attached. Correct surgically if large. • Internet resources: American Manchester Terrier Club:
Reported at a frequency of 1.75% in the Manchester Terrier Health http://clubs.akc.org/mtca
and Genetics Survey. Unknown mode of inheritance.1 Canadian Manchester Terrier Club:
www.canadamt.com
Deafness: Congenital sensorineural deafness can be unilateral British Manchester Terrier Club:
of bilateral. Diagnosed by BAER testing. Reported at a frequency www.british-manchester-terrier-club.co.uk
of 1.46% in the Manchester Terrier Health and Genetics Survey.
Unknown mode of inheritance.1 References
1. American & Canadian Manchester Terrier Clubs: Manchester Terrier
Cataracts: Too few Manchester Terriers have been CERF eye Health and Genetics Survey. 2002.
examined to determine an accurate frequency in the breed. 2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Reported in 3.81% of Manchester Terriers presented to veterinary 3. Vasseur PB, Foley P, Stevenson S, et. al.: Mode of inheritance of Perthes’
teaching hospitals. Reported at a frequency of 1.36% in the disease in Manchester terriers. Clin Orthop Relat Res. 1989 Jul;(244):281-92.
Manchester Terrier Health and Genetics Survey.1,7,8 4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Diabetes Mellitus: Sugar diabetes. Caused by a lack of insulin Vet Med Assoc 2002 Feb 15;220(4):466-71.
production by the pancreas. Controlled by insulin injections, 5. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
diet, and glucose monitoring. Dorn reports a 8.81x odds ratio in Population and Animal Health, Michigan State University. April, 2007.
6. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
Manchester Terriers versus other breeds.6
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
Juvenile Cardiomyopathy: Several Manchester Terriers under the
7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
age of one year have died in heart failure with a post-mortum College of Veterinary Ophthalmologists. ACVO, 2007.
diagnosis of juvenile cardiomyopathy. Research at Prince Edward 8. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
Island and the University of Pennsylvania is looking into the cause the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
of this disorder. 9. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p.228, AAHA Press, 1999.
Other Ocular Disorders: Too few Manchester Terriers have been 10. Robinson FL, Misizin AP, O’Brien DP, et. al.: Myotubular Myopathy in a
CERF examined to determine an accurate breed frequency of ocular Family of Manchester Terrier Dogs. Proceedings, 2008 ACVIM Forum. 2008.
disorders.7 11. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p.396-400.
Cleft Lip/Palate, Cutaneous Asthenia, Hydrocephalus, Lens
Luxation, Oligodontia, Progressive Retinal Atrophy, and
Retained Primary Teeth are reported.9
Genetic Tests
Tests of Genotype: Direct test for vWD is available from VetGen.
308
Mastiff
Points of Conformation: A massive well muscled and heavily
boned dog with an equally massive square head, the Mastiff is a
picture of brute strength. Medium-sized eyes are dark brown in
color and no nictitans should be showing. Ears are v-shaped with
rounded tips and possess fairly fine leather. They lie close to the
cheeks at rest. A prominent furrow up the center of the forehead is
present. The stop is moderate. The muzzle is short, blunt and deep,
and forehead wrinkles appear when alerted. The nose is always
dark, and the lips somewhat pendulous. The neck is muscular and
medium in length, with little loose skin. The topline is straight, until
gently curving down over the croup, and the thorax is deep and
The Breed History wide. There is a moderate abdominal tuck up. The tail reaches to
This popular and widespread breed was known in England for a the tarsus or a bit longer. The Tail tapers and is straight to slightly
few centuries as a pit fighter and watchdog. In ancient times they curved. The limbs are straight boned and wide set, feet are large
likely originated in Southwest Asia, moving through Tibet to the and toes well knuckled up. The gait is best described as smooth and
west of the continent. Phoenicians were thought to have brought ground covering.
Molosser and Alaunt type dogs westward to Britain by 2000 years
BC. Other breeds deriving from the ancient Molosser type dogs
include Tibetan Mastiff, Bullmastiff, Neopolitan Mastiff, Dogue de
Recognized Behavior Issues and Traits
Reported breed characteristics include: Courageous but docile to
Bordeaux and Fila Brasileiro. First written accounts of this breed in
handle represents the ideal breed temperament. A dignified manner
England date to 55 BC when Caesar made note of them during his
is also selected for. They are loyal, and well-developed guarding
invasions. Many were sent back to Italy, and became fighting dogs
instincts are the standard. They are wary of strangers and vigorous
in the Roman Empire. AKC recognition occurred in 1885.
in defense of perceived threats. Early socialization and obedience
The term Mastiff is actually a generic term for gigantic defense are essential. These dogs have high human companionship needs
dogs but over the Centuries types emerged, of which the English and need lots of room due to the large body size. High exercise
Mastiff, now simply termed Mastiff is one. At the times of the levels need to be allowed for. This dog, though calm with family is
World Wars of the twentieth century, they became almost extinct not recommended for toddlers due to massive size. They tend to
in England, but because of breeders sending dogs back from North drool significantly. Grooming needs are low.
America, the breed was revived.
Normal Physiologic Variations
Breeding for Function None reported
Pit fighting, police and military work, war cart dog and watchdog
According to a study in the UK 64.6% of Mastiff litters were born
duties are the best-known historical duties. Importantly, the
via cerserean section.1
peasant class kept these dogs to help with guarding, vermin and
wolf control. Many were kept by butchers who were able to afford
the high cost of feeding them because they fed the Mastiff dogs Drug Sensitivities
their meat scraps. The other function that the breed was prized for None reported
was as group hunting dogs for lion and deer. Power, courage and
agility are characteristics thoroughly bred into the Mastiff. Inherited Diseases
Hip Dysplasia: Polygenically inherited trait causing degenerative
Physical Characteristics joint disease and hip arthritis. OFA reports 19.4% affected.2
Height at Withers: female 27.5” (70 cm), male 30” minimum (76 cm).
Elbow Dysplasia: Polygenically inherited trait causing elbow
Weight: 170-190 lb (79-86 kg). arthritis. OFA reports 14.7% affected. Reported 48.4x odds ratio for
fragmented coronoid process, and 20.2x odds ratio for ununited
Coat: The double coat consists of very dense short undercoat and anconeal process forms of elbow dysplasia versus other breeds.2,3
an outer coat consisting of straight, coarse and moderately short
hairs. Brindle, apricot and fawn are accepted colors, and in brindle Multifocal Retinopathy/Retinal Dysplasia: Autosomal recessive
the background should be fawn or apricot. There is generally a black retinal pigment epithelial dysplasia causing localized multifocal
mask and ear coloration irrespective of coat coloration. retinal detachments. Age of onset from 11 to 13 weeks of age. Can
lead to blindness. Reported in 7.63% of Mastiffs CERF examined by
Longevity: Approximately 8-9 years. veterinary ophthalmologists between 2000-2005. A genetic test is
available.4
309
Dominant Progressive Retinal Atrophy (PRA): An autosomal Cataracts: Anterior cortex punctate cataracts predominate in the
dominant PRA exists in the breed, with an onset of 6 months breed. Identified in 2.82% of Mastiffs CERF examined by veterinary
to 3-1/2 years of age. Causes blindness. Optigen reports 1% of ophthalmologists between 2000-2005.4
Mastiffs are affected based on the available genetic test.4,5
Idiopathic Epilepsy: Inherited seizures. Control with anti-seizure
Patella Luxation: Polygenically inherited laxity of patellar ligaments, medication. Onset of seizures from 6 months to 5 years of age.
causing luxation, lameness, and later degenerative joint disease. Reported at a frequency of 1.4% in the Mastiff Health Survey.6
Treat surgically if causing clinical signs. OFA reports 0.3% affected.2
Osteochondritis Dissecans (OCD): Polygenically inherited cartilage
defect. Causes joint pain and lameness in young growing dogs.
Disease Predispositions Mild cases can resolve with rest, while more severe cases require
Allergic Dermatitis (Atopy): Inhalant or food allergy. Presents
surgery. Reported 1006.8xx odds ratio for stifle OCD, and 11.9x
with pruritis and pyotraumatic dermatitis (hot spots). Reported at a
odds ratio for shoulder OCD versus other breeds. Shoulder OCD is
frequency of 10.2% in the Mastiff Health Survey.6
reported at a frequency of 1.30% in the Mastiff.3,13
Hypothyroidism: Inherited autoimmune thyroiditis. 8.7% positive
Corneal Dystrophy: Endothelial form occurs in the breed due to
for thyroid auto-antibodies based on testing at Michigan State
edema from the loss of the inner lining of the cornea. Results in
University. (Ave. for all breeds is 7.5%).7,8
keratitis and decreased vision. Identified in 1.02% of Mastiffs CERF
Persistent Pupillary Membranes: Strands of fetal remnant examined by veterinary ophthalmologists between 2000-2005.4
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
Panosteitis: Self-limiting disease of young, large breed dogs
In the Mastiff, the strands most often bridge from the iris to the
involving the diaphyseal and metaphyseal areas of the tubular long
cornea and may potentially cause vision impairment. Identified in
bones. Affected dogs show intermittent lameness. Reported 3.5x
7.63% of Mastiffs CERF examined by veterinary ophthalmologists
odds ratio versus other breeds.3
between 2000-2005. CERF does not recommend breeding a Mastiff
with any form of PPM.4 Cervical Malformation/Malarticulation (Wobblers disease):
A congenital anatomical disorder that causes compression of
Cranial Cruciate Ligament Rupture (ACL): Traumatic tearing of
the cervical spinal cord. Clinical signs include limb weakness,
the anterior cruciate ligament. The breed is found to be one with an
proprioceptive deficits, and paralysis. A breed predisposition is
increased incidence. Treatment is surgery. Reported at a frequency
found in the Mastiff. Unknown mode of inheritance.14,15
of 7.5% in the Mastiff Health Survey.6,9
Pulmonic Stenosis (PS) and Dysplasia of the Atrioventricular
Ectropion: Rolling out of eyelids, often with a medial canthal
Valves (DAV): Two congenital heart disorders identified in the
pocket. Can also cause conjunctivitis. Ectropion is reported in 6.26%
breed. Screen with auscultation and echocardiography. Unknown
of Mastiffs CERF examined by veterinary ophthalmologists between
mode of inheritance.16
2000-2005.4
Microphthalmia, Prognathism, and Subaortic Stenosis are
Cystine Urolithiasis/Cystinuria: Cystine uroliths are a sequela
reported.17
to cystinuria, an inherited renal tubular defect in reabsorption of
cystine and some other amino acids. The mode of inheritance in the
breed is not determined. Diagnosis with nitroprusside urine test. Isolated Case Studies
PennGen testing shows 9.9% of males and 0.2% of females tested Sacral Osteochondrosis: Several case reports of this condition
are affected.10,11 are in the literature. In one, a Mastiff dog showed chronic signs
of pain in its pelvic limbs. Radiography revealed a triangular
Entropion: Rolling in of eyelids, often causing corneal irritation mineralized opacity at the craniodorsal aspect of the sacrum
or ulceration. Entropion is reported in 4.18% of Mastiffs CERF consistent with sacral osteochondrosis. A T2-weighted spin-echo
examined by veterinary ophthalmologists between 2000-2005.4 MRI revealed dorsal and lateral compression of the cauda equina.
The osteochondral fragment was removed via a dorsal laminectomy,
Macroblepharon: Abnormally large eyelid opening; may lead to and the clinical signs resolved.18,19
secondary conditions associated with corneal exposure. Reported
in 4.11% of Mastiffs CERF examined by veterinary ophthalmologists Extradural Synovial Cyst Myelopathy: Three male Mastiffs presented
between 2000-2005.4 with progressive ataxia and tetraparesis. Degenerative arthritis of
the articular facet joints was noted on survey spinal radiographs.
Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting Myelography disclosed lateral axial compression of the cervical spinal
of the stomach within the abdomen. Requires immediate veterinary cord medial to the articular facets. Extradural compressive cystic
attention. Cause of 16.3% of deaths in Mastiffs in one survey. structures adjacent to articular facets were identified on magnetic
Reported at a frequency of 4.0% in the Mastiff Health Survey.6,12 resonance imaging (1 dog). Dorsal laminectomies cured all 3 dogs. The
cysts were identified as synovial cysts.20
Osteosarcoma (OSA): Malignant bone cancer, most often seen in
the humerus or femur. Reported at a frequency of 3.8% in the OFA Mesenchymal Chondrosarcoma: A young adult female Mastiff
on-line Mastiff Health Survey.2 dog developed a large retroperitoneal mass, pleural effusion, and
310
multiple pulmonary and pleural nodules. All masses were diagnosed osteochondritis dissecans of the humeral head in dogs : 44 cases [1982 to
as mesenchymal subtype chondrosarcomas, using histological and 1987]. J Am Anim Hosp Assoc 1990: 26[2]:173-178.
immunohistochemical criteria.21 14. Berry WL: Common Cervical Myelopathies. Proceedings, 2004 Western
Veterinary Conference. 2004.
15. Lyman R: Surgical Treatment of Caudal Cervical Spondylomyeopathy: A
Genetic Tests Discussion of the Controversy III. Proceedings, 2004 ACVIM Forum. 2004.
Tests of Genotype: Direct tests for PRA and Multifocal Retinopathy 16. Fernández del Palacio MJ: Congenital Heart Diseases: Part I.
are available from Optigen. Proceedings, 2002 WSAVA Congress. 2002.
17. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Tests of Phenotype: CHIC Certification: Required testing includes Ackerman. p. 228. AAHA Press, 1999.
hip and elbow radiographs, CERF eye examination (minimum of 18. Glyde M, Doyle R, McAllister H, et. al.: Magnetic resonance imaging
2 years) and congenital cardiac evaluation. Optional tests include in the diagnosis and surgical management of sacral osteochondrosis in a
thyroid profile including autoantibodies, and nitroprusside urine mastiff dog. Vet Rec. 2004 Jul 17;155(3):83-6.
test for cystinuria from PennGen. (See CHIC website; www. 19. Snaps FR, Heimann M, Saunders J, et. al.: Osteochondrosis of the sacral
bone in a mastiff dog. Vet Rec. 1998 Oct 24;143(17):476-7.
caninehealthinfo.org).
20. Levitski RE, Chauvet AE, Lipsitz D: Cervical myelopathy associated
with extradural synovial cysts in 4 dogs. J Vet Intern Med. 1999
Recommend patella evaluation.
May-Jun;13(3):181-6.
21. Munday JS, Prahl A: Retroperitoneal extraskeletal mesenchymal
Miscellaneous chondrosarcoma in a dog. J Vet Diagn Invest. 2002 Nov;14(6):498-500.
• Breed name synonyms: Old English Mastiff, English Mastiff, 22. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Alan/Alaunts (historical terms in Italian-French). Book House, NY 2006. p. 293-297.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 28 (6,657 dogs registered)
• Internet resources: Mastiff Club of America Inc.:
http://mastiff.org/
Canadian Mastiff Club: www.mastiffcanada.org
Old English Mastiff Club (UK): www.mastiffclub.com
References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010 .
3. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
5. Kijas JW, Miller BJ, Pearce-Kelling SE, et. al.: Canine models of
ocular disease: outcross breedings define a dominant disorder present
in the English mastiff and bull mastiff dog breeds. J Hered. 2003
Jan-Feb;94(1):27-30.
6. Mastiff Club of America: Mastiff Health Survey; preliminary statistics –
first 570. 2005.
7. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
8. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
9. Duval JM, Budsberg SC, Flo GL, et. al.: Breed, sex, and body weight as risk
factors for rupture of the cranial cruciate ligament in young dogs. J Am Vet
Med Assoc. 1999 Sep 15;215(6):811-4.
10. Osborne CA, Sanderson SL, Lulich JP, et. al: Canine cystine urolithiasis.
Cause, detection, treatment, and prevention. Vet Clin North Am Small Anim
Pract. 1999 Jan;29(1):193-211, xiii.
11. Case LC, Ling GV, Franti CE, et. al.: Cystine-containing urinary
calculi in dogs: 102 cases (1981-1989). J Am Vet Med Assoc. 1992 Jul
1;201(1):129-33.
12. Evans KM & Adams VJ: Mortality and morbidity due to gastric
dilatation-volvulus syndrome in pedigree dogs in the UK. J Small Anim
Pract. 2010 Jul;51(7):376-81.
13. Rudd RG, Whitehair JG, Margolis JH: Results of management of
311
Miniature Bull Terrier
an early introduction to children (and small pets or other dogs) in
the household. Needs human companionship, has low grooming
needs and is a low shedder. Good in town or country but has high
energy levels so adequate exercise and mental gymnastics are
recommended to prevent boredom vices.
312
Hypothyroidism: Inherited autoimmune thyroiditis. 4.5% positive • Internet resources: Miniature Bull Terrier Club of America:
for thyroid auto-antibodies based on testing at Michigan State www.minibull.org
University. (Ave. for all breeds is 7.5%).8,9 Miniature Bull Terrier Club UK:
www.miniaturebullterrierclub.co.uk
Deafness: Congenital deafness can be unilateral or bilateral. Miniature Bull Terrier Club of Canada:
Diagnosed by BAER testing. Reported at a frequency of 3.80% in www.minibullyclub.com
the 2002-2004 MBTCA Breed Health Survey. Unknown mode of
inheritance.5
References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
Corneal Dystrophy: Endothelial form occurs in the breed due to
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
the edema from the loss of the inner lining of the cornea. Results in 2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
keratitis and decreased vision. Identified in 1.49% of Miniature Bull 3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Terriers CERF examined by veterinary ophthalmologists between College of Veterinary Ophthalmologists. ACVO, 2007.
2000-2005.3 4. Curtis R, Barnett KC, Startup FG: Primary lens luxation in the miniature
bull terrier. Vet Rec. 1983 Apr 2;112(14):328-30.
Vitreous Degeneration: Liquefaction of the vitreous gel which may 5. Miniature Bull Terrier Club of America: 2002-2004 Health Survey Report.
predispose to retinal detachment. Identified in 1.49% of Miniature 2004.
Bull Terriers CERF examined by veterinary ophthalmologists 6. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing
between 2000-2005.3 lens luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
7. Hood JC, Craig AJ: Hereditary nephritis in a miniature bull terrier. Vet Rec.
Cataracts: Anterior cortex and capsular punctate cataracts 1994 Aug 6;135(6):138-40.
predominate in the breed. Identified in 1.19% of Miniature Bull 8. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
Terriers CERF examined by veterinary ophthalmologists between hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
2000-2005. CERF does not recommend breeding any Miniature Bull Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
9. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Terrier with a cataract.3
Population and Animal Health, Michigan State University. April, 2007.
10. Moon-Fanelli AA, Dodman NH: Description and development of
Left Ventricular Outflow Tract Obstruction (LVOTO): Reported
compulsive tail chasing in terriers and response to clomipramine treatment.
as a problem in the breed. Screen by echocardiography. The MBTCA J Am Vet Med Assoc. 1998 Apr 15;212(8):1252-7.
recommends only breeding dogs with LVOT rates of less than 2.2 m/ 11. Dodman NH, Knowles KE, Shuster L, et. al.: Behavioral changes
sec with no multiple minor or any major structural defects present. associated with suspected complex partial seizures in bull terriers. J Am Vet
Med Assoc. 1996 Mar 1;208(5):688-091.
Compulsive Tail Chasing and Spinning: Disorder of persistent 12. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
spinning observed in the breed. Possibly a behavioral compulsion, Book House, NY 2006. p. 401-403.
as 75% of affected dogs respond to clomipramine administration.
However a neurological partial seizure disorder cannot be ruled out,
as some dogs have abnormal electroencephalograms and respond
to anticonvulsants.10,11
Genetic Tests
Tests of Genotype: Direct genetic test for Lens Luxation is available
from OFA and AHT.
Miscellaneous
• Breed name synonyms: Mini Bull
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 124 (236 dogs registered)
313
Miniature Pinscher
brave against dogs much larger, curious, extremely high activity levels,
good with sensible, quiet gentle children, moderately good trainability,
good escape artists, and should not be off leash unless in a fenced
enclosure. They are known to have a moderate barking tendency.
Color-Dilution Alopecia: Condition seen in some blue or fawn Direct test for black and chocolate coat color is available from VetGen.
(dilute) colored Miniature Pinschers. Starts as a gradual onset of dry,
Tests of Phenotype: Recommend patella examination, CERF eye
dull and poor hair coat quality. Progresses to poor hair regrowth,
examination, hip and elbow radiographs, thyroid profile including
follicular papules and comedomes. Hair loss and comedome
autoantibodies, and cardiac evaluation.
formation are usually most severe on the trunk. Dorn reports an
8.54x odds ratio for developing alopecia versus other breeds.1,4,13
Miscellaneous
Optic Nerve Hypoplasia/Micropapilla: Congenital defect of optic • Breed name synonyms: MinPin, Zwergpinscher, Reh Pinscher,
nerve development affecting vision, or a small optic disc. Identified King of Toys (nickname).
in 1.34% of Miniature Pinschers CERF examined by veterinary • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ophthalmologists between 2000-2005.9 ANKC (Australian National Kennel Club), NKC (National Kennel Club).
• AKC rank (year 2008): 32 (5,848 dogs registered)
Inherited Epilepsy: Grand-mal seizures. Control with anticonvulsant • Internet resources: Miniature Pinscher Club of America:
medication. Dorn reports a 5.39x odds ratio versus other breeds. www.minpin.org
Unknown mode of inheritance.4 The Canadian Miniature Pinscher Club:
www.cdn-miniaturepinscherclub.com
Demodicosis: Demodectic mange dermatitis has an underlying Miniature Pinscher Club of Great Britain:
immunodeficiency in its pathogenesis. Dorn reports a 1.95x odds www.miniaturepinscherclub.co.uk
ratio versus other breeds. Unknown mode of inheritance.4
316
Miniature Schnauzer
Recognized Behavior Issues and Traits
Reported breed characteristics include: Grooming requirements are
moderate, and they are low shedding dogs, though the coat must
be stripped at least every 6 months; ideally they should not be
clipped to maintain the outer coat. Daily grooming, with emphasis
on limbs and whiskers should be done. Whiskers need a wash clean
after meals. The Miniature Schnauzer dogs are obedient and friendly
and like close human companionship. They are of high intelligence,
possess high trainability, are active, affectionate, and are good with
children. They do well in both city and country, and do well with
The Breed History other dogs; considered less scrappy than the other terriers. They
possess a well-developed guarding instinct. Easy to train, but like to
In artwork of the 15th century, a dog with features consistent
alarm bark; some lines have nervous temperaments. When off leash,
with the Miniature Schnauzer is pictured. By 1900, the breed was
should be in a fenced enclosure.
well established and was being shown. The origin of this dog is
thought to be a mixture of Standard Schnauzer, with perhaps
Poodle, Miniature pinscher, and Affenpinscher. They were brought to Normal Physiologic Variations
America around the year 1925. The name derives from the German Idiopathic Hyperlipoproteinemia: Miniature Schnauzers have a
word for nose (schnauzer). The AKC recognized this breed in 1933. non-pathological condition of hypertriglyceridemia, characterized by
increased very low density lipoproteins with or without accompanying
Breeding for Function chylomicronemia. Both the prevalence and severity of hypertriglyc-
These dogs were widely used on the farm to control vermin such eridemia increase with age. Dogs with high serum triglyceride
as rats, but the temperament of this breed varies from the classic concentrations can also have associated high serum alkaline
terrier. Currently, they serve primarily as companion animals. phosphatase (AlkP) and alanine aminotransferase (ALT)levels.1,2,3
Coat: The double wiry, thick coat is commonly seen in salt and Drug Sensitivities
pepper (black and white intermixed in bands on some hairs to Miniature Schnauzers are overrepresented for adverse reactions
produce a grey appearance). Silver and black, and solid black to potentiated sulfonamides. Clinical signs included hypersensi-
are also seen. A small white patch is sometimes found on the tivity, thrombocytopenia and hepatopathy, and infrequently can
black-coated dogs. Coat color may fade with age. The undercoat include neutropenia, keratoconjunctivitis sicca, hemolytic anemia,
varies widely in color and can be beige, black, or gray. arthropathy, uveitis, skin and mucocutaneous lesions, proteinuria,
facial palsy, suspected meningitis, hypothyroidism, pancreatitis,
Longevity: 14 years facial edema, and pneumonitis.5
Points of Conformation: This alert expressive terrier-type dog
is similar in appearance to the Standard Schnauzer. Miniature Inherited and Congenital Diseases
Schnauzers are stocky in build, and the head is rectangular, and Myotonia Congenita: Autosomal recessive disorder causing
the flat forehead is free of wrinkles. The stop is slight, and oval hypertrophic skeletal muscles, difficulty in rising after a period of
ears are small, triangular, high-set, and lie close to the head. Some rest, a stiff and stilted gait when walking, and a bunnyhop-type
ears are cropped to have pointed tips, and to rest pricked up; if not movement when running. In addition, there are increased
cropped they fold forward. The eyes, overlain with bushy brows are respiratory sounds, difficulty when swallowing, ptyalism, dental
dark brown, deep-set and small. Body skin is pigmented. Whiskers abnormalities, and superior prognathism. Worldwide genetic testing
on the chin are left long to accentuate the face. The black nose is in the breed shows 20.4% carriers and 1.1% affected. A genetic test
prominent with wide nostrils. The neck is well muscled and arched, is available.6,7
and no throatiness is evident. The topline is straight but descends
slightly as it goes toward the rear, the thorax is deep and ribs well Hip Dysplasia and Legg-Calve Perthes Disease: Polygenically
sprung. No tuck up of abdomen is evident. The tail is carried up, and inherited traits causing degenerative hip joint disease and arthritis.
often docked short. Limbs are straight boned and feet are round, Too few Miniature Schnauzers have been screened by OFA to
with well-arched toes and possessing thick, black pads. The gait is determine an accurate frequency.8
quick and agile.
317
Patella Luxation: Polygenically inherited laxity of patellar ligaments, developing cataracts versus other breeds mean age of onset
causing luxation, lameness, and later degenerative joint disease. Treat of 5.4 years. Identified in 1.54% of Miniature Schnauzers CERF
surgically if causing clinical signs. Too few Miniature Schnauzers examined by veterinary ophthalmologists between 2000-2005.
have been screened by OFA to determine an accurate frequency.8 CERF does not recommend breeding any Miniature Schnauzer with
a cataract.10,21,22,23
Type-A Progressive Retinal Atrophy (PRA)/Photoreceptor
Dysplasia (PD): Partially dominant form of PRA identified in Hyperadrenocorticism (Cushing’s disease): Caused by a functional
Miniature Schnauzers causing progressive blindness with age of adrenal or pituitary tumor. Clinical signs may include increased
onset around three years of age. Dogs homozygous for the mutated thirst and urination, symmetrical truncal alopecia, and abdominal
gene are always affected. Heterozygous dogs can be clinically distention. Dorn reports a 3.77x odds ratio versus other breeds.
normal or affected. A genetic test for Type-A PRA is available. Reported in 4.3% of Miniature Schnauzers examined at veterinary
There are other forms of PRA in the breed that are not caused by school hospitals.17,20
Type-A PRA, and that do not have a genetic test. CERF does not
recommend breeding any Miniature Schnauzer with PRA.9,10 Diabetes Mellitus: Sugar diabetes. Control with insulin injection,
diet, and glucose monitoring. Reported in 4.0% of Miniature
Retinal Dysplasia: Autosomal recessive congenital disorder of Schnauzers examined at veterinary school hospitals. Odds ratios
the retina causing regional retinal dysplasia and associated retinal versus other breeds range from 10.01x (Dorn) to 9.87x (Hess).
detachment leading to blindness. The disorder is also associated Genetic predisposition is linked to mutations in the CTLA4
with a mild unilateral or bilateral persistent hyperplastic primary promotior. Unknown mode of inheritance.14,17,20,24,25
vitreous (PHPV). CERF does not recommend breeding any Miniature
Schnauzer with retinal dysplasia. There is no genetic test for Chronic Mitral Valve Disease/Mitral Prolapse: Systolic heart
carriers.10,11 murmurs caused by chronic mitral valve disease. Can progress to
congestive heart failure. Screen with auscultation. Reported in 3.9%
Elbow Dysplasia: Polygenically inherited trait causing elbow of Miniature Schnauzers examined at veterinary school hospitals.
arthritis. Too few Miniature Schnauzers have been screened by OFA Unknown mode of inheritance.20
to determine an accurate frequency.8
Pancreatitis: Inflammation of the pancreas causing vomiting and
Congenital Cataracts and Microphthalmia: A simple autosomal peritonitis. Can be life threatening if severe. Hypertriglyceridemia in
recessive disorder of congenital cataract and microphthalmia the breed is not a risk factor for pancreatitis. Reported in 3.5% of
occurs in the breed caused by a mutation in the MISRII receptor Miniature Schnauzers examined at veterinary school hospitals. Dorn
gene. The opacity is primarily in the lens nucleus and posterior reports a 55.06x odds ratio versus other breeds. Breed prevalence
cortex. There is no test for carriers.12,13 may be related to mutations in the SPINK 1 gene.17,20,26,27
Persistent MÜllerian Duct Syndrome: Autosomal recessive Persistent Pupillary Membranes: Strands of fetal remnant
intersex disorder in the breed caused by a mutation in the MISRII connecting; iris to iris, cornea, lens, or involving sheets of tissue.
gene. Genetically normal males have a normal male karyotype The later three forms can impair vision, and dogs affected with
(78, XY), bilateral testes, and a complete Mullerian duct system these forms should not be bred. Identified in 2.78% of Miniature
(oviducts, uterus, cervix and cranial vagina). A genetic test is Schnauzers CERF examined by veterinary ophthalmologists between
available.14,15,16 2000-2005.10
Mucopolysaccharidosis VI (MPS VI): PennGen reports MPS Distichiasis: Abnormally placed eyelashes that irritate the cornea
VI identified in the Miniature Schnauzer. This is an autosomal and conjunctiva. Can cause secondary corneal ulceration. Identified
recessive disorder causing skeletal deformities, including defects in in 1.93% of Miniature Schnauzers CERF examined by veterinary
the sternum, vertebrae and particularly the hip joints. To varying ophthalmologists between 2000-2005.10
degrees they may also experience corneal cloudiness and facial
dysmorphia. A genetic test is available. Schnauzer Comedome Syndrome: The breed is prone to
developing follicular dermatitis with comedones (blackheads); hair
follicles filled with keratin and sebum.28
Disease Predispositions
Urolithiasis: The breed has a high incidence of bladder stones Sick Sinus Syndrome: Arrhythmia characterized by sinus
compared to other breeds. Reported in 5.9% of Miniature bradycardia and sinoatrial arrest due to abnormal firing of the
Schnauzers examined at veterinary school hospitals. Of bladder sinoatrial node. Clinical signs include lethargy and syncopy. Occurs
stone submissions from Miniature Schnauzers in a Canadian study, at an increased frequency in older Miniature Schnauzers. Treatment
61.2% were Calcium Oxalate, 23.1% were Struvite, and 1.7% were is with a pacemaker. Reported in 1.9% of Miniature Schnauzers
Urate. Mean age of recognition of bladder stones in the breed is 4.9 examined at veterinary school hospitals.20,29
years. Dorn reports a 7.77x odds ratio versus other breeds.17,18,19,20
Hypothyroidism: Inherited autoimmune thyroiditis. 1.3% positive
Cataracts: Anterior or posterior intermediate and punctate for thyroid auto-antibodies based on testing at Michigan State
cataracts occur in the breed. Unknown mode of inheritance. University. (Ave. for all breeds is 7.5%.)30,31
4.98% of Miniature Schnauzers presented to veterinary teaching
hospitals had cataracts. The breed has a 3.7x odds ratio for Portosystemic Shunt (PSS, Liver Shunt): Undetermined mode
318
of inheritance. Vessels can be intrahepatic or extrahepatic. Causes some cases may culminate with death. Thought to be caused by a
stunting, with abnormal behavior and possible seizures. Diagnose severe contact dermatitis to elements in shampoo.45,46,47
with paired fasted and feeding serum bile acid and/or ammonium
levels, and abdominal ultrasound. In one study, 23% of Miniature Aquired Aurotrichia, Allergic Inhalant Dermatitis, Anterior
Schnauzers with PSS were not diagnosed until they were over 7 Crossbite, Base narrow Canines, Brachygnathism, Cleft Lip/
years of age (due to hepatic encephalopathy). Treatment of PSS Palate, Cryptorchidism, Cutaneous Asthenia, Deafness, Factor
includes partial ligation and/or medical and dietary control of VII Deficiency, Fanconi Syndrome, Glaucoma, IgA Deficiency,
symptoms. Reported in 1.3% of Miniature Schnauzers examined at Keratoconjunctivitis Sicca, Muscular Dystrophy, OCD Stifle,
veterinary school hospitals with an odds ratio of 19.8x versus other Optic Nerve Hypoplasia, Prognathism, Seasonal Flank Alopecia,
breeds.20,32,33,34 von Willebrand’s Disease, and Wry Mouth are reported.48
Superficial Suppurative Necrolytic Dermatitis (SSND): Rare, Direct test for Myotonia Congenita is available from PennGen and
cutaneous and systemic reaction consisting of erythematous HealthGene.
papules and plaques that progress to necrosis and ulcers. Systemic
signs consist of fever, depression and leucocytosis. Most cases of Direct test for Persistent Mullerian Duct Syndrome is available from
SSND improve in 1 to 2 weeks with symptomatic treatment, but the Meyers-Wallen lab: 607-256-5683, vnm1@cornell.edu.
319
Direct test for MPS is available from PennGen. 14. Meyers-Wallen VN: Genetics of sexual differentiation and anomalies in
dogs and cats. J Reprod Fertil Suppl. 1993;47:441-52.
Direct test for black color and mask is available from HealthGene 15. Pujar S & Meyers-Wallen VN: A molecular diagnostic test for
and VetGen. persistent Müllerian duct syndrome in miniature schnauzer dogs. Sex Dev.
2009;3(6):326-8.
Tests of Phenotype: CHIC Certification: CERF eye examination, 16. Wu X, Wan S, Pujar S, et. al.: A single base pair mutation encoding a
and cardiac evaluation. Optional testing includes the genetic test for premature stop codon in the MIS type II receptor is responsible for canine
myotonia congenita. (See CHIC website; www.caninehealthinfo.org). persistent Müllerian duct syndrome. J Androl. 2009 Jan-Feb;30(1):46-56.
17. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
Recommend patella evaluation, hip and elbow radiographs, and veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
thyroid profile including autoantibodies.
18. Houston DM & Moore AE: Canine and feline urolithiasis: examination of
over 50 000 urolith submissions to the Canadian veterinary urolith centre
Miscellaneous from 1998 to 2008. Can Vet J. 2009 Dec;50(12):1263-8.
• Breed name synonyms: Zwergschauzer. 19. Klausner JS, Osborne CA, Clinton CW, et. al.: Mineral composition of
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), urinary calculi from miniature schnauzer dogs. J Am Vet Med Assoc. 1981
ANKC (Australian National Kennel Club), NKC (National Kennel Club). May 15;178(10):1082-3.
• AKC rank (year 2008): 11 (17,040 dogs registered) 20. Veterinary Medical Database, Purdue University: Search of diagnoses for
Miniature Schnauzers. July 18, 2000.
• Internet resources: The American Miniature Schnauzer Club
21. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
Inc.: http://amsc.us
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
Miniature Schnauzer Club of Canada: www.mscc.ca 22. Adkins EA, Hendrix DV: Outcomes of dogs presented for cataract
The Miniature Schnauzer Club (UK): evaluation: a retrospective study. J Am Anim Hosp Assoc. 2005
http://the-miniature-schnauzer-club.co.uk Jul-Aug;41(4):235-40.
Schnauzer Club of Great Britain: www.schnauzerclub.co.uk 23. Park SA, Yi NY, Jeong MB, Kim WT, et. al.: Clinical manifestations of
cataracts in small breed dogs. Vet Ophthalmol. 2009 Jul-Aug;12(4):205-10.
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25. Short AD, Saleh NM, Catchpole B, et. al.: CTLA4 promoter
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34. Mertens M, Fossum TW, Willard MD, et. al.: Diagnosis of congenital
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41. Palmer DN, Tyynela J, van Mil HC, et. al.: Accumulation of sphingolipid
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42. Jolly RD, Sutton RH, Smith RI, e. al.: Ceroid-lipofuscinosis in miniature
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43. Morton LD, Sanecki RK, Gordon DE, et. al.: Juvenile renal disease in
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45. Rosenkrantz WS, Griffin CE & Walder E: Superficial suppurative
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46. Gross TL, Ihrke PJ, Walder EJ, et. al.: Sterile pustular erythroderma
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54. Santos NR, Krekeler N, Schramme-Jossen A, et. al.: The knobbed
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55. Vanhaesebrouck AE, Couturier J, Cauzinille L, et. al.: Demyelinating
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321
Neopolitan Mastiff
set, with large overhanging dorsal palpebral, and lower palpebral
sags, showing the third eyelid. Eye color and rim synchronize with
coat color, and usually are brown to amber. Ears may be cropped to
a triangular shape. The neck is short and well muscled. The thorax
is deep and ribs are well sprung. The topline is level. The abdomen
is not tucked up. Front dewclaws are not to be removed but rear
ones are. Feet are large, round and the front feet are slightly turned
out. Tail is tapered, and docked to 1/3 of the length to the tarsus.
Carriage is horizontal to slightly elevated when working. The gait is
slow, steady and a rolling swaying attitude is normal, especially if
pace rather than trot. The head is carried just above the topline level
The Breed History usually, and front feet may paddle a bit. There is a low shedding
This is an ancient breed with reports dating back 5000 years, tendency except during seasonal coat turnover.
but only recognized as a distinct breed since the 1940s. Very
early origins trace back to the war dogs (Macedonian, Sumerian,
Assyrian) in the middle east and Asia. Alexander the Great was
Recognized Behavior Issues and Traits
Breed attributes ascribed include: Loyal—even devoted, gentle, well
reported to have crossed war dogs with short-haired Indian dogs,
tempered, calm yet wary of strangers, fearsome when provoked.
giving rise to the Molossus. The Romans crossed these Molossus
Not recommended for young children due to extreme large size and
dogs with English Mastiffs when they invaded, increasing their
weight. They are droolers. Tolerate cool weather better than hot.
size. In southern Italy in the Neapolitan region, these crossbreds
Need enough room to move around. They are not well suited to
were further selected for guarding and inbred over the years. Breed
small apartments. Low to moderate need for exercise.
characteristics that define the Neapolitan Mastiff include extensive
loose skin, enormous body and head, and a smooth lumbering gait.
First reported imports to the USA occurred in the 1970s, and now Normal Breed Variations
estimates are that 6000 dogs are in the country, especially along Late maturing—about 3 years of age
the eastern seaboard. AKC recognition occurred in 2004.
Tend to need cesarian section and occasionally cannot breed
without artificial insemination. In a UK study, 36.4% of litters were
Breeding for Function delivered via Cesarian section.1
These dogs fulfilled many roles including guard dog, war dog,
hunting dog, and draft dog.
Drug Sensitivities
None reported
Physical Characteristics
Height at Withers: female 24-29” (61-74 cm), male 26-31”
(66-79 cm) Inherited Diseases
Hip Dysplasia: Polygenically inherited trait causing degenerative
Weight: bitches: 110 lb (50 kg), dogs 150 lb (68 kg) joint disease and hip arthritis. Reported at a frequency of 60% in a
Polish study. OFA reports 47.7% affected.2,3
Coat: Smooth, short (1”) and dense, the hairs are straight. Lacks
furnishings anywhere. Colors include black, tawny, mahogany, grey Elbow Dysplasia: Polygenically inherited trait causing elbow
(also termed blue). Sometimes brindling may occur, but must be arthritis. OFA reports 37.5% affected.2
tan. Any white markings must meet the breed standard—if outside
defined areas, these are a disqualification. Blue color is most desired Patella Luxation: Polygenically inherited laxity of patellar ligaments,
as he blends into the shadows during guarding. causing luxation, lameness, and later degenerative joint disease.
Treat surgically if causing clinical signs. Too few Neopolitan Mastiffs
Longevity: 8-10 years have been screened by OFA to determine an accurate frequency.2
327
Norfolk Terrier
Recognized Behavior Issues and Traits
Reported breed characteristics include: Enjoys the company of
people, possesses a stable temperament, fearless, a good guard dog,
good in both rural and urban environments. He is a loyal dog with a
charming personality, independently minded, moderately trainable;
one should start obedience training early. Introduce to children,
cats and other pets early. This terrier will view small pets as prey.
Generally, they are very good with children. A Norfolk must be
exercised in a fenced enclosure if off the leash.
Coat: The weather resistant coat is wiry and straight and about Elbow Dysplasia: Polygenically inherited trait causing elbow
1.5-2” (3.75-5 cm) in length, lies close, and the undercoat is arthritis. Too few Norfolk Terriers have been screened by OFA to
short and dense. Coat colors include red, grizzle, black and tan determine an accurate frequency.1
and wheaten. They may have dark points. White markings are
Epidermolytic Hyperkeratosis (Ichthyosis): An autosomal
undesirable. The male has a longer thick ruff. Regular brushing is
recessive cornification defect in Norfolk Terriers causing
important and stripping is usually performed twice a year. They are
hyperpigmented skin with scaling following mild trauma. The
moderate shedding dogs.
lesions are generalized but most prominent in the glabrous skin of
Longevity: 12-15 years the axillary and inguinal regions. A genetic test is available.2,3
Points of Conformation: The skull is wide and roundish, the Disease Predispositions
muzzle wedge-shaped, the face fox-like and the stop is well defined. Mitral Valve Disease (MVD): Norfolk Terriers are prone to early
Eyes are small and oval in shape, dark, and the palpebral margins age mitral regurgitation. This condition may eventually lead to
are black. The ears, which are the distinguishing feature of the breed congestive heart disease, cardiac arrhythmias (irregular heart beats)
fold forward and are small and triangular, with slightly rounded and cardiac failure. Unknown mode of inheritance.
tips. They possess a compact conformation, are longer than tall, and
fairly heavily boned. The neck is medium in length and well muscled, Persistent Pupillary Membranes: Strands of fetal remnant
the topline level, and thorax rounded with well-sprung ribs. The tail connecting; iris to iris, cornea, lens, or involving sheets of tissue.
is high set and usually docked. They have short fairly straight limbs, The later three forms can impair vision, and dogs affected with
with short metacarpals and metatarsals. The feet are compact, these forms should not be bred. Identified in 17.57% of Norfolk
round and nails are black. The gait is low and smooth. Terriers CERF examined by veterinary ophthalmologists between
2000-2005.4
328
Cataracts: Posterior cortex punctate cataracts predominate in the
breed. Identified in 3.38% of Norfolk Terriers CERF examined by
Miscellaneous
• Breed name synonyms: Jones Terrier (historical), Norfolk.
veterinary ophthalmologists between 2000-2005. CERF does not • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
recommend breeding any Norfolk Terrier with a cataract.4 ANKC (Australian National Kennel Club).
• AKC rank (year 2008): 115 (314 dogs registered)
Optic Nerve Coloboma: A congenital cavity in the optic nerve
• Internet resources: The Norfolk Terrier Club:
which, if large, may cause blindness or vision impairment.
www.norfolkterrierclub.org
Identified in 3.04% of Norfolk Terriers CERF examined by veterinary
American Norfolk Terrier Association:
ophthalmologists between 2000-2005. CERF does not recommend
http://www.norfolkterrier.org/
breeding any affected Norfolk Terrier.4
Norfolk Terrier Club of Great Britain:
Optic Nerve Hypoplasia: A congenital defect of the optic www.norfolkterrierclub.co.uk/
nerve causing blindness. Reported in 2.70% of Norfolk Terriers Norfolk Terrier Club of Canada:
CERF-examined by veterinary ophthalmologists between www.norfolkterrierclubofcanada.ca
2000-2005.4
References
Hypothyroidism: Inherited autoimmune thyroiditis. 1.1% positive 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
for thyroid auto-antibodies based on testing at Michigan State 2. Barnhart KF, Credille KM, Ambrus A, et. al.: A heritable keratinization
University. (Ave. for all breeds is 7.5%).5,6 defect of the superficial epidermis in norfolk terriers. J Comp Pathol. 2004
May;130(4):246-54.
Retinal Dysplasia: Retinal folds are recognized in the breed. Can 3. Credille KM, Barnhart KF, Minor JS, et. al.: Mild recessive epidermolytic
lead to retinal detachment and blindness. Reported in 1.01% of hyperkeratosis associated with a novel keratin 10 donor splice-site
Norfolk Terriers CERF-examined by veterinary ophthalmologists mutation in a family of Norfolk terrier dogs. Br J Dermatol. 2005
between 2000-2005.4 Jul;153(1):51-8.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Portosystemic shunt (PSS, liver shunt): Congenital abnormal blood College of Veterinary Ophthalmologists. ACVO, 2007.
5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
vessel connecting the portal and systemic circulation. More frequently
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
intrahepatic in this breed versus extrahepatic. Causes stunting,
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
abnormal behavior, possible seizures, and secondary ammonium urate 6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
urinary calculi in the breed. Treatment of PSS includes partial ligation Population and Animal Health, Michigan State University. April, 2007.
and/or medical and dietary control of symptoms. Reported to occur at 7. Center S: Portosystemic Vascular Anomalies & Hepatic MVD: Evidence of
an increased frequency in the breed.7 Common Genetics in Small Dogs. Proceedings, 2008 ACVIM Forum. 2008.
8. Ketring KL: Schirmer Testing & Tonometry Are “Good Medicine”.
Glaucoma: Primary, narrow angle glaucoma occurs in the breed. Proceedings, 2005 Western Veterinary Conference. 2005.
Can cause secondary lens luxation. Screen with gonioscopy and 9. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
tonometry. Frequency and mode of inheritance in the breed has not Ackerman. p. 229 AAHA Press, 1999.
been determined.8 10. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 409-411 .
Progressive Retinal Atrophy (PRA): Inherited retinal degeneration
leading to complete blindness. Onset between 2 and 3 years of age
with initial loss of night vision. Undetermined mode of inheritance.4
Genetic Tests
Tests of Genotype: Direct test for Ichthyosis is available from the
Venta Lab at Michigan State University (517-355-6463 x1552).
Weight: females 26.5-35.5 pounds (12-16 kg), males 31-40 pounds Patella Luxation: Polygenically inherited laxity of patellar
(14-18 kg). ligaments, causing luxation, lameness, and later degenerative joint
disease. Treat surgically if causing clinical signs. Too few Norwegian
Coat: Outer coat is thick and hard, but rather smooth lying. The Buhunds have been screened by OFA to determine an accurate
under coat is soft and dense. The coat on the head and front of the frequency.1
legs is comparatively short. The coat on the neck, chest and back
of the thighs is longer. Acceptable coat colors are: Wheaton (pale
cream to bright orange) with or without a black mask, or black Disease Predispositions
without too much bronzing. As little white as possible is permissible Cataracts: Besides the dominant nuclear cataracts, posterior
around the neck, face, chest, toes, or tail tip. cortical cataracts predominate in the breed. Identified in 11.93% of
Norwegian Buhunds CERF examined by veterinary ophthalmolo-
Longevity: 13-15 years. gists between 2000-2005. CERF does not recommend breeding any
Norwegian Buhund with a cataract.2
Points of Conformation: The Buhund is square in profile. The skull is
wedge-shaped, almost flat, and parallel with the bridge of the nose. Hypothyroidism: Inherited autoimmune thyroiditis. Too few
The lips should be black and tightly closed. The teeth should meet Norwegian Buhunds have been test for thyroid autoantibodies at
in a scissors bite. The eyes are oval shaped, color as dark as possible, Michigan State University to determine an accurate frequency for
with black eye rims. The ears are medium sized, prick ears with the breed. (Ave. for all breeds is 7.5%).4,5
pointed tips. The nose is black. The back is level; croup with as little
slope as possible. The tail is set high, tightly curled and carried over Isolated Case Studies
the center line of the back. The feet are oval in shape with tightly None Reported
closed toes. The action is free and effortless. The topline remains level
while moving. Sound movement is essential for working ability.
330
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: Norwegian Sheepdog, Norsk Buhund,
Nordiske Sitz-hunde.
• Registries: AKC, UKC, KCGB (Kennel Club of Great Britain), ANKC
(Australian National Kennel Club), NKC (National Kennel Club), FCI.
• AKC rank: (None) Became an AKC recognized breed Jan. 2009.
Entire studbook registered.
• Internet resources: Norwegian Buhund Club of America:
www.buhund.org
Norwegian Buhund Club (UK): www.norwegian-buhund.org.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Bjerkås E & Haaland MB: Pulverulent nuclear cataract in the Norwegian
buhund. J Small Anim Pract. 1995 Nov;36(11):471-4.
4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
5. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
6. AKC Breed Website: www.akc.org/breeds/norwegian_buhund/ Last
accessed July 1, 2010.
331
Norwegian Elkhound
Recognized Behavior Issues and Traits
Reported breed attributes include: Intelligent, reliable, enjoys close
human companionship, loyal, friendly, good alarm barker and
watchdog, and will capably protect home and family. These dogs
are eager to please. They have very high exercise needs. Noted to
be sensitive, independent and headstrong, this type of dog needs
mental stimulation to prevent boredom vices. Though needing
human companionship, they are aloof with strangers. They are good
with older, mature children, and may see small pets as prey. If off
leash, they must be in a fenced enclosure because they are prone to
The Breed History roaming.
Six thousand years ago is the estimated timeline given for the
origins of this ancient breed, also termed the “Dog of the Vikings”. Normal Physiologic Variations
Archeological records show skeletal remains that match the breed in Tendency to become obese without dietary restriction.
size and constitution dating from between 4000-5000 BC alongside
stone weapon remnants. The first breed standard was drawn up in Drug Sensitivities
1877. This is one of the Scandinavian elkhounds (Swedish Elkhound, None reported
Norwegian Buhund are others) included in the Spitz dog family. AKC
recognition occurred in1913.
Inherited Diseases
Hip Dysplasia: Polygenically inherited trait causing degenerative
Breeding for Function joint disease and hip arthritis. OFA reports 19.5% affected. Reported
Working as a chicken and duck herder, a guard dog, hunter for
at a frequency of 23% in the NEAA Health Survey 2007 Summary.1,2
moose, elk, lynx, raccoon, fox and bear and as a sled dog, this
was truly a versatile dog. Courageous enough to defend against Patella Luxation: Polygenically inherited laxity of patellar ligaments,
bear and wolf, but gentle enough to be a companion. Stamina causing luxation, lameness, and later degenerative joint disease. Treat
is a hallmark of the breed rather than extreme speed. Their surgically if causing clinical signs. Too few Norwegian Elkhounds
short-coupled stature allows them the agility to hold quarry at bay; have been screened by OFA to determine an accurate frequency.1
avoiding harm while sounding a strong voice for the hunter.
Elbow Dysplasia: Polygenically inherited trait causing elbow
Physical Characteristics arthritis. Too few Norwegian Elkhounds have been screened by OFA
Height at Withers: female 19.5” (49.5 cm), male 20.5” (cm) to determine an accurate frequency.1
Weight: females 48 lb (22 kg), males 55 lb (25 kg) Early Retinal Degeneration (ERD): An autosomal recessive
early onset form of progressive retinal atropy. Affected dogs are
Coat: They have a distinctive double gray coat. Hairs are straight, nightblind by 6 weeks of age, and become totally blind between
and the coat lies smoothly. The overcoat hairs are black-tipped. The 12- and 18 months. No genetic test is available. CERF does not
undercoat is wooly and dense and silvery shaded as is the underside recommend breeding affected dogs.3,4
and legs of the dog. There is a black tip on the tail; ears and muzzle
are also black. They undergo twice-yearly shedding and have Rod Dysplasia (RD): An autosomal recessive form of PRA
moderate grooming needs and no doggy odor. manifested by night blindness by 6 months of age, and total
blindness at 3-5 years. No genetic test is available. CERF does not
Longevity: 12-13 years recommend breeding affected dogs.4,5
Points of Conformation: These dogs possess heavy bone and Chondrodysplasia: Autosomal recessive dwarfism in the Norwegian
well-developed musculature and a compact conformation. The Elkhound occurrs due to a generalized disturbance in endochondral
wedge-shaped head is broad and ears are held pricked up. The ossification. Radiographic changes included flaring and increased
high-set tail is carried curled over the back. Eyes are medium-sized, width of the distal metaphyses of the radius and ulna, delayed
oval, and dark brown in color. The stop is clearly defined, skull is ossification of the cuboid bones of the carpus, and reduction in
broad, and the muzzle tapers. The neck is muscular, of medium length of the vertebral bodies. A direct genetic test is available.6
length and slightly arched, without throatiness. The thorax is large
and deep, and the ribs well sprung. The topline gradually slopes Sry Negative XX Sex-Reversal: Autosomal recessive disorder of
down to the rear. The legs are straight boned, dewclaws are usually sexual differentiation. Affected dogs can appear to be female with
left on, and paws are small with a compact oval shape. The gait is enlarged clitori, or male with bilateral aspermatogenic testes. All
smooth and ground covering.
332
have a 78 XX karyotype. Gonads can be ovotestes, but lack Sry, the Juvenile Renal Disease: A kidney basement membrane disorder
testis-determining gene. No genetic test is available.7 causing an impaired ability to concentrate urine, and progressive
azotemia. Periglomerular and interstitial fibrosis are the earliest
Disease Predispositions renal lesions. Results of glomerular counts, kidney size, and
Sebaceous Cysts: Benign accumulation of sebum within plugged dissection of the nephron indicated that nephron numbers and size
hair follicles. Reported at a frequency of 20.8% in the NEAA Health are adequate early in the disease, but that numbers decrease as
Survey 2007 Summary.2 the disease progresses. Dorn reports a 9.41x odds ratio for kidney
disease versus other breeds. Unknown mode of inheritance.10,13,14,15,16
Allergies: Inhalant or food allergy. Presents with pruritis (itching)
and pyotraumatic dermatitis (hot spots). Reported at a frequency of Renal Glucosuria/Fanconi Syndrome: Causes glucosuria,
5.2% in the NEAA Health Survey 2007 Summary.2 hyposthenuria, metabolic acidosis, hyperchloremia, and reduction
in glomerular filtration rate. May be part of Norwegian Elkhound
Cataracts: Posterior and equatorial cortex intermediate cataracts juvenile renal disease, or a separate inherited disorder. In a study
predominate in the breed. Age of onset 1-3 years. Identified in of Norwegian Elkhounds at dog show in Norway, 27.3% had
3.87% of Norwegian Elkhounds CERF examined by veterinary glucosuria. Dorn reports a 9.41x odds ratio for kidney disease versus
ophthalmologists between 2000-2005. Reported at a frequency of other breeds. Unknown mode of inheritance. Diagnose by finding
12.3% in the NEAA Health Survey 2007 Summary. CERF does not glucosuria with normal blood glucose levels, and urine amino acids.
recommend breeding any Norwegian Elkhound with a cataract.2,4 A phenotypic test is available.10,15,16,17
Hypothyroidism: Inherited autoimmune thyroiditis. 3.1% positive Diabetes Mellitus: Sugar diabetes caused by a lack of insulin
for thyroid auto-antibodies based on testing at Michigan State production by the pancreas. Controlled by insulin injections, diet,
University. (Ave. for all breeds is 7.5%). Reported at a frequency of and glucose monitoring. Reported at an increased frequency versus
2.4% in the NEAA Health Survey 2007 Summary.2,8,9 other breeds, with a female predominance. Unknown mode of
inheritance.18
Primary (Narrow Angle) Glaucoma: Ocular condition causing
increased pressure within the eyeball, and secondary blindness Intracutaneous Cornifying Epithelioma: Benign skin tumors
due to damage to the retina. The breed can have primary consisting of keratin-filled crypts in the dermis and subcutis that
goniodysgenesis with pectinate ligament dysplasia and/or open to the skin surface. Most of these tumors occur on the back,
trabecular meshwork dysplasia. Many affected dogs have cystic neck, sides of the thorax, and the shoulders. Usually occur prior to
degeneration of the iridociliary epithelial and/or peripheral retina. 5 years of age, with a male predominance. Etretinate treatment is
Age of onset of 4-7 years. Classified as an open-angle, closed-cleft successful in 50% of affected dogs.19,20
glaucoma. Diagnose with tonometry and gonioscopy. Dorn reports a
3.48x odds ratio for glaucoma versus other breeds. Incidence in the Brachygnathism, Ciliary Dyskenesia, Entropion, Oligodontia,
Norwegian Elkhound is estimated at 1.98%.10,11,12 Osteochondrodysplasia, Osteogenesis Imperfecta, and
Prognathism are reported.21
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. Isolated Case Studies
The later three forms can impair vision, and dogs affected with None Reported
these forms should not be bred. Identified in 1.83% of Norwegian
Elkhounds CERF examined by veterinary ophthalmologists between
2000-2005.4
Genetic Tests
Tests of Genotype: Direct test for chondrodysplasia is available
Idiopathic Epilepsy: Inherited seizures. Control with anticonvulsant from Genoscoper: www.genoscoper.com.
medication. Seizures are reported at a frequency of 1.8% in the
Tests of Phenotype: CHIC Certification: Required testing includes
NEAA Health Survey 2007 Summary.2
hip radiograph, CERF eye examination (minimum 5 years of age),
Distichiasis: Abnormally placed eyelashes that irritate the cornea thyroid profile including autoantibodies (minimum 5 years of age),
and conjunctiva. Can cause secondary corneal ulceration. Identified and kidney disease screening with urine protein:creatinine ratio
in 1.63% of Norwegian Elkhounds CERF examined by veterinary (minimum of 5 years of age). Optional recommended tests include
ophthalmologists between 2000-2005.4 elbow radiographs, patella examination, and urine amino acid test
for Fanconi syndrome from PennGen. (See CHIC website; www.
Mast Cell Tumor (MCT): Skin tumors that produce histamine, caninehealthinfo.org).
causing inflammation and ulceration. They can reoccur locally or
with distant metastasis. Reported at a frequency of 1.6% in the Recommend cardiac examination.
NEAA Health Survey 2007 Summary.2
Urine amino acid test for Fanconi syndrome is available from
Irritable Bowel Syndrome: Causes chronic bouts of diarrhea. PennGen.
Control with diet and/or medications. Reported at a frequency of
1.4% in the NEAA Health Survey 2007 Summary.2
333
Miscellaneous 21. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 229. AAHA Press, 1999.
• Breed name synonyms: Elkhound, Norsk Elghund, Grahund, Gray 22. The Complete Dog Book, 20th Ed. The American KennelClub. Howell Book
Norwegian Elkhound, Norsk Elghund (Gra). House, NY 2006. p. 192-195.
• Registries: AKC, UKC, CKC, ANKC (Australian National Kennel
Club), NKC (National Kennel Club)
• AKC rank (year 2008): 100 (544 dogs registered)
• Internet resources: Norwegian Elkhound Association of
America: www.neaa.net
Norwegian Elkhound Club of Canada: www.elkhounds.net/necc/
Norwegian Elkhound Club of Great Britain: www.necgb.co.uk/
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Norwegian Elkhound Association of America: NEAA Health Survey 2007
Summary. Sept. 18, 2007.
3. Acland GM, Aguirre GD: Retinal degenerations in the dog: IV. Early
retinal degeneration (erd) in Norwegian elkhounds. Exp Eye Res. 1987
Apr;44(4):491-521.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
5. Aguirre GD, Rubin LF: Progressive retinal atrophy (rod dysplasia in the
Norwegian Elkhound. J Am Vet Med Assoc. 1971 Jan 15;158(2):208-18.
6. Bingel SA, Sande RD: Chondrodysplasia in the Norwegian Elkhound. Am J
Pathol. 1982 May;107(2):219-29.
7. Melniczek JR, Dambach D, Prociuk U, et. al.: Sry-negative XX sex
reversal in a family of Norwegian Elkhounds. J Vet Intern Med. 1999
Nov-Dec;13(6):564-9.
8. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University, April, 2007.
9. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
10. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
11. Oshima Y, Bjerkas E, Peiffer RL Jr: Ocular histopathologic observations in
Norwegian Elkhounds with primary open-angle, closed-cleft glaucoma. Vet
Ophthalmol. 2004 May-Jun;7(3):185-8.
12. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
in pure-bred dogs in North America. Vet Ophthalmol. 2004
Mar-Apr;7(2):97-111.
13. Wiersma AC, Millon LV, van Dongen AM, et. al.: Evaluation of Canine
COL4A3 and COL4A4 as Candidates for Familial Renal Disease in the
Norwegian Elkhound. J Hered. 2005 Nov-Dec;96(7):739-44.
14. Finco DR, Kurtz HJ, Low DG, et. al.: Familial renal disease in Norwegian
Elkhound dogs. J Am Vet Med Assoc. 1970 Mar 15;156(6):747-60.
15. Finco DR: Familial renal disease in Norwegian Elkhound dogs:
physiologic and biochemical examinations. Am J Vet Res. 1976
Jan;37(1):87-91.
16. Finco DR, Duncan JD, Crowell WA, et. al.: Familial renal disease in
Norwegian Elkhound dogs: morphologic examinations. Am J Vet Res. 1977
Jul;38(7):941-7.
17. Heiene R, Bjørndal H, & Indrebø A: Glucosuria in Norwegian elkhounds
and other breeds during dog shows. Vet Rec. 2010 Apr 10;166(15):459-62.
18. Fall T, Hamlin HH, Hedhammar A, et. al.: Diabetes mellitus in a
population of 180,000 insured dogs: incidence, survival, and breed
distribution. J Vet Intern Med. 2007 Nov-Dec;21(6):1209-16.
19. Stannard AA, Pulley LT: Intracutaneous cornifying epithelioma
(keratoacanthoma) in the dog: a retrospective study of 25 cases. J Am Vet
Med Assoc. 1975 Sep 1;167(5):385-8.
20. White SD, Rosychuk RA, Scott KV, et. al.: Use of isotretinoin and
etretinate for the treatment of benign cutaneous neoplasia and cutaneous
lymphoma in dogs. J Am Vet Med Assoc. 1993 Feb 1;202(3):387-91.
334
Norwegian Lundehund
Points of Conformation: The Lundehund should be athletic and
agile. The head is wedge-shaped, tapering gradually to the end of
the muzzle. Nose and lips are black. Scissors bite is preferred, but
level and reverse scissors bite are permitted. Missing premolars on
both sides of the upper and lower jaws are common and allowed.
Eyes are almond-shaped, light yellow-brown to brown with a
brown ring around the pupil. Eye rims are dark and complete. Ears
are medium-size, triangular, and carried erect. Level back, short loin
and slightly sloping croup. The tail is high-set. When moving, the
tail may be carried trailing or in a graceful arch over the back. When
at rest, the tail hangs with a slight curve. Moderate angulation
The Breed History with very elastic shoulders so that the front legs can extend out to
The name Lundehund is a combination of the Norwegian words the side. The legs are straight with slightly outward-turned feet.
“lunde,” the Puffin bird, and “hund,” meaning dog. Originally, they The forefeet are oval with at least six fully developed toes, five
were bred to hunt and retrieve the Puffin, a meat and feather of which should reach the ground. Eight pads on each foot. The
crop for the Norwegian farmer of past centuries living along the additional toes consist of one three jointed toe, like a thumb, and
fjords and on the islands off the west coast. Written references one two-jointed toe along with corresponding tendons and muscles
to the breed date back to the fifteenth century. When the Puffin that give the foot a strong appearance. Strong muscular upper and
bird became a protected species in the 1800’s, the dogs were no lower thighs. Hind feet are oval, slightly outward turned with a
longer useful to the farmers and breed numbers were allowed to minimum of six toes, of which four support the dog’s weight. There
dwindle. The breed was saved from near extinction after World are seven pads with the center pad elongated. When viewed from
War II through the friendship of two concerned Norwegians, but behind, the rear legs are close but parallel. An elastic gait with a
even today there are a thousand dogs worldwide. AKC recognition unique rotary front movement.
occurred in 2011.
Recognized Behavior Issues and Traits
Breeding for Function A Lundehund is alert, very energetic, loyal and protective. He can
Their unique foot structure (at least six toes on each foot and be wary of strangers but never aggressive toward people. He is
elongated rear foot pads) and unusual flexibility enabled them to playful, curious, and intelligent. May be difficult to house train. Has
climb the steep, rocky cliffs and navigate the small burrows and a tendancy to barking. Can be stubborn.
crevices where Puffins nest. They have an elastic neck that allows
the head to bend backward to touch the spine, letting the dog turn
around in narrow puffin bird caves; and shoulders flexible enough
Normal Physiologic Variations
At least six toes on each foot and elongated rear foot pads.
to allow the front legs to extend flat to the side in order to hug the
cliffs. This shoulder structure produces a peculiar rotary movement.
Finally, the ears close and fold forward or backward to protect from Drug Sensitivities
debris. None reported
335
Disease Predispositions References
Gastroenteropathy (Lundehund Syndrome): The collective 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
term for a group of gastrointestinal disorders that include 2. Berghoff N, Ruaux CG, Steiner JM, et. al.: Gastroenteropathy in
chronic atrophic gastritis, intestinal lymphangiectasia, and Norwegian Lundehunds. Compend Contin Educ Vet. 2007 Aug;29(8):456-65,
lymphoplasmacytic enteritis. Secondary disease includes 468-70; quiz 470-1.
3. Landsverk T & Gamlem H: Intestinal lymphangiectasia in the Lundehund.
bacterial overgrowth in the small intestine, and protein-losing
Scanning electron microscopy of intestinal mucosa. Acta Pathol Microbiol
enteropathy (PLE) which causes abnormal protein loss in the Immunol Scand A. 1984 Sep;92(5):353-62.
intestines. Clinical signs are intermittent diarrhea, vomiting, 4. Kolbjørnsen O, Press CM & Landsverk T: Gastropathies in the
weight loss, lethargy, ascites, and subcutaneous edema of the Lundehund. I. Gastritis and gastric neoplasia associated with intestinal
hind legs. Laboratory changes include hypoalbuminemia (with lymphangiectasia. APMIS. 1994 Sep;102(9):647-61.
or without hypoglobulinemia), hypocalcemia, a decrease in the 5. Flesjå K & Yri T: Protein-losing enteropathy in the Lundehund. J Small
serum cobalamin concentration, and an increase or decrease in Anim Pract. 1977 Jan;18(1):11-23.
the serum folate concentration; reflecting microbial synthesis or 6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
malabsorption respectively. Pathology includes chronic atrophic Population and Animal Health, Michigan State University. April, 2007.
gastritis, segmental distention of lymphatics, atrophy, fusion and 7. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
balloon-like swelling of villi with occasional rupture of lacteals. hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
Undetermined mode of inheritance. Studies suggest that the
8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
majority of the breed is affected to some extent. Treatment is College of Veterinary Ophthalmologists. ACVO, 2007.
symptomatic.2,3,4,5 9. Qvigstad G, Kolbjørnsen Ø, Skancke E, et. al.: Gastric neuroendocrine
carcinoma associated with atrophic gastritis in the norwegian lundehund. J
Hypothyroidism: Inherited autoimmune thyroiditis. Not enough Comp Pathol. 2008 Nov;139(4):194-201.
samples have been submitted for thyroid auto-antibodies to 10. AKC Breed Website: www.akc.org/breeds/norwegian_lundehund Last
Michigan State University to determine an accurate frequency. (Ave. accessed July 1, 2010.
for all breeds is 7.5%).6,7
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: Lundehund, Norwegian Puffin Dog,
Norsk Lundehund, Lundies
• Registries: AKC, UKC, CKC, FCI, NKC (National Kennel Club)
• AKC rank (none): AKC recognized in January, 2011. Entire stud
book entered.
• Internet resources: Norwegian Lundehund Association of
America: www.nlaainc.com
Norwegian Lundehund Club Of America: www.lundehund.com
American Norwegian Lundehund Club:
www.americannorwegianlundehundclub.com
336
Norwich Terrier
with a charming personality, independently minded, and moderately
trainable so it is important to start obedience training early.
Introduce to children, cats and other pets early. This terrier will view
small pets as prey. Generally, they are very good with children. A
Norwich must be exercised in a fenced enclosure if off the leash.
They are moderate shedding dogs. They enjoy playing and they have
moderate exercise requirements. Norwich terriers like close human
contact and have a moderate barking tendency. These dogs may
bark or dig if bored. They are easy to housetrain.
Genetic Tests
Tests of Genotype: none
338
Nova Scotia Duck
Tolling Retriever
Points of Conformation: A sturdy well balanced conformation is
the hallmark of this medium-sized powerful working dog. Smallest
of all of the retriever type dogs, utility has dictated all aspects of
conformation. They possess a broad slightly wedge-shaped and
rounded skull, a strong profile with moderate stop, the muzzle tapers
and lips are tight, and the broad nose matches the coat color or is
black. Cheeks are flat. Ears are high and wide set and well back on the
skull. Ears are medium in size and length, triangular, and held slightly
erect. Eyes are wide set and almond shaped. Eye and eyelid margin
color should match the coat or be darker. Rims can also be black.
The Breed History The neck is strong and medium in thickness and length, without
In the southern tip of Nova Scotia in Yarmouth in the early part of throatiness. Deep-chested, back is short and straight, abdomen
the 19th century, the Toller was developed to toll or decoy (lure) has moderate tuck. The tail is richly feathered, broader at its base,
the waterfowl and then retrieve them. The dogs will play at the reaching to the tarsus and is carried above the back while active,
water’s edge in response to thrown balls and sticks, and this activity and held following the curve of the croup when resting. Medium
engages the attention of the ducks. They will then come into range in bone, these dogs should be slightly longer than high. Feet are
for the gunner and once the job is done, the dog swims out to medium-sized, webbed, oval and well knuckled up in the toes. Pads
bring in the bird. Breed origins are sketchy, but the Europeans may are thick, and the front dewclaws can be removed. Rear dewclaws
have brought with them the red decoy dog which was crossed disqualify. Moves with a springy gait, with straight alignment.
with the local retriever and spaniel types. The first registry to
accept this breed, affectionately called “the little red dog” was the
Canadian Kennel Club (1945). The AKC first accepted the dog into
Recognized Behavior Issues and Traits
Breed attributes ascribed include: Agile, keen to work, quick to learn,
the Miscellaneous Class in 2001 and accepted it into the Sporting loves to please. Very intense attitude is typical while working. Highly
group in 2003. This is the official dog of the province of origin, intelligent, good with children, affectionate, some puppies may be
Nova Scotia. reserved but shyness is a fault. Outgoing in the field. Training—can
be easily distracted and bored—need to keep sessions short and fun.
Breeding for Function
Strictly bred for hunter function, these dogs have continued to be
encouraged to prove in field tests (Working Certificates WC, WCI,
Normal Physiologic Variations
Sometimes the ears are taped to maintain proper folding if they
WCX) to ensure that their original suitability for the tolling and
become wonky (folded, rosebud). This frequently occurs when the
retrieving is maintained. They are gradually gaining in popularity
pup is around 3-4 months of age, and the taping is left on for
as a companion animal. While working, they usually keep their
about 1 month. Sometimes a second one month application is
feathered tail in motion.
required. The abnormal folding of the ear may be an inherited trait.
341
Old English Sheepdog
gait is long and elastic and they tend to do a rolling pace, or amble
much like a bear’s way of going.
345
Otterhound
and broad, and toes webbed. The Otterhound gait is long, low and
smooth and appears effortless. The walk is loose and shuffling.
Coat: The rough-coated double oily coat makes him almost Glanzmann’s Thrombasthenia (GT): This autosomal recessive
waterproof. It sits close, not flat, and the hairs are hard, crisp and defect causes frequent epistaxis, and gingival bleeding during
broken in texture. The outer coat is 1.5-2” (3.75-5 cm) long though teething in young dogs. Caused by a defect in intrinsic platelet
hairs are longer over the back (up to 6” or 15 cm). The undercoat function involving glycoprotein complex IIb-IIIa. Affected dogs have
is dense, short and wooly. Blue and white is the favored coat color, normal platelet numbers, and normal coagulation panels. A genetic
but they also commonly appear as black and tan grizzle and many test is available.3,4
other combinations.
Patella Luxation: Polygenically inherited laxity of patellar
Longevity: 12-13 years ligaments, causing luxation, lameness, and later degenerative
joint disease. Treat surgically if causing clinical signs. Too few
Points of Conformation: These large dogs are noted for their Otterhounds have been screened by OFA to determine an accurate
excellent nose and are of sturdy constitution, being both well frequency.1
muscled and boned. The large narrow head is well covered with
hair, the stop is not obvious, and the dark eyes are deeply set with
minimal nictitans exposure. Long, pendulous ears fold in hound
Disease Predispositions
Sebaceous Cysts: Benign accumulation of sebum within
fashion and are low set and close hanging. There is a square muzzle, plugged hair follicles. OHCA 2003 health survey reports 46.2% of
the flews are deep and the darkly pigmented nose is large. The Otterhounds develop sebaceous cysts.2
neck is muscular, and the topline level. The thorax is deep, ribs are
well sprung, and chest depth extends well back. The high set tail Allergic Dermatitis (Atopy): Inhalant or food allergy. Presents
is tapering, feathered and held up but not over the back when with pruritis and pyotraumatic dermatitis (hot spots). Reported at a
alert; the tail is arched and reaches the tarsus. Limbs are straight frequency of 15.1% in the 2003 OHCA Health Survey.2
boned, fore and rear dewclaws may be removed, the feet are large
346
Hypothyroidism: Inherited autoimmune thyroiditis. 2.3% positive 5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
for thyroid autoantibodies based on testing at Michigan State hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
University. (Ave. for all breeds is 7.5%). Reported at a frequency of Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
11.8% in the 2003 OHCA Health Survey.2,5,6 6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
Idiopathic Epilepsy: Inherited seizures can be generalized or partial 7. Evans KM & Adams VJ: Mortality and morbidity due to gastric
dilatation-volvulus syndrome in pedigree dogs in the UK. J Small Anim
seizures. Control with anticonvulsant medication. Reported at a
Pract. 2010 Jul;51(7):376-81
frequency of 10.0% in the 2003 OHCA Health Survey.2 8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007
Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting 9. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
of the stomach within the abdomen. Requires immediate veterinary Ackerman. p. 230 AAHA Press, 1999.
attention. Reported breed prevalence of 9.0%, and cause of death 10. Teske E, de Vos JP, Egberink HF, et. al.: Clustering in canine malignant
of 7.4% of Otterhounds in a UK study.7 lymphoma. Vet Q. 1994 Jul;16(2):134-6.
11. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Cataracts: Reported at a frequency of 5.04% in the 2003 OHCA Book House, NY 2006. p. 196-199.
Health Survey.2
Genetic Tests
Tests of Genotype: Direct test for Glannzmann’s thrombasthenia
(GT) is available from the Boudreaux Lab: http://www.
vetmed.auburn.edu/faculty/pathobiology-faculty/boudreaux
(334-844-2692).
Miscellaneous
• Breed name synonyms: none
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
• AKC rank (year 2008): 154 (36 dogs registered)
• Internet resources: The Otterhound Club of America:
http://clubs.akc.org/ohca/
The Otterhound Club (UK): www.otterhoundclub.co.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Otterhound Club of America: 2003 Otterhound Health Survey. 2003.
3. Boudreaux MK, Lipscomb DL: Clinical, biochemical, and molecular aspects
of Glanzmann’s thrombasthenia in humans and dogs. Vet Pathol. 2001
May;38(3):249-60.
4. Boudreaux MK, Catalfamo JL: Molecular and genetic basis for
thrombasthenic thrombopathia in otterhounds. Am J Vet Res. 2001
Nov;62(11):1797-804.
347
Papillon
Recognized Behavior Issues and Traits
Descriptions of the breed traits include: Good in rural or urban
environments, tolerate temperature extremes well, friendly and likes
to be a lapdog, playful.
Vitreous Degeneration: A liquefaction of the vitreous gel which Recommend hip and elbow radiographs, and thyroid profile
may predispose to retinal detachment resulting in blindness. including autoantibodies.
Identified in 2.93% of Papillions CERF examined by veterinary
ophthalmologists between 2000-2005.6 Miscellaneous
• Breed name synonyms: Pap, Continental Toy Spaniel, Phalene,
Persistent Pupillary Membranes: Strands of fetal remnant Epagneul Nain Continental, Dwarf Spaniel (historical)
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
later three forms can impair vision, and dogs affected with these ANKC (Australian National Kennel Club), NKC (National Kennel Club)
forms should not be bred. Identified in 2.70% of Papillions CERF • AKC rank (year 2008): 37 (4,396 dogs registered)
examined by veterinary ophthalmologists between 2000-2005.6 • Internet resources: Papillon Club of America:
www.papillonclub.org
Cataracts: Anterior cortex intermediate and punctate cataracts
Papillion Canada: www.papilloncanada.org
predominate in the breed. Age of onset 1.5-3 years. Identified in
Papillion (Buterfly Dog) Club UK: www.papillonclub.co.uk/
2.17% of Papillons CERF examined by veterinary ophthalmolo-
gists between 2000-2005. CERF does not recommend breeding any
Papillion with a cataract.6 References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Distichiasis: Abnormally placed eyelashes that irritate the cornea 2. Papillon Club of America: 2002 PCA Health Survey. 2002.
and conjunctiva. Can cause secondary corneal ulceration. Identified 3. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
in 1.67% of Papillions CERF examined by veterinary ophthalmolo-
Sep-Oct;38(5):467-77.
gists between 2000-2005.6 4. Narfstrom K, Wrigstad A: Clinical, electrophysiological and morphological
changes in a case of hereditary retinal degeneration in the Papillon dog. Vet
Deafness: Congenital deafness can be unilateral or bilateral. Ophthalmol. 1999;2(1):67-74.
Diagnosed by BAER testing. Reported to occur in the breed by 5. Narfstrom K, Ekesten B: Electroretinographic evaluation of Papillons
Strain, possibly associated with the piebald gene. Reported at a with and without hereditary retinal degeneration. Am J Vet Res. 1998
frequency of 1% in the 2002 PCA Health Survey.2,9 Feb;59(2):221-6.
6. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Birth Defects: Open Fontanels, Hydrocephalus, and Cleft Palate College of Veterinary Ophthalmologists. ACVO, 2007.
are reported as birth defects in the breed, according to the 2002 7. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
PCA Health Survey.2 hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
Neuroaxonal Dystrophy: Affected dogs present with pelvic limb 8. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
ataxia, hypermetria and depressed postural reflexes affecting all Population and Animal Health, Michigan State University. April, 2007.
9. Strain GM: Deafness prevalence and pigmentation and gender associations
four limbs. Affected dogs show clinical signs by 14 weeks of age,
in dog breeds at risk. The Veterinary Journal 2004; 167(1):23-32.
with deterioration to euthanasia by 5 months of age. Pathological 10. Franklin RJ, Jeffery ND, Ramsey IK: Neuroaxonal dystrophy in a litter of
examination revealed changes include widespread changes in papillon pups. J Small Anim Pract. 1995 Oct;36(10):441-4.
the dorsolateral white matter of the spinal cord, characterized by 11. Nibe K, Kita C, Morozumi M, et. al.: Clinicopathological features of canine
axonal swellings typical of neuroaxonal dystrophy.10,11,12,13 neuroaxonal dystrophy and cerebellar cortical abiotrophy in Papillon and
Papillon-related dogs. J Vet Med Sci. 2007 Oct;69(10):1047-52.
Black Hair Follicular Dysplasia, Inguinal Hernia, and Retained 12. Diaz JV, Duque C, & Geisel R: Neuroaxonal dystrophy in dogs: case report
Primary Teeth are reported.14 in 2 litters of Papillon puppies. J Vet Intern Med. 2007 May-Jun;21(3):531-4.
13. Nibe K, Nakayama H, Uchida K, et. al.: Immunohistochemical features of
Isolated Case Studies dystrophic axons in Papillon dogs with neuroaxonal dystrophy. Vet Pathol.
2009 May;46(3):474-83.
Cerebellar Cortical Abiotrophy (CCA): Reported in a 6 month old 14. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
male Papillion with broad-based stance, pelvic limb ataia, truncal Ackerman. p. 230. AAHA Press, 1999.
ataxia, head tremor, intension tremor, and loss of menace response. 15. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
Pathology showed loss of Purkinji cells and thinning of the granular House, NY 2006. p. 491-494.
349
Parson Russell Terrier
Points of Conformation: Jack Russell Terriers are medium-boned
and well muscled with almost square conformation. They possess
a keen expression and lively attitude. The eyes are moderate in size,
dark in color and almond-shaped. They have small triangular ears
with moderately thick leathers, pointed tips, and ears are folded
forward with the fold at the level of the top of the skull or slightly
higher. The head is also characterized by a flat skull, well-defined
stop and black nose. The moderately long and arched neck is free
of throatiness. The topline is level, abdomen is moderately tucked
up, and the thorax is moderate in depth and narrow. The tail is high
set and thick and normally docked to provide a handhold length at
The Breed History maturity (4” or 10 cm), Limbs are straight boned, feet are compact
with tough pads, and the gait is powerful with long strides.
The breed was cultivated for over 200 years in the south of England.
The breed progenitors are thought to be the extinct Black-and-Tan
terrier and the Old English White Terrier. The first Jack Russell terrier Recognized Behavior Issues and Traits
dogs were brought to America around 1930. Breed nomenclature Reported breed attributes include: High activity, sometmes
is quite confusing. Parson Jack Russell Terrier was often used as a hyperactive in fact, happy, but can be snappy or aggressive with
synonym for this breed, but in England and in the UKC standard, moving targets and other dogs. May see small pets as prey even
the Parson Jack Russell Terrier breed is different. Differences in after being socialized to them. Also described as intelligent, bouncy,
the Parson terrier standard include inclusion of three coat types, springy, lively (exuberant), friendly with family and strangers,
longer legs and shorter body, and being larger in stature. In those though some are aloof with strangers. They have low grooming
constituencies, the Jack Russell Terrier breed name is limited to needs. Considered good in town or country but not for condo or
terriers standing less than twelve inches. apartment life. They have a moderate shedding tendency. They
are diggers, and have high exercise needs. Fences need to be high
Parson John Russell was considered to be the original breeder of and secure since they can climb over and dig under fences quite
this general type of terriers. The Jack Russell terrier breed is popular effectively. They like close human companionship, and activities that
with the horsy set, and further gained popularity following feature provide mental stimulation to help prevent boredom vices. They
roles in television series as the Eddie and Wishbone characters. have a high barking tendency, and are good alarm barkers. Their
assertive nature means that early socialization to children and other
pets, and obedience training are important. Not recommended for
Breeding for Function homes with children under 6 years of age since they do not always
Fox hunting and ratting was the original purpose for which the tolerate young children well.
breed determination, fearlessness and agility were bred into them.
They were baying terriers, and were not developed to kill the quarry,
just bolt them out. Normal Physiologic Variations
None reported
Physical Characteristics Drug Sensitivities
Height at Withers: AKC ideal size is for the male, 14” (35.5 cm),
and female 13” (33 cm) None reported
350
Deafness: Polygenically inherited congenital deafness can be
unilateral or bilateral. Diagnosed by BAER testing. Strain reports
Disease Predispositions
Hypothyroidism: 4.1% positive for thyroid auto-antibodies based
16.1% testing unilaterally or bilaterally deaf based on BAER on testing at Michigan State University. (Ave. for all breeds is
testing. Heritability is between 0.22-0.31. There is a pigmentation 7.5%).17,18
association with deafness in this breed, as mostly white dogs are
more likely to be deaf.7,8 Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
Hip Dysplasia and Legg-Calve Perthes Disease: Polygenically later three forms can impair vision, and dogs affected with these
inherited traits causing degenerative hip joint disease and arthritis. forms should not be bred. Identified in 3.47% of Parson Russell
OFA reports 4.0% affected with hip dysplasia, and 3.0% affected terriers CERF-examined by veterinary ophthalmologists between
with Legg-Calve-Perthes disease.1 2000-2005.2
Elbow Dysplasia: Polygenically inherited trait causing elbow Secondary Glaucoma: Increased intraocular pressure can cause
arthritis. OFA reports 2.7% affected.1 retinal deterioration and blindness. Can occur after cataract
formation, lens luxation, or uveitis. Screen with tonometry. One
Cataracts: Polygenically inherited in this breed. Posterior cortex
report found an odds ratio of 7.1x for secondary glaucoma in Jack
intermediate cataracts predominate in the breed. Heritability
Russell Terriers.19
estimate of 0.73. Identified in 3.78% of Parson Russell terriers
CERF-examined by veterinary ophthalmologists between Autoimmune Hemolytic Anemia (AIHA): Auto-immune
2000-2005. CERF does not recommend breeding any Parson Russell destruction of red blood cells. Parson Russell terriers have a 2.8x
Terrier with a cataract.2,3 risk of developing AIHA versus other breeds. Females are more
frequently affected than males. Clinical features included pale
Patella Luxation: Polygenically inherited laxity of patellar
mucous membranes, weakness, lethargy and collapse. Treatment
ligaments, causing luxation, lameness, and later degenerative joint
with prednisone is successful in most cases.20
disease. Treat surgically if causing clinical signs. OFA reports 0.8%
affected.1 Distichiasis: Abnormally placed eyelashes that irritate the cornea
and conjunctiva. Can cause secondary corneal ulceration. Identified
Hereditary Ataxia (Axonopathy, Neuroaxonal Dystrophy): An
in 2.42% of Parson Russell terriers CERF-examined by veterinary
inherited axonopathy in the breed produces a gait disturbance
ophthalmologists between 2000-2005.2
between 2-9 months of age with symmetric generalized ataxia
and hypermetric and spastic movements. Seizures and respiratory Primary (Narrow Angle) Glaucoma: Ocular condition causing
distress can also occur. Pathological lesions occur throughout the increased pressure within the eyeball, and secondary blindness due
central nervous system. The disorder appears to have a polygenic to damage to the retina. Diagnose with tonometry and gonioscopy.
mode of inheritance.9,10 Diagnosed in 1.37% of Parson Russell Terriers presented to
veterinary teaching hospitals.5
Hyperuricosuria (HUU)/Urate Bladder Stones: An autosomal
recessive mutation in the SLC2A9 gene causes urate urolithiasis and Pulmonic Stenosis: Clinical signs can include exercise intolerance,
can predispose male dogs to urinary obstruction. Estimated at a stunting, dyspnea, syncope and ascites, leading to heart failure.
carrier frequency of 7.75% in the breed. A genetic test is available.36 Diagnosis by auscultation for a heart murmer, and echocardiography.
Parson Russell Terriers are overrepresented versus other breeds.21
Myasthenia Gravis: An autosomal recessive, congenital form of
myasthenia gravis occurs in Parson Russell terriers. Clinical signs Portosystemic Shunt (PSS, Liver Shunt): Abnormal blood vessels
are evident from six to eight weeks of age, and include exercise connecting the systemic and portal blood flow. Vessels can be
induced weakness without megaesophagus. Raised antibody levels intrahepatic or extrahepatic. Causes stunting, abnormal behavior,
to acetylcholine receptor do not occur, although the amount of possible seizures, and secondary ammonium urate urinary calculi.
receptor in the end-plates is decreased.11,12 Diagnose with paired fasting and post-feeding bile acids and blood
ammonia, and abdominal ultrasound. Tobias reports a 8.5x odds
Severe Combined Immunodeficiency (SCID): Autosomal recessive
ratio versus other breeds. Undetermined mode of inheritance.22,23
disorder, where affected dogs cannot generate antigen-specific
immune responses. Parson Russell terrier puppies with SCID Malassezia Pachydermatis infection: Yeast skin infection. Affected
succumb to infections at a few months of age. A commercial dogs present with pruritus, alopecia and lichenification. Parson
genetic test is not available.13,14 Russell terriers are significantly overrepresented versus other breeds.
Can also be secondary to ichthiosis in the breed.24
Nonepidermolytic Ichthyosis: A rare, autosomal recessive disease
in Jack Russell Terriers presenting with congenital, non-alopecic Episodic Myokymia and Neuromyotonia: Jack Russell Terriers
or pruritic, thick, adherent, scales. As adults, the scales persist and affected with Hereditary Ataxia can develop episodes of generalized
secondary infections with coccoid bacteria and yeasts are common. muscle stiffness and delayed muscle relaxation resulting in collapse
Pathology reveals orthokeratotic hyperkeratosis that extends into into lateral recumbency. Episodes can be preceded by intense
follicular infundibula. The disease is caused by an insertion of a facial rubbing, and can be associated with severe hyperthermia. An
LINE-1 into the TGM1 gene. A genetic test is not available.15,16 underlying neuronal ion channel dysfunction is suspected.25,26
351
Black Hair Follicular Dysplasia, Brachygnathism, Compulsive Tail Recommended tests include hip and elbow radiographs, thyroid
Chasing, Epilepsy, Oligodontia, Prognathism, and Progressive profile including autoantibodies, and cardiac examination.
Retinal Atrophy, are reported.27
Miscellaneous
Isolated Case Studies • Breed name synonyms: Jack Russell, JRT, Jack, Parson Jack
Sry-Negative XX Sex Reversal (Hermaphrodism): Identified in Russell Terrier, English Jack Russell Terrier
a Parson Russell terrier. An autosomal recessive disorder, where • Registries: AKC, UKC (Parson Russell Terrier), KCGB (Kennel
outwardly male dogs are chromosomal females (XX), and there is an Club of Great Britain) (also as Jack Parson Russell Terrier), ANKC
absence of male causing SRY.28 (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 84 (802 dogs registered)
Colonic Duplication: Identified in a 4-month-old male Parson • Internet resources: Parson Russell Terrier Association of
Russell terrier because of stranguria and tenesmus.29 America: www.prtaa.org
The Parson Russell Terrier Club (UK):
Factor X Deficiency: Deficiency in Factor X (Stuart-Prower factor) www.parsonrussellterrierclub.co.uk
was identified in a 7-month-old spayed female Parson Russell Association of Parson Russell Terrier Fanciers (Canada):
terrier following recurrent bleeding episodes. Low Factor X was http://aprtf.webs.com
also identified in the father and paternal grandmother. Factor English Jack Russell Terrier Club Alliance Inc.: www.ejrtca.com
X deficiency may be an autosomal dominant trait with variable (under 12” height dog registry)
expression.30 Jack Russell Terrier Club of America: www.therealjackrussell.com
Jack Russell Terrier Club of Canada: www.jrtca.com
Mitochondrial Myopathy: A stunted, thin four month old
Parson Russell terrier with a stilted gait and progressive exercise
intolerance was examined. The dog had raised lactate levels before References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
and after feeding and a raised lactate/pyruvate ratio after feeding,
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
indicating a metabolic abnormality. Ultrastructural examination College of Veterinary Ophthalmologists. ACVO, 2007.
of the muscle confirmed the presence of subsarcolemmal 3. Oberbauer AM, Hollingsworth SR, Belanger JM, et. al.: Inheritance of
accumulations of mitochondria.31 cataracts and primary lens luxation in Jack Russell Terriers. Am J Vet Res.
2008 Feb;69(2):222-7.
Mitochondrial Encephalomyopathy: A 10-month-old female 4. Johnsen DA, Maggs DJ, Kass PH: Evaluation of risk factors for
Parson Jack Russell terrier was euthanized because of therapy-re- development of secondary glaucoma in dogs: 156 cases (1999-2004). J Am
sistant ataxia, hypermetria, and deafness that had first been Vet Med Assoc. 2006 Oct 15;229(8):1270-4.
observed at 10 weeks of age. Pathological findings included severe, 5. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas
bilateral, symmetrical neuronal degeneration and mineralization in pure-bred dogs in North America. Vet Ophthalmol. 2004
of the brain, and hepatocytes and cardiac myocytes with increased Mar-Apr;7(2):97-111.
numbers of enlarged or misshapen mitochondria.32 6. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing
lens luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
Acute Necrotising Pulmonary Vasculitis: Identified in a 5 7. Strain GM: Deafness prevalence and pigmentation and gender
month-old female Jack Russell terrier with acute lethargy, associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
8. Famula TR, Cargill EJ, & Strain GM: Heritability and complex segregation
coughing, and respiratory distress. Tests revealed severe pulmonary
analysis of deafness in Jack Russell Terriers. BMC Vet Res. 2007 Nov 13;3:31.
hypertension, cor pulmonale and right-sided heart failure. 9. Wessmann A, Goedde T, Fischer A, et. al.: Hereditary ataxia in the Jack
Pathology revealed acute necrotising pulmonary arteritis without Russell Terrier--clinical and genetic investigations. J Vet Intern Med. 2004
any cardiac abnormalities or immune complex disease.33 Jul-Aug;18(4):515-21.
10. Sacre BJ, Cummings JF, De Lahunta A: Neuroaxonal dystrophy in a Jack
Myotonia Congenita: A 4-month-old male Jack Russell terrier Russell terrier pup resembling human infantile neuroaxonal dystrophy.
was evaluated for non-painful muscle spasms and exercise induced Cornell Vet. 1993 Apr;83(2):133-42.
hindquarter bunny-hopping and collapse. He had non-painful 11. Wallace ME, Palmer AC: Recessive mode of inheritance in myasthenia
hypertrophic muscles, and was found to have a mutation in the gravis in the Jack Russell terrier. Vet Rec. 1984 Apr 7;114(14):350.
chloride ion channel gene for MC.34 12. Palmer AC, Goodyear JV: Congenital myasthenia in the Jack Russell
terrier. Vet Rec. 1978 Nov 4;103(19):433-4.
13. Perryman LE: Molecular pathology of severe combined immunodefi-
Genetic Tests ciency in mice, horses, and dogs. Vet Pathol. 2004 Mar;41(2):95-100.
Tests of Genotype: Direct test for lens luxation is available from 14. Bell TG, Butler KL, Stickle JE, et. al.: Autosomal recessive severe
OFA and AHT. combined immunodeficiency of Jack Russell terriers. J Vet Diagn Invest
2002; 14:194-204.
Direct test for HUU is available from the UC-Davis VGL and the 15. Credille KM, Minor JS, Barnhart KF, et. al.: Transglutaminase 1-deficient
Animal Health Trust. recessive lamellar ichthyosis associated with a LINE-1 insertion in Jack
Russell terrier dogs. Br J Dermatol. 2009 Aug;161(2):265-72.
Tests of Phenotype: CHIC Certification: Required testing includes 16. Lewis DT, Ford MJ, & Kwochka KW: Characterization and management
CERF eye examination, patella examination, and BAER test for of a Jack Russell terrier with congenital ichthyosis. Vet Dermatol 1998;
deafness. (See CHIC website; www.caninehealthinfo.org). 9:111–18.
17. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
352
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
18. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
19. Johnsen DA, Maggs DJ, Kass PH: Evaluation of risk factors for
development of secondary glaucoma in dogs: 156 cases (1999-2004). J Am
Vet Med Assoc. 2006 Oct 15;229(8):1270-4.
20. Miller SA, Hohenhaus AE, Hale AS: Case-control study of blood type,
breed, sex, and bacteremia in dogs with immune-mediated hemolytic
anemia. J Am Vet Med Assoc. 2004 Jan 15;224(2):232-5.
21. Baumgartner C, Glaus TM: Congenital cardiac diseases in dogs: a
retrospective analysis. Schweiz Arch Tierheilkd. 2003 Nov;145(11):527-33,
535-6.
22. Hunt GB: Effect of breed on anatomy of portosystemic shunts resulting
from congenital diseases in dogs and cats: a review of 242 cases. Aust Vet
J. 2004 Dec;82(12):746-9.
23. Tobias KM, Rohrbach BW: Association of breed with the diagnosis of
congenital portosystemic shunts in dogs: 2,400 cases (1980-2002). J Am
Vet Med Assoc. 2003 Dec 1;223(11):1636-9.
24. Carlotti DN: Malassezia Dermatitis in the Dog. Proceedings 2005 World
Small Animal Veterinary Association World Congress. 2005.
25. Van Ham L, Bhatti S, Polis I, et. al.: “Continuous muscle fibre activity” in
six dogs with episodic myokymia, stiffness and collapse. Vet Rec. 2004 Dec
11;155(24):769-74.
26. Vanhaesebrouck AE, Van Soens I, Poncelet L, et. al.: Clinical and
electrophysiological characterization of myokymia and neuromyotonia in
jack russell terriers. J Vet Intern Med. 2010 Jul-Aug;24(4):882-9.
27. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 224. AAHA Press, 1999.
28. Kuiper H, Bunck C, Gunzel-Apel AR, et. al.: SRY-negative XX sex reversal
in a Jack Russell Terrier: a case report. Vet J. 2005 Jan;169(1):116-7.
29. Arthur EG, Fox DB, Essman SC, et. al.: Surgical treatment of
noncommunicating duplication of the colon in a dog. J Am Vet Med Assoc.
2003 Jul 15;223(2):210-4, 196.
30. Cook AK, Werner LL, O’Neill SL, et. al.: Factor X deficiency in a Jack
Russell terrier. Vet Clin Pathol. 1993;22(3):68-71.
31. Olby NJ, Chan KK, Targett MP, et. al.: Suspected mitochondrial myopathy
in a Jack Russell terrier. J Small Anim Pract. 1997 May;38(5):213-6.
32. Gruber AD, Wessmann A, Vandevelde M, et. al.: Mitochondriopathy with
regional encephalic mineralization in a Jack Russell Terrier. Vet Pathol. 2002
Nov;39(6):732-6.
33. Russell NJ, Irwin PJ, Hopper BJ, et. al.: Acute necrotising pulmonary
vasculitis and pulmonary hypertension in a juvenile dog. J Small Anim
Pract. 2008 Jul;49(7):349-55.
34. Lobetti RG: Myotonia congenita in a Jack Russell terrier. J S Afr Vet
Assoc. 2009 Jun;80(2):106-7.
35. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 415-418.
36. Karmi N, Brown EA, Hughes SS, et. al.: Estimated frequency of the
canine hyperuricosuria mutation in different dog breeds. J Vet Intern Med.
2010 Nov-Dec;24(6):1337-42.
353
Pekingese
the radius. Feet are outturned, large, flat and well feathered. Gait is
rolling in front and not fast moving.
357
Pembroke Welsh Corgis should not be bred together, and should Intervertebral Disc Disease (IVDD): Serious neurological condition
only be bred to normal-tailed dogs. This will produce 50% bob-tail where disk degeneration and rupture into spinal nerves and the
and 50% normal-tail offspring.2,3,4 spinal cord causes pain and possible paralysis. Requires immediate
veterinary attention. Occurs at an increased frequency in the breed.
Fluffy Coat Length: An autosomal recessive condition causing a
long, fluffy coat exists in the Pembroke Welsh Corgi. Dogs with this Degenerative Myelopathy (DM): Affected dogs show an insidious
coat type are not eligible for competition. A genetic test is available. onset of upper motor neuron (UMN) paraparesis at an average
age of 11.4 years. The disease eventually progresses to severe
In a UK study, 35.7% of litters were born via Cesarean section.5 tetraparesis. Affected dogs have normal results on myelography,
MRI, and CSF analysis. Necropsy confirms the condition. Reported
Drug Sensitivities at a frequency of 0.58% in Pembroke Welsh Corgis. Unknown mode
None reported of inheritance. A direct genetic test for an autosomal recessive DM
susceptibility gene is available. All affected dogs are homozygous
for the gene, however, only a small percentage of homozygous dogs
Inherited Diseases develop DM. OFA testing shows 39% carrier and 52% homozygous
Hip Dysplasia: Polygenically inherited trait causing degenerative
“at risk” for the DM susceptability gene.11,12,13,14
joint disease and hip arthritis. OFA reports 18.4% affected.6
Bladder Stones: The breed has a predisposition to develop bladder
von Willebrand’s Disease Type 1 (vWD): Autosomal recessive
stones. Stone composition is not identified. Dorn reports a 4.20x
genetic disorder causing a mild bleeding syndrome. A direct genetic
increased odds ratio versus other breeds.7,15,16
test is available from VetGen, reporting 6% affected, and 37%
carrier in the breed. Cystinuria/Cystine Bladder Stones: Caused by a metabolic
abnormality in cystine metabolism. Welsh Corgis have an
Elbow Dysplasia: Polygenically inherited trait causing elbow
increased risk for developing cystine bladder stones. Treat with
arthritis. OFA reports 3.0% affected.6
surgical removal and life-long medical therapy. Unknown mode of
Patella Luxation: Polygenically inherited laxity of patellar ligaments, inheritance in this breed.17
causing luxation, lameness, and later degenerative joint disease. Treat
Perineal Hernia: An Australian study identified the Corgi breed as
surgically if causing clinical signs. Too few Pembroke Welsh Corgis
most commonly affected with perineal hernias. The mean age of
have been screened by OFA to determine an accurate frequency.6
affected dogs was 9.4 years. Treatment is herniorrhaphy surgery.18
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: PBGV, Small Vendeen Basset, Little
Griffon Vendeen Basset, Roughies or Griffs (England nicknames),
Petites or Griffs (nickname in Denmark) and in America, Petites.
(pl. Petits Bassets Griffons Vendeens)
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club)
• AKC rank (year 2008): 119 (275 dogs registered)
• Internet resources: Petit Basset Griffon Vendéen Club of
America: www.pbgv.org
Petit Basset Griffon Vendeen Fanciers of Canada:
www.angelfire.com/bc2/PBGVFC/ClubInfo.html
Basset Griffon Vendeen Club (UK): www.bgvclub.co.uk
361
Pharaoh Hound
is minimal. The neck is long and muscular, with a small degree of
arching and no throatiness. The topline is level, except for a slight
slope down the croup. The tail is tapering and whip-like at the
terminus, reaching below the tarsus while at rest. The thorax is
deep, ribs are well sprung, and there is moderate tucking up of the
abdomen. Limbs are straight boned, and the feet are medium in size
with well knuckled up toes and strong large pads. Dewclaws fore
and hind may be removed. The gait is long striding and smooth,
and appears both powerful and effortless. When compared with the
Ibizan hound, the Pharaoh hounds are smaller, have less extreme
conformation and less white marking.
The Breed History
This breed is among the most ancient and mimics the depictions of
the Egyptian god, Anubis, the guide for the souls of the departed.
Recognized Behavior Issues and Traits
Reported breed characteristics include: Intelligent, easily trained,
First records date back to around 3000 BC. Skeletal remains that
friendly, and love children. They remain playful even as adults. They
match Pharaoh hound body structure date back to about 5000 BC.
need close human contact. Pharaoh hounds have low grooming
Paintings and many Egyptian hieroglyphs depict this dog. So highly
needs and don’t get doggy odor even after becoming wet. They
prized were these dogs that some were mummified along with the
are active dogs and without adequate exercise they become obese
nobility. Some of these dogs were exported to the Isle of Malta,
easily. Not considered an apartment dog. They should be off leash
where they were carefully bred for over 2000 years. This rare breed
in a fenced enclosure only. They are not considered watch or guard
is the National Dog of Malta. It was not until 1983 that the AKC
dogs, though they are aloof with strangers generally.
registered the breed.
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: Kelb-tal Fenek (means rabbit dog),
Pharoah Hound, Pharaoh.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain)-P,
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
• AKC rank (year 2008): 148 (72 dogs registered)
• Internet resources: Pharaoh Hound Club of America:
www.ph-club.org
The Pharaoh Hound Club (UK): www.pharaohhoundclub.co.uk
363
Plott Hound
deep with well sprung ribs. The topline is higher at the withers than
the hip, merging into slightly arched loins and a well tucked up
abdomen. They possess fine, medium length straight boned limbs,
with compact feet, toes well knuckled up. Nails are usually dark, but
if white feet markings are present, there may be white nails and in
brindles, reddish brown is permissible. A very long, medium weight
curving tail tapers, and is normally held high in a saber like carriage.
There can be a slight brush. Their gait is long, low, rhythmic, smooth
and appearing tireless.
Genetic Tests
Tests of Genotype: Direct test for MPS is available from PennGen.
Miscellaneous
• Breed name synonyms: Plotts.
• Registries: AKC, UKC, CKC, NKC (National Kennel Club).
• AKC rank (year 2008): 127 (220 dogs registered)
• Internet resources: The Plott Hound:
http://www.akc.org/breeds/plott/index.cfm
Plott Dogs: www.plottdogs.com
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Spellacy E, Shull RM, Constantopoulos G, et. al.: A canine model of
human alpha-L-iduronidase deficiency. Proc Natl Acad Sci U S A. 1983
Oct;80(19):6091-5.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
6. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 700-702.
365
Pointer
(SYN: English Pointer)
long, slightly arched and well muscled. Limbs are straight boned
and long bones are oval in cross section. The thorax is deep, ribs
well sprung, and topline slightly descending towards the rear with
a slight arch though loin and croup. The abdomen is moderately
tucked up. The tapering tail reaches no longer than the tarsus and
is carried slightly above the topline when active. Feet are compact
and oval, have well knuckled up toes. Dewclaws on forelimbs may
be removed.
367
hereditary sensory neuropathy. Am J Pathol. 1983 Jul;112(1):136-8.
5. Sillevis Smitt PA, de Jong JM: Animal models of amyotrophic
lateral sclerosis and the spinal muscular atrophies. J Neurol Sci. 1989
Jul;91(3):231-58.
6. O’Brien DP, Shibuya H, Zhou T: X-Linked Cerebellar Ataxia in English
Pointer Dogs: Phenotype and Linkage Data. Proceedings, 1997 AKC Canine
Health Foundation Canine Health Conference. 1997.
7. Coppens AG, Gilbert-Gregory S, Steinberg SA, et. al.: Inner ear
histopathology in “nervous Pointer dogs” with severe hearing loss. Hear
Res. 2005 Feb;200(1-2):51-62.
8. Steinberg SA, Klein E, Killens RL, et. al.: Inherited deafness among
nervous pointer dogs. J Hered. 1994 Jan-Feb;85(1):56-9.
9. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
10. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
11. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
12. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
13. American Pointer Club: 2002 APC Health & Research Survey. 2002.
14. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 231 AAHA Press, 1999.
15. Morrison WB, Wilsman NJ, Fox LE, et. al.: Primary ciliary dyskinesia in
the dog. J Vet Intern Med. 1987 Apr-Jun;1(2):67-74.
16. Cantile C, Baroni M, Tartarelli CL, et. al.: Intramedullary
hemangioblastoma in a dog. Vet Pathol. 2003 Jan;40(1):91-4.
17. Rallis TS, Tontis DK, Soubasis NH, et. al.: Immunohistochemical
study of a granular cell tumor on the tongue of a dog. Vet Clin Pathol.
2001;30(2):62-66.
18. Reese WG, Newton JE, Angel C, et. al.: Induced immobility in nervous
and normal Pointer dogs. J Nerv Ment Dis. 1982 Oct;170(10):605-13.
19. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 20-23.
368
Polish
Lowland Sheepdog
to 2 vertebrae in length. The tail is low set. The gait is long and low
striding with an ambling appearance. These dogs may tend to toe in
somewhat.
Weight: 30-35 lb (13.5-16 kg). Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Coat: The double coat is accepted in any color. The coarse profuse disease. Treat surgically if causing clinical signs. Too few Polish
outer coat is shaggy and long, and the inner coat short, dense Lowland Sheepdogs have been screened by OFA to determine an
and wooly. Colors may include white with black, or gray or sandy accurate frequency.1
patches, gray and white, or chocolate. A fading factor (dominant
inheritance) results in puppy coats fading as they mature; this does Disease Predispositions
not affect white puppies. Hypothyroidism: Inherited autoimmune thyroiditis. 28.4% positive
for thyroid autoantibodies based on testing at Michigan State
Longevity: 13-15 years University. (Ave. for all breeds is 7.5%).2,3
Points of Conformation: In general appearance, they are often Persistent Pupillary Membranes: Strands of fetal remnant
considered to be a small version of the Bearded Collie, a breed connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
that the PON may have acted as an ancestor for. Their overall later three forms can impair vision, and dogs affected with these
conformation is slightly longer than tall, cobby and heavily boned. forms should not be bred. Identified in 6.50% of Polish Lowland
The skull is heavy and broad and slightly domed. The hair normally Sheepdogs CERF examined by veterinary ophthalmologists between
covers the brown or hazel oval shaped eyes. The head appears 2000-2005.4
to be larger than it really is because of profuse hair, especially in
the brows, moustache and beard. The muzzle is long. The nose is Corneal Dystrophy: Epithelial/stromal form causes a bilateral
large and dark brown or black. Ears are moderate in size, hanging non-inflammatory corneal opacity (white to gray). Identified in
down and well covered in hair. The neck is short and strong. These 3.11% of Polish Lowland Sheepdogs CERF-examined by veterinary
dogs possess a broad level topline, and the legs are well haired. ophthalmologists between 2000-2005.4
The thorax is deep with moderately sprung ribs and the abdomen
is moderately tucked up. Limbs are straight boned and the feet Cataracts: Anterior cortex punctate cataracts predominate in
are oval, compact, and the forefeet are larger than the rear feet. the breed. Identified in 2.26% of Polish Lowland Sheepdogs CERF
Puppies may be born tailless; if a tail is present, it is usually docked examined by veterinary ophthalmologists between 2000-2005.
369
CERF does not recommend breeding any Polish Lowland Sheepdog Ackerman. p. 231. AAHA Press, 1999.
with a cataract.4 9. McConnell JF, Platt S, Smith KC: Magnetic resonance imaging findings of
an intracranial medulloblastoma in a Polish Lowland Sheepdog. Vet Radiol
Neuronal Ceroid Lipofuscinosis (NCL, CL): A slowly progressive Ultrasound. 2004 Jan-Feb;45(1):17-22.
disorder, beginning with retinal degeneration and nyctalopia from 10. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 680-683
6 months to 4-5 years of age. Affected dogs then progress to
cerebellar ataxia and dementia. Stored material in nerve and retinal
cells consisting of sphingolipid activation proteins. Suspected
autosomal recessive mode of inheritance.5,6,7
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: Polski Owczarek Nizinny, Valee
Sheepdog, Nizinny, PON.
• Registries: AKC, UKC (as Polski Owczarek Nizinny), KCGB (Kennel
Club of Great Britain), ANKC (Australian National Kennel Club).
• AKC rank (year 2008): 145 (78 dogs registered)
• Internet resources: The American Polish Lowland Sheepdog
Club: www.aponc.org
Canadian Polish Lowland Sheepdog Club: www.cponc.com
Polish Lowland Sheepdog Club (UK): www.plsc.org.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
3. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
4. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
5. Wrigstad A, Nilsson SE, Dubielzig R, et. al.: Neuronal ceroid lipofuscinosis
in the Polish Owczarek Nizinny (PON) dog. A retinal study. Doc Ophthalmol.
1995;91(1):33-47.
6. Narfstrom K, Wrigstad A: Clinical, electrophysiological, and
morphological findings in a case of neuronal ceroid lipofuscinosis in the
Polish Owczarek Nizinny (PON) dog. Vet Q. 1995 Apr;17 Suppl 1:S46.
7. Narfström K, Wrigstad A, Ekesten B, et. al.: Neuronal ceroid
lipofuscinosis: clinical and morphologic findings in nine affected Polish
Owczarek Nizinny (PON) dogs. Vet Ophthalmol. 2007 Mar-Apr;10(2):111-20.
8. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
370
Pomeranian
particularly during the shedding season. They enjoy learning games,
tricks and obedience training.
Drug Sensitivities
None reported
Inherited Diseases
The Breed History Patella Luxation: Polygenically inherited laxity of patellar
Pomeranians are a Spitz-type breed that originated from sled dogs ligaments, causing luxation, lameness, and later degenerative joint
in Iceland and Lapland. They were bred down from much larger disease. Treat surgically if causing clinical signs. Dorn reports a
dogs in Pomerania and Germany. They are similar in type to the 10.15x odds ratio in Pomeranians versus other breeds. Another
modern Klein German Spitz. Queen Victoria brought them into the study reports an 18.6x odds ratio versus other breeds. OFA reports
limelight in Britain. 42.6% affected.1,2,3
Breeding for Function Hip Dysplasia and Legg-Calve Perthes Disease: Polygenically
Bred for companionship after downsizing, though early in breed inherited traits causing degenerative hip joint disease and arthritis.
development they were used for sheep herding. Too few Pomeranians have been screened by OFA to determine an
accurate incidence.1
Physical Characteristics Elbow Dysplasia: Polygenically inherited trait causing elbow
Height at Withers: 8-11” (20-28 cm) arthritis. Reported 3.7x odds ratio for ununited anconeal process
form of elbow dysplasia versus other breeds. Too few Pomeranians
Weight: 3-7 lb (1.5-3 kg). have been screened by OFA to determine an accurate incidence.1,3
Coat: Double coated, with a profuse fluffy glossy outer coat Patent Ductus Arteriosus (PDA): Polygenically inherited
consisting of long harsh hairs, and a soft dense undercoat. congenital heart disorder, where a fetal vessel remains open after
Feathering includes a frill over neck and chest, and limb and birth, causing a mixing of oxygenated and unoxygenated blood.
tail feathering. All colors and patterns are allowed, though the Affected dogs are usually stunted, and have a loud heart murmur.
red-orange coat is most popular. It takes a few years for the coat to Diagnosis with Doppler ultrasound. Treat with surgery. Dorn reports
reach full density and length. a 10.15x odds ratio in Pomeranians versus other breeds.2,4
Longevity: 15 years. Hyperuricosuria (HUU)/Urate Bladder Stones: An autosomal
recessive mutation in the SLC2A9 gene causes urate urolithiasis and
Points of Conformation: Sturdy, compact conformation, high
can predispose male dogs to urinary obstruction. Estimated at a
head carriage, profusely plumed tail sits flat over the short back,
carrier frequency of 1.12% in the breed. A genetic test is available.24
expression is described as fox-like, wide set eyes are large and
dark, almond shaped and set low on the skull. The top of the skull
is mildly domed, and the muzzle short and fine. Ears are high and Disease Predispositions
pricked, the stop well defined, nose and eyelid margins are black (or Tracheal Collapse: Caused by diminished integrity of the cartilage
self in some colors such as blue and brown). The short neck is well rings in the trachea. Can produce increased coughing, stridor, and
muscled and the back is short. The topline is level, thorax fairly deep respiratory distress, especially when excited. Usually occurs in
with well sprung ribs, limbs are straight and short, feet are compact middle-aged to older dogs. Usually poorly responsive to surgery.
and straight. Dewclaws are often removed. The gait is smooth, quick Many cases can be controlled medically. Dorn reports a 11.61x odds
and active. ratio for tracheal collapse versus other breeds.2,5
371
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The Globoid Cell Leukodystrophy, Intervertebral Disk Disease,
later three forms can impair vision, and dogs affected with these Oligodontia, Prognathism, and Sebaceous Adenitis are reported.18
forms should not be bred. Identified in 3.31% of Pomeranians CERF
examined by veterinary ophthalmologists between 2000-2005.6 Isolated Case Studies
Vitamin D-Resistant Rickets: A female Pomeranian was followed
Cataracts: Anterior and posterior cortex punctate and intermediate
from 2 to 8.5 months of age with low Vitamin D levels, progressive
cataracts predominate in the breed. Identified in 2.76% of
hypocalcemia, secondary hyperparathyroidism, hypomineralization
Pomeranians CERF examined by veterinary ophthalmologists
and fracture of bones, rickets, and alopecia that was not responsive
between 2000-2005. CERF does not recommend breeding any
to Vitamin D supplementation. An autosomal recessive mutation
Pomeranian with a cataract.6
was identified in the vitamin D receptor gene.19
Hypothyroidism: Inherited autoimmune thyroiditis. 2.5% positive
Congenital Methemoglobinemia: A six-month-old Pomeranian
for thyroid autoantibodies based on testing at Michigan State
was referred for evaluation of cyanosis, occurring since it was
University. (Ave. for all breeds is 7.5%).7,8
acquired at six weeks of age. Blood assays diagnosed methemoglo-
Alopecia-X (Black Skin Disease, BSD, Coat Funk, Severe Hair binemia due to deficiency of methemoglobin reductase enzyme.20
Loss, SHL): Progressive, symmetrical, non-pruritic, truncal hair
Occipital Dysplasia: Congenital malformation of the foramen
loss usually beginning in early adulthood. ACTH stimulation test,
magnum was diagnosed in a 4-year-old Pomeranian dog, causing
low-dose dexamethazone suppression test, and thyroid panel
caudal displacement of the cerebellum and hydrocephalus.21
results are normal. Urinary corticoid:creatinine ratio may be normal
to elevated. Elevated blood concentrations of 17-hydroxypro- Hydrocephalus and Secondary Syringomyelia: A 7-year-old
gesterone (17-OHP) have been seen post ACTH stimulation. Oral spayed female Pomeranian with a 6-month history of progressive
trilostane reverses the condition in some cases. The disorder paraparesis was determined to have syringomyelia secondary to
appears familial, with a male predilection.9,10,11 hydrocephalus. Magnetic resonance imaging clearly revealed severe
syringomyelia in the cervical portion of the spinal cord, which
Chronic Valvular Heart Disease: Heart failure due to valvular
was directly connected to the marked dilated fourth ventricle.
insufficiency, usually involving the mitral valve. Treat with heart
Laminectomy provided partial amelioration of clinical signs, without
medications. Pomeranians have a high odds ratio for chronic
further deterioration.22
valvular disease versus other breeds.12
Progressive Retinal Atrophy (PRA): Inherited degeneration of Direct test for HUU is available from the UC-Davis VGL and the
the retina resulting in blindness. Unknown mode of inheritance in Animal Health Trust
this breed. Generalized or suspicious PRA was identified in 1.66%
of Pomeranians CERF examined by veterinary ophthalmologists Tests of Phenotype: CHIC Certification: Required testing includes
between 2000-2005.6 CERF eye examination, congenital cardiac examination (with
re-evaluation between 3 and 5 years of age), and patella evaluation.
Hydrocephalus: Congenital increased volume of cerebrospinal Optional recommended testing includes hip radiographs and
fluid (CSF), with a concurrent dilation of the ventricular system and thyroid profile including autoantibodies. (See CHIC website; www.
reduction of brain tissue. Can have an associated open fontanel. caninehealthinfo.org).
Can cause behavior changes, visual defects, impaired motor
function, or seizures.13 Recommend elbow radiographs.
373
Poodle
Standard
Height at Withers: female 15 “ (38 cm) or more, male 15” (38 cm)
or more.
Standard Weight: females 45-60 lb (20-27 kg), males 45-70 lb
(20-32 kg).
Coat: All solid colors accepted (e.g., apricot, black, gray, silver, blue,
café-au-lait, cream) and the coat is dense, wiry and curly. If left
unclipped, it tends to form ringlets (cording) and waves. There are
specific clips used in show, and their coat is a distinguishing breed
feature.
The Breed History
“Poodle” likely derives from Pudel, a German term describing one Longevity: 12-15 years. The smaller types may reach 15-17 years
who plays and splashes in water or puddles. The exact lines of on average.
genetic origin are obscured, but ancient breeds such as the Irish
water spaniel, Rough haired water dog and others contribute to Points of Conformation: A long face, with medium-sized and
the type, and perhaps the first of the smaller types of poodles leathered triangular ears lying flat, and wide, almond-shaped
originated by crosses with terrier type for use in truffle hunting. dark brown eyes, a slight stop, and fairly narrow muzzle typify the
German history records poodle type dogs in the 15th century. The poodle head. They possess a level topline, feet are compact and
toy version of poodle first widely entered the history record in the webbed, and they have straight limbs with the dewclaws generally
18th century. Very early records in the Mediterranean place poodle removed. Tails are usually docked to one half length, and they are
type dogs in the first century. Though often referred to as the proportioned to be as high as they are long. Their gait is lively and
French poodle, the breed is not though to have originated there. elastic, and they move straight.
AKC recognition occurred in 1887.
Recognized Behavior Issues and Traits
Breeding for Function Extreme intelligence, sociability, and excellent trainability are well
known poodle traits. Very lively, they do tend to bark, and need to
Originally these dogs were bred as gundogs for waterfowl hunting,
as a water retriever. The origins of the fancy coat clips trace back be socialized to other pets and people or else they can potentially
to early times when the hunters clipped the bulk of the dog coat so be nippy. They need close human companionship and tend to be
that they would dry quickly, and to minimize the weight of the wet aloof with strangers. They are good alarm barkers.The poodles
hair for ease of swimming, but they left fur over bony prominences require regular clip and grooming (every 6-8 weeks), and are low
to help insulate joints from the cold. In France, the dog was also shedding and low allergy dogs. They tend to need more frequent
used extensively as a circus dog. Toy, miniature, and standard dental care. They do well in town or country and need moderate
levels of exercise. They are high activity around the house, though
poodles are all popular as companion dogs, and the smaller types
the standard poodles are often less active indoors.
were bred down in size from the standard; it was the larger
standard poodle that was originally used for hunting. Guide dogs,
therapy dogs, police work and obedience and agility competitions Normal Physiologic Variations
round out some of their modern functions.
Echocardiographic Normal Values
for Miniature Poodles:1
Physical Characteristics
All three types share the same breed standard, only the size and Parameter Median (Range)
weight varies between the three. Weight (kg) 3 (1.4-9)
Heart rate (bpm) 150 (100-200)
Toy LVPWD (mm) 5 (4-6)
Height at Withers: female up to 10” (25.4 cm), male up to 10” LVPWS (mm) 8 (6-10)
LVD (mm) 20 (16-28)
(25.4 cm)
LVS (mm) 10 (8-16)
Weight: females 6-9 lb (2.5-4 kg), males 6-9 lb (2.5-4 kg).
FS (%) 47 (35-57)
EPSS (mm) 0 (0-2)
Miniature RVd (mm) 4 (2-9)
Height at Withers: female 10-15” (25.5-38 cm), male 10-15” IVSd (mm) 5 (4-6)
(25.5-38 cm) IVSs (mm) 8 (6-10)
Miniature Weight: females 15-17 lb (7-8 kg), males 15-17 lb (7-8 kg). AOD (mm) 10 (8-13)
LAS (mm) 12 (8-18)
N 20
374
LVPWD, LV posterior wall dimension at end-diastole; LVPWS, LV Mucopolysaccharidosis VI (MPS VI): PennGen reports MPS VI
posterior wall thickness at end-systole; LVD, LV chamber dimension identified in the Miniature and Toy Poodle. This is an autosomal
at end-diastole; LVS, LV chamber dimension at end-systole; FS, recessive disorder causing skeletal deformities, including defects in
percent fractional shortening; EPSS, E-point septal separation; RVD, the sternum, vertebrae and particularly the hip joints. To varying
RV chamber dimension at end-diastole; IVSd, interventricular septal degrees they may also experience corneal cloudiness and facial
thickness at end-diastole; IVSs, interventricular septal thickness at dysmorphia. A genetic test is available.
end-systole; AOD, aortic root at end-diastole; LAS, left atrium at
end-systole; N, number of animals. Disease Predispositions
Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting
Drug Sensitivities of the stomach within the abdomen. Requires immediate veterinary
None Reported attention. There is a 25.3% lifetime risk of developing GDV in
Standard Poodles, with 6.3% of all Standard Poodles dying from the
Inherited Diseases condition.16,17,18
Hip Dysplasia: Polygenically inherited trait causing degenerative
Epiphora: Ocular tear drainage with hair staining is reportedly a
joint disease and hip arthritis. OFA reports 12.3% affected.2
common occurrence in Toy Poodles. Can occur secondary to medial
Patella Luxation: Polygenically inherited laxity of patellar canthal trichiasis and/or entropion. Treat by keeping hair clipped
ligaments, causing luxation, lameness, and later degenerative joint short, and daily cleaning. Medial canthoplasty is curative in severe
disease. Treat surgically if causing clinical signs. Reported 9.7x odds cases.19
ratio in Toy Poodles, 4.1x odds ratio in Miniature Poodles, and 3.2x
Distichiasis: Abnormally placed eyelashes that irritate the cornea
odds ratio in Standard Poodles versus other breeds. OFA reports
and conjunctiva. Can cause secondary corneal ulceration. Identified
4.4% affected.2,3
in 11.72% of Toy Poodles, 9.08% of Miniature Poodles, and 1.04%
Progressive Retinal Atrophy (PRA): Autosomal recessive of Standard Poodles CERF examined by veterinary ophthalmologists
progressive rod cone degeneration (prcd) form seen in Minature between 2000-2005.5
and Toy Poodles. Age of onset between 3-8 years of age, eventually
Cataracts: Cortical and nuclear cataracts predominate in the
causing blindness. Optigen reports 3% testing affected, and 28%
breed. Reported at a frequency of 10.79% in Miniature Poodles,
testing carrier in Miniature Poodles, and 5% testing affected, and
10.21% in Toy Poodles, and 7.00% in Standard Poodles. Reported
29% testing carrier in Toy Poodles. Dorn reports a 9.71x odds ratio
at a frequency of 13.8% in Toy Poodles in Brazil. Dorn reports a
versus other breeds. A genetic test is available.4,5,6,7,8
3.10x odds ratio in Standard Poodles versus other breeds. One
Elbow Dysplasia: Polygenically inherited trait causing elbow study showed a 6.1x odds ratio for Toy Poodles, and a 4.3x odds
arthritis. OFA reports 2.8% affected.2 ratio for Miniature Poodles versus other breeds. Mean age at onset
of 9.6 years in Miniature and Toy Pooodles. Identified in 3.95% of
Legg-Perthes Disease: Polygenically inherited aseptic necrosis Toy Poodles, 3.63% of Standard Poodles, and 2.82% of Miniature
of the femoral head seen in Toy and Miniature Poodles. Causes Poodles CERF examined by veterinary ophthalmologists between
degenerative joint disease and hip arthritis. Usually presents 2000-2005. CERF does not recommend breeding any Poodle with a
unilaterally. Reported 22.4x odds ratio in Toy Poodles, and 12.1x cataract.4,5,20,21,22,23
odds ratio in Miniature Poodles for Legg-Calve-Perthes versus other
breeds. OFA reports 1.0% affected.2,3,9 Periodontal Disease: Miniature and Toy Poodles are found to be
predisposed to periodontal disease and tooth loss.24
von Willebrand’s Disease Type 1 (vWD): Autosomal recessive
genetic disorder causing a mild bleeding syndrome. A direct genetic Persistent Pupillary Membranes: Strands of fetal remnant
test is available from VetGen, reporting 1% affected, and 9% carrier connecting; iris to iris, cornea, lens, or involving sheets of tissue.
in the breed.10 The later three forms can impair vision, and dogs affected with
these forms should not be bred. Identified in 5.54% of Miniature
Hypoadrenocorticism (Addison’s disease): Controlled by a major Poodles, 4.12% of Toy Poodles, and 2.08% of Standard Poodles CERF
autosomal recessive gene, but not a simple recessive disorder. examined by veterinary ophthalmologists between 2000-2005.5
Immune mediated destruction of the adrenal gland seen in
Standard Poodles. Typical presentation of lethargy, poor appetite, Bronchiectasis: Clinical signs of chronic cough with excessive
vomiting, weakness, and dehydration occuring from 4 months airway mucous. Diagnosis with radiographs. Reported at a
to several years of age. Can also present with painful muscle frequency of 5.2% and an odds ratio of 2.99x in the Miniature
cramping. Treatment with DOCA injections or oral fludrocortisone. Poodle, and a frequency of 2.4% and an odds ratio of 1.83x in the
Heritabililty of 0.75 in the breed. No genetic test is available.11,12,13,14 Toy Poodle versus other breeds. Treatment is with bronchodilators
and possibly corticosteroids.25
Neonatal Encephalopathy: Rare, autosomal recessive disorder
causing poor growth, ataxia, whole body tremor, and tonic-clonic Hypothyroidism: Inherited autoimmune thyroiditis. 4.2% positive
seizures between 1-5 weeks of age. A genetic test is available.15 for thyroid autoantibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5).26,27
375
Otitis Externa (Chronic Ear Infection): Bacterial, yeast, or mixed (predominantly Standard Poodles). One report found an odds ratio
infections. Miniature Poodles are one of the breeds with the highest of 4.7x for secondary glaucoma in Poodles.42,43
incidence. In one study, 39.29% of dogs with Malassezia (yeast) ear
infection were Poodles.28,29 Vitreous Degeneration: A liquefaction of the vitreous gel which
may predispose to retinal detachment and/or glaucoma. Identified
Tracheal Collapse: Seen in Toy and Miniature Poodles. Causes in 1.85% of Toy Poodles CERF examined by veterinary ophthalmolo-
persistent “honking” cough, especially when excited. Dorn reports a gists between 2000-2005.5
5.92x odds ratio for tracheal collapse versus other breeds. Usually
occurs in middle-aged to older dogs. Usually poorly responsive to Primary (Narrow Angle) Glaucoma: Ocular condition causing
surgery. Many cases can be controlled medically.4,30 increased pressure within the eyeball, and secondary blindness due
to damage to the retina. Diagnose with tonometry and gonioscopy.
Mitral Valve Disease (MVD): Elderly Miniature and Toy Poodles Diagnosed in 1.68% of Miniature Poodles, 1.20% of Toy Poodles,
are prone to mitral valvular regurgitation, at an average age of 9.8 and 0.73% of Standard Poodles presented to veterinary teaching
years. Can lead to congestive heart disease, cardiac arrhythmias hospitals. CERF does not recommend breeding any Poodle with
(irregular heartbeats) and cardiac failure. Treat with heart drugs.31 glaucoma.5,44
Cryptorchidism (Retained Testicles): Can be unilateral or bilateral. Patent Ductus Arteriosus (PDA): Polygenically inherited
Reported at an increased frequency in all three varieties of Poodle; congenital heart disorder; affected dogs are usually stunted, and
with a significant risk in Toy Poodles, moderate risk in Miniature have a loud heart murmur. Diagnosis is via Doppler ultrasound.
Poodles, and increased risk in Standard Poodles versus other breeds.32 Treatment is surgical. Miniature and Toy Poodles have an increased
incidence versus other breeds.45
Atrial Septal Defect (ASD): Limited echocardiographic screening
of Standard Poodles show approximately 5% affected with an Calcium Oxalate Urolithiasis: Miniature and Toy Poodles have a
ostium secundum atrial septal defect. Some families have up to predisposition to develop calcium oxalate bladder stones, with a
40% of dogs affected. If small, an ASD may not produce clinical 3.85x odds ratio versus other breeds.46
disease. Medium to large ASD have hemodynamically significant
left to right shunting resulting in right atrial and ventricular Lens Induced Uveitis: Occurs secondary to cataract formation.
enlargement and clinical signs of heart failure. Screen with Doppler 35% of all cases are in Toy and Miniature Poodles, with a mean
echocardiography. Undetermined mode of inheritance.33,34 age of 9.0 years. One-third of cases are bilateral. Can progress to
glaucoma.47
Sebaceous Adenitis: Disorder of immune mediated sebaceous
gland destruction, presenting with hair loss, hyperkeratosis and Juvenile Renal Disease: Young Standard Poodles can develop a
seborrhoea, usually beginning with the dorsal midline and ears. progressive renal dysfunction. Typically presents with increased
Diagnosis by skin biopsy. Treat with isotretinoin. An autosomal drinking and urination, weight loss or unthriftiness, consistently
recessive mode of inheritance is suspected. Poodles are reported at dilute urine, and elevated kidney blood tests. Late in the disease,
a frequency of 0.9% in Sweden. OFA reports 2.8% affected.2,35,36 affected dogs can leak urinary protein, have non-regenerative
anemia, and fibrous osteodystrophy. Onset from weeks of age to
Idiopathic Epilepsy: Inherited Seizures can be generalized or partial over a year in age. Some dogs remain with mild signs, while others
seizures. In a study of one family, 93% had focal-onset seizures rapidly progress to kidney failure. Unknown mode of inheritance.
with a median age of onset of 3.7 years, an equal sex ratio, and Diagnosis by kidney biopsy or pathology.48
a possible simple autosomal mode of inheritance. In Standard
Poodles, 17.1% start as generalized seizures, and 68.3% begin as Mammary Gland Osteosarcoma: Female Miniature Poodles have
partial seizures (with the rest mixed) at a mean age of 2.8 years. predisposition to develop this malignant cancer, with an odds ratio
81% of affected Standard Poodles progress to generalized seizures. of 2.7x versus other breeds.49
Control with anticonvulsant medications.37,38
Alopecia-X/ Hyperadrenocorticism Associated with Sex Steroid
Diabetes Mellitus: Caused by a lack of insulin production by Excess (Black Skin Disease, BSD, Coat Funk, Severe Hair
the pancreas. Controlled by insulin injections, diet, and glucose Loss, SHL): Miniature Poodles are overrepresented. Progressive,
monitoring. Miniature Poodles have an odds ratio of 4.01x, and Toy symmetrical, non-pruritic, truncal hair loss usually beginning in
Poodles have an odds ratio of 3.27x versus other breeds.39 early adulthood. ACTH stimulation test, low-dose dexamethazone
suppression test, and thyroid panel results are normal. Alkaline
Hyperadrenocorticism (Cushing’s disease): Hyperfunction of the phosphatase and ALT are elevated. Urinary corticoid:creatinine
adrenal gland caused by a pituitary or adrenal tumor. Clinical signs ratio may be normal to elevated. Elevated blood concentrations
may include increased thirst and urination, symmetrical truncal of 17-hydroxyprogesterone (17-OHP) have been seen post ACTH
alopecia, and abdominal distention. Reported at an increased stimulation. Oral trilostane reverses the condition in some cases.
frequency in Poodles, representing 38.14% of all cases. Dorn reports The disorder appears familial, with a male predilection.50,51,52
a 2.72x odds ratio versus other breeds.4,40,41
Dilated Cardiomyopathy: Can present with ventricular
Secondary Glaucoma: Increased intraocular pressure and blindness arrhythmias, leading to cardiac dilation and heart failure. Increased
can occur after cataract formation, lens luxation (predominantly incidence reported in Standard Poodles. There is a two to one ratio
Miniature Poodles), hyphema (predominantly Toy Poodles), or uveitis of affected males to females.53
376
Perineal Hernia: Miniature Poodles have a predisposition to Nodular Panniculitis, Oligodontia, Pancreatitis, Prognathism,
developing perineal hernias. Treatment is surgery.54 Prolapsed Nictitans, Proliferative Episcleritis, Prekallikrein
Deficiency, Pseudohermaphrodism, Retinal Dysplasia, Shoulder
Optic Nerve Hypoplasia/Micropapilla: Failure of development Osteochondritis Dessicans, Sphingomyelinosis, Tetralogy of
of the optic nerve. Identified in 0.90% of Miniature Poodles CERF Fallot, Vertebral Stenosis, and Wry Mouth are reported.62
examined by veterinary ophthalmologists between 2000-2005. CERF
does not recommend breeding any Poodle with the condition.5
Isolated Case Studies
Digital Squamous Cell Carcinoma (SCC): Subungual squamous Chronic Hepatitis: Three related Standard Poodles with chronic
cell carcinoma occurs at increased frequency in black dogs. Treat liver disease were pathologically diagnosed with lobular dissecting
with digital amputation. Standard Poodles account for 14.3% of all hepatitis.63
cases.55
Nonspherocytic Hemolytic Anemia: A family of Miniature Poodles
developed nonspherocytic hemolytic anemia, marked reticulocy-
Shoulder Instability: In a one study, the most frequent breed was
tosis, hepatosplenomegaly, hemosiderosis of reticuloendothelial
Standard Poodles, representing 13% of all cases. Clinical signs
organs, bone marrow myelofibrosis, and osteosclerosis by 1 year of
included pain and muscle atrophy. Surgerical stabilization provided
age. The disease was fatal by 3 years of age. A pathogenesis was not
the best outcome.56
determined.64
Lingual Squamous Cell Carcinoma (SCC): Poodles have a 4.61x
Congenital Ectodermal Defect: X-linked recessive disorder
odds ratio versus other breeds of developing this cancer. Females
reported in male Miniature Poodle siblings. Affected dogs are born
are overrepresented in one study.57
without hair (hypotrichosis), have a reduced number or absence of
Degenerative Myelopathy (DM): Identified as a rare disorder sweat glands, and missing or malformed teeth.65,66
in Standard Poodles, though Miniature Poodles have also been
Amelogenesis Imperfecta/Familial Enamel Defect: A multi-gener-
pathologically diagnosed. Affected dogs show an insidious onset
ational family of Standard Poodles in Sweden was identified with
of upper motor neuron (UMN) paraparesis at an average age of
discolored teeth due to enamel malformation. Defective enamel
11.4 years. The disease eventually progresses to severe tetraparesis.
mineralization was documented histologically.67
Affected dogs have normal results on myelography, MRI, and CSF
analysis. Necropsy confirms the condition. Unknown mode of Junctional Epidermolysis Bullosa: A newborn Toy Poodle
inheritance. A direct genetic test for an autosomal recessive DM developed vesicles and bullae on the pads of the feet, oral mucous
susceptibility gene is available from OFA showing 17% carrier and membranes, and skin if the ventral abdomen. The lesions progressed
1% homozygous genes “at risk” in Poodles. All affected dogs are rapidly, and the pup was euthanized on day 2.68
homozygous for the gene, however, only a small percentage of
homozygous dogs develop DM.2,58
Genetic Tests
Atresia Ani (Imperforate Anus): An increased incidence of this Tests of Genotype: Direct test for pcrd-PRA is available from
congenital condition is reported in Miniature and Toy Poodles, with a Optigen.
frequency of 0.02%, and an odds ratio of 4.28x. Treatment is surgery.59
Direct test for von Willebrand’s disease (vWD) is available from
Polymicrogyria: Affected Standard Poodles present between 7 VetGen
weeks and 4 months of age with clinical signs that can include
blindness, behavior changes, hypermetric gait, complex partial Direct test for neonatal encephalopathy is available from the OFA.
motor seizures, delayed proprioceptive hopping, and resting
nystagmus. (1/5), and decreased pupillary light response. Some A direct test for an autosomal recessive DM susceptibility gene is
dogs also demonstrated progressive aggression toward the owner. available from the OFA.
EEG readings were abnormal. Imaging, and gross and histological
Direct test for MPS is available from PennGen.
examination revealed polymicrogyria that variously involved
the occipital, temporal, or entire cerebral lobes of the brain. Direct tests for black, brown, cream, white, red, and apricot coat
Undetermined mode of inheritance.60,61 colors, and black and brown nose are available from HealthGene
and VetGen.
Allergic Inhalant Dermatitis, Anterior Crossbite, Base-Narrow
Canines, Brachygnathism, Cerebellar Abiotrophy, Ceroid Tests of Phenotype: Miniature Poodles: CHIC Certification:
Lipofuscinosis, Corneal Dystrophy, Cystinuria, Deafness, Required testing includes hip radiographs, CERF eye examination,
Entropion, Factor VIII Deficiency, Factor XII Deficiency, Fibrinoid direct test for prcd-PRA, and patella evaluation. (See CHIC website;
Leukodystrophy, Globoid Cell Leukodystrophy, Growth Hormone www.caninehealthinfo.org).
Responsive Dermatosis, Hemeralopia, Hydrocephalus, Ichthyosis,
Intervertebral Disc Disease, Keratoconjunctivits Sicca, Lafora Recommend thyroid profile including autoantibodies, elbow
Body Disease, Leukodystrophy Lymphedemamacrocytosis/ radiographs, and cardiac evaluation.
Dyshematopoiesis, Methemaglobin Reductase Deficiency,
Microphthalmia, Osteogenesis Imperfecta, Narcolepsy, Standard Poodles: CHIC Certification: Required testing includes
377
hip radiographs, CERF eye examination, and one of the following: findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). J Am
thyroid profile including autoantibodies, biopsy for sebaceous Vet Med Assoc. 1996 Jan 1;208(1):85-91.
adenitis, or cardiac evaluation including echocardiogram. (See CHIC 14. Shaker E, Hurvitz AI & Peterson ME: Hypoadrenocorticism in a family of
website; www.caninehealthinfo.org). Standard poodles. J Am Vet Med Assoc. 1988 Apr 15;192(8):1091-2.
15. Chen X, Johnson GS, Schnabel RD, et. al.: A neonatal encephalopathy
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canine ortholog of ATF2. Neurogenetics. 2008 Feb;9(1):41-9.
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in the years 1975 to 1991 at the Institute for Veterinary Pathology of hemolytic anemia in poodles. Am J Vet Res. 1986 Mar;47(3):687-95.
the Free University of Berlin. Berl Munch Tierarztl Wochenschr. 1992 Sep 65. Selmanowitz VJ, Kramer KM & Orentreich N: Congenital ectodermal
1;105(9):305-11. defect in miniature poodles. J Hered. 1970 Sep-Oct;61(5):196-9.
41. Ling GV, Stabenfeldt GH, Comer KM, et. al.: Canine hyperadrenocor- 66. Selmanowitz VJ, Kramer KM, Orentreich N, et. al.: Congenital ectodermal
ticism: pretreatment clinical and laboratory evaluation of 117 cases. J Am dysplasia in male miniature poodle siblings. Arch Dermatol. 1970
Vet Med Assoc. 1979 Jun 1;174(11):1211-5. May;101(5):613-5.
42. Johnsen DA, Maggs DJ, Kass PH: Evaluation of risk factors for 67. Mannerfelt T & Lindgren I: Enamel defects in standard poodle dogs in
development of secondary glaucoma in dogs: 156 cases (1999-2004). J Am Sweden. J Vet Dent. 2009 Winter;26(4):213-5.
Vet Med Assoc. 2006 Oct 15;229(8):1270-4. 68. Dunstan RW, Sills RC, Wilkinson JE, et. al.: A disease resembling
43. Gelatt KN, MacKay EO: Secondary glaucomas in the dog in North. Vet junctional epidermolysis bullosa in a toy poodle. Am J Dermatopathol. 1988
Ophthalmol. 2004 Jul-Aug;7(4):245-59. Oct;10(5):442-7.
44. Gelatt KN, MacKay EO: Prevalence of the breed-related glaucomas 69. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
in pure-bred dogs in North America. Vet Ophthalmol. 2004 Mar-Apr; Book House, NY 2006. p 503-506 TOY, p 579-587 MINIATURE, STANDARD.
7(2):97-111.
45. Ackerman N, Burk R, Hahn AW, et. al.: Patent ductus arteriosus in the
dog: a retrospective study of radiographic, epidemiologic, and clinical
findings. Am J Vet Res. 1978 Nov;39(11):1805-10.
46. Lekcharoensuk C, Lulich JP, Osborne CA, et. al.: Patient and
environmental factors associated with calcium oxalate urolithiasis in dogs.
J Am Vet Med Assoc. 2000 Aug 15;217(4):515-9.
47. van der Woerdt A, Nasisse MP & Davidson MG: Lens-induced
uveitis in dogs: 151 cases (1985-1990). J Am Vet Med Assoc. 1992 Sep
15;201(6):921-6.
48. DiBartola SP, Chew DJ & Boyce JT: Juvenile renal disease in related
Standard Poodles. J Am Vet Med Assoc. 1983 Sep 15;183(6):693-6.
49. Langenbach A, Anderson MA, Dambach DM, et. al.: Extraskeletal
osteosarcomas in dogs: a retrospective study of 169 cases (1986-1996). J
Am Anim Hosp Assoc. 1998 Mar-Apr;34(2):113-20.
50. Greco DS: Hyperadrenocorticism associated with sex steroid excess. Clin
Tech Small Anim Pract. 2007 Feb;22(1):12-7.
51. Cerundolo R, Lloyd DH, Persechino A, et. al: Treatment of canine
Alopecia X with trilostane. Vet Dermatol. 2004 Oct;15(5):285-93
52. Cerundolo R, Lloyd DH, Vaessen MM, et. al.: Alopecia in pomeranians
and miniature poodles in association with high urinary corticoid:creatinine
ratios and resistance to glucocorticoid feedback. Vet Rec. 2007 Mar
24;160(12):393-7.
53. Tidholm A, Jonsson L : A retrospective study of canine dilated
cardiomyopathy (189 cases). J Am Anim Hosp Assoc. 1997
Nov-Dec;33(6):544-50.
54. Hosgood G, Hedlund CS, Pechman RD, et. al.: Perineal herniorrhaphy:
perioperative data from 100 dogs. J Am Anim Hosp Assoc. 1995
Jul-Aug;31(4):331-42.
55. O’Brien MG, Berg J & Engler SJ: Treatment by digital amputation of
subungual squamous cell carcinoma in dogs: 21 cases (1987-1988) J Am
Vet Med Assoc. 1992 Sep 1;201(5):759-61.
56. Pucheu B & Duhautois B: Surgical treatment of shoulder instability. A
retrospective study on 76 cases (1993-2007). Vet Comp Orthop Traumatol.
2008;21(4):368-74.
57. Dennis MM, Ehrhart N, Duncan CG, et. al.: Frequency of and risk factors
associated with lingual lesions in dogs: 1,196 cases (1995-2004).
58. Matthews NS & de Lahunta A: Degenerative myelopathy in an adult
379
Portuguese Water Dog
or brown. The neck is short and strongly muscled, head carriage is
high, and the throat is clean. Thorax is deep, the ribs are well sprung
and moderate tuck up of abdomen is evident. The well-plumed tail
extends to just above or just to the tarsus. When alert, the tail is
held over the croup in a ring. Limbs are well muscled and straight
boned. Dewclaws may be removed on the forelimbs. There are
no rear dewclaws. Feet are flat and round in shape and are well
covered in hair. The energetic gait is short-strided and quick.
Hypoadrenocorticism (Addison’s Disease): Immune mediated Malignant Cancer: Based on the 2005 PWD Health Survey, 3.1%
destruction of the adrenal gland. Typical presentation of lethargy, were diagnosed with hemangiosarcoma, 1.6% with lymphosarcoma,
poor appetite, vomiting, weakness, and dehydration can occur from 1.4% with mammary gland cancer (some of which may be benign),
4 months to several years of age. Treatment with DOCA injections and 1.1% with mast cell cancer.1
or oral fludrocortisone. Heritabililty of 0.49. Reported incidence of
1.5% affected. Controlled by a major autosomal recessive gene, Distichiasis: Abnormally placed eyelashes that irritate the cornea
but not a simple recessive disorder. No genetic test is available. and conjunctiva. Can cause secondary corneal ulceration. Identified
Reported at a frequency of 1.7% in the 2005 PWD Health in 3.04% of Portuguese Water Dogs CERF examined by veterinary
Survey.1,9,10,11 ophthalmologists between 2000-2005. Reported at a frequency of
1.2% in the 2005 PWD Health Survey.1,5
Juvenile Dilated Cardiomyopathy (JDCM): Fatal autosomal
recessive disorder causing sudden death between 2-32 weeks of Cataracts: Anterior cortex punctate cataracts predominate in the
age from congestive heart failure. Echocardiograms are normal breed. Identified in 2.87% of Portuguese Water Dogs CERF examined
until 3-7 days prior to death. Occurring at a low frequency in the by veterinary ophthalmologists between 2000-2005. Reported at a
breed. A direct genetic test is available, showing a 12% carrier frequency of 5.9% in the 2005 PWD Health Survey. CERF does not
frequency worldwide.12,13,14,15,16 recommend breeding any Portuguese Water Dog with a cataract.1,5
Patella Luxation: Polygenically inherited laxity of patellar Umbilical Hernia: Congential body wall defect at the umbilicus.
ligaments, causing luxation, lameness, and later degenerative joint Correct surgically if large. Reported in 2.7% of litters in the 2005
disease. Treat surgically if causing clinical signs. Reported at a high PWD Health Survey.1
frequency by OFA, but too few Portuguese Water Dogs have been
screened to determine an accurate frequency.3 Cleft Palate: Congenital disorder of incomplete closure of the
maxillary processes to form the roof of the mouth. Reported in
2.3% of litters in the 2005 PWD Health Survey.1
Disease Predispositions
Sebaceous Cysts: Benign subcutaneous cysts of sebaceous material. Inflammatory Bowel Disease (IBD): Inflammatory condition
Reported at a frequency of 10.0% in the 2005 PWD Health Survey.1 of the gastrointestinal tract causing chronic vomiting, diarrhea,
and/or weight loss. A low frequency of Portuguese Dogs suffers
Cryptorchidism: Undescended testicles can be unilateral or from IBD. Affected dogs can usually be controlled with diet and/
bilateral. This is a sex-limited disorder with an unknown mode of or medications. Reported at a frequency of 2.1% in the 2005 PWD
inheritance. Reported in 10.0% of litters in the 2005 PWD Health Health Survey.1
Survey.1
Bladder Stones: Based on the 2005 PWD Health Survey, 2.1%
Aggression and Behavior: Based on the 2005 PWD Health Survey, developed bladder stones. The composition of the stones was not
7.4% show dog to dog aggression, and 3.4% show aggression indicated.1
towards people. 7.1% show noise phobia, and 5.7% show shyness.1
Seizures/Epilepsy: Generalized or partial seizures. Based on the
Allergies: Presents with pruritis and pyotraumatic dermatitis (hot 2005 PWD Health Survey, 1.7% are reported with seizures or
spots). Based on the 2005 PWD Health Survey, 6.2% show food epilepsy.1
allergy and 3.4% show inhalant allergies.1
Keratoconjunctivitis Sicca (KCS, Dry Eye): Ocular condition
Persistent Pupillary Membranes: Strands of fetal remnant causing lack of tear production and secondary conjunctivitis,
connecting; iris to iris, cornea, lens, or involving sheets of tissue. corneal ulcerations, and vision problems. Reported at a frequency of
The later three forms can impair vision, and dogs affected with 1.2% in the 2005 PWD Health Survey.1
these forms should not be bred. Identified in 5.52% of Portuguese
Water Dogs CERF examined by veterinary ophthalmologists Follicular Dysplasia (Hair Loss): Inherited, non-inflammatory,
between 2000-2005. Reported at a frequency of 1.6% in the 2005 truncal, symmetrical, cyclic hair loss. Only occurs in curly dogs from
PWD Health Survey.1,5 two curly parents. Unknown mode of inheritance. Reported at a
frequency of 0.62% in the 2005 PWD Health Survey.1,19
Otitis Externa (Chronic Ear Infections): Can be bacterial or yeast
infection. Reported at a frequency of 5.4% in the 2005 PWD Health Coat Dilution Alopecia and Microphthalmia are reported.20
Survey.1
381
Gastrinoma and Somatostatinoma: Case study of a ten year old normal canine beta-galactosidase gene and its mutation in a dog model of
Portuguese Water Dog with multiple endocrine tumors consisting GM1-gangliosidosis. J Inherit Metab Dis. 2000 Sep;23(6):593-606.
of a pancreatic islet cell somatostatinoma, and a gastrinoma in the 9. Peterson ME, Kintzer PP, Kass PH: Pretreatment clinical and laboratory
mesenteric lymph nodes and liver.21 findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). J Am
Vet Med Assoc. 1996 Jan 1;208(1):85-91.
10. Chase K, Sargan D, Miller K, et. al.: Understanding the genetics of
Genetic Tests autoimmune disease: two loci that regulate late onset Addison’s disease in
Tests of Genotype: Direct test for JDCM is available from PennGen. Portuguese Water Dogs. Int J Immunogenet. 2006 Jun;33(3):179-84.
11. Oberbauer AM, Bell JS, Belanger JM, et. al.: Genetic evaluation of
Direct tests for prcd-PRA and improper coat are available from Addison’s disease in the Portuguese Water Dog. BMC Vet Res. 2006 May
Optigen. 2;2:15.
12. Alroy J, Rush JE, Freeman L, et. al.: Inherited infantile dilated
Direct test for GM1-Gangliosidosis available from New York cardiomyopathy in dogs: genetic, clinical, biochemical, and morphologic
University Neurogenetics Laboratory: http://www.pwdca.org/health/ findings. Am J Med Genet. 2000 Nov 6;95(1):57-66.
tests/instructions/GM1TestInstructions.html. 13. Sleeper MM, Henthorn PS, Vijayasarathy C, et. al.: Dilated
cardiomyopathy in juvenile Portuguese Water Dogs. J Vet Intern Med. 2002
Test for black and brown colors, and black or brown nose is Jan-Feb;16(1):52-62.
available from HealthGene and VetGen. 14. Alroy J, Rush JE, Sarkar S: Infantile dilated cardiomyopathy in
Portuguese water dogs: correlation of the autosomal recessive trait with
Tests of Phenotype: CHIC Certification: Hip radiographs, CERF low plasma taurine at infancy. Amino Acids. 2005 Feb;28(1):51-6.
15. Werner P, Raducha MG, Prociuk U, et. al.: A novel locus for dilated
eye examination (annually until age 10), and direct genetic tests
cardiomyopathy maps to canine chromosome 8. Genomics. 2008
for GM-1 and prcd-PRA. Optional tests include congenital cardiac Jun;91(6):517-21.
evaluation by a cardiologist, elbow radiographs, thyroid profile 16. Dambach DM, Lannon A, Sleeper MM, et. al.: Familial dilated
including autoantibodies, skin biopsy for sebaceous adenitis, patella cardiomyopathy of young Portuguese water dogs. J Vet Intern Med. 1999
evaluation, and genetic test for JDCM. (See CHIC website; www. Jan-Feb;13(1):65-71.
caninehealthinfo.org). 17. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
Miscellaneous hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
18. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
• Breed name synonyms: Portie, Cão de Agua, Cão de Agua for Population and Animal Health, Michigan State University. April, 2007.
de Pelo Ondulado (longhaired variety), Cão de Agua de Pelo 19. Miller Jr WH, & Scott DW: Follicular Dysplasia of the Portuguese Water
Encaradolado (curly-coated variety). Dog. Vet Dermatol. 1995:6[2]:67-74.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 20. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
ANKC (Australian National Kennel Club). Ackerman. p. 233-234 AAHA Press, 1999.
• AKC rank (year 2008): 64 (1,427 dogs registered) 21. Hoenerhoff M, Kiupel M: Concurrent gastrinoma and somatostatinoma
• Internet resources: Portuguese Water Dog Club of America: in a 10-year-old Portuguese water dog. J Comp Pathol. 2004
www.pwdca.org May;130(4):313-8.
Portuguese Water Dog Club of Canada: www.pwdcc.org 22. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Portuguese Water Dog Club of Great Britain: Book House, NY 2006. p. 308-313.
www.portuguesewaterdogs.org.uk
Portuguese Water Dog Health Foundation:
www.pwdfoundation.org
References
1. Slater M: The 2005 Portuguese Water Dog Health Survey. July 1, 2010.
2. Parker HG, Chase K, Cadieu E, et. al.: An insertion in the RSPO2 gene
correlates with improper coat in the Portuguese water dog. J Hered. 2010
Sep-Oct;101(5):612-7.
3. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
4. Chase K, Lawler DF, Adler FR, et. al.: Bilaterally asymmetric effects of
quantitative trait loci (QTLs): QTLs that affect laxity in the right versus left
coxofemoral (hip) joints of the dog (Canis familiaris). Am J Med Genet A.
2004 Jan 30;124(3):239-47.
5. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
6. Zangerl B, Goldstein O, Philp AR, et. al.: Identical mutation in a novel
retinal gene causes progressive rod-cone degeneration in dogs and retinitis
pigmentosa in humans. Genomics. 2006 Nov;88(5):551-63.
7. Shell LG, Potthoff AI, Carithers R, et. al.: Neuronal-visceral GM1
gangliosidosis in Portuguese water dogs. J Vet Intern Med. 1989
Jan-Mar;3(1):1-7.
8. Wang ZH, Zeng B, Shibuya H, et. al.: Isolation and characterization of the
382
Pug
minded, stable, liking lots of human companionship.
Coat: The fine short double glossy coat lies flat and breed colors Disease Predispositions
include fawn and apricot, black, and silver. Markings follow a set Brachycephalic Complex: Can cause dyspnea, and collapse.
pattern and are black or dark including ears, muzzle and sometimes Includes Elongated Soft Palate, Stenotic Nares, Hypoplastic
a line is present down the back. Trachea, and Everted Laryngeal Saccules. Clinical signs are
associated with bronchial collapse. Nasopharyngeal turbinates may
Longevity: 13-15 years. also play a role. Surgery is indicated in severe cases. Identified in
26.0% of Pugs in an Australian study. Dorn reports a 13.3x odds
Points of Conformation: Their cobby, stout, and compact square ratio in Pugs versus other breeds.4,5,6,7,8
constitution gives them a lot of apparent substance for their size.
Though they are classed as a toy, their heavy build makes them look Entropion: A rolling in of the eyelids that can cause corneal
larger. The head is massive and round, the high set ears are soft, irritation and ulceration. Dorn reports a 2.94x odds ratio in Pugs
the leather is thin and ears either in a rose or button type. Muzzle versus other breeds. Entropion is reported in 21.00% of Pugs CERF
is very short and square and the bite is mildly undershot. Top of the examined by veterinary ophthalmologists between 2000-2005.4,9
head has prominent forehead wrinkles, eyes are dark, shallow set,
and very large. Neck is short and strong, topline level, the thorax Exposure Keratopathy Syndrome/Pigmentary Keratitis: Corneal
is barrel shaped, tail is high set and ideally, doubly curled to rest reactivity and drying from ocular exposure secondary to shallow
tightly over the hip joint. Legs are straight, moderate in length, orbits, exophthalmos, and lagophthalmos. Identified in 16.55%
and feet are moderately sized and oval in shape, toenails are black of Pugs CERF examined by veterinary ophthalmologists between
and dewclaws are generally removed. Their gait is strong, free, and 2000-2005.9
hindquarters typically have some roll.
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
Recognized Behavior Issues and Traits The later three forms can impair vision, and dogs affected with
These dogs have been described as being: Loving of children and these forms should not be bred. Identified in 9.87% of Pugs CERF
family, good alarm barkers, playful, “pugnacious”, independently examined by veterinary ophthalmologists between 2000-2005.9
383
Distichiasis: Abnormally placed eyelashes that irritate the cornea stones. Stone composition is not identified.20,21
and conjunctiva. Can cause secondary corneal ulceration. Identified
in 8.62% of Pugs CERF examined by veterinary ophthalmologists Diabetes Mellitus: Sugar diabetes caused by a lack of insulin
between 2000-2005.9 production by the pancreas. Controlled by insulin injections, diet,
and glucose monitoring. Identified as a breed at increased risk of
Hypothyroidism: Inherited autoimmune thyroiditis. 5.6% positive developing diabetes, with an odds ratio of 3.87x versus other breeds.22
for thyroid autoantibodies based on testing at Michigan State
University. (Ave. for all breeds is 7.5%).10,11 Hemivertebra and Butterfly Vertebra: Malformed veterbra can
cause scoliosis, pain or spinal cord compression if severe. Can
Allergic Dermatitis (Atopy): Inhalant or food allergy. Presents produce Spina Bifida or Sacrocaudal Dysgenesis. Associated with
with pruritis and pyotraumatic dermatitis (hot spots). Pugs have a selection for the screw tail. Seen at an increased frequency in the
significantly increased risk for atopy versus other breeds.12 breed. Undetermined mode of inheritance.23,24
Chronic Superficial Keratitis (Pannus): Chronic corneal Pigmented Plaques: Pugs are predisposed to the development of
inflammatory process that can cause vision problems due to deeply pigmented, slightly elevated hyperkeratotic noncancerous
corneal pigmentation. Treatment with topical ocular lubricants and plaques on the abdomen and limbs. A novel papilloma virus (CPV4)
anti-inflammatory medication. Identified in 3.20% of Pugs CERF has been isolated from these plaques.25
examined by veterinary ophthalmologists between 2000-2005.
CERF does not recommend breeding any Pug with the condition.9 Lung Lobe Torsion: Pugs have a predisposition for spontaneous
lung lobe torsion. Median age of 1.5 years, with a male prevalence.
Macroblepharon: Abnormally large eyelid opening; may lead to Histories included increased weakness, increased respiratory effort,
secondary conditions associated with corneal exposure. Identified tachypnea, acute collapse, lethargy, anorexia, and cyanosis. Surgical
in 3.06% of Pugs CERF examined by veterinary ophthalmologists correction is curative, though one reported case had another lobe
between 2000-2005.9 torsion 2 years later.26,27,28,29
Mast Cell Tumor (MCT): Histamine producing skin tumors that Hydrops Fetalis: A previously unreported syndrome of transient
produce inflammation and ulceration. Can metastasize or reoccur mid-gestational hydrops fetalis identified by ultrasound was
locally following surgical removal. Pugs have a 4 to 8 times greater diagnosed in 16 litters of 16 different Pugs. There was 7.4% fetal
risk for developing cutaneous mast cell tumors than other breeds.13 resorption, 8.4% abortion, 8.0% stillbirths, 15% neonatal mortality,
and 9.6% congenital abnormalities. Pugs were significantly (22.8
Cataracts: Anterior, posterior, intermediate and punctate cataracts times) more likely to be affected than other breeds.30
occur in the breed. Unknown mode of inheritance. Reported in
2.28% of Pugs presented to veterinary teaching hospitals. Identified Degenerative Myelopathy (DM): Affected dogs show an insidious
in 1.53% of Pugs CERF examined by veterinary ophthalmologists onset of upper motor neuron (UMN) paraparesis. The disease
between 2000-2005. CERF does not recommend breeding any Pug eventually progresses to severe tetraparesis. Affected dogs have
with a cataract.9,14 normal results on myelography, MRI, and CSF analysis. Necropsy
confirms the condition. Unknown mode of inheritance. A direct
Portosystemic Shunt (PSS, Liver Shunt): Abnormal blood vessels genetic test for an autosomal recessive DM susceptibility gene is
connecting the systemic and portal blood flow. Vessels can be available. All affected dogs are homozygous for the gene, however
intrahepatic, extrahepatic or microvascular dysplasia. Causes only a small percentage of homozygous dogs develop DM. OFA
stunting, abnormal behavior and possible seizures. Diagnose with reports DM susceptibility gene frequencies of 29% carrier, and 2%
paired fasted and feeding serum bile acid and/or ammonium levels, homozygous “at-risk”.2
and abdominal ultrasound. Treatment of PSS includes partial
ligation and/or medical and dietary control of symptoms. The Pug is Brachygnathism, Cleft Palate, Cryptorchidism, Demodicosis,
a breed at increased risk of having PSS, with an incidence of 1.3% Fold Dermatitis, Lentigo, Oligodontia, and Progressive Retinal
and an odds ratio of 26.2x versus other breeds. Undetermined mode Atrophy are reported.31
of inheritance.15
Weight: 30-40 lb (13.5-18 kg). Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Coat: An off-black, which is tinged with bronze or grey is the disease. Treat surgically if causing clinical signs. OFA reports 5.2%
standard breed color, though especially in Hungary, white and affected.1
gray are seen. A small white spot on the chest is allowed. Body
skin is darkly pigmented. The undercoat is wooly, short and soft. Disease Predispositions
It naturally intermingles with the long outer coat. As the puppy Persistent Pupillary Membranes: Strands of fetal remnant
matures, the tangle evolves into the cords that characterize the connecting; iris to iris, cornea, lens, or involving sheets of tissue.
adult coat. Cording normally begins around the time of sexual The later three forms can impair vision, and dogs affected with
maturity. This adult coat development process can take 4 or 5 years these forms should not be bred. Identified in 26.88% of Pulik CERF
to complete. Cords may reach the ground if untrimmed. The dog examined by veterinary ophthalmologists between 2000-2005.2
may be shown corded or groomed.
Retinal Dysplasia: Retinal folds, geographic, and generalized
Longevity: 11-14 years retinal dysplasia with detachment are recognized in the breed. Can
progress to blindness. Reported in 7.50% of Pulik CERF examined by
Points of Conformation: The profuse corded coat is the trademark veterinary ophthalmologists between 2000-2005.2
feature of this breed. The compact, square, medium build is hard to
assess through the profuse coat. The head is medium in size, large, Cataracts: Anterior cortex punctate cataracts predominate in the
and the almond shaped eyes are dark brown with dark palpebral breed. Unknown mode of inheritance. Identified in 3.44% of Pulik
margins. Cords normally hang over the eyes in mature dogs. Ears CERF examined by veterinary ophthalmologists between 2000-2005.
are medium sized, triangular, high set, and hang down beside the CERF does not recommend breeding any Puli with a cataract.2
head. The stop is average, skull is slightly domed, and the nose is
386
Hypothyroidism: Inherited autoimmune thyroiditis. 2.9% positive 8. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
for thyroid autoantibodies based on testing at Michigan State House, NY 2006. p. 684-687.
University. (Ave. for all breeds is 7.5%).3,4
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: Hungarian Puli, Hungarian Water Dog.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
• AKC rank (year 2008): 142 (102 dogs registered)
• Internet resources: The Puli Club of America: www.puliclub.org
Puli Canada: www.pulicanada.ca
Hungarian Puli Club of Great Britain:
www.hungarianpuliclubofgb.co.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Hannah SS: Genetic Considerations in Companion Animal Nutrition.
Proceedings, 2003 Tufts’ Canine and Feline Breeding and Genetics
Conference. 2003.
6. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
7. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 234. AAHA Press, 1999.
387
Pyrenean Shepherd
Points of Conformation: The dog in good working condition is
lightly boned and sinewy. In rough faced dogs the body is clearly
long in proportion to the height of the dog, whereas Smooth-Faced
dogs appear much more square. The head is triangular in shape,
and small in proportion to the size of the dog. The eyes are
almond-shaped and dark brown in color, except in merles where
blue or partially blue eyes are acceptable. Eye rims must be black.
Ears can be cropped and erect, or natural and semi-prick. The
head is a triangular wedge shape, with no stop. The nose is black.
The back is level. The tail can be docked, natural bob, or long. The
feet are oval, with double, single, or no rear dewclaws. The gait is
The Breed History flowing, with the feet barely leaving the ground.
Evidence of sheepdogs in the Pyrenean mountains dates back to
6000 BC. Pyrenean Sheepdogs were used solely for herding and Recognized Behavior Issues and Traits
companionship, and not for protection; that role was left to the The Pyrenean Shepdog is a high energy, intelligent, and mischievous
Great Pyrenees. It is believed that when the Virgin Mary appeared dog that is always on alert, suspicious, ready for action. An ardent
to the young shepherdess Bernadette Soubirous in the grotto at herder of all kinds of livestock. The Pyr Shep is naturally distrustful
Lourdes in 1858, her little Pyrenean Shepherd was by her side. of strangers, but when well-socialized from a young age, he or she
They are often referred to as “the dog that saw God.” Pyrenean has a very lively, cheerful disposition. He is very affectionate with the
Shepherds distinguished themselves in the Pyrenees during World members of his immediate family. He has the tendency to become
War II as couriers, and search and rescue dogs. The smooth-faced passionately attached to his owner to the complete exclusion of
variety was used to establish the Australian Shepherd breed. The all others and is astonishingly sensitive to his owner’s moods. As a
majority of Pyrenean Shepherd breeding stock was imported to the companion, he is very active and enthusiastic and insists upon being
US in the 1970s and 1980s. AKC recognition occurred in 2009. involved in the day’s activities whatever they may be.
Coat: Rough-Faced: The Rough-Faced dog’s coat can be of long or Elbow Dysplasia: Polygenically inherited trait causing elbow
demi-long hair. Demi-long dogs have culottes on the rump, while arthritis. Too few Pyrenean Shepherds have been screened by OFA
the long-haired dogs are more heavily furnished with woollier to determine an accurate frequency.3
hair that may cord. Smooth-Faced: The muzzle is covered with
short, fine hairs. The hair becomes longer on the sides of the head, Patella Luxation: Polygenically inherited laxity of patellar
blending into a modest ruff. The hair on the body is fine and soft, ligaments, causing luxation, lameness, and later degenerative joint
attaining a maximum length of no more than 3 inches for the disease. Treat surgically if causing clinical signs. Reported as a breed
ruff and culottes, 2 inches along the back. Various shades of fawn problem on the Pyrenean Shepherd Club of America website. Too
from tan to copper, with or without a mixture of black hairs; grey, few Pyrenean Shepherds have been screened by OFA to determine
ranging from charcoal to silver to pearl grey; merles of diverse an accurate frequency.3
tones; brindle; black; black with white markings not exceeding 30%
of the body surface. A little white is acceptable on the chest, head, Disease Predispositions
and feet. Cataracts: Anterior cortex punctate cataracts predominate in the
breed. Reported in 7.14% of Pyrenean Shepherds CERF examined
Longevity: 9-12 years.
388
by veterinary ophthalmologists between 2000-2005. CERF does not
recommend breeding any Pyrenean Shepherd with a cataract.5
Miscellaneous
• Breed name synonyms: Berger Des Pyrenees, Petit Berger, Labrit
• Registries: AKC, Canadian Kennel Club, UKC, KCGB (Kennel Club
Choroidal Hypoplasia: Inadequate development of the choroid
of Great Britain), FCI.
present at birth and non-progressive. This condition is more
• AKC rank: (None) Became an AKC recognized breed Jan. 2009.
commonly identified in the Collie breed where it is a manifestation
Entire studbook registered.
of “Collie Eye Anomaly”. CERF does not recommend breeding
• Internet resources: Pyrenean Shepherd Club of America:
any Pyrenean Shepherd affected with the disorder. No genetic
www.pyrshep.com
test is available in the breed. Identified in 5.36% of Pyrenean
The Pyrenean Sheepdog Club of Great Britain:
Shepherds CERF examined by veterinary ophthalmologists between
www.pyreneansheepdog.co.uk/
2000-2005.5
Genetic Tests
Tests of Genotype: None
389
Redbone Coonhound
brush and saber-like. The gait should have good reach and drive.
Breeding for Function Patella Luxation: Polygenically inherited laxity of patellar ligaments,
The Redbone has been bred for the purpose of treeing raccoon and causing luxation, lameness, and later degenerative joint disease. Treat
small game, and is acclaimed for its speed and agility from lowlands surgically if causing clinical signs. Too few Redbone Coonhounds
to steep, rocky hills. An excellent swimmer with a pleasant, if not have been screened by OFA to determine an accurate frequency.1
constant voice.
Disease Predispositions
Physical Characteristics Hypothyroidism: Inherited autoimmune thyroiditis. Not enough
Height at withers: Males - 22 to 27 inches (56-69 cm). Females - samples have been submitted for thyroid auto-antibodies to
21 to 26 inches (53-66 cm). Michigan State University to determine an accurate frequency. (Ave.
for all breeds is 7.5%).2,3
Weight: 50-70 pounds (23-32 kg).
Coonhound Paralysis (polyradiculoneuritis): Disorder of acute
Coat: Short, smooth, coarse enough to provide protection. Solid red paralysis due to transient demyelination, similar to Guillain-Barré
preferred. Dark muzzle and small amount of white on brisket and syndrome. Caused by exposure to raccoon saliva in genetically
feet permissible. susceptible dogs. Affected dogs can recover, but must be supported
during remyelinization.4,5
Longevity: 11-12 years.
Inherited Ocular Disorders: Too few Redbone Coonhounds have
Points of Conformation: Should be equal in height from highest been CERF examined by veterinary ophthalmologists to determine
point of the shoulder blade to the ground as long measured from an accurate frequency of inherited ocular disorders.6
sternum to the buttocks. Slightly taller at shoulder than at hips.
Pleading. Eyes - Dark brown to hazel in color, dark preferred. Set Ectropion, Entropion, and Progressive Retinal Atrophy are
well apart. No drooping eyelids. Eyes round in shape. Ears are set reported.7
moderately low, and fine in texture. The muzzle is square, and
nostrils wide. Nose is black. Deep broad chest with ribs well sprung.
Shoulder angulation should have a perfect 90-degree angle or close.
Isolated Case Studies
None Reported
Legs are straight and well boned. Tail is medium length, very slight
390
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: Redbone
• Registries: AKC, UKC, CKC, NKC (National Kennel Club)
• AKC rank: (none) AKC recognized in Dec. 2009. Entire stud book
entered.
• Internet resources: Redbone Coonhound Association of
America: www.redbonecaa.com
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Cummings JF, Haas DC: Coonhound paralysis. An acute idiopathic
polyradiculoneuritis in dogs resembling the Landry-Guillain-Barre
syndrome. J Neurol Sci. 1966 Jan-Feb;4(1):51-81.
5. Holmes DF, Schultz RD, Cummings JF, et. al.: Experimental coonhound
paralysis: animal model of Guillain-Barre syndrome. Neurology. 1979
Aug;29(8):1186-7.
6. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
7. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 234. AAHA Press, 1999.
8. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 703-705.
391
Rhodesian Ridgeback
Recognized Behavior Issues and Traits
This dog is protective, gentle and loyal. He is easily trained,
even-tempered and enjoys a family with children. They are known
to be wary with strangers, and only rarely bark. Gentle obedience
training should be combined with socialization to people and
other pets when the dog is young. They need regular exercise and
stimulation to prevent boredom. Average shedders, they require
minimal grooming. They are not ideal city dogs, unless they get
vigorous exercise.
Allergic Dermatitis (Atopy): Inhalant or food allergy. Presents Acute Nonlymphocytic Leukemia: Diagnosed in a 1-year-old
with pruritis and pyotraumatic dermatitis (hot spots). Reported at a Rhodesian Ridgeback. Clinical signs of disease included weight
frequency of 4.6% in the RRCUS Health Survey 2001 Update.1 loss, anorexia, lethargy, lymphadenopathy, splenomegaly, and
hepatomegaly.23
Mast Cell Tumor (MCT): Skin tumors that produce histamine and
cause inflammation and ulceration. Can reoccur locally or with Myotonic Dystrophy: A mature female Rhodesian Ridgeback had
distant metastasis. Reported at a frequency of 4.1% in the RRCUS a progressive degenerative myopathy, associated with myotonia,
Health Survey 2001 Update.1 dysphagia, and marked muscle wasting. Clinical findings revealed
percussion dimpling, creatine kinase elevation, and a paroxysmal
Cataracts: Posterior cortex intermediate and punctate cataracts atrial tachycardia.24
predominate in the breed. Age of onset 3 years. Identified in 3.41%
of Rhodesian Ridgebacks CERF examined by veterinary ophthalmol- Renal Adenocarcinoma: Concurrent renal adenocarcinoma and
ogists between 2000-2005. CERF does not recommend breeding polycythemia were diagnosed in a 19-month-old, female Rhodesian
any Rhodesian Ridgeback with a cataract.15 ridgeback. Clinical signs included brick-red mucous membranes,
lethargy, a periodic systolic heart murmur, and engorged retinal
Distichiasis: Abnormally placed eyelashes that irritate the cornea vessels. A large retroperitoneal mass and pulmonary metastatic
and conjunctiva. Can cause secondary corneal ulceration. Identified nodules were found. Polycythemia was the result of excessive
in 2.73% of Rhodesian Ridgebacks CERF examined by veterinary erythropoietin production.25
ophthalmologists between 2000-2005.15
Osteochondrosarcoma of the Hard Palate: A 14-year-old
Soft Tissue Sarcoma: The Rhodesian Ridgeback is a breed at castrated male Rhodesian Ridgeback was presented with a history
increased risk for developing soft tissue sarcomas, with 5.7% of of sneezing and epistaxis. A multilobular osteochondrosarcoma of
all STS cases in one study occurring in Rhodesian Ridgebacks. the hard palate with pulmonary metastases was diagnosed.26
Aggressive surgical management is associated with a low incidence
of local recurrence.16 Spinal Meningioma: A 5-month-old male Rhodesian Ridgeback
was diagnosed with a meningothelial meningioma with focal
Secondary Glaucoma: Rhodesian Ridgebacks are listed as having mineralization that extended from the cervical to the lumbosacral
a 4.1x risk for developing secondary glaucoma versus other breeds. spine. There was a concurrent hydrocephalus.27
Causes of secondary glaucoma include anterior uveitis, lens
luxation, and cataract.17
Genetic Tests
Degenerative Myelopathy (DM): Affected dogs show an insidious Tests of Genotype: Direct test for an autosomal recessive DM
onset of upper motor neuron (UMN) paraparesis at an average susceptibility gene is available from the OFA.
age of 11.4 years. The disease eventually progresses to severe
tetraparesis. Affected dogs have normal results on myelography, The genes for ridgelessness, deafness, and hemophilin B have been
MRI, and CSF analysis. Necropsy confirms the condition. Reported identified, however, commercial tests have not yet been developed.
at a frequency of 0.74% in Rhodesian Ridgebacks. Unknown mode
Tests of Phenotype: CHIC certification: Required testing includes
393
hip and elbow radiographs, CERF eye examination (annually to age 9), Vet Med Assoc. 2006 Oct 15;229(8):1270-4.
and thyroid profile including autoantibodies (at age 2, 3, 4, 5, 6 and 18. Coates JR: Degenerative Myelopathy of Pembroke Welsh Corgi Dogs.
8). Optional recommended tests include cardiac evaluation, and BAER Proceedings, 2005 ACVIM Forum. 2005.
testing for deafness (minimum age of 12 months). (See CHIC website; 19. Awano T, Johnson GS, Wade CM, et. al.: Genome-wide association
analysis reveals a SOD1 mutation in canine degenerative myelopathy that
www.caninehealthinfo.org).
resembles amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A. 2009 Feb
24;106(8):2794-9.
Recommend patella evaluation.
20. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p.234, AAHA Press, 1999.
Miscellaneous 21. Lobetti RG, Pearson J, Jimenez M: Renal dysplasia in a Rhodesian
• Breed name synonyms: African Lion Hound, Ridgeback ridgeback dog. J Small Anim Pract. 1996 Nov;37(11):552-5.
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), 22. Chieffo C, Stalis IH, Van Winkle TJ, et. al.: Cerebellar Purkinje’s cell
ANKC (Australian National Kennel Club), NKC (National Kennel Club) degeneration and coat color dilution in a family of Rhodesian Ridgeback
• AKC rank (year 2008): 50 (2,199 dogs registered) dogs. J Vet Intern Med. 1994 Mar-Apr;8(2):112-6.
23. Hamlin RH, Duncan RC: Acute nonlymphocytic leukemia in a dog. J Am
• Internet resources: Rhodesian Ridgeback Club of the United
Vet Med Assoc. 1990 Jan 1;196(1):110-2.
States: www.rrcus.org 24. Simpson ST, Braund KG: Myotonic dystrophy-like disease in a dog. J Am
RRCUS Health Website: www.rhodesianridgebackhealth.org Vet Med Assoc. 1985 Mar 1;186(5):495-8.
Rhodesian Ridgeback Club of Canada: www.rrclubofcanada.org 25. Crow SE, Allen DP, Murphy CJ, et. al.: Concurrent renal
Rhodesian Ridgeback Club of Great Britain: adenocarcinoma and polycythemia in a dog. J Am Anim Hosp Assoc. 1995
www.rhodesianridgebacks.org Jan-Feb;31(1):29-33.
26. Banks TA, Straw RC: Multilobular osteochondrosarcoma of the hard
References palate in a dog. Aust Vet J. 2004 Jul;82(7):409-12.
27. Yeomans SM: SHORT PAPER - extensive spinal meningioma in a young
1. Pethick BJ, Brown DS: Rhodesian Ridgeback Club of the United States,
dog. J Comp Pathol. 2000 May;122(4):303-6.
Inc. 1996 National Health Survey Update. April 2001.
28. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
2. Hillbertz NH, Andersson G: Autosomal dominant mutation causing the
Book House, NY 2006. p. 209-213.
dorsal ridge predisposes for dermoid sinus in Rhodesian ridgeback dogs. J
Small Anim Pract. 2006 Apr;47(4):184-8.
3. Salmon Hillbertz NH, Isaksson M, Karlsson EK, et. al.: Duplication of FGF3,
FGF4, FGF19 and ORAOV1 causes hair ridge and predisposition to dermoid
sinus in Ridgeback dogs. Nat Genet. 2007 Nov;39(11):1318-20.
4. Karlsson EK, Baranowska I, Wade CM, et. al.: Efficient mapping of
mendelian traits in dogs through genome-wide association. Nat Genet.
2007 Nov;39(11):1321-8.
5. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
6. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
7. Neff M: Personal communication. UC-Davis Veterinrary Genetics
Laboratory. May, 2007.
8. Mischke R, Kühnlein P, Kehl A, et. al.: G244E in the canine factor IX
gene leads to severe haemophilia B in Rhodesian Ridgebacks. Vet J. 2011
Jan;187(1):113-8.
9. Sist MD, Refsal KR, & Nachreiner RF: A Laboratory Survey of
Autoimmune Thyroiditis and Hypothyroidism in Selected Sight Hound
Breeds. Proceedings, 2009 Tufts’ Canine and Feline Breeding and Genetics
Conference. 2009.
10. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
11. Hillbertz NH: Inheritance of dermoid sinus in the Rhodesian ridgeback. J
Small Anim Pract. 2005 Feb;46(2):71-4.
12. Kasa F, Kasa G, Kussinger S: Dermoid sinus in a Rhodesian ridgeback.
Case report. Tierarztl Prax. 1992 Dec;20(6):628-31.
13. Antin IP: Dermoid sinus in a Rhodesian Ridgeback dog. J Am Vet Med
Assoc. 1970 Oct 1;157(7):961-2.
14. Mann GE, Stratton J: Dermoid sinus in the Rhodesian Ridgeback. J Small
Anim Pract. 1966 Oct;7(10):631-42.
15. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
16. Baker-Gabb M, Hunt GB, France MP: Soft tissue sarcomas and mast cell
tumours in dogs; clinical behaviour and response to surgery. Aust Vet J.
2003 Dec;81(12):732-8.
17. Johnsen DA, Maggs DJ, Kass PH: Evaluation of risk factors for
development of secondary glaucoma in dogs: 156 cases (1999-2004). J Am
394
Rottweiler
well muscled and slightly arched without throatiness. The topline
is level. The thorax is deep and broad, and the ribs well sprung.
Slight tuck up in the abdomen is standard. In North America, the
tail is normally closely docked. The tail is carried slightly above
horizontal while moving. Limbs are straight and heavily boned. Feet
are compact, and round with well-arched toes. Dewclaws may be
removed. Nails are black and the pads are thick and tough.
Cranial Cruciate Ligament (ACL) Rupture: Traumatic tearing Multicentric Lymphoma (Lymphosarcoma): Malignant cancer
of the ACL in the stifle, causing lameness and secondary arthritis. of lymphocytes, expecially B-cells in the breed. Studies show an
Treat with surgery. Dorn reports a 2.19x odds ratio versus increased prevalence in the breed, with a 6.01x odds ratio versus
other breeds. Affected dogs have a significantly greater tibial other breeds. Treatment is with chemotherapy. Reported at a
plateau angle (TPA). TPA measurements may be helpful to screen frequency of 3.3% in the Rottweiler Health Foundation Health
prospective breeding dogs. Reported at a frequency of 9.1% in the Survey.7,19,20,21
Rottweiler Health Foundation Health Survey.6,7,8
Gastric Dilation/Volvulus (GDV, Bloat): Polygenically inherited,
Cataracts: Posterior polar cataracts predominate in the breed. life-threatening twisting of the stomach within the abdomen.
Identified in 8.22% of Rottweilers CERF-examined by veterinary Requires immediate veterinary attention. There is a 3.9% lifetime
ophthalmologists between 2000-2005. Possible autosomal risk of developing GDV in Rottweilers. Risk of death from GDV
dominant inheritance, with incomplete penetrance. Reported at after prophylactic gastropexy decreased 2.2x fold. Reported at a
a frequency of 6.6% in the Rottweiler Health Foundation Health frequency of 2.6% in the Rottweiler Health Foundation Health
Survey. CERF does not recommend breeding any Rottweiler with a Survey.7,22,23
cataract.7,9,10
Umbilical Hernia: Congenital opening in the body wall from
Hypothyroidism: Inherited autoimmune thyroiditis. 7.7% positive where the umbilical cord was attached. Correct surgically if
for thyroid autoantibodies based on testing at Michigan State large. Reported at a frequency of 2.3% in the Rottweiler Health
University. (Ave. for all breeds is 7.5%). Reported at a frequency of Foundation Health Survey.7
7.2% in the Rottweiler Health Foundation Health Survey.7,11,12
Inflammatory Bowel Disease (IBD)/Protein-Losing Enteropathy
Osteosarcoma (OSA): Malignant bone cancer. Rottweilers are a (PLE): Immune mediated inflammatory disease of the intestines
breed with a predisposition for developing osteosarcoma versus resulting in malabsorbtion. Rottweilers can present with a severe
other breeds. Mean age of appendicular OSA in the breed is 8.3 years, form of protein-losing enteropathy due to lymphoplasmacellular
with preference for the forelimbs, and a breed frequency of 5.3%. enteritis, with lymphangiectasia and eosinophil infiltration. Affected
Affected Rottweilers tend to have an increased immunohistochemical dogs present with chronic diarrhea, anorexia and weight loss, and a 1
expression of p53 protein, and breed specific tumor chromosomal year survival rate of 47% despite treatment with immunosuppressive
changes. Reported at a frequency of 7.3% in the Rottweiler Health drugs. IBD is reported at a frequency of 2.1% in the Rottweiler Health
Foundation Health Survey.7,13,14,15,16 Foundation Survey.7,24,25
Panosteitis: Self-limiting disorder of intermittent lameness Idiopathic Epilepsy: Inherited seizures can be generalized or partial
involving the diaphyseal and metaphyseal areas of the tubular seizures. Control with anticonvulsant medication. Reported at a
long bones in young dogs prior to skeletal maturation. Reported frequency of 2.0% in the Rottweiler Health Foundation Health
at a frequency of 5.0% in the Rottweiler Health Foundation Health Survey.7
Survey.7
Demodicosis, Generalized: Overgrowth of demodex mites in
Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis hair follicles due to an underlying immunodeficiency. Causes hair
and pyotraumatic dermatitis. Food allergy reported at a frequency loss and inflammation. Reported at a frequency of 1.9% in the
of 5.0%, and inhalant at 3.2% in the Rottweiler Health Foundation Rottweiler Health Foundation Health Survey.7
Health Survey.7
Persistent Pupillary Membranes: Strands of fetal remnant
Sebaceous Cysts: Benign skin cysts filled with sebum. Reported at connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
a frequency of 4.7% in the Rottweiler Health Foundation Health later three forms can impair vision, and dogs affected with these
Survey.7 forms should not be bred. Identified in 1.42% of Rottweilers CERF
examined by veterinary ophthalmologists between 2000-2005.9
396
Cryptorchidism: Retained testicles. Can be unilateral or bilateral. Hypoadrenocorticism (Addison’s Disease): Immune-mediated
Reported at a frequency of 1.3% in the Rottweiler Health destruction of the adrenal glands. Cited as a breed at significantly
Foundation Health Survey.7 higher risk. Treat with life-long medication. Unknown mode of
inheritance.37
Intervertebral Disc Disease (IVDD): Expulsion of disc material
into the spinal cord causing pain, and spinal weakness or paralysis. Juvenile Nephropathy: Young affected Rottweilers present with
Requires immediate veterinary attention. Reported at a frequency severe polyuria and polydipsia, and progress to chronic renal failure.
of 1.3% in the Rottweiler Health Foundation Health Survey.7 Histopathology included immature glomeruli and/or tubules, and
persistent mesenchyme. A type IV collagen defect is suspected.
Retinal Dysplasia: Retinal folds, geographic, and generalized Undetermined mode of inheritance.38,39,40
retinal dysplasia with detachment are recognized in the breed.
Can progress to blindness. Reported in 1.05% of Rottweilers Calcinosis Circumscripta: Calcinosis circumscripta is an
CERF-examined by veterinary ophthalmologists between uncommon syndrome of dystrophic, metastatic or iatrogenic
2000-2005.9 mineralization of calcium salts in soft tissues. Lesions usually occur
on the hind feet or tongue in 1-4 year old dogs. Thirteen percent of
Corneal Dystrophy: Rottweilers can have an epithelial/stromal canine cases occur in Rottweilers.41
form of corneal dystrophy. Identified in 0.98% of Rottweilers CERF
examined by veterinary ophthalmologists between 2000-2005.9 Bronchiectasis: Rottweilers in Brazil have been reported with
severe diffuse bronchiectasis with a history of chronic cough,
Entropion: A rolling in of the eyelids that can cause corneal respiratory distress, and progressive weight loss. Radiographic signs
irritation and ulceration. Reported in 0.73% of Rottweilers include lung lob consolidation, mild pleural effusion, and bilateral,
CERF-examined by veterinary ophthalmologists between diffuse saccular bronchiectasis.42
2000-2005. Dorn reports a 1.53x odds ratio versus other breeds.6,9
Neuronal Vacuolation and Spinocerebellar Degeneration: Rare,
Progressive Retinal Atrophy (PRA): Inherited degeneration of the inherited disorder of Rottweilers presenting with generalized
retina resulting in blindness. CERF does not recommend breeding weakness, ataxia, and laryngeal paralysis starting at six weeks of
any Rottweiler with PRA. Undetermined mode of inheritance in the age, and progressing to severe placing deficits, knuckling, severe
breed.9 ataxia, and quadraparesis by eight months of age. Pathology
includes intracytoplasmic neuronal vacuolation in the cerebellar
Susceptibility to Parvovirus Infection: Rottweilers have a 6.0x roof nuclei and extrapyramidal system, and symmetrical spinal cord
odds ratio for parvovirus enteritis versus other breeds. This is axonal degeneration. Undetermined mode of inheritence.43,44,45
assumed to be due to an inherited immune impairment.26
Neuroaxonal Dystrophy: Rare, inherited disorder of Rottweilers
Hypereosinophilia: Rottweilers are a breed found with presenting with progressive four limb ataxia and head tremors of
higher frequencies of hypereosinophilia. Causes include several months to years duration. There is no weakness associated
pulmonary infiltrates with eosinophils, gastrointestinal disease, with this disorder. Pathology shows neuroaxonal dystrophy,
meningoencephalitis, and idiopathic hypereosinophilic syndrome and immunoreactivity shows disruption of axonal transport.
(IHES).27,28,29,30,31 Undetermined mode of inheritence.46,47
Metacarpal Sesamoid Disease: Young Rottweilers have a Spinal Subarachnoid Cysts/Pseudocysts: Studies show Rottweilers
propensity for lameness due to forelimb sesamoid inflammation. under 12 months of age can have a predisposition to form cystic
Lameness resolves with rest. Many Rottweilers have subclinical lesions in the subarachnoid space that can compress the spinal cord
sesamoid disease based on X-rays.32 causing weakness and ataxia. Diagnosis with CT or MRI. Treatment
is with surgery.48,49
Histiocytic Sarcomas: Rottweilers are a breed at increased risk for
developing disseminated histiocytic sarcomas of the eye, synovium, Leucoencephalomyelopathy: Rare, inherited disorder of
subcutis, extremities, spleen, lung, brain, nasal cavity, and bone Rottweilers presenting with progressive ataxia and paresis from
marrow. Histiocytic sarcoma should be considered as a differential 1.5 to 3.5 years of age. In most dogs the forelimbs were affected
diagnosis when a soft tissue mass is associated with a bone lesion prior to the hind limbs. Pathology reveals demyelinating lesions
on radiographs or myelography in Rottweilers over 5 years of age, in the cervical spinal cord and brain stem. Undetermined mode of
or with aggressive periarticular, vertebral, or proximal humeral bone inheritence.50
lesions.33,34,35
Juvenile Distal Myopathy/Muscular Dystrophy: Rare disorder
Cervical Spondylomyelopathy/Vertebral Instability (Wobbler observed in multiple Rottweilers with decreased activity, plantigrade
Syndrome): Presents with UMN spasticity and ataxia. Imaging and palmigrade stance and splayed forepaw digits. Electromyo-
studies suggest that the primary lesion is foramenal stenosis and graphy reveals a primary myopathy. Pathology revealed myofiber
intervertebral instability at C6-7. MRI is superior to myelography atrophy of the distal muscles.51
in determining site, severity, and nature of the spinal cord
compression. Seen an an increased frequency versus other breeds. Distal Sensorimotor Polyneuropathy: Rare, slowly progressive
Undetermined mode of inheritance.36 paraparesis that progresses to tetraparesis, spinal hyporeflexia
and hypotonia, and appendicular muscle atrophy in 1.5 to 4 year
397
old Rottweilers. Histopathology suggests a dying-back distal 5. Malm S, Fikse WF, Danell B, et. al.: Genetic variation and genetic trends in
sensorimotor polyneuropathy.52 hip and elbow dysplasia in Swedish Rottweiler and Bernese Mountain Dog.
J Anim Breed Genet. 2008 Dec;125(6):403-12.
Brachygnathism, Ciliary Dyskenesis, Deafness, Hemivertebra, 6. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
Hypertrophic Osteodystrophy, Incomplete Ossification veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
of the Humeral Condyle, Leukodystrophy, Lymphedema, 2000.
7. Rottweiler Health Foundation, Slater MR: Rottweiler Health Foundation
Microphthalmia, Oligodontia, Prognathism, Seasonal Flank
Health Survey. 2001.
Alopecia, Spinal Muscular Atrophy, Ulcerative Keratitis,
8. Morris E, Lipowitz AJ: Comparison of tibial plateau angles in dogs with
Vasculitis, Vitiligo, von Willebrand’s Disease, and Wry Mouth are and without cranial cruciate ligament injuries. J Am Vet Med Assoc. 2001
reported.53 Feb 1;218(3):363-6.
9. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Isolated Case Studies College of Veterinary Ophthalmologists. ACVO, 2007.
Aortic Bulb/Valve Mineralization: Seven of 20 affected dogs were 10. Bjerkas E, Bergsjo T: Hereditary cataract in the Rottweiler dog. Progress
in Veterinary and Comparative Ophthalmol 1991;1:7.
Rottweilers in one study. The mineralization is visible radiographi-
11. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum
cally, but does not cause clinical signs.54
thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
Narcolepsy: Case report of a one year old female Rottweiler with
12. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
narcolepsy and cataplexy responsive to imipramine.55 for Population and Animal Health, Michigan State University. April, 2007.
13. Misdorp W, Hart AA: Some prognostic and epidemiologic factors in
Congenital Holoprosencephaly/Otocephaly: A stillborn Rottweiler canine osteosarcoma. J Natl Cancer Inst. 1979 Mar;62(3):537-45.
puppy was born with severe craniofacial malformations including 14. Loukopoulos P, Thornton JR, Robinson WF: Clinical and pathologic
absence of the eyes, upper and lower jaws, mouth, teeth and relevance of p53 index in canine osseous tumors. Vet Pathol. 2003
tongue. Repeat breedings of the parents produced similarly affected May;40(3):237-48.
pups.56 15. Rosenberger JA, Pablo NV, Crawford PC, et. al.: Prevalence of and
intrinsic risk factors for appendicular osteosarcoma in dogs: 179 cases
(1996-2005). J Am Vet Med Assoc. 2007 Oct 1;231(7):1076-80.
Genetic Tests 16. Thomas R, Wang HJ, Tsai PC, et. al.: Influence of genetic background on
Tests of Genotype: None tumor karyotypes: evidence for breed-associated cytogenetic aberrations in
canine appendicular osteosarcoma. Chromosome Res. 2009;17(3):365-77.
Tests of Phenotype: CHIC Certification: Required testing includes 17. Wisner ER, Berry CR, Morgan JP, et. al.: Osteochondrosis of the lateral
hip and elbow radiographs, CERF eye examination, and cardiac trochlear ridge of the talus in seven Rottweiler dogs. Vet Surg. 1990
evaluation. (See CHIC website; www.caninehealthinfo.org). Nov-Dec;19(6):435-9.
18. Kienle RD, Thomas WP, Pion PD: The natural clinical history of canine
Recommended thyroid profile including autoantibodies, and patella congenital subaortic stenosis. J Vet Intern Med. 1994 Nov-Dec;8(6):423-31.
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study of the incidence and prognostic factors of multicentric lymphoma
in dogs (1998-2000). J Vet Med A Physiol Pathol Clin Med. 2002
Miscellaneous Oct;49(8):419-24.
• Breed name synonyms: Rottweiler Metzgerhund (means butcher 20. Pastor M, Chalvet-Monfray K, Marchal T, et. al.: Genetic and
dog) Rottie, Rottwieler. environmental risk indicators in canine non-Hodgkin’s lymphomas:
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), breed associations and geographic distribution of 608 cases
ANKC (Australian National Kennel Club), NKC (National Kennel Club). diagnosed throughout France over 1 year. J Vet Intern Med. 2009
• AKC rank (year 2008): 14 (13,059 dogs registered) Mar-Apr;23(2):301-10.
• Internet resources: American Rottweiler Club (AKC parent 21. Lobetti RG: Lymphoma in 3 related Rottweilers from a single household.
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Rottweiler Club of Canada: www.rottclub.ca 22. Glickman LT, Glickman NW, Schellenberg DB, et. al.: Incidence of and
breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet
The Rottweiler Club (UK): www.therottweilerclub.co.uk
Med Assoc. 2000 Jan 1;216(1):40-5.
United States Rottweiler Club: www.usrconline.org
23. Ward MP, Patronek GJ, Glickman LT: Benefits of prophylactic gastropexy
Rottweiler Health Foundation: www.rottweilerhealth.org for dogs at risk of gastric dilatation-volvulus. Prev Vet Med. 2003 Sep
12;60(4):319-29.
References 24. Dijkstra M, Kraus JS, Bosje JT, et. al.: Protein-losing enteropathy in
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010. Rottweilers. Tijdschr Diergeneeskd. 2010 May 15;135(10):406-12.
2. Meyer-Lindenberg A, Langhann A, Fehr M, et. al.: Prevalence of 25. Lecoindre P, Chevallier M & Guerret S: Protein-losing enteropathy of
fragmented medial coronoid process of the ulna in lame adult dogs. Vet non neoplastic origin in the dog: a retrospective study of 34 cases. Schweiz
Rec. 2002 Aug 24;151(8):230-4. Arch Tierheilkd. 2010 Mar;152(3):141-6.
3. LaFond E, Breur GJ & Austin CC: Breed susceptibility for 26. Glickman LT, Domanski LM, Patronek GJ, et. al.: Breed-related risk
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002 factors for canine parvovirus enteritis. J Am Vet Med Assoc. 1985 Sep
Sep-Oct;38(5):467-77. 15;187(6):589-94.
4. Heine A, Hamann H, Tellhelm B, et. al.: Estimation of population genetic 27. Lilliehook I, Tvedten H: Investigation of hypereosinophilia and potential
parameters and breeding values for elbow dysplasia in Rottweilers. Berl treatments. Vet Clin North Am Small Anim Pract. 2003 Nov;33(6):1359-78,
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28. Sykes JE, Weiss DJ, Buoen LC, et. al.: Idiopathic hypereosinophilic
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syndrome in 3 Rottweilers. J Vet Intern Med. 2001 Mar-Apr;15(2):162-6. 53. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
29. Olivier AK, Parkes JD, Flaherty HA, et. al.: Idiopathic eosinophilic Ackerman. p. 235. AAHA Press, 1999.
meningoencephalomyelitis in a Rottweiler dog. J Vet Diagn Invest. 2010 54. Douglass JP, Berry CR, Thrall DE, Malarkey DE, Spaulding KA:
Jul;22(4):646-8. Radiographic features of aortic bulb/valve mineralization in 20 dogs. Vet
30. Lyles SE, Panciera DL, Saunders GK, et. al.: Idiopathic eosinophilic Radiol Ultrasound. 2003 Jan-Feb;44(1):20-7.
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Jul-Aug;23(4):818-23. narcolepsy. J Am Vet Med Assoc. 1989 Mar 15;194(6):791-2.
31. James FE & Mansfield CS: Clinical remission of idiopathic hypereosino- 56. Martínez JS, Velázquez IR, Reyes H, et. al.: Congenital holoprosen-
philic syndrome in a Rottweiler. Aust Vet J. 2009 Aug;87(8):330-3. cephaly with severe otocephaly in a rottweiler puppy. Vet Rec. 2006 Apr
32. Read RA, Black AP, Armstrong SJ, et. al.: Incidence and clinical 15;158(15):518-9.
significance of sesamoid disease in rottweilers. Vet Rec. 1992 Jun 57. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
13;130(24):533-5. Book House, NY 2006. p. 314-318.
33. Affolter VK, Moore PF: Localized and disseminated histiocytic sarcoma
of dendritic cell origin in dogs. Vet Pathol. 2002 Jan;39(1):74-83.
34. Schultz RM, Puchalski SM, Kent M, et. al.: Skeletal lesions of
histiocytic sarcoma in nineteen dogs. Vet Radiol Ultrasound. 2007
Nov-Dec;48(6):539-43.
35. Naranjo C, Dubielzig RR, & Friedrichs KR: Canine ocular histiocytic
sarcoma. Vet Ophthalmol. 2007 May-Jun;10(3):179-85.
36. Casimiro da Costa R: Cervical Spondylomyelopathy: Recent Advances.
Proceedings, World Small Animal Veterinary Association World Congress.
2009.
37. Peterson ME, Kintzer PP, Kass PH: Pretreatment clinical and laboratory
findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). J Am
Vet Med Assoc. 1996 Jan 1;208(1):85-91.
38. Peeters D, Clercx C, Michiels L, et. al.: Juvenile nephropathy in a
boxer, a rottweiler, a collie and an Irish wolfhound. Aust Vet J. 2000
Mar;78(3):162-5.
39. Cook SM, Dean DF, Golden DL, et. al.: Renal failure attributable to
atrophic glomerulopathy in four related rottweilers. J Am Vet Med Assoc.
1993 Jan 1;202(1):107-9.
40. Wakamatsu N, Surdyk K, Carmichael KP, et. al.: Histologic and
ultrastructural studies of juvenile onset renal disease in four Rottweiler
dogs. Vet Pathol. 2007 Jan;44(1):96-100.
41. Tafti AK, Hanna P, Bourque AC: Calcinosis circumscripta in the dog: a
retrospective pathological study. J Vet Med A Physiol Pathol Clin Med. 2005
Feb;52(1):13-7.
42. Duarte R: Severe Bronchiectasis in Rottweilers: An Unnamed Disease.
Proceedings, 2009 World Small Animal Veterinary Association World
Congress. 2009.
43. Salvadori C, Tartarelli CL, Baroni M, et. al.: Peripheral nerve pathology
in two rottweilers with neuronal vacuolation and spinocerebellar
degeneration. Vet Pathol. 2005 Nov;42(6):852-5.
44. Kortz GD, Meier WA, Higgins RJ, et. al.: Neuronal vacuolation and
spinocerebellar degeneration in young Rottweiler dogs. Vet Pathol. 1997
Jul;34(4):296-302.
45. Mahony OM, Knowles KE, Braund KG, et. al.: Laryngeal paralysis-
polyneuropathy complex in young Rottweilers. J Vet Intern Med. 1998
Sep-Oct;12(5):330-7.
46. Siso S, Ferrer I, Pumarola M: Juvenile neuroaxonal dystrophy in a
Rottweiler: accumulation of synaptic proteins in dystrophic axons. Acta
Neuropathol (Berl). 2001 Nov;102(5):501-4.
47. Chrisman CL, Cork LC, Gamble DA: Neuroaxonal dystrophy of Rottweiler
dogs. J Am Vet Med Assoc. 1984 Feb 15;184(4):464-7.
48. Gnirs K, Ruel Y, Blot S, et. al.: Spinal subarachnoid cysts in 13 dogs. Vet
Radiol Ultrasound. 2003 Jul-Aug;44(4):402-8.
49. Jurina K, Grevel V: Spinal arachnoid pseudocysts in 10 rottweilers. J
Small Anim Pract. 2004 Jan;45(1):9-15.
50. Wouda W, van Nes JJ: Progressive ataxia due to central demyelination
in Rottweiler dogs. Vet Q. 1986 Apr;8(2):89-97.
51. Hanson SM, Smith MO, Walker TL, et. al.: Juvenile-onset distal myopathy
in Rottweiler dogs. J Vet Intern Med. 1998 Mar-Apr;12(2):103-8.
52. Braund KG, Toivio-Kinnucan M, Vallat JM, et. al.: Distal sensorimotor
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May;31(3):316-26.
399
Saint Bernard
Longevity: 8-9 years
References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
4. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
5. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
6. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
7. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
8. Glickman LT, Glickman NW, Perez CM, et. al.: Analysis of risk factors for
gastric dilatation and dilatation-volvulus in dogs. J Am Vet Med Assoc.
1994 May 1;204(9):1465-71.
9. Duval JM, Budsberg SC, Flo GL, et. al.: Breed, sex, and body weight as risk
factors for rupture of the cranial cruciate ligament in young dogs. J Am Vet
Med Assoc. 1999 Sep 15;215(6):811-4.
10. Bech-Nielsen S, Haskins ME, Reif JS, et. al.: Frequency of osteosarcoma
among first-degree relatives of St. Bernard dogs. J Natl Cancer Inst. 1978
Feb;60(2):349-53.
11. Taylor GN, Lloyd RD, Mays CW, et. al.: Relationship of natural
incidence and radiosensitivity for bone cancer in dogs. Health Phys. 1997
Oct;73(4):679-83.
12. Egenvall A, Nødtvedt A & von Euler H: Bone tumors in a population of
400 000 insured Swedish dogs up to 10 y of age: incidence and survival.
Can J Vet Res. 2007 Oct;71(4):292-9.
13. Bishop L: Ultrastructural investigations of cardiomyopathy in the dog. J
Comp Pathol. 1986 Nov;96(6):685-98.
14. Patterson EN: Clinical Characteristics and Inheritance of Idiopathic
Epilepsy. Proceedings, 2007 Tufts’ Canine and Feline Breeding and Genetics
Conference. 2007.
15. Jones BR, Alley MR: Primary idiopathic hypoparathyroidism in St.
Bernard dogs. N Z Vet J. 1985 Jun;33(6):94-7.
16. Russell NJ, Bond KA, Robertson ID, et. al.: Primary hypoparathy-
402
Saluki
Points of Conformation: Long, with a very lean athletic build,
exceptionally smooth and graceful bounding movements
characterize Saluki dogs. Their ability to accelerate very quickly to
speed allows them to be effective in gazelle hunts. The skull is long
and narrow, the stop is not very pronounced, and the nose is either
black or liver colored. The eyes are large, oval and colored dark
brown to hazel. The ears are long, pendulous and fine-leathered
with very long feathers. The neck is long and muscular, the thorax is
somewhat narrow but very deep. The legs are straight and long. Tarsi
are placed low on the hind limb. Feet are moderately arched, with
good feathering between the toes. The inner digits can be longer
The Breed History than the outer digits. The tail is long, tapering, feathered on the
This breed is thought to be one of the most ancient breeds of underside, and carried in a curve. The back is broad with a slightly
domesticated dogs. Excavations of ancient settlements (6500 BC, arched loin. They normally have prominent hip bones and the caudal
Sumerian empire), and Egyptian tomb carvings of 2100 BC reflect rib cage is also clearly evident when they are in fit condition.
the presence of a distinctly “Saluki type” dog. They were highly
esteemed and mummified remains of this type of dog have been
found, attesting to their important status in Egyptian society.
Recognized Behavior Issues and Traits
Reported breed characteristics include: Very athletic, and require
Muslim religion classed dogs as unclean, and termed them kelb but
lots of exercise and activity, friendly, clean, and they enjoy a soft
the Saluki on the other hand, was termed the “noble one” or El Hor,
bed inside the home. Saluki dogs are intelligent. Training should be
and accorded sacred status.
started early, and socialization should be emphasized to counteract
Originating in the region that includes Egypt, Arabia, Syria any nervous or shy/high strung tendencies. Introduce them to
and Persia, and accompanying the Bedouin tribes, the first children, small dogs and household cats early. They thrive on close
specimens were brought to England in the year 1840. The smooth human companionship. They are sensitive, and obedience training
(non-feathered) variety of Saluki is very much like the Sloughi dog. is strongly recommended. Free exercise should only occur in a
The latter was thought to have originated from the town of Saloug high fenced enclosure. They are somewhat independent minded.
in Yemen. The Saluki likely originated in the town of Saluk, Yemen. Though they do not like fetch type activities, they love to chase, so
The AKC recognized this breed in 1927. care should be taken to keep small animals such as cats out of their
reach. Destructive behavior can occur if they become bored. Their
coat has average care needs and they are average shedders. They will
Breeding for Function alarm bark, but are not considered defense dogs. Some recommend
Because of the harsh climate in which these dogs were kept, they
a snood, or ear hood to help prevent soiling of hair at mealtime.
became hardy and tolerated temperature extremes. They were also
particularly sure-footed in rough going. Their speed, agility and
endurance allowed them to hunt all day over difficult terrain. Arabs Normal Physiologic Variations
used these dogs to hunt gazelle, though they were also capable Thyroid Hormone Levels: Sighthounds have lower normal ranges
hunters of foxes, wild boar, and hares. In Europe and England for T4 and T3 concentrations compared to other breeds. Median
the sport of saluki racing (which required clearing hurdles) was (reference limits) serum concentrations in Salukis are:1,2
undertaken. They are found nowadays mostly in companionship Total T(4): 13.0 nmol/L (2.8 to 40.0 nmol/L)
and lure coursing or open field coursing roles. Free T(4): 12.0 pmol/L (2.0 to 30.3 pmol/L)
Total T(3): 1.0 nmol/L (0.4 to 2.1 nmol/L)
Physical Characteristics Free T(3): 4.0 pmol/L (1.6 to 7.7 pmol/L)
Height at Withers: female 22-26” (56-66 cm), male 23-28” TSH: 0.18 ng/mL (0 to 0.86 ng/mL)
(58.5-71 cm)
Drug Sensitivities
Weight: females 31-40 lb (14-18 kg), males 40-55 lb (18-25 kg). Anesthesia: Sight hounds require particular attention during
anesthesia. Their lean body conformation with high surface-area-to-
Coat: Their coat is fine and silky, shorter over the body and volume ratio predisposes them to hypothermia during anesthesia.
well-developed feathers are present. Colors include white, cream, Impaired biotransformation of drugs by the liver results in prolonged
golden, red, fawn, grizzle and tan, black-and-tan, and tri-color. A recovery from barbiturate and thiobarbiturate intravenous
smooth variety of this breed has the same body coat but without anesthetics. Propofol, and ketamine/diazepam combination are
the feathers. recommended induction agents.3
Longevity: 12 years
403
Inherited Diseases Ceroid Lipofuscinosis: Rare, fatal degenerative neurological
disease. Onset 1-2 years. Unknown mode of inheritance.11
Hip Dysplasia: Polygenically inherited trait causing degenerative
joint disease and hip arthritis. OFA reports 1.6% affected.4
Brachygnathism, Color Dilution Alopecia, and Prognathism, are
Elbow Dysplasia: Polygenically inherited trait causing elbow reported.12
arthritis. Too few Salukis have been screened by OFA to determine
an accurate frequency.4 Isolated Case Studies
Motor Neuron Abiotrophy: A nine-week-old saluki puppy
Patella Luxation: Polygenically inherited laxity of patellar presented for progressive, generalized weakness and bilateral
ligaments, causing luxation, lameness, and later degenerative joint forelimb deformities. Histopathology revealed a diffuse,
disease. Treat surgically if causing clinical signs. Too few Salukis symmetrical, degenerative motor neuronopathy of the ventral horn
have been screened by OFA to determine an accurate frequency.4 of the spinal cord.13
405
Samoyed
tail reaches the tarsus when held down, is profusely covered with
hair, and when moving or alert, should be over the back and to one
side. The proper gait is a trot, not a pace, and strides are quick and
agile; springiness and speed are valued.
408
Schipperke
makes the dog appear higher in the withers than it really is. Thorax
is broad and the ribs are well sprung. Though some are born tailless,
those born with tails are usually docked to within 1” of the body
wall. Dewclaws are usually removed on forelegs and are removed
from the hind limbs. Limbs are straight boned, feet are compact and
small. Nails are black. The gait is smooth, low and fast.
410
treatment of avascular necrosis of the femoral head in a dog. J Am Vet Med
Assoc. 1990 Oct 1;197(7):868-70.
4. Knowles K, Alroy J, Castagnaro M, et. al.: Adult-onset lysosomal storage
disease in a Schipperke dog: clinical, morphological and biochemical
studies. Acta Neuropathol (Berl). 1993;86(3):306-12.
5. Ellinwood NM, Wang P, Skeen T, et. al.: A model of mucopolysaccharidosis
IIIB (Sanfilippo syndrome type IIIB): N-acetyl-alpha-D-glucosaminidase
deficiency in Schipperke dogs. J Inherit Metab Dis. 2003;26(5):489-504.
6. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
7. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
9. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
10. Patterson EN: Clinical Characteristics and Inheritance of Idiopathic
Epilepsy. Proceedings, 2007 Tufts’ Canine and Feline Breeding and Genetics
Conference. 2007.
11. Ihrke PJ, Stannard AA, Ardans AA, et. al.: Pemphigus foliaceus in dogs: a
review of 37 cases. J Am Vet Med Assoc. 1985 Jan 1;186(1):59-66.
12. Kimmel SE, Ward CR, Henthorn PS, et al. Familial insulin-dependent
diabetes mellitus in samoyed dogs. J Am Anim Hosp Assoc 2002;38:235-238
13. Carlotti DN: Non-Hormonal Alopecia. Proceedings, World Small Animal
Veterinary Association Congress, 2005.
14. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 236 AAHA Press, 1999.
15. Frykman OF: Spinal arachnoid cyst in four dogs: diagnosis,
surgical treatment and follow-up results. J Small Anim Pract. 1999
Nov;40(11):544-9.
16. Delauche AJ, Cuddon PA, Podell M, et. al.: Nemaline rods in canine
myopathies: 4 case reports and literature review. J Vet Intern Med. 1998
Nov-Dec;12(6):424-30.
17. Stephens JA, Parnell NK, Clarke K, et. al.: Subcutaneous emphysema,
pneumomediastinum, and pulmonary emphysema in a young schipperke. J
Am Anim Hosp Assoc. 2002 Mar-Apr;38(2):121-4.
18. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 588-592.
411
Scottish Deerhound
and straight boned with a lithe build, and feet are compact with
well-arched toes, with little hair. The topline is arched through the
loin, and drops off to the tail, which is long and tapering, reaching
about 1/2 way down the metatarsals, and is gently curved. The gait
is strong, long and low and appears effortless.
Inhalant Allergies (Atopy): Presents with pruritis and Congenital Hypothyroidism: Two Scottish Deerhound full-siblings
pyotraumatic dermatitis (hot spots). Reported at a frequency of 6% had clinical and pathological features of congenital non-goitrous
in the 2000 SDCA Health Survey.7 hypothyroidism. The puppies were smaller, had shorter limbs and
shorter, broader heads than their littermates. They also had histories
Dilated Cardiomyopathy (DCM)/Atrial Fibrillation: A high of weakness, difficulty in walking and somnolence. Radiographically,
percentage of affected dogs initially present with atrial fibrillation, epiphyseal growth centers were absent. Both had depressed serum
and progress to biventricular dilated cardiomyopathy. Clinical signs thyroxine (T4) levels and one did not respond to exogenous thyroid
include sudden death, passing out, exercise intolerance, pulmonary stimulating hormone.20
edema, or ascites. Average age of onset of heart failure is 6-1/2
years of age. Not all dogs with atrial fibrillation will develop DCM, Orthostatic Tremor: A four-year-old male Scottish deerhound was
but these dogs should be carefully followed for the development of presented with a two-year history of pelvic limb tremors, which
DCM and perhaps should be held out of breeding programs. DCM progressed to the thoracic limbs. Primary OT was diagnosed from
occurs in male Scottish Deerhounds 4x the frequency in females. the clinical signs, typical electrophysiological findings and the
DCM is reported at a frequency of 5-8%, heart failure at 5% and absence of other identifiable disease.21
arrhythmia at 4% in the 2000 SDCA Health Survey. The mode of
inheritance is not determined.7,11
Genetic Tests
Hypothyroidism: Inherited autoimmune thyroiditis. 4.5% positive Tests of Genotype: Direct genetic test for Factor VII deficiency is
for thyroid autoantibodies based on testing at Michigan State available from PennGen and VetGen.
University. (Ave. for all breeds is 7.5%). Reported at a frequency of
Tests of Phenotype: CHIC Certification: Required testing
4% in the 2000 SDCA Health Survey.7,12,13
includes a congenital cardiac evaluation by a cardiologist with
Portosystemic Shunt (PSS, Liver Shunt): Abnormal blood vessels echocardiography, and direct test for Factor VII deficiency. Optional
connecting the systemic and portal blood flow can be intrahepatic recommended test is serum bile acid test at Texas A&M. (See CHIC
website; www.caninehealthinfo.org).
413
Recommend hip and elbow radiographs, CERF eye examination, Scottish Deerhound puppies. Aust Vet J. 1988 Dec;65(12):386-9.
patella evaluation, and thyroid profile including autoantibodies. 21. Platt SR, De Stefani A, & Wieczorek L: Primary orthostatic tremor in a
Scottish deerhound. Vet Rec. 2006 Oct 7;159(15):495-6.
22. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Miscellaneous Book House, NY 2006. p. 218-222.
• Breed name synonyms: Royal Dog of Scotland, Rough
Greyhound, Highland Deerhound (all historical), Deerhound,
Scotch Greyhound.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
• AKC rank (year 2008): 133 (153 dogs registered)
• Internet resources: Scottish Deerhound Club of America:
www.deerhound.org
The Deerhound Club (UK): www.deerhound.co.uk
References
1. Kintzer PP & Peterson ME: Progress in the Diagnosis and Treatment of
Canine Hypothyroidism. 2007. Proceedings, ACVIM 2007
2. Vollmar, A: Echocardiographic examinations in Deerhounds, reference
values for echocardiography. Kleintierpraxis. 1998. 43: 7, 497-508.
3. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
4. Court MH: Anesthesia of the sighthound. Clin Tech Small Anim Pract
1999 Feb;14(1):38-43.
5. Huff A, Seng A, Tuneva J, et. al.: Molecular, Metabolic, and Hematologic
Screening for Hereditary Diseases at the University of Pennsylvania
(PennGen). Proceedings, 2007 Tufts’ Canine and Feline Breeding and
Genetics Conference. 2007.
6. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
7. Dillberger J: SDCA Health Survey. Scottish Deerhound Club of America.
2000.
8. Phillips J: Genetic analysis of osteosarcoma in the Scottish Deerhound.
Proceedings Veterinary Cancer Society Meeting. 2003.
9. Phillips JC, Stephenson B, Hauck M, et. al.: Heritability and segregation
analysis of osteosarcoma in the Scottish deerhound. Genomics. 2007
Sep;90(3):354-63.
10. Phillips JC, Lembcke L & Chamberlin T: A novel locus for canine
osteosarcoma (OSA1) maps to CFA34, the canine orthologue of human
3q26. Genomics. 2010 Oct;96(4):220-7.
11. Meurs K: Inherited Heart Disease in the Dog. Proceedings Tufts’ Canine
and Feline Breeding and Genetics Conference, 2003.
12. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
13. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
14. Maxwell A, Hurley K, Burton C, et. al.: Reduced Serum Insulin-Like
Growth Factor (IGF) and IGF-Binding Protein-3 Concentrations in Two
Deerhounds with Congenital Portosystemic Shunts. J Vet Internal Med.
2000: 14 (5) : 542-545.
15. Kinzel S, Hein S, Buecker A, et. al.: Diagnosis and Treatment of
Arthrosis of Cervical Articular Facet Joints in Scottish Deerhounds: 9 Cases
(1998-2002). J Am Vet Med Assoc. Nov 1’03; 223[9]:1311-1315.
16. Osborne CA, Sanderson SL, Lulich JP, et. al.: Canine cystine urolithiasis.
Vet. Clinics of North America: Small Animal Practice. 1999:29:193-211.
17. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
18. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 238. AAHA Press, 1999.
19. Breur GJ, Zerbe CA, Slocombe RF, et. al.: Clinical, radiographic,
pathologic, and genetic features of osteochondrodysplasia in Scottish
deerhounds. J Am Vet Med Assoc. 1989 Sep 1;195(5):606-12.
20. Robinson WF, Shaw SE, Stanley B, et. al.: Congenital hypothyroidism in
414
Scottish Terrier
aggression. This is also a protective dog for the home, being a keen
alarm barker. The Scottie needs firm, gentle training at an early age.
Scotties are considered a low shedder and require regular grooming
and periodic clipping. They require moderate exercise.
Cataracts: Anterior, posterior, intermediate and punctate cataracts Demodicosis: Overgrowth of demodex mites in hair follicles due to
are seen in the breed. Identified in 6.99% of Scottish Terriers CERF an underlying immunodeficiency. Dorn reports a 1.73x odds ratio of
examined by veterinary ophthalmologists between 2000-2005. developing demodectic mange versus other breeds. Reported at a
Reported at a frequency of 1.4% in the 2005 STCA Health Survey. frequency of 1.1% in the 2005 STCA Health Survey.8,24
CERF does not recommend breeding any Scottish Terrier with a
cataract.8,16 Corneal Dystrophy: Either the epithelial/stromal, or endothelial
form of corneal dystrophy can be seen in the breed. Identified
Hypothyroidism: Inherited autoimmune thyroiditis. 6.7% positive in 1.08% of Scottish Terriers CERF examined by veterinary
for thyroid autoantibodies based on testing at Michigan State ophthalmologists between 2000-2005.16
University. (Ave. for all breeds is 7.5%). Reported at a frequency of
3.9% in the 2005 STCA Health Survey.8,18,19 Distichiasis: Abnormally placed eyelashes that irritate the
cornea and conjunctiva. Can cause secondary corneal ulceration.
Transitional Cell Carcinoma (TCC, Bladder Cancer): Scottish Identified in 1.08% of Scottish Terriers CERF examined by veterinary
Terriers have an 18x greater risk of developing TCC versus ophthalmologists between 2000-2005.16
other breeds. Glickman et. al. found an increased risk for TCC in
Scottish Terriers exposed to phenoxy-based lawn herbicides, and Acquired Myasthenia Gravis: Scottish Terriers are a breed
a decreased risk for TCC in Scottish Terriers that consumed green at increased risk of developing generalized or focal acquired
leafy or yellow-orange vegetables three times a week. TCC is a myasthenia gravis. The most common presenting signs were
malignant cancer that can be controlled with surgery and piroxicam generalized weakness, with or without megaesophagus. Diagnosis
treatment. Reported at a frequency of 4.6% in the 2005 STCA is by identifying acetylcholine receptor antibodies.Undetermined
Health Survey.8,20,21,22,23 mode of inheritance.26
Hyperadrenocorticism (Cushing’s disease): Hyperfunction of the Superficial Necrolytic Dermatitis (Hepatocutaneous syndrome):
adrenal gland caused by a pituitary or adrenal tumor. Clinical signs Three Scottish Terriers were identified in a study of 36 dogs
may include increased thirst and urination, symmetrical truncal with diagnoses of superficial necrolytic dermatitis, suggesting a
alopecia, and abdominal distention. Dorn reports a 3.97x odds ratio breed prevalence. Affected dogs present with erythema, crusting,
versus other breeds. Reported at a frequency of 3.5% in the 2005 exudation, ulceration and alopecia involving footpads, peri-ocular
STCA Health Survey.8,24 or peri-oral regions, anal–genital regions, and pressure points
on the trunk and limbs. Average age of presentation is 10 years.
Vitreous Degeneration: Liquefaction of the vitreous gel which may Diagnosis is by biopsy.27
416
Brachygnathism, Copper Toxicosis, Cystinuria, Fibrinoid Recommend hip and elbow radiographs, and cardiac examination.
Leukodystrophy, Lens Luxation, Progressive Retinal Atrophy,
Renal Glycosuria, Seasonal Flank Alopecia, and Sebaceous Miscellaneous
Adenitis are reported.28 • Breed name synonyms: Scottie, Aberdeen Terrier (historical)
• Registries: CKC, AKC, UKC,, KCGB (Kennel Club of Great Britain),
Isolated Case Studies ANKC(Australian National Kennel Club), NKC (National Kennel Club)
Idiopathic Multifocal Osteopathy: Fatal disease identified in four • AKC rank (year 2008): 49 (2,429 dogs registered)
related Scottish Terriers between 16 months and 4.5 years of age • Internet resources: Scottish Terrier Club of America:
presented with reluctance to move, stiff/stilted gait, carpal valgus/ http://clubs.akc.org/stca
laxity, and drooling/dysphagia. Histopathology showed osteoclastic The Scottish Terrier Club (England): www.stcengland.co.uk
osteolysis and replacement of bone with fibrous tissue in the skull, The Canadian Scottish Terrier Club:
cervical spine, and proximal radii, ulna, and femora.29 www.canadianscottishterrierclub.org
418
Sealyham Terrier
Normal Physiologic Variations
None reported
Drug Sensitivities
None reported
Inherited Diseases
Patella Luxation: Polygenically inherited laxity of patellar ligaments,
causing luxation, lameness, and later degenerative joint disease.
Treat surgically if causing clinical signs. Too few Sealyham Terriers
The Breed History have been screened by OFA to determine an accurate frequency.1
A small town in Wales called Sealyham was the first recorded home
of the breed. In the late 1800s, crosses to breeds such as Dandie Primary Lens Luxation (PLL) and Secondary Glaucoma: An
Dinmont, Corgi, Westie, and perhaps Wirehaired Fox Terriers were autosomal recessive gene causes primary lens luxation. Homozygous
done to develop this hardy athletic stock. AKC registration first affected dogs usually develop lens luxation between 3-5 years of
occurred in 1911, and it was about that time also that the breed age. Rarely, heterozygous carriers can develop lens luxation, but
was first brought to North America. at a later age. Lens luxation can lead to secondary glaucoma and
blindness. A genetic mutation has been identified, and a genetic
Breeding for Function test is available. OFA testing shows 38% carrier, and 5% affected.
Hunting, defense, tracking of mid-sized quarry such as otter, badger Identified in 1.79% of Sealyham Terriers CERF examined by
and fox were some of the tasks these dogs were bred for. Digging veterinary ophthalmologists between 2000-2005. CERF does not
and endurance, combined with lightning speed contributed to the recommend breeding any Sealyham Terrier with lens luxation.1,2,7
success of the hunt.
Retinal Dysplasia: Autosomal recessive inheritance. Congenital
retinal folds, geographic, and generalized retinal dysplasia with
Physical Characteristics detachment is seen in Sealyham Terriers. Can progress to blindness.
Height at Withers: ideal is 10.5” (26.5 cm) Identified in 2.98% of Sealyham Terriers CERF examined by
veterinary ophthalmologists between 2000-2005. CERF does not
Weight: females 22 lb (10 kg), males 23-24 lb (10.5-11 kg). recommend breeding any Sealyham Terrier with retinal dysplasia.
There is no genetic test.2,3
Coat: White to creamy white, the coarse haircoat is variably marked
with small areas of beige or so-called lemon or badger distributed Hip Dysplasia: Polygenically inherited trait causing degenerative
mostly around the head. joint disease and hip arthritis. Too few Sealyham Terriers have been
screened by OFA to determine an accurate frequency.1
Longevity: 14-16 years.
Elbow Dysplasia: Polygenically inherited trait causing elbow
Points of Conformation: Their slightly convex skulls, moderate
arthritis. Too few Sealyham Terriers have been screened by OFA to
stop and strong jaws contribute to the tough terrier image. Dark,
determine an accurate frequency.1
deep and widely set oval eyes, black nose, and small triangular ears
folded down with fine leather characterize their faces. Tails may be
docked, and are carried vertical. A medium neck, large compact feet Disease Predispositions
with arched toes and short-coupled stocky muscular body with a Persistent Pupillary Membranes: Strands of fetal remnant
deep chest, level topline, and powerful build behind complete the connecting; iris to iris, cornea, lens, or involving sheets of tissue.
image. Their way of going is quick, agile, and straight. The later three forms can impair vision, and dogs affected with
these forms should not be bred. Identified in 5.95% of Sealyham
Recognized Behavior Issues and Traits Terriers CERF examined by veterinary ophthalmologists between
2000-2005.2
Reported breed traits include: Alert intelligence, a calculating
stubborn streak, loyalty and adaptability to both country and city Cataracts: Anterior cortex punctate, and anterior or posterior
living make them a great companion. Their fanciers sometimes cortex intermediate cataracts predominate in the breed. Identified
attribute to them a sense of humor. They thrive on close human in 3.57% of Sealyham Terriers CERF examined by veterinary
contact and lots of attention. They enjoy barking, and are of ophthalmologists between 2000-2005. CERF does not recommend
medium trainability. They need moderate exercise and are breeding any Sealyham Terrier with a cataract.2
considered low activity dogs and low shedders. Regular clipping,
grooming or plucking will keep the coat in top form.
419
Distichiasis: Abnormally placed eyelashes that irritate the cornea 4. Ackerman L: Managing Inhalant Allergies. Proceedings, Tufts Animal Expo
and conjunctiva. Can cause secondary corneal ulceration. Identified 2002.
in 3.57% of Sealyham Terriers CERF examined by veterinary 5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
ophthalmologists between 2000-2005.2 hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
Allergic Dermatitis (Atopy): Inhalant or food allergy presents with 6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
pruritis and pyotraumatic dermatitis (hot spots). Sealyham Terriers
7. Nasisse MP: Diseases of the Lens and Cataract Surgery. Proceedings,
are over-represented with atopy versus other breeds.4 Waltham/OSU Symposium, Small Animal Ophthalmology, 2001.
8. Strain GM: Deafness prevalence and pigmentation and gender
Hypothyroidism: Inherited autoimmune thyroiditis. 2.0% positive associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
for thyroid autoantibodies based on testing at Michigan State 9. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
University. (Ave. for all breeds is 7.5%).5,6 Ackerman. p 238, AAHA Press, 1999.
10. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Vitreous Degeneration: A liquefaction of the vitreous gel which Book House, NY 2006. p 424-427.
may predispose to retinal detachment resulting in blindness.
Identified in 1.90% of Sealyham Terriers CERF examined by
veterinary ophthalmologists between 2000-2005.2
Genetic Tests
Tests of Genotype: Direct genetic test for lens luxation is available
from OFA.
Miscellaneous
• Breed name synonyms: Sealyham
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 152 (56 dogs registered)
• Internet resources: American Sealyham Terrier Club:
http://clubs.akc.org/sealy
Sealyham Terrier Club of Canada:
www.sealyhamcanada.com
Sealyham Terrier Breeders Association (UK):
www.davmar.freeuk.com/sealyhambreedersassoc.html
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
3. Dietz HH: Retinal dysplasia in dogs—a review. Nord Vet Med. 1985
Jan-Feb;37(1):1-9.
420
Shetland Sheepdog
Recognized Behavior Issues and Traits
Reported breed attributes include: Their alert intelligence means
that they learn quickly, and they are also docile and quick to
obey. They are loyal and very affectionate, love to please and
need contact with their owners. An aloof attitude to strangers is
expected, but timid or snappy behavior is unacceptable. They are
alarm barkers, and noble defenders. Their training should start early,
and socialization is important. As a minimum, they require a careful
weekly grooming with prompt removal of any matting. They need
daily exercise, and for mental stimulation, active playtime should be
The Breed History integrated.
This small rough collie-type dog is likely related to the collie
(which in turn originated from the Border collie of Scotland), but Normal Physiologic Variations
though some sources report that shelties were collies selected Merle Coat Color: Caused by a dominant mutation in the SILV
for progressively smaller body stature, others claim the breed is gene. Breeding two merle dogs together should be avoided, as
distinct. The Sheltie, as the Shetland sheepdog is often called traces homozygous dogs can be born with multiple defects, including
back to the Shetland Islands off of the coast of Scotland where blindness, deafness, and heart anomalies.1
small and hardy are the trademark of all species able to survive that
harsh environment. The first AKC registration was in 1911. Hyperlipidemia: Shetland Sheepdogs can have a non-pathological
hyperlipidemia and hypercholesterolemia, that can increase with
age. This can also progress to hypertriglyceridemia.2
Breeding for Function
These dogs were bred for sheep herding work in rough
environments, and they are cherished for both their herding ability Drug Sensitivities
and their companionship. They excel in obedience trials due to their MDR1 Mutation (Ivermectin/Drug Toxicity): Autosomal
high intelligence, trainability, and willingness. Newer sports such as recessive disorder in the MDR1 gene allows high CNS drug levels
agility, tracking and performing tricks suit their talents as well. of ivermectin, doramectin, loperamide, vincristine, moxidectin, and
other drugs. Causes neurological signs, including tremors, seizures,
and coma. A genetic test is now available for the mutated gene,
Physical Characteristics showing 1.3% of Shetland sheepdogs are affected, and 10.5%
Height at Withers: 13-16” (33-40.5 cm) carrier. In Germany, 8% test homozygous affected, and 43% test as
carriers.3,4,5
Weight: females 12-16 lb (5.5-7 kg), males 14-18 lb (6-8 kg).
Coat: The double coat is thick and smooth, with a very full mane in Inherited Diseases
males. Some feathering on limbs occurs, and coat volume thickens Collie Eye Anomaly/Choroidal Hypoplasia/Coloboma (CEA/CH):
over the tail. Colors range from sable (golden brown to mahogany) Autosomal recessive disorder of eye development that can lead to
marked with white or tan to black, and blue merle. Bi-black and retinal detachment and blindness. Reported in 0.79% of Shetland
bi-blue are accepted. Brindle or white-predominant coats are sheepdogs CERF-examined by veterinary ophthalmologists between
disqualified. 1991-1999. A Swiss study showed 13.1% with CH, and 1.8% with
CH and coloboma. A genetic test is available through Optigen,
Longevity: 12-15 years. which reports 11% of Shetland sheepdogs test as affected, and 34%
test as carriers. CERF does not recommend breeding any Shetland
Points of Conformation: The dog is compact, with a Sheepdogs affected with CEA/CH.6,7,8,9
dolichocephalic skull, slight stop—overall forming a long blunt
tapering profile. Eyes are oblique, almond-shaped and pigmented Hip Dysplasia: Polygenically inherited trait causing degenerative
dark except in merle coated dogs, where blue or merle is permitted. joint disease and hip arthritis. OFA reports 4.7% affected. Listed as a
The ears are small, and break about three quarters of the way up. significantly reported disorder in the 2000 ASSA Health Survey.10,11
Black nose pigmentation is standard. The neck is muscular, arched
and of moderate length. The topline is level, and the chest is deep Elbow Dysplasia: Polygenically inherited trait causing elbow
but narrows underneath, with moderate abdomen tuck. The tail arthritis. OFA reports 3.1% affected.10
when resting reaches the tarsus. Dewclaws may be removed.
Compact arched toes in a small foot, and straight limbs contribute Patella Luxation: Polygenically inherited laxity of patellar
to a low, smooth gait and agility on rough ground. ligaments, causing luxation, lameness, and later degenerative joint
disease. Treat surgically if causing clinical signs. Reported at a high
421
frequency of Shetland sheepdogs screened by OFA, but too few Autoimmune Hemolytic Anemia (AIHA): Autoimmune
have been examined for statistical accuracy.10 destruction of red blood cells. Shetland sheepdogs have a 4.8x
risk of developing AIHA versus other breeds. Females are more
Von Willebrand’s Disease (vWD): Shetland sheepdogs can have frequently affected than males. Clinical features included pale
the severe bleeding Type III form of autosomal recessive vWD. A mucous membranes, weakness, lethargy and collapse. Treatment
genetic test is available that shows 0.3% affected and 7.7% carrier with prednisone is successful in most cases.22
in the breed.12,13,14
Vesicular Cutaneous Lupus Erythematosus: Adult onset vesicular
Disease Predispositions form of lupus that causes annular, polycyclic and serpiginous
Hypothyroidism: Inherited autoimmune thyroiditis. 12.7% positive ulcerations distributed over sparsely haired areas of the body. These
for thyroid autoantibodies based on testing at Michigan State especially occur during the summer months due to ultraviolet
University. (Ave. for all breeds is 7.5%). Dorn reports a 1.32x odds exposure. Treatment is with immunosuppressive drugs and
ratio versus other breeds. Listed as a significantly reported disorder sunscreen. Shetland Sheepdogs are a breed at increased risk.23
in the 2000 ASSA Health Survey.11,15,16,17
Idiopathic Epilepsy: The breed has a form of frontal lobe epilepsy
Dermatomyositis: Inherited disorder causing patches of scaling, with an onset between 2-5 years of age, often progressing to status
crusting and alopecia over the muzzle, periorbital skin and epilepticus. Control with anticonvulsant medication. Frequency and
distal limbs, and an associated myositis especially affecting the mode of inheritance not known.24,25
masticatory muscles. Onset between 3-6 months of age. Thought
Gall Bladder Mucoceles: Gall bladder mucoceles and concurrent
to be immune mediated, however specific autoantibodies have
dyslipidemia or dysmotility are reported at a 7.2x odds ratio versus
not been identified. Mode of inheritance is unknown, though
other breeds at a median age of 9 years. Treatment is surgery, and
some researchers suspect autosomal dominant with incomplete
a more successful outcome is found in Shetland Sheepdogs who
penetrance. Listed as a significantly reported disorder in the 2000
undergo surgery prior to the onset of clinical signs. In case studies,
ASSA Health Survey.11,18,19,20
9.3% of dogs diagnosed with gall bladder mucoceles were Shetland
Distichiasis: Abnormally placed eyelashes that irritate the cornea Sheepdogs. The disease is associated with a heterozygous mutation
and conjunctiva. Can cause secondary corneal ulceration. In in the ABCB4 gene.26,27
Shelties, usually involves stiff lashes which require permanent
Patent Ductus Arteriosus (PDA): Inherited congenital heart
epilation. Identified in 5.51% of Shetland Sheepdogs CERF examined
disorder; affected dogs are usually stunted, and have a loud heart
by veterinary ophthalmologists between 2000-2005.7
murmur. Diagnosis is via Doppler ultrasound. Treatment is surgical.
Persistent Pupillary Membranes: Strands of fetal remnant Shetland sheepdogs have an increased incidence versus other
connecting; iris to iris, cornea, lens, or involving sheets of tissue. breeds.28
The later three forms can impair vision, and dogs affected with
Rostally Displaced Maxillary Canine Teeth: Shetland Sheepdogs
these forms should not be bred. Identified in 5.01% of Shetland
can have this abnormal dentition occur. They can also have
sheepdogs CERF-examined by veterinary ophthalmologists between
abnormal (small) upper third incisors. Undetermined mode of
2000-2005.7
inheritance. Reported on the ASSA website.
Corneal Dystrophy: Shetland sheepdogs can have an ulcerative
Superficial Necrolytic Dermatitis: Inherited skin disorder caused
stromal epithelial form of corneal dystrophy. Identified in 2.45% of
by a metabolic hepatopathy causing increased hepatic catabolism
Shetland sheepdogs CERF-examined by veterinary ophthalmologists
of amino acids and hypoaminoacidaemia.29
between 2000-2005.7,21
Distal Tibial Valgus Deformity: Distal hind limb deformity possibly
Cataracts: Anterior and posterior cortex intermediate and punctate
due to premature closure of the lateral aspect of the distal tibial
cataracts predominate in the breed. Identified in 1.05% of Shetland
physis. Correct surgically. Reported at a 12.3x odds ratio versus
sheepdogs CERF examined by veterinary ophthalmologists between
other breeds.30
2000-2005. CERF does not recommend breeding any Shetland
sheepdog with a cataract.7
Lateral Luxation of The Superficial Digital Flexor Tendon: This
Uveodermatologic (VKH-Like) Syndrome: This is an autoimmune disorder occurs with increased frequency in Shetland sheepdogs.
disease manifested by progressive uveitis and depigmenting Breeding studies suggest an autosomal recessive mode of
dermatitis that closely resembles the human Vogt-Koyanagi-Harada inheritance.31,32
syndrome. The disease presents between 1-1/2 and 4 years of age,
Brachygnathism, Central PRA, Color Dilution Alopecia,
and can progress to blindness. Treatment is with steroids. CERF
Cryptorchidism, Factor VII Deficiency, Factor IX Deficiency,
does not recommend breeding any Shetland Sheepdog with the
Fanconi Syndrome, Mucinosis, Muscular Dystrophy,
condition.7
Oligodontia, Optic Nerve Hypoplasia, Peripheral Vestibular
Kidney Disease: No specific kidney diseases are documented in the Disease, Posterior Crossbite, Progressive Retinal Atrophy, and
literature, but Dorn reports a 17.82x odds ratio versus other breeds.15 Uveal Hypopigmentation are reported.33
422
Isolated Case Studies References
Leukodystrophy: Rare, inherited mitochondrial disorder, where 1. Clark LA, Wahl JM, Rees CA, et. al.: Retrotransposon insertion in SILV is
affected dogs develop tremors at two to nine weeks of age followed responsible for merle patterning of the domestic dog. Proc Natl Acad Sci U
by progressive neurological worsening with ataxia, paresis, paralysis, S A. 2006 Jan 31;103(5):1376-81.
spasticity, and cranial nerve dysfunction. Affected dogs had severe 2. Mori N, Lee P, Muranaka S, et. al.: Predisposition for primary
hyperlipidemia in Miniature Schnauzers and Shetland sheepdogs as
diffuse spongy degeneration of the white matter of the brain and
compared to other canine breeds. Res Vet Sci. 2010 Jun;88(3):394-9.
spinal cord.34,35 3. Neff MW, Robertson KR, Wong AK, et. al.: Breed distribution and history
of canine mdr1-1Delta, a pharmacogenetic mutation that marks the
Gastric Leiomyosarcoma: A 7-1/2 year old female Shetland emergence of breeds from the collie lineage. Proc Natl Acad Sci U S A. 2004
Sheepdog presented with weight loss and bloody vomiting and Aug 10;101(32):11725-30.
diarrhea. A pleomorphic leiomyosarcoma was found in the pyloric 4. Mealey KL & Meurs KM: Breed distribution of the ABCB1-1Delta
stomach.36 (multidrug sensitivity) polymorphism among dogs undergoing ABCB1
genotyping. J Am Vet Med Assoc. 2008 Sep 15;233(6):921-4.
Renal Agenesis: Two cases of bilateral renal agenesis were 5. Gramer I, Leidolf R, Döring B, et. al.: Breed distribution of the nt230(del4)
identified from related litters.37 MDR1 mutation in dogs. Vet J. 2011 Jul;189(1):67-71.
6. Bedford PG: Collie eye anomaly in the United Kingdom. Vet Rec. 1982
Erythrocyte Fragility with Pigmenturia: A two year-old spayed Sep 18;111(12):263-70.
female Shetland sheepdog had recurrent episodes of discolored 7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
urine correlating with stressful situations or excessive activity. College of Veterinary Ophthalmologists. ACVO, 2007.
Alkaline and osmotic fragility tests determined that an increase 8. Lowe JK, Kukekova AV, Kirkness EF, et. al.: Linkage mapping of the primary
in erythrocyte fragility was the underlying cause of the recurrent disease locus for collie eye anomaly. Genomics. 2003 Jul:82(1):86-95.
pigmenturia.38 9. Walser-Reinhardt L, Hässig M & Spiess B: Collie Eye Anomaly in
Switzerland. Schweiz Arch Tierheilkd. 2009 Dec;151(12):597-603.
10. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Genetic Tests 11. American Shetland Sheepdog Association: 2000 ASSA Health Survey
Tests of Genotype: Direct test for CEA/CH is available from Results. 2000.
Optigen. 12. Pathak EJ: Type 3 von Willebrand’s disease in a Shetland sheepdog. Can
Vet J. 2004 Aug;45(8):685-7.
Direct test for MDR1 (ivermectin sensitivity) gene is available from 13. Raymond SL, Jones DW, Brooks MB, et. al.: Clinical and laboratory
Washington State Univ.-VCPL. features of a severe form of von Willebrand disease in Shetland sheepdogs.
J Am Vet Med Assoc. 1990 Nov 15;197(10):1342-6.
Direct test for vWD is available from VetGen. 14. Loechel RH, Springer K, & Brewer GJ: VWD and VetGen: Ten Years of
Genetic Test Results. Proceedings, 2007 Tufts’ Canine and Feline Breeding
Direct test for bicolor, tricolor and sable colors is available from and Genetics Conference. 2007.
Health Gene and VetGen. 15. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Tests of Phenotype: CHIC Certification: Required testing includes 2000.
hip radiographs, CERF eye examination (annually until age 5, then 16. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
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hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
tests for vWD and MDR1, thyroid profile including autoantibodies 17. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
(at 2, 4, and 7 years), direct gene test for CEA/CH, and elbow for Population and Animal Health, Michigan State University. April, 2007.
radiographs. Optional recommended tests include cardiac 18. Ferguson EA, Cerundolo R, Lloyd DH, et. al.: Dermatomyositis in
evaluation by a specialist and temperament test. (See CHIC website; five Shetland sheepdogs in the United Kingdom. Vet Rec. 2000 Feb
www.caninehealthinfo.org). 19;146(8):214-7.
19. Clark LA, Credille KM, Murphy KE, et. al.: Linkage of dermatomyo-
Recommend patella examination. sitis in the Shetland Sheepdog to chromosome 35. Vet Dermatol. 2005
Dec;16(6):392-4.
Miscellaneous 20. Wahl JM, Clark LA, Skalli O, et. al.: Analysis of gene transcript profiling
and immunobiology in Shetland sheepdogs with dermatomyositis. Vet
• Breed name synonyms: Sheltie, Miniature Collie, Toy Collie Dermatol. 2008 Apr;19(2):52-8.
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain), 21. Cooley PL, Dice PF 2nd: Corneal dystrophy in the dog and cat. Vet Clin
ANKC (Australian National Kennel Club), NKC (National Kennel Club) North Am Small Anim Pract. 1990 May;20(3):681-92.
• AKC rank (year 2008): 19 (10,188 dogs registered) 22. Miller SA, Hohenhaus AE, Hale AS: Case-control study of blood type,
• Internet resources: American Shetland Sheepdog Association: breed, sex, and bacteremia in dogs with immune-mediated hemolytic
www.assa.org anemia. J Am Vet Med Assoc. 2004 Jan 15;224(2):232-5.
Canadian Shetland Sheepdog Association: 23. Jackson HA: Eleven cases of vesicular cutaneous lupus erythematosus in
www.canadianshelties.ca Shetland sheepdogs and rough collies: clinical management and prognosis.
The English Shetland Sheepdog Club: www.essc.org.uk Vet Dermatol. 2004 Feb;15(1):37-41.
24. Morita T, Shimada A, Takeuchi T, et. al.: Cliniconeuropathologic findings
of familial frontal lobe epilepsy in Shetland sheepdogs. Can J Vet Res. 2002
Jan;66(1):35-41.
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25. Morita T, Takahashi M, Takeuchi T, et. al.: Changes in extracellular
neurotransmitters in the cerebrum of familial idiopathic epileptic
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immunohistochemical study for glutamate metabolism. J Vet Med Sci. 2005
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26. Aguirre AL, Center SA, Randolph JF, et. al.: Gallbladder disease in
Shetland Sheepdogs: 38 cases (1995-2005). J Am Vet Med Assoc. 2007 Jul
1;231(1):79-88.
27. Mealey KL, Minch JD, White SN, et. al.: An insertion mutation in ABCB4
is associated with gallbladder mucocele formation in dogs. Comp Hepatol.
2010 Jul 3;9:6.
28. Ackerman N, Burk R, Hahn AW, et. al.: Patent ductus arteriosus in the
dog: a retrospective study of radiographic, epidemiologic, and clinical
findings. Am J Vet Res. 1978 Nov;39(11):1805-10.
29. Outerbridge CA, Marks SL, Rogers OR: Plasma amino acid
concentrations in 36 dogs with histologically confirmed superficial
necrolytic dermatitis. Vet Dermatol. 2002 Aug;13(4):177-86.
30. Jaeger GH, Marcellin-Little DJ, & Ferretti A: Morphology and
correction of distal tibial valgus deformities. J Small Anim Pract. 2007
Dec;48(12):678-82.
31. Solanti S, Laitinen O, Atroshi F: Hereditary and clinical characteristics
of lateral luxation of the superficial digital flexor tendon in Shetland
sheepdogs. Vet Ther. 2002 Spring;3(1):97-103.
32. Mauterer JV Jr, Prata RG, Carberry CA, et. al.: Displacement of
the tendon of the superficial digital flexor muscle in dogs: 10 cases
(1983-1991). J Am Vet Med Assoc. 1993 Oct 15;203(8):1162-5.
33. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p.238-9, AAHA Press, 1999.
34. Wood SL, Patterson JS: Shetland Sheepdog leukodystrophy. J Vet Intern
Med. 2001 Sep-Oct;15(5):486-93.
35. Li FY, Cuddon PA, Song J, et. al.: Canine spongiform leukoencepha-
lomyelopathy is associated with a missense mutation in cytochrome b.
Neurobiol Dis. 2006 Jan;21(1):35-42.
36. Park CH, Ishizuka Y, Tsuchida Y, et. al.: Gastric pleomorphic
leiomyosarcoma in a Shetland sheepdog. J Vet Med Sci. 2007
Aug;69(8):873-6.
37. Brownie CF, Tess MW, Prasad RD: Bilateral renal agenesis in two litters
of Shetland sheepdogs. Vet Hum Toxicol. 1988 Oct;30(5):483-5.
38. LeGrange SN, Breitschwerdt EB, Grindem CB, et. al.: Erythrocyte fragility
and chronic intermittent pigmenturia in a dog. J Am Vet Med Assoc. 1995
Apr 1;206(7):1002-6
39. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 688-693.
424
Shiba Inu
tarsus when straightened; normal carriage is over the back curled
or sickled. Limbs are straight boned and the feet are compact, with
toes well knuckled up. Front dewclaws may be removed; there are
no rear declaws. They possess an athletic, agile, springy gait.
426
14. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
15. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
16. Abbott JA, Hawkes K, Small MT, et. al.: Retrospective Description of
Canine Ventricular Septal Defect. Proceedings, 2008 ACVIM Forum. 2008.
17. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p 239. AAHA Press, 1999.
18. Takemura N: Successful long-term treatment of congenital nephrogenic
diabetes insipidus in a dog. J Small Anim Pract. 1998 Dec;39(12):592-4.
19. Fox E, Lee K, Lamb CR, et. al.: Congenital oesophageal stricture in a
Japanese shiba inu. J Small Anim Pract. 2007 Dec;48(12):709-12.
20. Tanaka R, Hoshi K, Shimizu M, et. al.: Surgical correction of cor
triatriatum dexter in a dog under extracorporeal circulation. J Small Anim
Pract. 2003 Aug;44(8):370-3.
21. Kamiie J, Yasuno K, Ogihara K, et. al.: Collagenofibrotic glomeruloneph-
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22. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p 593-596.
427
Shih Tzu
They are moderate shedders, and some owners prefer to have
them clipped once to twice annually. They do well with children in
the household. They enjoy close human contact, and have low to
moderate exercise needs. They tolerate heat poorly.
Drug Sensitivities
None reported
The Breed History
The name means “lion” in Chinese. This dog perhaps originated Inherited Diseases
in the Byzantine Empire or Tibet, though they are known to have Renal Dysplasia: Autosomal dominant disease with incomplete
reached China in the Tang Dynasty. Earliest records go back to penetrance causing renal failure. Affected dogs can succumb to
about the year 625. Though they were brought to North America renal failure from birth to two years of age. Mildly affected dogs
during World War II, they did not join AKC registry until 1969. It can live with compensated renal insufficiency. Biopsy studies
is possible the modern breed originated from Pekingese and Pug suggest that a majority of the breed is affected, although only a
crossed with Tibetan dogs such as Lhasa Apso. Only 14 foundation small percentage die from the condition. Dorn reports a 12.10x odds
dogs are thought to have been the source of the breed outside ratio for kidney disease in Shih Tzus versus other breeds. A direct
China since the 1900s. genetic test for a susceptibility gene is available. (Affected dogs all
have one copy of the gene, but most dogs with the gene will not
Breeding for Function develop kidney failure.)1,2,3,4
They were bred for companionship and as a lapdog for the Chinese
and Tibetan royalty. Hip Dysplasia and Legg-Calve-Perthes Disease: Polygenically
inherited traits causing degenerative hip joint disease and arthritis.
OFA reports 19.4% affected.5
Physical Characteristics
Height at Withers: female 9-10.5” (23-26.5 cm), male 9-10.5” Patella Luxation: Polygenically inherited laxity of patellar ligaments,
(23-26.5 cm), causing luxation, lameness, and later degenerative joint disease.
Treat surgically if causing clinical signs. OFA reports 2.4% affected.5
Weight: females 9-16 lb (4-7 kg), males 9-16 lb (4-7 kg).
Elbow Dysplasia: Polygenically inherited trait causing elbow
Coat: Their dense, long, straight double coat can be any color. arthritis. Too few Shih Tzus have been screened by OFA to determine
an accurate frequency.5
Longevity: 13-15 years.
Points of Conformation: In these toy dogs, the tail is carried over Disease Predispositions
the back, head carriage is high and the topline is straight. Though Distichiasis: Abnormally placed eyelashes that irritate the cornea
a toy breed, the Shih Tzu is built with solid stature and they are and conjunctiva. Can cause secondary corneal ulceration. Identified
longer than high. The large dark round eyes are not prominent, in 15.59% of Shih Tzus CERF-examined by veterinary ophthalmolo-
eyelid and lip margins are pigmented darkly. Skull is brachycephalic gists between 2000-2005. Dorn reports a 3.13x odds ratio in Shih
and the small muzzle is about one inch long. The nose is black Tzus versus other breeds.1,6
except for the liver and blue dogs, where they are liver and blue
to match. They have large pendulous ears, a definite stop and a Primary (Narrow Angle) Glaucoma: Ocular condition causing
prognathic jaw. The abdomen has no waist, and the chest consists increased pressure within the eyeball, and secondary blindness
of a deep moderately sprung ribcage. Dewclaws may be taken off, due to damage to the retina. Can also predispose to lens luxation.
and the legs are straight. Their gait is powerful and straight. Screen with gonioscopy and tonometry. Reported at a frequency
of 16.5% in Japan. Diagnosed in 1.58% of Shih Tzus presented to
veterinary teaching hospitals.7,8
Recognized Behavior Issues and Traits
These dogs are reported to be intelligent, very alert, and friendly. Brachycephalic Complex: The brachycephalic complex includes
Their docile nature is a high priority in breeding programs because Stenotic Nares, Elongated Soft Palate, Everted Laryngeal
they are used solely as companion dog. They are alarm barkers. Saccules, Laryngeal Collapse, and occasionally Hypoplastic
Their profuse coat should be groomed daily and may require a Trachea. Can cause respiratory distress, apnea, and hypoxia. Early
regular bath. Hair above the eyes is either trimmed or tied up. surgical correction of severe stenotic nares is recommended.9,10
428
Epiphora: Ocular tear drainage with hair staining. Can occur Chronic Superficial Keratitis (Pannus): Chronic corneal
secondary to medial canthal trichiasis and/or entropion. Shih Tzu inflammatory process that can cause vision problems due to
are listed as the most frequently affected breed. Treat by keeping corneal pigmentation. Treatment with topical ocular lubricants
hair clipped short, and daily cleaning. Medial canthoplasty is and anti-inflammatory medication. Identified in 1.05% of Shih
curative in severe cases.11 Tzus CERF-examined by veterinary ophthalmologists between
2000-2005.6
Entropion: Rolling in of eyelids, often causing corneal irritation
or ulceration. Identified in 7.88% of Shih Tzus CERF examined by Intervertebral Disc Disease (IVDD): Shih Tzus have an increased
veterinary ophthalmologists between 2000-2005.6 risk of developing spinal cord disease due to prolapsed disk
material. Clinical signs include back pain, scuffing of paws, spinal
Vitreous Degeneration: Liquefaction of the vitreous gel which ataxia, limb weakness, and paralysis. In a Japanese study, 11.4%
may predispose to retinal detachment. Identified in 7.36% of Shih of dogs with IVDD were Shih Tzus, primarily affecting the cervical
Tzus CERF-examined by veterinary ophthalmologists between spinal cord at an average age of 10 years.18,19
2000-2005.6
Portosystemic Shunt (PSS, Liver Shunt): Can be intrahepatic,
Cataracts: Juvenile and adult onset. Anterior or posterior extrahepatic or microvascular dysplasia. Causes stunting, abnormal
intermediate cataracts predominate in the breed. Median age of 6.5 behavior, possible seizures, and secondary ammonium urate urinary
+/- 3.4 years. In one large study, 4.14% of Shih Tzus had cataracts. calculi. Diagnose with paired fasted and feeding serum bile acid
Identified in 5.43% of Shih Tzus CERF-examined by veterinary and/or ammonia levels, and abdominal ultrasound. 0.78% of Shih
ophthalmologists between 2000-2005. CERF Does not recommend Tzus (odds ratio of 15.4x) presented to veterinary teaching hospitals
breeding any Shih Tzu with a cataract.6,12,13 had PSS.20,21,22
Eury/Macroblepharon: An exceptionally large palpebral fissure. Keratoconjunctivitis Sicca (KCS, Dry Eye): Ocular condition
With laxity, may lead to lower lid ectropion and upper lid entropion. causing lack of tear production and secondary conjunctivitis,
Either of these conditions may lead to severe ocular irritation. corneal ulcerations, and vision problems. In one study, 4.8% of
Identified in 3.50% of Shih Tzus CERF-examined by veterinary dogs with KCS were Shih Tzus. Usually presents in the breed at
ophthalmologists between 2000-2005.6 0-2 years of age, or 4-6 years of age. Treat with ocular lubricants
and anti-inflammatory medications. CERF does not recommend
Exposure Keratopathy Syndrome/Pigmentary Keratitis: Corneal breeding any Shih Tzu with KCS.6,23
reactivity and drying from ocular exposure secondary to shallow
orbits, exophthalmos, and lagophthalmos. Identified in 3.50% of Urinary Calculi: The breed is found to be at an increased risk of
Shih Tzus CERF-examined by veterinary ophthalmologists between developing struvite and oxalate calculi. Dorn reports a 2.74x odds
2000-2005.6 ratio in Shih Tzus versus other breeds.1,24,25
Hypothyroidism: Inherited autoimmune thyroiditis. 3.0% positive Optic Nerve Hypoplasia: Congenital malformation of the optic
for thyroid autoantibodies based on testing at Michigan State nerve causing blindness. 23% of reported cases are Shih Tzus. CERF
University. (Ave. for all breeds is 7.5%).14,15 does not recommend breeding any Shih Tzu with the condition.6,26
Ectopic Cilia: Hair emerging through the eyelid conjunctiva. Allergic Inhalant Dermatitis, Cleft Lip/Palate, Dermoid
Ectopic cilia can cause discomfort and corneal disease. Identified in Sinus, Hydrocephalus, Malassezia Dermatitis, Oligodontia,
1.93% of Shih Tzus CERF-examined by veterinary ophthalmologists Prognathism, Sebaceous Adenitis, Tricuspid Valve Dysplasia, and
between 2000-2005.6 von Willebrand’s Disease are reported.27
429
consistent with a lesion affecting the cervicothoracic (C6 through serum thyroid hormone autoantibodies in dogs with clinical signs of
T2) spinal cord. MRI identified symmetric lesions in the C5-C7 spinal hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
cord, caudal colliculi, and vestibular and cerebellar nuclei. Pathology 15. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
revealed polioencephalomyelopathy, similar to that seen in the for Population and Animal Health, Michigan State University. April, 2007.
16. Young MD: Umbilical hernias in shih tzus. Vet Rec. 1991 Aug
mitochondrial disorder in Australian Cattle Dogs, and humans with
31;129(9):204.
Leigh disease.32
17. Herrera D: Surgery of the Eyelids. 2005. Proceedings, World Small
Animal Veterinary Association Congress, 2005.
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Tests of Genotype: Direct test for a renal dysplasia susceptibility Proceedings, Western Veterinary Conference.
gene is available from Dogenes (www.dogenes.com). 19. Itoh H, Hara Y, Yoshimi N, et. al.: A retrospective study of intervertebral
disc herniation in dogs in Japan: 297 cases. J Vet Med Sci. 2008
Direct test for coat color is available from VetGen. Jul;70(7):701-6.
20. Hunt GB: Effect of breed on anatomy of portosystemic shunts resulting
Tests of Phenotype: Recommended tests are; CERF eye from congenital diseases in dogs and cats: a review of 242 cases. Aust Vet
examination, hip and elbow radiographs, patella examination, J. 2004 Dec;82(12):746-9.
21. Tobias KM, Rohrbach BW: Association of breed with the diagnosis of
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genetic test for renal dysplasia susceptibility.
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22. Center SA: Portosystemic Vascular Anomalies & Hepatic MVD: Evidence
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24. Houston DM & Moore AE: Canine and feline urolithiasis: examination of
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
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• AKC rank (year 2008): 10 (20,219 dogs registered)
from 1998 to 2008. Can Vet J. 2009 Dec;50(12):1263-8.
• Internet resources: American Shih Tzu Club: www.shihtzu.org 25. Lekcharoensuk C, Lulich JP, Osborne CA, et. al.: Patient and
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26. da Silva EG, Dubielzig R, Zarfoss MK, et. al.: Distinctive histopathologic
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11. Yi NY, Park SA, Jeong MB, et. al.: Medial canthoplasty for epiphora
in dogs: a retrospective study of 23 cases. J Am Anim Hosp Assoc. 2006
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12. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
13. Park SA, Yi NY, Jeong MB, et. al.: Clinical manifestations of cataracts in
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Siberian Husky
muscling with a slight arch. The thorax is deep and somewhat
laterally flattened; ribs are well sprung. The topline is level. They
possess straight limbs which are moderately boned and muscled.
Foreleg dewclaws may be removed, while the rear ones are usually
removed. Feet are oval, medium sized and possess plenty of fur
between the toes. Pads are thick.
432
Tests of Phenotype: CHIC Certification: Required tests are; CERF 17. Slater MR, Erb HN: Effects of risk factors and prophylactic treatment
eye examination (minimum of 1 year of age), and hip dysplasia on primary glaucoma in the dog. J Am Vet Med Assoc. 1986 May
radiograph. (See CHIC website: www.caninehealthinfo.org) 1;188(9):1028-30.
18. White SD, Bourdeau P, Rosychuk RA et. al.: Zinc-responsive dermatosis
Recommend elbow radiograph, patella evaluation, thyroid profile in dogs: 41 cases and literature review. Vet Dermatol. 2002 Feb;13(1):63.
including autoantibodies, and cardiac examination. 19. Brellou GD, Kleinschmidt S, Meneses F, et. Al.: Eosinophilic
Granulomatous Gastroenterocolitis and Hepatitis in a 1-year-old Male
Siberian Husky. Vet Pathol. 2006 Nov;43(6):1022-5.
Miscellaneous 20. Vercelli A, Cornegliani L, Portigliotti L: Eyelid eosinophilic granuloma in
• Breed name synonyms: Husky, Arctic Husky. a Siberian husky. J Small Anim Pract. 2005 Jan;46(1):31-3.
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), 21. Lilliehook I, Tvedten H: Investigation of hypereosinophilia and potential
ANKC (Australian National Kennel Club), NKC (National Kennel Club). treatments. Vet Clin North Am Small Anim Pract. 2003 Nov;33(6):1359-78,
• AKC rank (year 2008): 23 (8,465 dogs registered) viii.
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23. Glaze MB: Canine and Feline Uveitis. Proceedings, 2004 Northeast
Siberian Husky Club of Canada: Veterinary Conference. 2004.
www.siberianhuskyclubofcanada.com 24. Sigle KJ, McLellan GJ, Haynes JS, et. Al.: Unilateral uveitis in a
Siberian Husky Club of Great Britain: dog with uveodermatologic syndrome. J Am Vet Med Assoc. 2006 Feb
www.siberianhuskyclub.com 15;228(4):543-8.
25. Frank LA, Hnilica KA, Oliver JW: Adrenal steroid hormone concentrations
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melatonin and mitotane. Vet Dermatol. 2004 Oct;15(5):278-84.
1. Lawler DF, Keltner DG, Hoffman WE et. al.: Benign familial
hyperphosphatasemia in Siberian huskies. Am J Vet Res. 1996 26. Frank LA, Hnilica KA, Rohrbach BW, et. al.: Retrospective evaluation of
May;57(5):612-7. sex hormones and steroid hormone intermediates in dogs with alopecia.
2. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at Vet Dermatol. 2003 Apr;14(2):91-7.
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation. 27. McLaughlin R Jr, Miller CW: Urinary incontinence after surgical repair of
2000. ureteral ectopia in dogs. Vet Surg. 1991 Mar-Apr;20(2):100-3.
3. Siberian Husky Club of America: 2006 Siberian Husky Health Survey. 28. Puerto DA, Brockman DJ, Lindquist C, et. al.: Surgical and nonsurgical
2006. management of and selected risk factors for spontaneous pneumothorax
4. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in in dogs: 64 cases (1986-1999). J Am Vet Med Assoc. 2002 Jun
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11. 1;220(11):1670-4.
5. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American 29. Chavkin MJ, Roberts SM, Salman MD, et. al.: Risk factors for
College of Veterinary Ophthalmologists. ACVO, 2007. development of chronic superficial keratitis in dogs. J Am Vet Med Assoc.
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8. Genevois JP, Remy D, Viguier E, et. al.: Prevalence of hip dysplasia of blue-eyed dogs: an immunohistochemical study. Vet Pathol. 2007
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13. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
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15. Hawkins EC, Basseches J, Berry CR, et. al.: Demographic, clinical, and
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433
Silky Terrier
Normal Physiologic Variations
None reported
Drug Sensitivities
None reported
Inherited Diseases
Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
disease. Treat surgically if causing clinical signs. Reported 16.0x
The Breed History odds ratio versus other breeds. OFA reports 1.6% affected. Reported
The breed origins trace to Australia in the late 1800s and early at a frequency of 1.1% in the 2002 STCA Health Survey.1,2,3
1900s. They were developed as a result of crosses between Yorkshire
terriers and native Australian terriers. The AKC recognized the breed Legg-Perthes Disease and Hip Dysplasia: Polygenically inherited
in 1955. traits causing degenerative hip joint disease and arthritis. Too few
Silky Terriers have been screened by OFA to determine an accurate
Breeding for Function frequency. Legg-Perthes disease is reported at a frequency of 0.8%
Early in breed development, the Silky terriers were used for vermin in the 2002 STCA Health Survey.1,2
control, but this breed was primarily developed for companionship.
Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. Too few Silky Terriers have been screened by OFA to
Physical Characteristics determine an accurate frequency.1
Height at Withers: 9-10 “ (23-25.5 cm)
Ocular Disorders: Too few Skye Terriers have been CERF examined
to determine accurate frequencies for inherited ocular disorders.
All Skye Terriers considered for breeding should have a CERF
examination.9
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: Skye
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 143 (88 dogs registered)
• Internet resources: The Skye Terrier Club of America:
http://clubs.akc.org/skye/
Skye Canada: www.skyecanada.ca
The Skye Terrier Club (UK): www.skyeterrierclub.org.uk
The Skye Terrier Foundation: www.skyeterrier.org
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hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc. 2002 Feb 15;220(4):466-71.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. McGrotty YL, Ramsey IK, Knottenbelt CM: Diagnosis and management
of hepatic copper accumulation in a Skye terrier. J Small Anim Pract. 2003
Feb;44(2):85-9.
6. Haywood S, Rutgers HC, Christian MK: Hepatitis and copper
accumulation in Skye terriers. Vet Pathol. 1988 Nov;25(6):408-14.
7. Fuentealba IC, Aburto EM: Animal models of copper-associated liver
437
Smooth Fox Terrier
Terrier. Gait is quick and agile, springy, with a ground-covering
stride.
Physical Characteristics Elbow Dysplasia: Polygenic trait causing elbow arthritis. Too few
Height at Withers: Less than 15.5” (39.5 cm) Smooth Fox Terriers have been screened by OFA to determine an
accurate frequency.1
Weight: male 18 lb (8 kg), female 16 lb (7 kg)
Congenital Myasthenia Gravis: A lethal, autosomal recessive
Coat: Short, hard hairs are dense. These predominantly white dogs disorder in the breed. Presents within 5 weeks of birth with muscle
have well demarcated color patches. Brindle and red-liver are not weakness, megaesophagus, and secondary aspiration pneumonia.2,3,4
favored as the second color. Black and tan is most common.
Genetic Tests
Tests of Genotype: Direct test for coat color is available from
VetGen.
Miscellaneous
• Breed name synonyms: Fox Terrier, Smooth Fox, Smooth-haired
Fox Terrier
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
• AKC rank (year 2008): 106 (415 dogs registered)
• Internet resources: American Fox Terrier Club: www.aftc.org
The Smooth Fox Terrier Association (UK):
www.smoothfoxterrierassociation.co.uk
439
Soft Coated
Wheaten Terrier
Recognized Behavior Issues and Traits
Reported breed characteristics include: Intelligent, responsive,
a merry disposition, and loving. They are considered more
even-tempered and obedient than some of the other terrier breeds.
Grooming needs are high. The Wheaten needs moderate exercise.
They are energetic, but less so than some of the terriers. Good with
children, good alarm barkers. Some suggest this dog is better for
older children (not toddlers) because of the high energy level. If off
leash, they should be in a fenced enclosure. It is recommended that
obedience training be started early, and some dogs are headstrong.
The Breed History They like to jump vertically in place, they can also tend to be leash
pullers. If bored, the Wheaten Terrier may dig or chew. Considered
Breed records dating back to the 1700s in Ireland (counties Kerry
good with other dogs and cats if raised together, but as a terrier,
and Cork) may not reflect the earliest days of the breed. They are
they may chase small pets. They tend to keep their puppy-like
closely related to Irish terriers and contributed to the development
exuberance well into middle age (5-7 yrs).
of the Kerry Blue terrier. Wheatens were first brought to America in
1946, and first registered in the AKC studbook in 1973.
Normal Physiologic Variations
None reported
Breeding for Function
These dogs were widely used for hunting small game and vermin,
herding, and as a guard dog for the home and livestock. Today, they Drug Sensitivities
are primarily companion dogs. None reported
Weight: females 30-35 lb (13.5-16 kg), males 35-40 lb (16-18 kg). Hip Dysplasia: Polygenically inherited trait causing degenerative
joint disease and hip arthritis. OFA reports 4.8% affected.1
Coat: As the name suggests, the coat is very soft and is wheaten
in coloration. On some dogs, the ears and muzzle have blue-gray Patella Luxation: Polygenically inherited laxity of patellar ligaments,
shading. The hairs of the coat are silky and slightly wavy. The color causing luxation, lameness, and later degenerative joint disease.
and texture does not fully set until 1 1/2 to 2 years of age. From Treat surgically if causing clinical signs. OFA reports 4.0% affected.1
sexual maturity on, the coat is lighter wheaten. Puppies are often
dark wheaten and some puppies have black tips. This is a silky shiny Disease Predispositions
single coat. Protein-Losing Nephropathy (PLN): Inherited disease causing
protein loss through the kidneys. General clinical signs include
Longevity: 13-15 years vomiting, diarrhea, weight loss, and pleural and peritoneal
effusions. Laboratory findings include hypoalbuminemia,
Points of Conformation: They are a square, medium-sized terrier proteinuria, hypercholesterolemia, and azotemia. Renal lesions
with moderate bone and muscling. They move with smooth ground typically showed chronic glomerulonephritis and glomeruloscle-
covering strides. They are to move with tails held erect. The head has rosis, and less commonly end-stage renal disease. Average age of
a moderately long rectangular conformation, the muzzle is block and diagnosis is 6.3 years. Food hypersensitivity may play a role in the
there is a defined stop. The nose is large and both lip margins and disorder. This disease can present concurrently with PLE, and may
nose are pigmented black. Eyes are almond shaped and medium in share a genetic basis. Estimated to affect 10-15% of the breed.
size, brown, the palpebral margins are pigmented black and the eyes Reported at a frequency of 2.7% in the 2000 General Health Survey
are fairly wide set. Hair falls over the eyes to a significant extent. on Soft Coated Wheaten Terriers. Unknown mode of inheritance.
Ears are triangular and fold to hang parallel to the head. The neck Fecal perinuclear antineutrophilic cytoplasmic antibody (PANCA)
is medium in length, muscular and not throaty. The topline is level, can be used as a phenotypic screening test.2,3,4,5,6
and the back short. The thorax is deep and ribs are well sprung. The
tails are usually docked, and are set high. Legs straight boned and Allergies: Food Allergy was identified in 7.0% of dogs, and Inhalant
feet are compact and round in shape with black nails. Dewclaws are allergies were identified in 5.7% in the 2000 General Health Survey
removed in North America. Rear dewclaws are penalized. on Soft Coated Wheaten terriers. Dorn reports a 1.34x odds ratio for
allergic dermatitis versus other breeds.5,7
440
Persistent Pupillary Membranes: Strands of fetal remnant Persistent Hyaloid Artery (PHA): A congenital defect resulting
connecting; iris to iris, cornea, lens, or involving sheets of tissue. from abnormalities in the development and regression of the
The later three forms can impair vision, and dogs affected with hyaloid artery. Identified in 1.09% of Soft-coated Wheaten
these forms should not be bred. Identified in 3.96% of Soft-coated terriers CERF-examined by veterinary ophthalmologists between
Wheaten terriers CERF-examined by veterinary ophthalmologists 2000-2005.8
between 2000-2005.8
Ectopic Ureter: Congenital disorder where the ureters do not
Dental Issues: The 2000 General Health Survey on Soft Coated enter the urinary bladder, but instead deposit urine in the urethra
Wheaten terriers reports 3.9% with missing teeth, and 2.1% with or vestibule. Causes urinary incontinence, especially in females.
undershot bites.5 Reported at an increased incidence in the breed. Undetermined
mode of inheritance.14
Protein-Losing Enteropathy (PLE): Inherited disease causing
protein loss through the intestines. General clinical signs include XX-Sex Reversal: Sry-negative XX-sex reversal causes external
vomiting, diarrhea, weight loss, and pleural and peritoneal make characteristics of a prepuce and an enlarged clitoris, in
effusions. Laboratory findings include panhypoproteinemia and genetically female dogs. A uterus is usually present. Reported as a
hypocholesterolemia. Intestinal lesions include inflammatory bowel rare disorder in the breed. Presumed autosomal recessive mode of
disease, dilated lymphatics, and lipogranulomatous lymphangitis. inheritance.15
Average age of diagnosis is 4.7 years. Food hypersensitivity may
play a role in the disorder. This disease can present concurrently Anterior Crossbite, Brachygnathism, Cutaneous Asthenia,
with PLN, and may share a genetic basis. Reported at a frequency Microphthalmia, Optic Nerve Hypoplasia, Prognathism,
of 2.6% in the 2000 General Health Survey on Soft Coated Wheaten Progressive Retinal Atrophy, and von Willebrand’s Disease are
terriers. Unknown mode of inheritance. Perinuclear antineutro- reported.16
philic cytoplasmic antibody (pANCA) can be used as a pre-clinical
phenotypic screening test.2,3,6,9 Isolated Case Studies
Multiple Ocular Anomalies: Two related litters of wheaten terriers
Cataracts: Anterior cortex punctate cataracts predominate in the had various combinations abnormalities including; lens luxation,
breed. Identified in 2.40% of Soft-coated Wheaten terriers CERF persistent pupillary membranes, distichiasis, persistent right aortic
examined by veterinary ophthalmologists between 2000-2005. arch, hydronephrosis, atypical coloboma of the posterior segment,
CERF does not recommend breeding any Soft-coated Wheaten choroid hypoplasia, scleral thinning, posterior cortical cataract,
terrier with a cataract.8 anterior iris adhesion to the cornea, microphthalmia, strabismus,
limbic corneal edema, abnormal scleral outgrowth, and dermoid.17
Renal Dysplasia (RD): Affected Soft Coated Wheaten terriers
present between 4.5 to 30 weeks of age with polyuria, polydipsia, Pilomatricoma: Reported case studies of pilomatricona have been
isosthenuria, azotemia, and small kidneys. Proteinuria is not a published in the breed. These are usually subcutaneous calcifying
hallmark of the disease. Affected dogs die of progressive renal tumors of the skin, usually over the shoulders or extremeties.
failure by three years of age. Histopathologic changes include Surgical removal is usually curative, although one case report was
immature (fetal) glomeruli, persistent fetal mesenchyme, and on a malignant form in the pelvis that had spread to the lungs.18,19
tubular dilatation. There is no sex predilection. Some researchers
postulate an autosomal recessive mode of inheritance. A genetic Segmental Aplasia of the Caudal Vena Cava: A two year-old
test for a dominant susceptibility gene is available. (Affected dogs wheaten terrier with lethargy, exercise intolerance, and ascites was
all have one copy of the gene, but most dogs with the gene will not diagnosed with segmental aplasia of the caudal vena cava with
develop kidney failure.)4,10 azygos continuation, complicated by thrombus formation.20
Hypothyroidism: Inherited autoimmune thyroiditis. 1.7% positive Ichthyosiform Dermatosis: A wheaten terrier had patches of thick,
for thyroid autoantibodies based on testing at Michigan State scaly skin from birth. By three months of age, the scaling was
University. (Ave. for all breeds is 7.5%). Reported at a frequency of generalized and was accompanied by a greasy exudation which
2.5% in the 2000 General Health Survey on Soft Coated Wheaten matted the haircoat. Microscopically, the skin had patchy areas
Terriers.5,11,12 of ortho- and parakeratotic hyperkeratosis, follicular keratosis,
superficial perivascular dermatitis, and variable hypergranulosis.21
Distichiasis: Abnormally placed eyelashes that irritate the cornea
and conjunctiva. Can cause secondary corneal ulceration. Identified
in 1.20% of Soft-coated Wheaten terriers CERF-examined by Genetic Tests
veterinary ophthalmologists between 2000-2005.8 Tests of Genotype: Direct test for a renal dysplasia susceptibility
gene is available from Dogenes (www.dogenes.com).
Hypoadrenocorticism (Addison’s Disease): Typical presentation
of lethargy, poor appetite, vomiting, weakness, and dehydration Tests of Phenotype: CHIC Certification: Required testing includes
can occur from 4 months to several years of age. Cited as a breed CERF eye examination and hip radiograph. (See CHIC website; www.
at significantly higher risk. Treatment with DOCA injections or oral caninehealthinfo.org).
fludrocortisone. Unknown mode of inheritance.13
Recommend patella examination, elbow radiographs, thyroid
profile including autoantibodies, cardiac examination, and annual
441
screening for PLE/PLN (urine protein:creatinine ratios, fecal reversal in several breeds. Sexual Development. 2008;2(2):84-95.
alpha1-protease inhibitor concentrations and serum globulin, 16. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
albumin and creatinine levels). Ackerman. p. 240. AAHA Press, 1999.
17. van der Woerdt A, Stades FC, van der Linde-Sipman JS: Multiple Ocular
An open registry and DNA bank for Soft Coated Wheaten Terriers Anomalies in Two Related Litters of Soft Coated Wheaten Terriers. Vet
exists at the University of Pennsylvania Veterinary School.22 Comp Ophthalmol 1995: 5[2]:78-82. The Complete Dog Book, 19th Ed. The
American Kennel Club. Howell Book House, NY 1998. p. 392-95.
18. Jackson K, Boger L, Goldschmidt M, et. al.: Malignant pilomatricoma in a
Miscellaneous soft-coated Wheaten Terrier. Vet Clin Pathol. 2010 Jun;39(2):236-40.
• Breed name synonyms: Wheaten. 19. Holt TL & Mann FA: Carbon dioxide laser resection of a distal carpal
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain), pilomatricoma and wound closure using swine intestinal submucosa in a
ANKC (Australian National Kennel Club), NKC (National Kennel Club). dog. J Am Anim Hosp Assoc. 2003 Sep-Oct;39(5):499-505.
• AKC rank (year 2008): 60 (1,481 dogs registered) 20. Harder MA, Fowler D, Pharr JW, et. al.: Segmental aplasia of the caudal
• Internet resources: Soft Coated Wheaten Terrier Club of vena cava in a dog. Can Vet J. 2002 May;43(5):365-8.
21. Helman RG, Rames DS, Chester DK: Ichthyosiform Dermatosis in a
America: www.scwtca.org
Soft-Coated Wheaten Terrier. Vet Dermatol 1997: 8[1]:53-58.
Soft Coated Wheaten Terrier Association of Canada:
22. Littman MP & Smagala AJ: The Open Registry and DNA Bank for
www.scwtac.com Soft-Coated Wheaten Terriers at the University of Pennsylvania School of
Soft Coated Wheaten Terrier Club of Great Britain: Veterinary Medicine. Proceedings, 2009 Tufts’ Canine and Feline Breeding
www.wheaten.org.uk and Genetics Conference. 2009.
Wheaten Health Initiative: www.wheatenhealthinitiative.com 23. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 432-435.
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Littman MP, Dambach DM, Vaden SL, et. al.: Familial protein-losing
enteropathy and protein-losing nephropathy in Soft Coated
Wheaten Terriers: 222 cases (1983-1997). J Vet Intern Med. 2000
Jan-Feb;14(1):68-80.
3. Vaden SL, Hammerberg B, Davenport DJ, et. al.: Food hypersensitivity
reactions in Soft Coated Wheaten Terriers with protein-losing enteropathy
or protein-losing nephropathy or both: gastroscopic food sensitivity
testing, dietary provocation, and fecal immunoglobulin E. J Vet Intern Med.
2000 Jan-Feb;14(1):60-7
4. Lees, GE: Inherited Kidney Diseases in Dogs and Cats. Proceedings, 2005
Tufts’ Canine and Feline Breeding and Genetics Conference. 2005.
5. Slater MR & Harbison J: General Health Survey on Soft Coated Wheaten
Terriers. Soft Coated Wheaten Terrier Club of America. 2000.
6. Allenspach K, Lomas B, Wieland B, et. al.: Evaluation of perinuclear
anti-neutrophilic cytoplasmic autoantibodies as an early marker of
protein-losing enteropathy and protein-losing nephropathy in Soft Coated
Wheaten Terriers. Am J Vet Res. 2008 Oct;69(10):1301-4.
7. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
2000.
8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
9. Luckschander N, Allenspach K, Hall J, et. al.: Perinuclear antineutrophilic
cytoplasmic antibody and response to treatment in diarrheic dogs with
food responsive disease or inflammatory bowel disease. J Vet Intern Med.
2006 Mar-Apr;20(2):221-7.
10. Nash AS, Creswick JA: Familial nephropathy in soft-coated wheaten
terriers. Vet Rec. 1988 Dec 17;123(25):654-5.
11. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum
thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
12. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
13. Peterson ME, Kintzer PP, Kass PH: Pretreatment clinical and laboratory
findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). J Am
Vet Med Assoc. 1996 Jan 1;208(1):85-91.
14. Chew DJ & DiBartola SP: Urinary Incontinence in Dogs--Diagnosis and
Treatment. Proceedings, 2008 Atlantic Coast Veterinary Conference. 2008.
15. De Lorenzi L, Groppetti D, Arrighi S, et. al.: Mutations in the RSPO1
coding region are not the main cause of canine SRY-negative XX sex
442
Spinone Italiano
Eyes are yellow brown, with the depth of color well matched to the
coat. Wide-set, the eyes have tight fitting lids and eyes are closest
to round in shape and neither protrude or recess. Eyelid margins
match the coat, ranging from brown through flesh tone. The nose
is large and protrudes forward of the front lip profile. A scissors
or level bite is accepted. Occipital protuberance is prominent. The
muzzle is square, the stop is subtle. The profile is straight to slightly
Roman-nosed. The triangular fine-leathered ears with rounded tip
hang particularly low and back on the skull. The neck has a double
dewlap and is thick. A broad, deep thorax is evident, and the topline
drops down except for an arch over the loin area, with minimal
The Breed History abdominal tuck up. A square conformation and good solid bone
The breed harkens from the Piedmont region of Northern Italy. A characterize this strong hunter.
rare breed, this is a bird gundog in the AKC Sporting Dog group. It is
one of the most ancient of the Italian hunting dog breeds, with very The tail is thicker at the base, and carried below back level. Can
early records of a tough, bristly pointer meeting the description of be docked to 5.5-8” in length. The feet are large but well knuckled
the Spinone dating to a work in 500 BC. Works from the 13th to up—nails are dark but not black and the front and rear dewclaws
15th century describe very closely such a dog—then termed bristled may be removed. The rear feet are more oval than the front feet.
hound, bacco Spinoso or the rough-coated hound. AKC recognition The gait is a long easy trot that covers a great deal of ground with
occurred in 2000. each stride.
Weight: females 62-70 lb (28-32 kg) males 70-84 lb (32-38 kg) Normal Physiologic Variations
None reported
Coat: Harsh dense wired texture of haircoat and thick skin keep this
dog warm and comfortable in the field. Single-coated, with straight
to crimped hairs. Length is closely controlled, with 1.5-2.5” being
Drug Sensitivities
None reported
the breed standard, with a 0.5” tolerance outside the standard.
Not feathered but face is embellished with moustache, eyebrows
and beard to protect the dog from rough going. Colors are limited Inherited Diseases
to Capuchin Friar’s Frock, also called “monk’s habit” (a chestnut Hip Dysplasia: Polygenic trait causing degenerative joint disease
brown), white with brown markings, white, orange roan +/- orange and hip arthritis. OFA reports 15.5% affected.1
markings, brown roan, +/- brown markings.
Elbow Dysplasia: Polygenic trait causing elbow arthritis. OFA
Longevity: 12-14 years reports 5.8% affected.1
Points of Conformation: These large dogs have a very people-like Patella Luxation: Polygenically inherited laxity of patellar
expression. Skull is long, and expression is of gentle intelligence. ligaments, causing luxation, lameness, and later degenerative joint
443
disease. Treat surgically if causing clinical signs. Too few Spinone
Italianos have been screened by OFA to determine an accurate
Genetic Tests
Tests of Genotype: A linked-marker test is available for cerebellar
frequency.1 ataxia from the Animal Health Trust.
Cerebellar Ataxia (CA, Cerebellar Abiotrophy): Autosomal Tests of Phenotype: CHIC Certification: Required testing includes
recessive disease of progressive incoordination. Onset of hip and elbow radiographs, and CERF eye examination (beginning at
hypermetria and ataxia about 4-8 months of age. No affected 2 years of age). Optional recommended testing includes congenital
dogs survive past 1 year of age. Identified in Spinone in Italy, Great cardiac examination, and thyroid profile including autoantibodies
Britain, Denmark, Holland, and the US. All affected dogs trace (annually until year 6, then every other year until 10). (See CHIC
back to a common family. A linked-marker based genetic test is website; www.caninehealthinfo.org).
available.2,3
Recommend patella evaluation.
Disease Predispositions
Ectropion: A rolling out of the eyelids, can cause frequent Miscellaneous
conjunctivitis, and ocular discharge. Often with a medial canthus • Breed name synonyms: Spinone, Spinoni Italiani (pl), Italian
pocket. Reported in 17.5% of Spinones in the 1999 SCA Health Griffon, Italian Spinone.
Survey Report.4 • Registries: AKC, CKC, KCGB (Kennel Club of Great Britain), NKC
(National Kennel Club).
Allergies: Inhalent or food. Presents with pruritis and pyotraumatic • AKC rank (year 2008): 114 (318 dogs registered)
dermatitis (hot spots). Reported in 15.6% of Spinones in the 1999 • Internet Resources: Spinone Club of America:
SCA Health Survey Report.4 www.spinoneclubofamerica.com
Italian Spinone Club of Great Britain: www.italianspinone.co.uk
Hypothyroidism: 8.0% positive for thyroid autoantibodies based on
testing at Michigan State University. (Ave. for all breeds is 7.5%).5,6
References
Otitis Externa: Recurrent Ear Infection. Reported in 5.8% of 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
Spinones in the 1999 SCA Health Survey Report.4 2. Bianchi E, Corradi A, Dondi M, et. al.: Two Cases of Cerebellar Cortical
Abiotrophy in Italian Spinone. Proceedings World Small Animal Veterinary
Cataracts: Anterior cortex intermediate and nuclear punctate Association Congress 2002.
cataracts predominate in the breed. Identified in 3.87% of Spinone 3. Wheeler S & Rusbridge C: Neurological syndrome in Italian spinones. Vet
Italiani CERF examined by veterinary ophthalmologists between Rec. 1996 Mar 2;138(9):216.
4. Spinone Club of America: 1999 Spinone Club of America Health Survey
2000-2005. CERF does not recommend breeding any Spinone
Report. January, 2000.
Italiano with a cataract.7
5. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Inherited Epilepsy: Grand-mal or petit-mal seizures. Control with
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
anticonvulsant medication. Reported in 3.4% of Spinones in the 6. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
1999 SCA Health Survey Report.4,8 Population and Animal Health, Michigan State University. April, 2007.
7. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Persistent Pupillary Membranes: Strands of fetal remnant College of Veterinary Ophthalmologists. ACVO, 2007.
connecting; iris to iris, cornea, lens, or involving sheets of tissue. 8. Hill C: Primary epilepsy in the Italian spinone. Vet Rec. 2006 Sep
The later three forms can impair vision, and dogs affected with 9;159(11):368.
these forms should not be bred. Identified in 3.03% of Spinone 9. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Italiani CERF examined by veterinary ophthalmologists between Ackerman. AAHA Press, p. 240, 1999.
2000-2005.7 10. Boyd SP, Taugner FM, Serrano S, et. al.: Matrix “blues”: clue to a cranial
thoracic mass in a dog. Vet Clin Pathol. 2005 Sep;34(3):271-4.
Entropion: A rolling in of the eyelids that can cause corneal 11. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
irritation and ulceration. Identified in 2.53% of Spinone Italiani Book House, NY 2006. p. 115-119.
CERF examined by veterinary ophthalmologists between
2000-2005.7
They may see small pets or children as prey, may fight with other
dogs, will not back down in a fight and have a tenacious crushing
bite. They should be on leash unless in a fenced enclosure.
Electric fencing will not deter them. They are good diggers. They
need human companionship, and do not do well if left alone or
kenneled. They do not tolerate temperature extremes well. At least
The Breed History a basic level obedience training course is strongly advised. Early
Ancient lineage of all fighting dogs traces back to Roman war dogs, socialization to children and other pets should be done. They are
from which the Mastiff lines arose. The early Staffordshire arose generally tolerant, but should be supervised. They will guard family,
from Bulldog and Mastiff crosses, and were used for bull and bear but not the home. They may snore.
baiting. These were called Old Pit Bulls, or Pit Dogs. Manchester
terrier and English White terrier (now extinct) crosses were done
to make the dog smaller and quicker when dog fighting replaced Normal Physiologic Variations
baiting. These terrier crosses were termed Bull and Terrier, and None reported
eventually became known as Staffordshire Bull Terriers. The first
dogs to reach North America arrived in the 1880s. It was from Drug Sensitivities
these American imports that the American Staffordshire Terriers None reported
originated, which are taller and heavier in stature than the
Staffordshire bull. First AKC registry for Staffordshire Bull Terriers
occurred in 1974.
Inherited Diseases
Hip Dysplasia: Polygenically inherited trait causing degenerative
joint disease and hip arthritis. OFA reports 17.4% affected.1
Breeding for Function
Originally bred for bull and bear baiting, they were later bred for Elbow Dysplasia: Polygenically inherited trait causing elbow
dog fighting. They were also highly prized as ratters. Staffordshire arthritis. OFA reports 16.4% affected.1
Bull Terriers were sometimes called Nanny Dogs in Britain because
of their role as guardians of the home and family. Juvenile Cataracts (Hereditary Cataracts, HC): Autosomal
recessive disorder causing bilateral nuclear and cortical cataracts
with an onset around 3 months of age. Identified in 2.05% of
Physical Characteristics Staffordshire Bull Terriers CERF examined by veterinary ophthalmol-
Height at Withers: 14-16” (35.5-40.5 cm) ogists between 2000-2005. A genetic test is available. CERF does not
recommend breeding any Staffordshire Bull Terrier with a cataract.2,3
Weight: females 24-34 lb (11-15.5 kg), males 28-38 lb (12.5-17 kg).
L-2-Hydroxyglutaric Aciduria (L2-HGA): Autosomal recessive
Coat: The short, smooth glossy coat lies flat and colors accepted
disorder. Affected Staffordshire Bull Terriers present with seizures,
include brindle, brindle and white, black, red, white, fawn or blue.
ataxia, dementia, and tremors. Levels of L-2-hydroxyglutaric acid
Liver or Black and Tan are disqualifying colors.
are elevated in all body fluids evaluated (urine, plasma, and CSF). A
Longevity: 11-12 years genetic test is available.4,5
Points of Conformation: The breed is characterized by a compact, Patella Luxation: Polygenically inherited laxity of patellar
muscular square conformation. They possess a broad skull with ligaments, causing luxation, lameness, and later degenerative
prominent masseter muscles, a black nose, and short blocky muzzle. joint disease. Treat surgically if causing clinical signs. Too few
The stop is distinct. The eyes are front facing and moderate in size, Staffordshire Bull Terriers have been screened by OFA to determine
round and variable in color. Ears are small to medium in size, half an accurate frequency.1
pricked or rose. They have a short well-muscled neck, level topline,
and are broad through the chest. The thorax is barrel shaped and the Disease Predispositions
abdomen mildly tucked up. The low set tapering tail is carried low. Distichiasis: Abnormally placed eyelashes that irritate the cornea
Limbs are straight-boned, the feet are compact and medium in size. and conjunctiva. Can cause secondary corneal ulceration. Identified
Dewclaws may be removed. The hindquarters are well muscled. The in 10.25% of Staffordshire Bull Terriers CERF examined by veterinary
gait is strong, quick, moderate in stride length, and agility is evident. ophthalmologists between 2000-2005.2
445
Brachycephalic Complex: Includes Elongated Soft Palate, Congenital Laryngeal Paralysis: Reported at an increased
Stenotic Nares, Hypoplastic Trachea, and Everted Laryngeal frequency in the breed in the UK, with an average age of onset
Saccules. Causes dyspnea, and can cause collapse and death with of 4 to 6 months. Causes voice change or hoarse bark, exercise
extreme stress. Identified in 5.5% of Staffordshire Bull Terriers in an intolerance, gagging, coughing, stridor, dyspnea, cyanosis, collapse,
Australian study. Surgery is indicated in severe cases.6 and vomiting. Undetermined mode of inheritance.17
Hypothyroidism: Inherited autoimmune thyroiditis. Too Compulsive Tail Chasing, Epilepsy, Osteochondritis Dessicans-
few Staffordshire Bull Terriers have been tested for thyroid Stifle, and Prognathism are reported.18
autoantibodies at Michigan State University to determine an
accurate frequency. (Ave. for all breeds is 7.5%).7,8 Isolated Case Studies
Ciliary Dyskinesia: Primary ciliary dyskinesia was diagnosed in a
Tibial Tuberosity Avulsion Fracture: Traumatic avulsion seen
14-week old Staffordshire bull terrier that had a history of respiratory
in immature dogs, usually between 4-6 months of age. Requires
disease from 7 weeks of age. Pneumonia was diagnosed based on
surgical repair. Occurs in 3.3% of Staffordshire Bull Terriers, who
thoracic radiographs and trans-tracheal aspirate. Transmission
account for 85% of all cases seen.9
electron microscopy of the bronchi and trachea indicated the
Persistent Pupillary Membranes: Strands of fetal remnant presence of both primary and secondary ciliary dyskinesia.19
connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
Ocular Mixed Germ Cell Tumor: A 3-year-old female neutered
later three forms can impair vision, and dogs affected with these
Staffordshire Bull Terrier presented with a mixed germ cell tumor
forms should not be bred. Identified in 1.23% of Staffordshire Bull
involving the base of the iris and the ciliary body of the right eye.20
Terriers CERF examined by veterinary ophthalmologists between
2000-2005.2 Rhabdomyoma/Myxosarcoma: Separate case reports of;
a six-year-old Staffordshire bull terrier with right atrial
Demodicosis, Juvenile Generalized: Overgrowth of demodex mites
rhabdomyoma, a six-year-old Staffordshire bull terrier with a
in hair follicles due to an underlying immunodeficiency. Causes
lingual rhabdomyosarcoma, and a case of right atrial myxosarcoma
hair loss and inflammation. Reported 17.1 odds ratio versus other
in a Staffordshire bull terrier.21,22,23
breeds.10
446
Staffordshire Bull Terriers. J Vet Intern Med. 2003 Jul-Aug;17(4):551-6.
5. Scurrell E, Davies E, Baines E, et. al.: Neuropathological findings in a
Staffordshire bull terrier with l-2-hydroxyglutaric aciduria. J Comp Pathol.
2008 Feb-Apr;138(2-3):160-4.
6. Torrez CV & Hunt GB: Results of surgical correction of abnormalities
associated with brachycephalic airway obstruction syndrome in dogs in
Australia. J Small Anim Pract. 2006 Mar;47(3):150-4.
7. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
8. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
9. Gower JA, Bound NJ, Moores AP, et. al.: Tibial tuberosity avulsion fracture
in dogs: a review of 59 dogs. J Small Anim Pract. 2008 Jul;49(7):340-3.
10. Plant JD, Lund EM & Yang M: A case-control study of the risk factors for
canine juvenile-onset generalized demodicosis in the USA. Vet Dermatol.
2011 Feb;22(1):95-9.
11. Sullivan M, Lee R, Fisher EW, et. al.: A study of 31 cases of gastric
carcinoma in dogs. Vet Rec. 1987 Jan 24;120(4):79-83.
12. Baker-Gabb M, Hunt GB, France MP: Soft tissue sarcomas and mast
cell tumours in dogs; clinical behaviour and response to surgery. Aust Vet J.
2003 Dec;81(12):732-8.
13. Curtis R, Barnett KC, Leon A: Persistent hyperplastic primary vitreous in
the Staffordshire bull terrier. Vet Rec. 1984 Oct 13;115(15):385.
14. Allen LBA, Pratt A, Lulich J, et. al.: Canine Cystine Urolithiasis:
Investigation of Cases Identified in the United Kingdom. Proceedings, 2008
British Small Animal Veterinary Congress. 2008.
15. Wilson GJ: Inverted Canines in the Staffordshire Bull Terrier - A New
Clinical Condition. Aust Vet Pract 2003: 33[2]:83-85.
16. Clercx C: Chronic Non-Cardiac Cough in Dogs. Proceedings, 2010 World
Small Animal Veterinary Association World Congress. 2010.
17. Kirby BM: Laryngeal Paralysis Diagnosis and Management. Proceedings,
2008 World Small Animal Veterinary Association World Congress. 2008.
18. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 207 AAHA Press, 1999.
19. De Scally M, Lobetti RG, Van Wilpe E: Primary ciliary dyskinesia in a
Staffordshire bull terrier. J S Afr Vet Assoc. 2004 Sep;75(3):150-2.
20. Patterson-Kane JC, Schulman FY, Santiago N, et. al.: Mixed germ cell
tumor in the eye of a dog. Vet Pathol. 2001 Nov;38(6):712-4.
21. Mansfield CS, Callanan JJ, McAllister H: Intra-atrial rhabdomyoma
causing chylopericardium and right-sided congestive heart failure in a dog.
Vet Rec. 2000 Sep 2;147(10):264-7.
22. Lascelles BD, McInnes E, Dobson JM, et. al.: Rhabdomyosarcoma of the
tongue in a dog. J Small Anim Pract. 1998 Dec;39(12):587-91.
23. Briggs OM, Kirberger RM, Goldberg NB: Right atrial myxosarcoma in a
dog. J S Afr Vet Assoc. 1997 Dec;68(4):144-6.
24. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 436-438.
447
Standard Schnauzer
toes are well arched, with thick pads and black nails. Rear dewclaws
are generally taken off. The gait is quick, smooth and true.
Prognathism is reported.10
Genetic Tests
Tests of Genotype: Direct genetic test for PDP1 is available at the
University of Missouri and the Animal Health Trust.
Miscellaneous
• Breed name synonyms: Sussex
• Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
451
Swedish Vallhund
Recognized Behavior Issues and Traits
The breed is watchful, energetic, fearless, alert, intelligent, friendly,
eager to please, active, and steady, making a good herding and
companion dog. Sound temperament, neither vicious or shy.
Drug Sensitivities
None Reported
The Breed History
It is believed that the Swedish Vallhund goes back more than 1000
years to the days of the Vikings. During the eighth or ninth century,
Inherited Diseases
Patella Luxation: Polygenically inherited laxity of patellar
historians state, either the Swedish Vallhund was brought to Wales
ligaments, causing luxation, lameness, and later degenerative joint
or the Corgi was taken to Sweden, hence the similarities between
disease. Treat surgically if causing clinical signs. Reported at a high
the two breeds. By 1942, the breed was almost extinct, and a
frequency, however, too few Swedish Vallhunds have been screened
breeding program was started. In 1948, the Swedish Kennel Club
by OFA to determine an accurate frequency. Reported as a breed
recognized the breed. In 1974, the first Swedish Vallhund came to
problem on the SVCA website.2
England, and the Swedish Vallhund Society received approval from
the UK Kennel Club in 1980. The first litter was born in the US in Hip Dysplasia: Polygenically inherited trait causing degenerative
1986. The breed received AKC recognition in 2007. joint disease and hip arthritis. OFA reports 10.2% affected.2
Breeding for Function Elbow Dysplasia: Polygenically inherited trait causing elbow
The Swedish Vallhund is a small, powerful, fearless, sturdily built arthritis. OFA reports 2.4% affected.2
Spitz herding dog. Swedish Vallhunds are bred to work on farms
and ranches as a cattle/sheep herder. Their herding style is low to Disease Predispositions
the ground and they herd by rounding up and nipping at the hocks. Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue.
Physical Characteristics The later three forms can impair vision, and dogs affected with
Height at Withers: female 11.5 - 12.5” (29-32 cm), male 12.5 - these forms should not be bred. Identified in 15.15% of Swedish
13.5” (32-34.5 cm) Vallhunds CERF examined by veterinary ophthalmologists between
2000-2005.3
Weight: 25-35 lbs. (11.5-16 kg).
Cataracts: Punctate cataracts predominate in the breed. Identified
Coat: Medium length hair, harsh; topcoat close and tight. Undercoat in 4.85% of Swedish Vallhunds CERF examined by veterinary
is soft and dense. Hair is short on the head and the foreparts of the ophthalmologists between 2000-2005. CERF does not recommend
legs and slightly longer on the neck, chest and back parts of the breeding any Swedish Vallhund with a cataract.3
hind legs. A sable pattern is seen in colors of grey through red. Dark
muzzle/mask. White is permitted as a narrow blaze, neck spot, slight Vitreous Degeneration: Liquefaction of the vitreous gel which may
necklace, and white markings on the legs, and chest. White can not predispose to retinal detachment. Identified in 3.64% of Swedish
be in excess of one third of the dog’s total color. Vallhunds CERF examined by veterinary ophthalmologists between
2000-2005.3
Longevity: 12-14 years.
Distichiasis: Abnormally placed eyelashes that irritate the cornea
Points of Conformation: The relationship of height to length of and conjunctiva. Can cause secondary corneal ulceration. Identified
body should be 2:3. Viewed from above, the head forms an even in 3.03% of Swedish Vallhunds CERF examined by veterinary
wedge from skull to tip of the nose and is well filled-in under the ophthalmologists between 2000-2005.3
eyes. The eyes are medium size, oval in shape and dark brown with
black eye rims. Prick ears. Viewed from the side, the muzzle should Retinal Dysplasia: Focal retinal dysplasia/folds, and geographic
look rather square, slightly shorter than the skull. Scissors bite. Tails retinal dysplasia are recognized in the breed. The later can progress
may be long, stub, or bob. Dewclaws may be removed. The gait is to retinal detachment and blindness. Reported in 2.42% of Swedish
sound with strong reach and drive. Vallhunds CERF-examined by veterinary ophthalmologists between
2000-2005.3
452
Hypothyroidism: Inherited autoimmune thyroiditis. Too few
Swedish Vallhunds have been tested for thyroid autoantibodies
at Michigan State University to determine an accurate breed
frequency. (Ave. for all breeds is 7.5%).4,5
Genetic Tests
Tests of Genotype: none
Miscellaneous
• Breed name synonyms: Vasgotaspets, Swedish Cattle Dog, Viking
Dog, Spitz of the West Goths
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel
Club), FCI.
• AKC rank (year 2008): 149 (67 dogs registered)
• Internet resources: Swedish Vallhund Club of America:
http://swedishvallhund.com
Swedish Vallhund Club of Canada:
www.swedishvallhundclubofcanada.com
Swedish Vallhund Society (UK): www.swedishvallhunds.co.uk
References
1. Evans KM & Adams VJ: Proportion of litters of purebred dogs born by
caesarean section. J Small Anim Pract. 2010 Feb;51(2):113-8.
2. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
3. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
4. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
Vet Med Assoc 2002 Feb 15;220(4):466-71.
5. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
6. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell Book
House, NY 2006. p. 706-709.
453
Tibetan Mastiff
is embellished by a mane. The head is held high. The stop is
prominent. A curved tail is carried high over the dorsum, and is
not longer than the hock when measured. Moderate flews are
acceptable, and the facial skin may be somewhat wrinkled in the
mature animal. Wide set almond shaped eyes are pigmented brown,
and not prominent. Ears are triangular, covered with short hair, with
thick leather, and hanging to the head when resting, but high set
and carried high when active. A scissor or level bite is acceptable.
Some dewlap may be present. Straight level back, and thorax deep
and broad but not barrel. The abdomen is tucked up. The dog has
low set hocks, and tight large strong compact feet. A TM may single
The Breed History track during motion. Single dewclaws are present on the forefeet,
These massive quintessential guardians originated in Tibet, and single or double may be present on the hind feet. Rear dewclaw
were traditional guards of home and monastery. Though used for removal is optional.
livestock defense, they are territory guardians first and foremost.
Some consider these dogs to have been the original Mastiff-type
dog which was exported to develop other versions of the mastiff
Recognized Behavior Issues and Traits
Loyal to family and home, these dogs are generally aloof with
in Europe and the various mountain dogs. The first Mastiff is
strangers. Dogs of this breed need plenty of exercise and some
thought to have arrived in England around 1847, with a pair
people contact. They are too intelligent to be left alone and can be
arriving around1874. The year 1931 marked the first recognition
very destructive if bored and lonely. Lots of room in the home to
of the breed in the UK kennel club. In the early 1970s, breeding
accommodate their large stature, and plenty of room outdoors to
stock was introduced to the US. Because of the nomadic life style
run are essential. Can night bark. Instinct for protection of home is
of the Tibetans, regional variations in type occurred, so variation
strong. Socialize with children early. High intelligence and strong
in conformation and size is a hallmark of the native stock. The AKC
independence makes them a tougher dog to train than some. Some
accepted the breed as its 155th in 2006. DNA analysis suggests
refer to them as having a strong stubborn streak. Early socialization
that the breed is more ancient than other domestic dog breeds,
and plenty of training is essential. Crate training is important so
diverging from the grey wolf lineage approximately 58,000 years
the dog learns to be alone and comfortable in a safe “den”. Highly
ago.1
territorial, these dogs will defend vigorously. May be quite dominant
with other dogs, and must be supervised when introduced to new
Breeding for Function people or animals to prevent possible mishaps. They are capable
The Himalayas are a harsh mountainous region, with extremes climbers, so a high sturdy fence is necessary. Not for off leash,
of temperature and terrain. These hardy strong dogs were bred these independent dogs may not come when called. A dog may
exclusively for guardian function and to withstand the rigors of not allow visitors into a home without introduction so caution is
their environment. needed if children come to play. Can be destructive, especially when
young; with their strong jaws, they can chew extensively. Needs
Physical Characteristics daily brushing while blowing their coat using a rake, otherwise
Height at Withers: males 26-30in.” (66-76cm), females 24-28 in. a weekly slicker brush is usually adequate. Moderate exercise
(61-71 cm) requirements—are less active indoors, more active outdoors.
Genetic Tests
Tests of Genotype: Direct tests for coat color are available from
VetGen.
Drug Sensitivities
None reported
Inherited Diseases
The Breed History Patella Luxation: Polygenically inherited laxity of patellar
Tibetan Spaniels can be found in over 2000 years of recorded ligaments, causing luxation, lameness, and later degenerative joint
history. This breed was highly esteemed in the Tibetan Monasteries, disease. Treat surgically if causing clinical signs. OFA reports 9.4%
and these dogs nicknamed “Lion dog” were frequently given as affected. Reported at a frequency of 3.1% in the 2006 TSCA Health
gifts—never sold to visiting dignitaries. The Pekingese and Japanese Survey.1,2
Chin may be relatives of this dog. First exports to England occurred
in the late 1800s, and export to America occurred in the year 1965. Elbow Dysplasia: Polygenically inherited trait causing elbow
Breed registry with the AKC was established in 1984. arthritis. OFA reports 7.9% affected.1
Recognized Behavior Issues and Traits Hypothyroidism: Inherited autoimmune thyroiditis. 6.0% positive
Reported breed attributes include: Alarm barkers, friendly, for thyroid autoantibodies based on testing at Michigan State
active-high energy, cat-like disposition, loyal, intelligent, good University. (Ave. for all breeds is 7.5%).5,6
temperament but assertive and aloof with strangers. They need
456
Entropion: Rolling in of eyelids, often causing corneal irritation or hyperoxaluria since there was no exposure to agents capable of
ulceration. Entropion is reported in 4.82% of Tibetan Spaniels CERF producing secondary hyperoxaluria.11
examined by veterinary ophthalmologists between 2000-2005.4
Persistent Pupillary Membranes: Strands of fetal remnant Brachygnathism, Polydontia, Prognathism, Retinal Dysplasia,
connecting; iris to iris, cornea, lens, or involving sheets of tissue. and von Willebrand’s Disease are reported.25
The later three forms can impair vision, and dogs affected with
these forms should not be bred. Identified in 4.91% of Tibetan Isolated Case Studies
Terriers CERF examined by veterinary ophthalmologists between Recurrent Flank Alopecia (Seasonal Flank Alopecia): Case
2000-2005.8 report of a 2-year-old, male, neutered Tibetan Terrier with winter
flank alopecia. The disorder is characterized by episodes of truncal
Deafness: Congenital sensorineural deafness can be unilateral non-scarring alopecia (and often hyperpigmentation) that usually
of bilateral. Diagnosed by BAER testing. Reported at a frequency occur on a recurrent, seasonal basis. Diagnosis is by clinical signs
of 3.1% in the 2003 TTCA Health Survey. Unknown mode of and biopsy.26
inheritance.5,17
Malignant Histiocytosis: An 8-year-old male Tibetan Terrier
Missing Teeth: Reported at a frequency of 2.6% in the 2003 TTCA showed prolonged astasia, complete paralysis, tic-like signs,
Health Survey. Unknown mode of inheritance.5 and seizure and died 2 months after the onset of symptoms.
Histopathologic diagnosis was diffuse leptomeningeal malignant
Cataracts: Anterior cortex punctate cataracts predominate in the histiocytosis of the brain and spinal cord.27
breed. Non-congenital cataracts have a heritability of 0.13, and are
76% correlated to PRA in the breed. Reported in 5.92% of Tibetan
Terriers presented to veterinary teaching hospitals. Cataracts Genetic Tests
between 2-7 years of age are reported at a frequency of 2.2% in Tests of Genotype: A direct test for NCL is available from the OFA.
the 2003 TTCA Health Survey. Identified in 2.39% of Tibetan Terriers
A direct test for PLL is available from the OFA and Animal Health
CERF examined by veterinary ophthalmologists between 2000-2005.
Trust.
Unknown mode of inheritance. CERF does not recommend breeding
any Tibetan Terrier with a cataract.5,8,18,19 A direct test for a dominant renal dysplasia susceptibility gene is
available from Dogenes.
Distichiasis: Abnormally placed eyelashes that irritate the
cornea and conjunctiva. Can cause secondary corneal ulceration. Tests of Phenotype: CHIC Certification: Required testing includes
Identified in 1.47% of Tibetan Terriers CERF examined by veterinary hip radiographs, annual CERF eye examination and BAER testing
ophthalmologists between 2000-2005.8 for deafness. Recommended tests include patella evaluation, elbow
radiographs, and thyroid profile including autoantibodies. (See CHIC
Corneal Dystrophy: Epithelial/stromal form of corneal opacities.
website; www.caninehealthinfo.org).
Identified in 1.47% of Tibetan Terriers CERF examined by veterinary
ophthalmologists between 2000-2005.8 Recommended cardiac examination.
Diabetes Mellitus: Sugar diabetes due to immune mediated
destruction of the pancreatic beta cells. Treat with insulin injections, Miscellaneous
diet, and glucose monitoring. Identified as a breed at increased risk • Breed name synonyms: Dhokhi Apso
of developing diabetes.20,21 • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club)
Idiopathic Epilepsy: Inherited seizures can be generalized or partial • AKC rank (year 2008): 96 (626 dogs registered)
seizures. Control with anticonvulsant medication. Reported at a • Internet resources: Tibetan Terrier Club of America:
frequency of 0.5% in the 2003 TTCA Health Survey.5 www.ttca-online.org
Tibetan Terrier Club of Canada: www.tibetanterriercanada.com
Renal Dysplasia: Affected dogs can succumb to renal failure Tibetan Terrier Association of the U.K.: www.the-tta.org.uk
from birth to two years of age. Mildly affected dogs can live
with compensated renal insufficiency. A direct genetic test for a
459
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Katz ML, Narfstrom K, Johnson GS, et. al.: Assessment of retinal function
and characterization of lysosomal storage body accumulation in the retinas
and brains of Tibetan Terriers with ceroid-lipofuscinosis. Am J Vet Res. 2005
Jan;66(1):67-76.
3. Riis RC, Cummings JF, Loew ER, et. al.: Tibetan terrier model of canine
ceroid lipofuscinosis. Am J Med Genet. 1992 Feb 15;42(4):615-21.
4. Alroy J, Schelling SH, Thalhammer JG, et. al.: Adult onset lysosomal
storage disease in a Tibetan terrier: clinical, morphological and biochemical
studies. Acta Neuropathol (Berl). 1992;84(6):658-63.
5. Tibetan Terrier Club of America: 2003 TTCA Health Survey. 2004.
6. Katz ML, Sanders DN, Mooney BP, et. al.: Accumulation of glial fibrillary
acidic protein and histone H4 in brain storage bodies of Tibetan terriers
with hereditary neuronal ceroid lipofuscinosis. J Inherit Metab Dis. 2007
Nov;30(6):952-63.
7. Curtis R, Barnett KC, Lewis SJ: Clinical and pathological observations
concerning the aetiology of primary lens luxation in the dog. Vet Rec. 1983
Mar 12;112(11):238-46.
8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 1999.
9. Curtis R: Lens luxation in the dog and cat. Vet Clin North Am Small Anim
Pract. 1990 May;20(3):755-73.
10. Curtis R: Aetiopathological aspects of inherited lens dislocation in the
Tibetan Terrier. J Comp Pathol. 1983 Jan;93(1):151-63.
11. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing
lens luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
12. Akhmedov NB, Baldwin VJ, Zangerl B, et. al.: Cloning and
characterization of the canine photoreceptor specific cone-rod homeobox
(CRX) gene and evaluation as a candidate for early onset photoreceptor
diseases in the dog. Mol Vis. 2002 Mar 22;8:79-84.
13. Millichamp NJ, Curtis R, Barnett KC: Progressive retinal atrophy in
Tibetan terriers. J Am Vet Med Assoc. 1988 Mar 15;192(6):769-76.
14. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
15. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
16. White SD: Update on Allergies: Atopic Dermatitis. Proceedings,
Northeast Veterinary Conference 2004.
17. Strain GM: Deafness prevalence and pigmentation and gender
associations in dog breeds at risk. Vet J. 2004 Jan;167(1):23-32.
18. Ketteritzsch K, Hamann H, Brahm R, et. al.: Genetic analysis of presumed
inherited eye diseases in Tibetan Terriers. Vet J. 2004 Sep;168(2):151-9.
19. Gelatt KN, Mackay EO: Prevalence of primary breed-related cataracts in
the dog in North America. Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
20. Catchpole B, Ristic JM, Fleeman LM, et. al.: Canine diabetes mellitus: can
old dogs teach us new tricks? Diabetologia. 2005 Oct;48(10):1948-56.
21. Catchpole B, Kennedy LJ, Davison LJ, et. al.: Canine diabetes mellitus:
from phenotype to genotype. J Small Anim Pract. 2008 Jan;49(1):4-10.
22. Ter Haar G: Diseases of the Middle and Inner Ear. Proceedings, 2005
World Small Animal Veterinary Association Congress. 2005.
23. Bower JM: Head tilt in Tibetan terrier puppies. Vet Rec. 1983 Jan
8;112(2):46.
24. Weiss DJ: Hemophagocytic syndrome in dogs: 24 cases (1996-2005). J
Am Vet Med Assoc. 2007 Mar 1;230(5):697-701.
25. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 242. AAHA Press, 1999.
26. Bassett RJ, Burton GG, Robson DC: Recurrent flank alopecia in a Tibetan
Terrier. Aust Vet J. 2005 May;83(5):276-9.
27. Uchida K, Morozumi M, Yamaguchi R, et. al.: Diffuse leptomeningeal
malignant histiocytosis in the brain and spinal cord of a Tibetan Terrier. Vet
Pathol. 2001 Mar;38(2):219-22.
28. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 602-605.
460
Toy Fox Terrier
is not throaty. Well sloped shoulder and front of chest prominent.
Level topline smoothly merges with tail, thorax is deep and ribs well
sprung, abdomen has moderate tuck up. Limbs straight, the feet are
compact and small, with oval shape and well knuckled up, dewclaws
will usually be removed from rear limbs. Gait is long, low and
smooth—topline remains straight. The tail is high set and usually
docked to the 3-4th vertebra joint.
The AKC fully recognized the Toy Fox Terrier breed in 2003, as its
148th breed, in the Toy division.
Drug Sensitivities
None Reported
461
Elbow Dysplasia: Polygenic trait causing elbow arthritis. Too
few Toy Fox Terriers have been screened by OFA to determine an
Miscellaneous
• Breed name synonyms: American Toy
accurate frequency.1 • Registries: AKC, UKC, CKC, NKC (National Kennel Club).
• AKC rank (year 2008): 88 (731 dogs registered)
Disease Predispositions • Internet resources: American Toy Fox Terrier Club:
Cataracts: Too few Toy Fox Terriers have been CERF eye examined www.atftc.com
to determine an accurate frequency in the breed. Reported in 3.78% Toy Fox Terrier Club of Canada: www.tftcc.ca
of Toy Fox Terriers presented to veterinary teaching hospitals.6,7
Genetic Tests
Tests of Genotype: Direct test for Congenital Hypothyroidism is
available from the Fyfe laboratory at Michigan State University:
http://mmg.msu.edu/faculty/fyfe.htm (517-355-6463 x1559),
HealthGene, and PennGen.
Direct test for PLL is available from the OFA and Animal Health Trust.
462
Vizsla
very straight, the feet are small and very compact and the toes are
well arched. Dewclaws usually are removed if present. Gait is easy,
long-strided, very animated and elastic, and they are nimble-footed.
They will single track at a fast trot.
464
• Registries: AKC, CKC, KCGB (Kennel Club of Great Britain)
• AKC rank (year 2008): 44 (3,010 dogs registered)
• Internet resources: Vizsla Club of America: www.vcaweb.org
Vizsla Canada: www.vizslacanada.ca
Hungarian Vizsla Club (UK): www.hungarianvizslaclub.org.uk
References
1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
2. Dodds WJ: Bleeding Disorders in Animals. Proceedings, 2005 World Small
Animal Veterinary Association Congress. 2005.
3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
hormone autoantibodies in dogs with clinical signs of hypothyroidism. J
Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
Population and Animal Health, Michigan State University. April, 2007.
5. Gibbons TA, Ruffini L, & Rieger RH: The 2008 Vizsla Health Survey. West
Chester Statistics Institute, West Chester, PA: 2009.
6. Tarpataki N, Pápa K, Reiczigel J, et. al.: Prevalence and features of canine
atopic dermatitis in Hungary. Acta Vet Hung. 2006 Sep;54(3):353-66.
7. Patterson EE, Mickelson JR, Da Y, et. al.: Clinical characteristics and
inheritance of idiopathic epilepsy in Vizslas. J Vet Intern Med. 2003
May-Jun;17(3):319-25.
8. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
9. Bedford P: Inherited Disease of the Canine Eye. Proceedings, 2001 World
Small Animal Veterinary Association Congress. 2001.
10. White SD: When Hair Loss Isn’t an Infection: Sebaceous Adenitis and
Ischemic Dermatitis. Proceedings, 2004 Northeast Veterinary Conference.
2004.
11. Macklin, A: Immune-Mediated Hemolytic Anemia: Pathophysiology &
Diagnosis. Proceedings, 2009 Western Veterinary Conference. 2009.
12. McAlees TJ: Immune-mediated haemolytic anaemia in 110 dogs in
Victoria, Australia. Aust Vet J. 2010 Jan;88(1-2):25-8.
13. Haley AC, Platt SR, Kent R, et. al.: Breed Specific Polymyositis in the
Hungarian Vizsla Dog. Proceedings, 2009 ACVIM Forum. 2009.
14. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p 242, AAHA Press, 1999
15. Clooten JK, Woods JP, Smith-Maxie LL: Myasthenia gravis and
masticatory muscle myositis in a dog. Can Vet J. 2003 Jun;44(6):480-3.
16. Galac S, Kars VJ, Voorhout G, et. al.: ACTH-independent hyperadreno-
corticism due to food-dependent hypercortisolemia in a dog: a case report.
Vet J. 2008 Jul;177(1):141-3.
17. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p 120-123.
465
Weimaraner
chest and well-sprung rib cage, level loins, and a moderately tucked
waist. They possess fine long straight limbs, with small compact
feet well knuckled up and webbed. The tail is medium and tapering,
but often cropped to 6” (15 cm) adult length. Their gait is long and
straight, smooth but elastic.
Coat: The short single-layered glossy haircoat is only recognized in Patella Luxation: Polygenically inherited laxity of patellar
the color of silver-gray to mouse-gray with a “metallic sheen”; only ligaments, causing luxation, lameness, and later degenerative joint
one small spot of white is tolerated on the chest. Over the head, disease. Treat surgically if causing clinical signs. Reported at a high
and particularly the ears, a lighter metallic gray color is noted. frequency by the OFA, but too few Weimaraners have been screened
to determine an accurate frequency.1
Though the longhaired Weimaraner is not recognized, this subtype
was used for waterfowl hunting. This double-coated, medium Hyperuricosuria (HUU)/Urate Bladder Stones: An autosomal
length water resistant coat is feathered on legs and tail. There are recessive mutation in the SLC2A9 gene causes urate urolithiasis
variations in the length, texture and volume of undercoat. A genetic and can predispose male dogs to urinary obstruction. Weirmaraners
test is available. have a computed 0.15 frequency of the defective gene. A genetic
test is available.38
Longevity: 10-14 years.
Gastric Dilation/Volvulus (GDV, Bloat): Life-threatening twisting Exocrine Pancreatic Insufficiency: The Weimaraner breed
of the stomach within the abdomen. Requires immediate veterinary has a predisposition to maldigestion from exocrine pancreatic
attention. There is a 9.1% lifetime risk of developing GDV, with insufficiency based on cPLI testing.20
4.8% of all Weimaraners dying from the condition. Odds ratios of
4.6x to 6.2x for developing bloat versus other breeds have been Cervical Spondylomyelopathy (Wobbler Syndrome): Presents
computed. A UK study shows a 5% prevalence of GVD, with it being with neck pain, UMN spasticity and ataxia. Imaging studies suggest
the cause of death of 11.6% of Weimaraners.5,6,7,8 that the primary lesion is spinal cord compression at C5-6 or
C6-7. MRI is superior to myelography in determining site, severity,
Hypertrophic Osteodystrophy (HOD): Immune-mediated disorder and nature of the spinal cord compression. Seen at an increased
causing fever, and painful, swollen joints and bones in young incidence in the breed. Undetermined mode of inheritance.21
Weimaraners. Occurs mostly within 3-14 days post-vaccination.
The disorder is not linked to a specific type of vaccine. Age of Immunodeficiency: Rare, familial disorder expressed as low IgA,
onset is 8-16 weeks. Risk factor is 21x that of other breeds, with IgG, IgM and leading to recurrent infections of skin, GIT, and CNS.
an incidence of 5.4%. Reported 21.4x odds ratio versus other Unknown mode of inheritance.22,23,24
breeds. One study found distemper virus contained in the affected
growth plates. This breed is prone to a severe variant of HOD that XX-Sex Reversal: Sry-negative XX-sex reversal causes external
can result in death without steroid therapy. Unknown mode of make characteristics of a prepuce and an enlarged clitoris, in
inheritance, but the heritability of HOD in the breed is 0.68. Occurs genetically female dogs. A uterus is usually present. Reported as a
as a widespread disorder in the breed, with no familial line having a rare disorder in the breed. Presumed autosomal recessive mode of
greater risk.9,10,11,12,13 inheritance.25
Hormonal Urinary Incontinence: Weimaraners are found to be Immunodeficient Dwarfism: Immunodeficient dwarfism in an
a breed with increased risk for spayed females to develop urinary inbred line of Weimaraner dogs was characterized by failure to
incontinence. Treat with phenylpropanolamine.14 grow, emaciation, growth hormone (GH) deficiency, decreased
lymphocyte blastogenic responsiveness to mitogens, lack of thymus
Corneal Dystrophy: Epithelial/stromal form of corneal opacities. cortex, and recurrent infections usually resulting in death.26,27
Identified in 2.40% of Weimaraners CERF-examined by veterinary
ophthalmologists between 2000-2005.2 Corneal Dystrophy, Factor XI Deficiency, Lupoid Onychopathy,
Prognathism, and Tricuspid Valve Dysplasia are reported.28
Persistent Pupillary Membranes: Strands of fetal remnant
connecting; iris to iris, cornea, lens, or involving sheets of tissue. Isolated Case Studies
The later three forms can impair vision, and dogs affected with Factor VII Deficiency/Hemophilia A: Two males from a litter of
these forms should not be bred. Identified in 2.13% of Weimaraners Weimaraners were diagnosed with hemophilia A. No other relatives
CERF-examined by veterinary ophthalmologists between 2000-2005.2 tested as affected or carrier, indicating a recent mutation.29
Mast Cell Tumor (MCT): Skin tumors that produce histamine, and Muscular Dystrophy: A 2-year-old, male Weimaraner presented
can cause inflammation and ulceration. They can reoccur locally or with a slowly progressive form of muscular dystrophy with organ
with distant metastasis. Weimaraners have a 4-8 times greater risk agenesis. He showed generalized muscle atrophy of the limbs;
for developing cutaneous mast cell tumors than other breeds.15 hypertrophy of the neck, infraspinatus, and lingual muscles;
dysphagia; regurgitation; and unilateral renal agenesis, and hiatal
Everted Cartilage of the Third Eyelid: A scroll-like curling of
hernia.30
the cartilage of the third eyelid, usually everting the margin. Can
be unilateral or bilateral, and cause ocular irritation. Identified in Immune-Complex (Arthus-Type) Vasculitis: A 7-year-old
1.07% of Weimaraners CERF-examined by veterinary ophthalmolo- Weimaraner dog with multiple episodes of neurological illness was
gists between 2000-2005.2,16 euthanatized and submitted for postmortem examination. Lesions
in the white matter of the cerebral cortex and cervical spinal cord
Follicular Dysplasia: Affected young adult Weimaraners show
showed necrotizing vasculitis. More chronic changes consisted of
progressive alopecia of the trunk (head and limbs are spared)
perivascular demyelination.31
associated with recurrent folliculitis/furunculosis. Diagnosis by
histopathology. The lesions are similar to mild cases of color Pansteatitis: Three unrelated Weimaraners were identified with
dilution alopecia.17 pyrexia and multiple subcutaneous nodules. Clinical investigation
467
revealed inflammation of subcutaneous, mesenteric and falciform
fat, with histopathological findings of sterile pansteatitis. Unknown
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1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
mode of inheritance.32 2. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
Hypomyelination: Two litters of Weimaraners developed tremors 3. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of serum thyroid
by 3 weeks of age. Many axons in the brain and spinal cord were hormone autoantibodies in dogs with clinical signs of hypothyroidism. J Am
either thinly myelinated or nonmyelinated relative to controls, while Vet Med Assoc 2002 Feb 15;220(4):466-71.
the peripheral nervous system was normally myelinated. In all areas 4. Nachreiner R & Refsal K: Personal communication, Diagnostic Center for
of white matter evaluated, astrocytes subjectively outnumbered Population and Animal Health, Michigan State University. April, 2007.
oligodendrocytes, suggesting an abnormality in glial differentiation. 5. Ward MP, Patronek GJ, Glickman LT: Benefits of prophylactic gastropexy
Clinical signs in two dogs resolved.33 for dogs at risk of gastric dilatation-volvulus. Prev Vet Med. 2003 Sep
12;60(4):319-29.
Juvenile Nephropathy: A two-year-old Weimaraner bitch 6. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
presented in renal failure. Renal pathology consisted of tubular
2000
as well as glomerular lesions. There was also an inflammatory left
7. Glickman LT, Glickman NW, Perez CM, et. al.: Analysis of risk factors for
atrial wall necrotizing arteritis.34 gastric dilatation and dilatation-volvulus in dogs. J Am Vet Med Assoc. 1994
May 1;204(9):1465-71.
Endocardial Fibroelastosis: A 9-week-old Weimaraner presented 8. Evans KM & Adams VJ: Mortality and morbidity due to gastric
with left-sided heart failure. On necropsy, diffuse fibroplasia over dilatation-volvulus syndrome in pedigree dogs in the UK. J Small Anim
the left ventricular endocardium; small, deformed papillary muscles; Pract. 2010 Jul;51(7):376-81.
and pulmonary congestion were evident, consistent with congenital 9. Mee AP, Gordon, MT,May, C, Benett, D, Anderson, DC, and sharpe, PT
endocardial fibroelastosis.35 (1983). Canine distemper virus transcripts detected in the bone cells of
dogs with metaphysical osteopathy. Bone Vol. 14:59-67.
Narcolepsy: A 3-year-old male neutered Weimaraner dog presented 10. Munjar, TA, Austin, CC, and Bruer, GJ (1998). Comparison risk factors
with acute onset cataplectic attacks, triggered by emotional events for Hypertrophic Osteodystrophy, Craniomandibular Osteopathy and
such as playing or eating. The diagnosis of narcolepsy and cataplexy Canine Distemper Virus Infection. Veterinary Comparative Orthopedic
was made based on clinical signs and evaluation of cerebrospinal Traumatology, Vol. 11:37-437.
fluid (CSF) that contained a dramatically decreased hypocretin-1 11. Malik, R, Dowden, M, Davis, PE, Allan, GS, Barrs, VR, Canfield, PJ,
and Love, DN. (1995) Concurrent juvenile cellulites and metaphyseal
concentration.36
osteopathy: An atypical canine Distemper virus syndrome. Aust. Vet. Pract.
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Genetic Tests 12. Crumlish PT, Sweeney T, Jones B, et. al.: Hypertrophic osteodystrophy
Tests of Genotype: Direct genetic test for HUU is available from in the Weimaraner dog: lack of association between DQA1 alleles
UC-Davis VGL and the Animal Health Trust. of the canine MHC and hypertrophic osteodystrophy. Vet J. 2006
Mar;171(2):308-13.
Direct genetic test for long coat is available from the Animal Health 13. LaFond E, Breur GJ & Austin CC: Breed susceptibility for
Trust and VetGen. developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
Sep-Oct;38(5):467-77.
Tests of Phenotype: CHIC Certification: Required testing includes 14. Holt PE, Thrusfield MV: Association in bitches between breed, size,
hip radiographs, CERF eye examination, and thyroid profile including neutering and docking, and acquired urinary incontinence due to
incompetence of the urethral sphincter mechanism. Vet Rec. 1993 Aug
autoantibodies. Optimal testing includes genetic test for HUU. (See
21;133(8):177-80.
CHIC website; www.caninehealthinfo.org).
15. Moore AS: Cutaneous Mast Cell Tumors in Dogs. Proceedings, 2005
World Small Animal Veterinary Association Congress. 2005.
Recommend elbow radiographs, patella evaluation, and cardiac
16. Herrera D: Surgery of the Eyelids. Proceedings, 2005 World Small
examination. Animal Veterinary Association Congress. 2005.
17. Laffort-Dassot C, Beco L, Carlotti DN: Follicular dysplasia in five
Miscellaneous Weimaraners. Vet Dermatol. 2002 Oct;13(5):253-60.
• Breed name Synonyms: Vorsthund, Vorstenhund, Weimar 18. Confer AW, Ward, BC: Spinal Dysraphism: A Congenital Myelodysplasia
Pointer, Grey Ghost in the Weimaraner. J Am Vet Med Assoc. 1972 May 15;160(10):1423-6.
19. Engel HN, Draper DD: Comparative prenatal development of the spinal
• Registries: AKC, CKC, UKC, KCGB (Kennel Club of Great Britain),
cord in normal and dysraphic dogs: embryonic stage. Am J Vet Res. 1982
ANKC (Australian National Kennel Club), NKC (National Kennel Club)
Oct;43(10):1729-34.
• AKC rank (year 2008): 31 (8,732 dogs registered) 20. Williams DA, Minnich F: Canine exocrine pancreatic insufficiency--A
• Internet resources: Weimaraner Club of America: survey of 640 cases diagnosed by assay of serum trypsin-like immunoreac-
www.weimclubamerica.org tivity. J Vet Intern Med 1990: 4[2]:123
Weimaraner Association of Canada: www.weims.ca 21. da Costa RC & Parent J: Magnetic Resonance Imaging Findings in 60
Weimaraner Club of Great Britain: Dogs with Cervical Spondylomyelopathy. Proceedings, 2009 ACVIM Forum.
www.weimaranerclubofgreatbritain.org.uk 2009.
22. Couto, CG, Krakowka, S, Johnson, G, Ciekot, P, Hill, R, Lafrado, L and
Kociba, G (1989),. In vitro immunologic features of Weimaraner dogs with
neutrophil abnormalities and recurrent infections. Vet. Immunology and
Pathology, Vol. 23:103-112.
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23. Day, MJ, Power, C, Oleshenko, J, and Rose, M (1997) Low serum
immunoglobulin concentrations in related Weimaraner dogs. Journal of
Small Animal Practice, Vol. 38:311-315.
24. Hansen, P, Clerex, Henroteaux, M, Ritten, VPMG, and Bernadina, WE
(1995). Neutrophil phagocyte dysfunction in a Weimaraner with recurrent
infections. Journal Small Animal Practice Vol. 17:721-735.
25. Meyers-Wallen VN: Inherited Disorders of Sexual Development in Dogs
and Cats. Proceedings, 2007 Tufts’ Canine and Feline Breeding and Genetics
Conference. 2007.
26. Roth JA, Lomax LG, Altszuler N, et. al.: Thymic abnormalities and growth
hormone deficiency in dogs. Am J Vet Res. 1980 Aug;41(8):1256-62
27. Roth JA, Kaeberle ML, Grier RL, et. al.: Improvement in clinical
condition and thymus morphologic features associated with growth
hormone treatment of immunodeficient dwarf dogs. Am J Vet Res. 1984
Jun;45(6):1151-5.
28. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 242, AAHA Press, 1999.
29. Dunning MD, Averis GF, Pattinson H, et. al.: Haemophilia A (factor
VIII deficiency) in a litter of Weimaraners. J Small Anim Pract. 2009
Jul;50(7):357-9.
30. Baltzer WI, Calise DV, Levine JM, et. al.: Dystrophin-deficient
muscular dystrophy in a Weimaraner. J Am Anim Hosp Assoc. 2007
Jul-Aug;43(4):227-32.
31. Berrocal A, Montgomery DL, Pumarola M: Leukoencephalitis and
vasculitis with perivascular demyelination in a Weimaraner dog. Vet Pathol.
2000 Sep;37(5):470-2.
32. German AJ, Foster AP, Holden D, et. al.: Sterile nodular panniculitis
and pansteatitis in three weimaraners. J Small Anim Pract. 2003
Oct;44(10):449-55.
33. Kornegay JN, Goodwin MA, Spyridakis LK: Hypomyelination in
Weimaraner dogs. Acta Neuropathol (Berl). 1987;72(4):394-401.
34. Roels S, Schoofs S, Ducatelle R: Juvenile nephropathy in a Weimaraner
dog. J Small Anim Pract. 1997 Mar;38(3):115-8.
35. Bentley DM: Congenital endocardial fibroelastosis in a dog. Can Vet J.
1999 Nov;40(11):805-7.
36. Schatzberg SJ, Cutter-Schatzberg K, Nydam D, et. al.: The effect
of hypocretin replacement therapy in a 3-year-old Weimaraner with
narcolepsy. J Vet Intern Med. 2004 Jul-Aug;18(4):586-8.
37. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. P 124-127.
38. Karmi N, Brown EA, Hughes SS, et. al.: Estimated frequency of the
canine hyperuricosuria mutation in different dog breeds. J Vet Intern Med.
2010 Nov-Dec;24(6):1337-42.
469
Welsh
Springer Spaniel
The gait is smooth, long, and ground covering.
Genetic Tests
Tests of Genotype: None
471
Welsh Terrier
Recognized Behavior Issues and Traits
Reported breed characteristics include: Well mannered, gregarious,
good with other dogs; better than most terriers, though may see
small pets as prey. An extroverted personality, high activity levels,
high exercise needs and high intelligence characterize the Welsh
Terrier breed. The beard may need cleaning after meals. May tend to
dig, especially if bored. Should not be off leash unless in a fenced
enclosure. Low shedding dogs but the haircoat needs regular
grooming and stripping twice a year.
Coat: They possess a wiry coarse outer coat with distinctive black Elbow Dysplasia: Polygenically inherited trait causing elbow
and tan coloring. The undercoat is short, dense and wooly. Tan is arthritis. Too few Welsh Terriers have been screened by OFA to
found on the head, legs and belly. The black jacket can be grizzled. determine an accurate frequency.1
Puppies are often born almost all black.
Primary Lens Luxation (PLL) and Secondary Glaucoma:
Longevity: 10-14 years An autosomal recessive gene causes primary lens luxation.
Homozygous affected dogs usually develop lens luxation between
Points of Conformation: The Welsh Terrier has a compact square 4-8 years of age. Rarely, heterozygous carriers can develop lens
conformation, is medium sized, and the head is square. In overall luxation, but at a later age. Lens luxation can lead to secondary
type, they appear similar to a scaled down Airedale. The eyes are glaucoma and blindness. Relative risk of 7.20x versus other breeds.
small, dark and almond-shaped, deep and fairly wide set. The ears Reported in 0.58% of Welsh Terriers CERF-examined by veterinary
are triangular and small, and the fold sits above the top of the skull ophthalmologists between 2000-2005. CERF does not recommend
and fold forwards. The stop is slight, and the muzzle is square; breeding any Welsh Terrier with lens luxation. A genetic mutation
nose is black, lips are pigmented black also. The neck is moderate has been identified, and a genetic test is available. OFA testing
in muscling and thickness; slightly arching without throatiness. shows 36% carrier, and 1% affected.1,2,3
The topline is level, the thorax deep and ribs are well sprung. The
foreface furnishings include a well-developed moustache, brows Disease Predispositions
and beard. The high set tail is usually docked and is held high. The Persistent Pupillary Membranes: Strands of fetal remnant
limbs are straight boned and the feet are round and small; nails are connecting; iris to iris, cornea, lens, or involving sheets of tissue.
black. The stride is longer than with most terriers, and movement The later three forms can impair vision, and dogs affected with
projects an effortless appearance. these forms should not be bred. Identified in 10.40% of Welsh
Terriers CERF-examined by veterinary ophthalmologists between
2000-2005.2
472
Allergic Dermatitis: Inhalant or food allergy. Presents with
pruritis and pyotraumatic dermatitis (hot spots). Welsh Terriers are
Miscellaneous
• Breed name synonyms: none
significantly over-represented with atopy versus other breeds.4 • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
ANKC (Australian National Kennel Club), NKC (National Kennel Club).
Glaucoma: Primary, narrow angle glaucoma occurs in the breed.
• AKC rank (year 2008): 101 (534 registered)
Can cause secondary lens luxation. Age of onset 4-6 years. Screen
• Internet resources: Welsh Terrier Club of America:
with gonioscopy. There is a 2.6 to 1 female to male prevalence
http://clubs.akc.org/wtca/
in the breed, with an affected frequency of 3.6%. CERF does not
Welsh Terrier Club of Great Britain: www.welshterrierclub.co.uk
recommend breeding any Welsh Terrier with narrow angles.2,5,6
Genetic Tests
Tests of Genotype: Direct test for Lens Luxation is available from
OFA and Animal Health Trust.
Drug Sensitivities
None Reported
475
Sick Sinus Syndrome: Affected dogs present with episodic Ectrodactyly: A case of monomelic forelimb ectrodactyly
weakness and syncope. Electrocardiographic findings included (lobster-claw deformity) in a West Highland white terrier is
sinus bradycardia, sinus arrest with or without escape complexes, reported. The dog was treated with a soft tissue reconstruction. This
disturbances of atrioventricular conduction, paroxysmal was the second report of ectrodactyly in this breed.37
supraventricular tachycardia, or some combination of these
dysrhythmias. Reported at a frequency of 1.8% in the 2005 WHTCA Genetic Tests
Health Survey.2,28 Tests of Genotype: Direct test for Globoid Leukodystrphy is
available from the Jefferson Medical College (215-955-1666) and
Portosystemic Shunt (PSS, Liver Shunt): Abnormal blood vessels
HealthGene.
connecting the systemic and portal blood flow. Can be intrahepatic
extrahepatic or microvascular dysplasia. Causes stunting, abnormal Direct test for Pyruvate Kinase Deficiency is available from
behavior, possible seizures, and secondary ammonium urate urinary HealthGene, PennGen, and VetGen.
calculi. Diagnosis with paired fasted and feeding serum bile acid
and/or ammonium levels, and abdominal ultrasound. Reported Tests of Phenotype: CHIC Certification: CERF eye examination
6.0x odds ratio versus other breeds. Reported at a frequency of (annually until at least age 8 years), hip radiographs, and patella
1.5% in the 2005 WHTCA Health Survey. Undetermined mode of evaluation. (See CHIC website; www.caninehealthinfo.org).
inheritance.2,29
Recommend elbow radiographs, chest (lung) radiographs, thyroid
Cystic Calculi (Bladder Stones): West Highland White Terriers are profile including autoantibodies, and cardiac examination.
found to have a predisposition to forming bladder stones. Mineral
composition is not reported.30
Miscellaneous
Superficial Necrolytic Dermatitis: A metabolic hepatopathy. • Breed name synonyms: Roseneath Terrier (historical), Poltalloch
Increased hepatic catabolism of amino acids is hypothesized to Terrier (historical), Westie.
explain the hypoaminoacidaemia seen. Reported with at a higher • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
frequency in the breed. In one report, the median age was 10 years, ANKC (Australian National Kennel Club), NKC (National Kennel Club)
and 75% were male.31 • AKC rank (year 2008): 34 (4,755 dogs registered)
• Internet resources: West Highland White Terrier Club of
Deafness, Glaucoma, Ichthyosis, IgA Deficiency, America: www.westieclubamerica.com
Microphthalmia, Oligodontia, Prognathism, Pulmonic Stenosis, Canadian West Highland White Terrier Club:
and Retained Deciduous Teeth are reported.32 www.canadawestieclub.ca
The West Highland White Terrier Club of England:
www.thewesthighlandwhiteterrierclubofengland.co.uk
Isolated Case Studies Westie Health Foundation: www.westiefoundation.org
Polycystic Kidney and Liver Disease: Polycystic kidney and liver
disease was present in four of six female and three of five male
offspring born in two matings between the same pair of West References
Highland White Terriers. Clinical signs and serum biochemistry 1. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
analysis consistent with liver failure was evident by 5 weeks of 2. West Highland White Terrier Club of America & Grayson JK: 2005 West
Highland White Terrier Club of America Health Survey: Final Report. Feb 20,
age. Affected pups were euthanized because of their disease. An
2007.
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developmental orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002
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21. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
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22. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
for Population and Animal Health, Michigan State University. April, 2007.
23. Nett CS, Reichler I, Grest P, et. al.: Epidermal dysplasia and Malassezia
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24. Bond R, Ferguson EA, Curtis CF, et. al.: Factors associated with elevated
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interferon-gamma therapy. J Vet Med Sci. 2007 Apr;69(4):455-7.
26. Peterson ME, Kintzer PP, Kass PH: Pretreatment clinical and laboratory
findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). J Am
Vet Med Assoc. 1996 Jan 1;208(1):85-91.
27. Bagley RS: Differential Diagnosis of Animals with Peripheral Nervous
System Disease. Proceedings, 2002 Atlantic Coast Veterinary Conference.
2002.
28. Moneva-Jordan A, Corcoran BM, French A, et. al.: Sick sinus syndrome
in nine West Highland white terriers. Vet Rec. 2001 Feb 3;148(5):142-7.
29. Tobias KM & Rohrbach BW: Association of breed with the diagnosis of
congenital portosystemic shunts in dogs: 2,400 cases (1980-2002). J Am
Vet Med Assoc. 2003 Dec 1;223(11):1636-9.
30. Weichselbaum RC, Feeney DA, Jessen CR, et. al.: Evaluation of the
morphologic characteristics and prevalence of canine urocystoliths from a
regional urolith center. Am J Vet Res. 1998 Apr;59(4):379-87.
31. Outerbridge CA, Marks SL, Rogers QR: Plasma amino acid concentrations
in 36 dogs with histologically confirmed superficial necrolytic dermatitis.
Vet Dermatol. 2002 Aug;13(4):177-86.
32. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 243, AAHA Press, 1999.
33. McAloose D, Casal M, Patterson DF, et. al.: Polycystic kidney and liver
disease in two related West Highland White Terrier litters. Vet Pathol. 1998
Jan;35(1):77-81.
34. Kovacevic A, Little CJ, Lombard CW, et. al.: Heart failure in two West
Highland white terriers caused by congenital angiomatous cardiac anomaly.
Vet Rec. 2007 Aug 4;161(5):161-4.
35. Aresu L, D’Angelo A, Zanatta R, et. al.: Canine necrotizing encephalitis
associated with anti-glomerular basement membrane glomerulonephritis. J
Comp Pathol. 2007 May;136(4):279-82.
477
Whippet
back is broad and the loin is long. The topline is arched starting over
the loin. The thorax is deep and ribs are well sprung. They possess a
well tucked up abdomen. The tail is long, thin, tapering and carried
low between the legs. It is gently curved upwards, reaching to the
tarsus. Leg bones are straight, feet have hare-to-cat-like shape and
the pads are hard and thick; toes well arched. Dewclaws may be
removed. Metatarsals are short.
Physical Characteristics Vertebral Heart Size: In lateral views, the VHS was 11.0 +/- 0.5
Height at Withers: female 18-21” (45.5-53.5cm), male 19-22” vertebrae (mean +/- SD) on right-to-left lateral and 11.3 +/- 0.5
(48-56 cm). vertebrae on left-to-right lateral radiographs, being larger than the
9.7 +/- 0.5 vertebrae proposed by Buchanan (P < 0.0001). The VHS
Weight: females 14-25 lb (6-11 kg), males 17-28 lb (7.5-12.5 kg). was 10.5 +/- 0.6 vertebrae on dorsoventral radiographs and 11.1 +/-
0.6 vertebrae on ventrodorsal radiographs. Both values were larger
Coat: The very short coat is firm textured but not coarse, lays than the 10.2 +/- 1.5 vertebrae (dorsoventral) (P < 0.0082) or 10.2
flat and hairs are straight. Any colors are accepted. A longhaired +/- 0.8 vertebrae (ventrodorsal) (P < 0.0001) proposed by Buchanan.
whippet association exists, though the breed standard for AKC Dogs out of racing pedigree lines had a significantly larger VHS
or any other major registry does not mention these. They cannot than those out of show pedigree lines, and trained dogs had a
compete as whippets in racing and coursing etc. In the longhaired significantly larger VHS than nontrained dogs.4
standard, miniatures are described and for these dogs; the upper
size limit is 10 lb (4.5 kg). Electrocardiogram Normal Values: Whippets can have normal
ECG values that fall outside of the normal range for other breeds,
Longevity: 12-14 years probably relating to their vertebral heart size. These include:
P-amplitude (0.30 to 0.42), R-amplitude (3.02 to 4.32), ST-segment
Points of Conformation: They have a long narrow skull and (0.06 to 0.20) and T-amplitude (0.42 to 0.84).5
tapered muzzle, though the skull is wider between the eyes. The
stop is minimal. Their gait is graceful and smooth. They possess
light bone and lithe musculature. The nose is black, and eyes
must be same color and large, and dark with pigmented palpebral
margins. Small fine-leathered ears (rose ears) are carried back and
folded. The neck is arched, long and fine, though well muscled. The
478
atrophy in the homozygous state, and increased muscle mass and
Echocardiographic Normal Values6
athletic performance in the heterozygous state. Affected dogs
Parameter Mean Mean ±2SD Range can show intermittent cramping and stiffness. A genetic test is
Body weight (kg) 13.2 9.0-17.4 9.3-17.2 available.11,12
Body surface area (m2) 0.56 0.44-0.68 0.45-0.68
Heart rate (bpm) 93.9 48.5-139.3 54.0-158.0
M-mode (mm)
Disease Predispositions
Cryptorchidism (Retained Testicles): Can be bilateral or unilateral.
IVSd 9.4 7.0-11.8 7.1-12.9 Reported at a frequency of 19% in the Whippet Health Survey.13
LVDd 37.3 29.7-44.8 25.7-47.5
LVWd 8.8 6.6-10.9 6.4-11.5 Canine Pattern Baldness: Progressive alopecia developing at
IVSs 12.0 9.0-15.1 9.0-15.5 the post- and/or pre-auricular regions, along the ventral neck,
LVDs 26.9 19.8-34.1 17.0-36.1 thorax and abdomen, and on the caudomedial thighs. The hair
LVWs 12.4 9.3-15.4 8.6-17.2 loss starts around 6 months of age and gradually progresses over
EPSS 4.2 1.4-7.1 0.4-9.2 the following year, but remains restricted to the described areas.
2D Reported at a frequency of 12% in the Whippet Health Survey,
Ao(sa) (mm) 19.0 15.7-22.3 14.8-24.0 primarily affecting females.13,14
LA(sa) (mm) 26.5 20.2-32.8 18.4-33.7
Demodicosis: Overgrowth of demodex mites causing hairloss and
LA/Ao 1.4 1.1-1.7 1.1-1.7
dermatitis. The condition has an underlying immunodeficiency in its
LA(la) (mm) 32.0 26.5-37.6 23.5-38.7 pathogenesis. Reported at a frequency of 8% in the Whippet Health
Survey. Unknown mode of inheritance.13
M-mode measurements: IVSd, interventricular septal thickness in
diastole; LVDd, left ventricular internal diameter in diastole; LVWd, Vitreous Degeneration: A liquefaction of the vitreous gel which
left ventricular wall thickness in diastole; IVSs, interventricular may predispose to retinal detachment resulting in blindness.
septal thickness in systole; LVDs, left ventricular internal diameter Identified in 5.19% of Whippets CERF examined by veterinary
in systole; LVWs, left ventricular wall thickness in systole; EPSS, ophthalmologists between 2000-2005.15
E-point to septal separation. 2D measurements: Ao(sa), aortic root
diameter from short-axis view; LA(sa), left atrial diameter from Allergic Dermatitis: Inhalant or food allergy. Presents with pruritis
short-axis view; LA(la), left atrial diameter from long-axis view. and pyotraumatic dermatitis (hot spots). Reported at a frequency of
3% in the Whippet Health Survey.13
Drug Sensitivities Hypothyroidism: Inherited autoimmune thyroiditis. 2.9% positive
Anesthesia: Sight hounds require particular attention during
anesthesia. Their lean body conformation with high surface-ar- for thyroid auto-antibodies based on testing at Michigan State
ea-to-volume ratio predisposes them to hypothermia during University. (Ave. for all breeds is 7.5%).16,17
anesthesia. Impaired biotransformation of drugs by the liver
Deafness: Congenital sensorineural deafness can be unilateral of
results in prolonged recovery from barbiturate and thiobarbiturate
bilateral. Diagnosed by BAER testing. Not associated with a specific
intravenous anesthetics. Propofol, and ketamine/diazepam
color variety in this breed. Strain reports 2.4% bilaterally deaf
combination are recommended induction agents.7
Whippets through BAER testing. Reported at a frequency of 1% in
Drug Sensitivity: Longhaired Whippets can be homozygous for the the Whippet Health Survey. Undetermined mode of inheritance.13,18
autosomal recessive MDR1 mutation allowing toxicity due to high
Cataracts: Anterior cortex and nuclear punctate cataracts
CNS drug levels of ivermectin, doramectin, loperamide, vincristine,
predominate in the breed. Identified in 2.35% of Whippets CERF
moxidectin, and other drugs. Testing in the US shows 58% carriers
examined by veterinary ophthalmologists between 2000-2005. CERF
and in Germany shows 60% carrier and 15% affected. A genetic
does not recommend breeding any Whippet with a cataract.15
test is available.8,9
Persistent Pupillary Membranes: Strands of fetal remnant
Inherited Diseases connecting; iris to iris, cornea, lens, or involving sheets of tissue. The
Hip Dysplasia: Polygenically inherited trait causing degenerative later three forms can impair vision, and dogs affected with these
joint disease and hip arthritis. OFA reports 1.4% affected.10 forms should not be bred. Identified in 1.21% of Whippets CERF
examined by veterinary ophthalmologists between 2000-2005.15
Patella Luxation: Polygenically inherited trait causing stifle
instability and arthritis. Too few Whippets have been screened by Primary Lens Luxation: Occurs at an increased frequency in the
OFA to determine an accurate frequency.10 breed. Often progresses to secondary glaucoma and blindness.
Reported relative risk of 4.57x versus other breeds.19
Elbow Dysplasia: Polygenically inherited trait causing elbow
arthritis. Too few Whippets have been screened by OFA to determine Color Dilution Alopecia: Associated with the blue (dilute) coat
an accurate frequency.10 color in Whippets. Tardive alopecia occurs in areas covered by
darkly pigmented diluted hairs, while the non-pigmented or lightly
Gross Muscle Hypertrophy (Bully Whippets): An incomplete pigmented hairs remain unaffected.20
dominant mutation in the myostatin gene produces gross muscle
479
Hemangiosarcoma and Hemangioma: In one study, Whippets • Registries: AKC, UKC, CKC, KCGB (Kennel Club of Great Britain),
had an increased frequency of visceral and nonvisceral ANKC (Australian National Kennel Club), NKC (National Kennel
hemangiosarcoma and hemangiomas.21 Club).
• AKC rank (year 2008): 63 (1,435 dogs registered)
Brachygnathism, Corneal Dystrophy, Ectodermal Defect, Gastric • Internet resources: American Whippet Club:
Dilatation-Volvulus, Micropapilla, Osteochondritis Dessicans- www.americanwhippetclub.net
Shoulder, Prognathism, Progressive Retinal Atrophy, and von National Whippet Club of Canada: www.whippetcanada.com
Willebrand’s Disease are reported.22 The Whippet Club (UK): www.thewhippetclub.com
Longhaired Whippet Association:
Isolated Case Studies http://home.ica.net/~westwood/
Phosphofructokinase Deficiency: Two male Whippet littermates Whippet Health Foundation: www.whippethealth.org
presented at 1 year of age with pallor, tachycardia, systolic heart
murmur, dark yellow to orange feces, intermittent lethargy, References
pigmenturia, and muscle shivering or cramping after exercise. They 1. Kintzer PP & Peterson ME: Progress in the Diagnosis and Treatment of
were anemic, with increased serum creatine kinase activity and Canine Hypothyroidism. 2007. Proceedings, ACVIM 2007.
hyperkalemia. They were homozygous for the mutation in the PFK 2. van Geffen C, Bavegems V, Duchateau L, et. al.: Serum thyroid
gene found in English Springer Spaniel dogs with PFK deficiency.23 hormone concentrations and thyroglobulin autoantibodies in trained and
non-trained healthy whippets. Vet J. 2006 Jul;172(1):135-40.
Lung Lobe Torsion: A four-year-old, entire male whippet was 3. Caldin M, Carli E, Furlanello T, et. al.: A retrospective study of 60 cases of
presented with a three-day history of lethargy, inappetence, eccentrocytosis in the dog. Vet Clin Pathol. 2005 Sep;34(3):224-31.
occasional retching, a soft cough and intermittent episodes of 4. Bavegems V, Van Caelenberg A, Duchateau L, et. al.: Vertebral
heart size ranges specific for whippets. Vet Radiol Ultrasound. 2005
haemoptysis. Thoracic radiographs suggested a diagnosis of lung
Sep-Oct;46(5):400-3.
lobe torsion. A concurrent lung lobe torsion of the right cranial and 5. Bavegems V, Duchateau L, Ham LV, et. al.: Electrocardiographic reference
right middle lung lobes was confirmed at exploratory thoracotomy. values in whippets. Vet J. 2009 Oct;182(1):59-66.
Management included resection of both of the affected lung lobes.24 6. Bavegems V, Duchateau L, Sys SU, De Rick A: Echocardiographic
Reference Values in Whippets. Vet Radiol Ultrasound. 2007, 48(3):230-238.
Membranoproliferative Glomerulonephritis and Nephrotic 7. Court MH: Anesthesia of the sighthound. Clin Tech Small Anim Pract
Syndrome: A 2-year-old spayed female Whippet with proteinuria 1999 Feb;14(1):38-43.
and decreased serum albumin was diagnosed by kidney biopsy to 8. Mealey KL & Meurs KM: Breed distribution of the ABCB1-1Delta
have membranoproliferative glomerulonephritis.25 (multidrug sensitivity) polymorphism among dogs undergoing ABCB1
genotyping. J Am Vet Med Assoc. 2008 Sep 15;233(6):921-4.
Malignant Lymphoma: A 4-year-old Whippet was diagnosed with 9. Gramer I, Leidolf R, Döring B, et. al.: Breed distribution of the nt230(del4)
malignant lymphoma with cardiac and bone involvement, using MDR1 mutation in dogs. Vet J. 2011 Jul;189(1):67-71.
radiography, histology, nuclear scintigraphy of the skeleton and 10. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
heart, and cardiac ultrasonography.26 11. Shelton GD & Engvall E: Gross muscle hypertrophy in whippet dogs is
caused by a mutation in the myostatin gene. Neuromuscul Disord. 2007
Oct;17(9-10):721-2.
Genetic Tests 12. Mosher DS, Quignon P, Bustamante CD, et. al.: A mutation in the
Tests of Genotype: Direct test for MDR1 (ivermectin sensitivity) myostatin gene increases muscle mass and enhances racing performance in
is available from Washington State Univ. http://www.vetmed.wsu. heterozygote dogs. PLoS Genet. 2007 May 25;3(5):e79.
edu/depts-VCPL/test.asp (Longhaired Whippets). 13. Whippet Health Foundation, Inc.: 2000 Whippet Health Survey. 2000.
14. White SD: Update on Follicular Alopecias: “Pseudo-Endocrinopathies”.
Direct test for CEA/CH (Collie Eye Anomoly/Choroidal Hypoplasia) is Proceedings, 2005 ACVIM Forum. 2005.
available from Optigen (Longhaired Whippets). 15. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
College of Veterinary Ophthalmologists. ACVO, 2007.
Direct test for coat length gene is available from VetGen. 16. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of
serum thyroid hormone autoantibodies in dogs with clinical signs of
Direct test for Bully Whippet gene is available from DDC Veterinary. hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71.
17. Nachreiner R & Refsal K: Personal communication, Diagnostic Center
Tests of Phenotype: CHIC Certification: Required testing for Population and Animal Health, Michigan State University. April, 2007.
includes CERF eye examination, ECHOcardiogram by a cardiologist, 18. Strain GM: Deafness prevalence and pigmentation and gender
BAER testing for deafness, and entry into the Whippet Health associations in dog breeds at risk. Vet J 2004; Jan;167(1):23-32.
19. Sargan DR, Withers D, Pettitt L, et. al.: Mapping the mutation causing
Foundation database. Optional testing includes hip radiographs and
lens luxation in several terrier breeds. J Hered. 2007;98(5):534-8.
thyroid profile including autoantibodies. (See CHIC website; www. 20. Miller WH: Alopecia Associated with Coat Color Dilution in Two
caninehealthinfo.org). Yorkshire Terriers, One Saluki, and One Mixed-Breed Dog. J Am Anim Hosp
Assoc 1991: 27(1):39-43.
Recommend elbow radiographs and patella evaluation. 21. Schultheiss PC: A retrospective study of visceral and nonvisceral
hemangiosarcoma and hemangiomas in domestic animals. J Vet Diagn
Miscellaneous Invest. 2004 Nov;16(6):522-6.
• Breed name synonyms: Snap-dog (historical). 22. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Ackerman. p. 243-44. AAHA Press, 1999.
480
23. Gerber K, Harvey JW, D’Agorne S, et. al.: Hemolysis, myopathy, and
cardiac disease associated with hereditary phosphofructokinase deficiency
in two Whippets. Vet Clin Pathol. 2009 Mar;38(1):46-51.
24. White RN, Corzo-Menendez N: Concurrent torsion of the right cranial
and right middle lung lobes in a whippet. J Small Anim Pract. 2000
Dec;41(12):562-5.
25. Grauer GF, Frisbie DD, Snyder PS, et. al.: Treatment of membranopro-
liferative glomerulonephritis and nephrotic syndrome in a dog
with a thromboxane synthetase inhibitor. J Vet Intern Med. 1992
Mar-Apr;6(2):77-81.
26. Ogilvie GK, Brunkow CS, Daniel GB, et. al.: Malignant lymphoma with
cardiac and bone involvement in a dog. J Am Vet Med Assoc. 1989 Mar
15;194(6):793-6.
27. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
Book House, NY 2006. p. 223-226.
481
Wire Fox Terrier
length. It is high set and thick. Limbs are straight, metatarsals and
metacarpals heavy and short, feet small and compact and pads
tough. The toes are moderately arched. In body type in all respects
they are the same as the Smooth Fox Terrier.
483
Wirehaired
Pointing Griffon
expression; many eye colors are accepted including brown and
yellow. Ears are flat lying, medium sized and the nose is always
brown with wide nostrils. The nictitans should not show. The neck
is long and not throaty, and is slightly arched. The topline descends
slightly towards the rear. The thorax is deep with moderately sprung
ribs. The tail is carried horizontally or a bit higher when active, and
may be docked to about 1/3 to 1/2 of the normal length. Limbs
are straight boned, and the dewclaws are removed in America. The
feet are round; the toes webbed. The gait is smooth with ground
covering strides, and lots of natural agility.
Weight: females 35-50 lb (16-23 kg) males 50-60 lb (23-27 kg). Patella Luxation: Polygenically inherited laxity of patellar
ligaments, causing luxation, lameness, and later degenerative joint
Coat: The double coat consists of an undercoat of lighter colored disease. Treat surgically if causing clinical signs. Too few Wirehaired
soft dense hair overlaid by a very coarse wiry straight haircoat that Pointing Griffons have been screened by OFA to determine an
is medium in length. Black is not allowed, but brown, steel gray accurate frequency.1
with brown markings, roan and white, and orange or brown are
accepted. Disease Predispositions
Otitis Externa: Chronic or intermittent ear infections. Reported
Longevity: 10-13 years at a frequency of 22% in the AWPGA National Health Survey
2002-2003.2
Points of Conformation: The Wirehaired Pointing Griffon is
characterized by a very strong constitution, a medium size, and is Umbilical Hernia: Congenital opening of the body wall at
built slightly longer than he is tall. The head is square in shape, the the umbilicus. Should be closed surgically if large. Reported
stop is not well pronounced, and eyebrows, moustache and beard at a frequency of 3.3% in the AWPGA National Health Survey
are well developed. Eyes are rounded, large and have a friendly 2002-2003.2
484
Allergies: Inhalant or food. Presents with pruritis and pyotraumatic
dermatitis (hot spots). Inhalant allergy is reported at a frequency
Miscellaneous
• Breed name synonyms: Korthals’ Griffon, Griffon d’Arret a Poil
of 2.2%, and food allergy at 2.7% in the AWPGA National Health Dur, Griffon d’Arret Korthals, Pointing Griffon, Griff.
Survey 2002-2003.2 • Registries: AKC, UKC, CKC, NKC (National Kennel Club).
• AKC rank (year 2008): 105 (419 registered)
Hypothyroidism: Inherited autoimmune thyroiditis. 2.4% positive
• Internet resources: The American Wirehaired Pointing
for thyroid autoantibodies based on testing at Michigan State
Griffon: Association www.awpga.com
University. (Ave. for all breeds is 7.5%). Reported at a frequency of
Wirehaired Pointing Griffon Club of America: www.wpgca.org
2.2% in the AWPGA National Health Survey 2002-2003.2,3,4
Genetic Tests
Tests of Genotype: Direct tests for coat and nose colors, nose are
available from HealthGene and VetGen.
485
Xoloitzcuintli
Points of Conformation: This is a small finely put together dog
with a noble carriage, and similar to sight hounds in body structure.
Limbs are straight boned. The somewhat almond-shaped eyes are
wide set, dark brown, and moderate in size and depth of setting. The
muzzle tapers to a point, nose is black, ears are erect and triangular
with pointed tips, and sometimes traces of hair exist on the top of
the skull, on the tip of the tail and around the toes in the hairless
type. They have a moderately deep thorax, and the abdomen is well
tucked up. The fine tail hangs down and tapers to a point at the
tarsus. The long neck is slightly arched and finely built, and the feet
are hare-like in conformation. Their gait is quick and elastic.
The Breed History
Since the 1500s these unusual dogs have been reported, and are
thought to have originated in Mexico. Their history perhaps goes
Recognized Behavior Issues and Traits
Reported breed characteristics include: Active, a good alarm barker
back to ancient societies such as the Aztecs since dog skulls have
and good in apartments. Only suitable as an indoor dog, and needs
been found that resemble this breed’s in size and shape that date
a winter sweater unless in a sub-tropical or tropical environment.
to 3300 years ago in Central America. The name derives from the
The personality is similar to the terriers—like fox terriers particularly;
Aztec word for God “Xoloti” and “Itzcuintli”, the Aztec word for dog.
also quite playful. It may be necessary to bathe a Xolo periodically
Commonly, these dogs are referred to as the Mexican Hairless. AKC
and apply lotion to keep the skin moist. This is a type of dog that
recognition occurred in 2011.
has low exercise needs. Xolo dogs are good with children, but
Molecular genetic (mitochondrial DNA) results do not support a children need to be very gentle so as not to injure these dogs,
New World domestication of Xoloitzcuintli, or close association with especially the smallest variety. Good for some allergy sufferers
other hairless breeds of dogs. Despite their phenotypic uniformity, (hairless variety).
the Xoloitzcuintli has a surprisingly high level of mtDNA sequence
variation, suggesting that the breed was founded with a large Normal Physiologic Variations
number of dogs from outbred populations.1 Hairlessness is caused by a autosomal semidominant mutation in
the FOX13 gene that is lethal in utero in the homozygous state.
Breeding for Function This gene also produces variably expressed missing premolars in
Throughout their history, their prime purpose has been the heterozygous state. Because of the lethal homozygous state,
companionship; perhaps they were also the object of sacrifice in breeding two heterozygous hairless dogs together produces a
ancient Aztec, Toltec and Mayan civilizations. They were thought to 2:1 ratio of hairless to (homozygous normal) powderpuff dogs.
have healing powers because of their warm skin temperature and Breeding hairless to powderpuff dogs, produces a 1:1 ratio of
were used by arthritis sufferers for that purpose. hairless to powderpuff offspring.2,3,4
Xoloitzcuintli are very sensitive to heat and cold. The skin is thin,
Physical Characteristics and prone to lacerations, and dryness. They sweat through their
Toy skin so they do not pant as much as other breeds.
Height at Withers: 11-12” (28-31cm),
Weight: 9-18 lb (4-8 kg) Hairlessness is accompanied by early atrophy of the thymus after
birth, and is followed by poor accumulation of lymphocytes in the
Miniature thymus-dependent area of the spleen and the mesenteric lymph
Height at Withers: 12-15” (30-38 cm). nodes. This presentation is different from that seen in athymic
Weight: 13-22 lb (6-10kg) nude mice and rats. No immunodeficiency or diminished antibody
response has been documented in the breed.5
Standard
Height at Withers: 16-22.5” (41-57 cm) Drug Sensitivities
Weight: 20-31 lb (9-14 kg) None Reported
Coat: There are two haircoat types: Hairless and Powder Puff. The
latter is not accepted for show purposes. Colors include orange,
Inherited Disease
Incomplete Dentition: It is common to have variable expression
black, slate, liver, bronze, and charcoal.
of missing premolars with the autosomal dominant hairless
Longevity: 12-15 years phenotype.3
486
Patella Luxation: Polygenically inherited laxity of patellar AKC rank: (None) Became an AKC recognized breed Jan. 2011.
ligaments, causing luxation, lameness, and later degenerative Entire studbook registered.
joint disease. Treat surgically if causing clinical signs. Too few • Internet resources: Xoloitzcuintli Club of America:
Xoloitzcuintli have been evaluated by the OFA to determine an www.xoloitzcuintliclubofamerica.com
accurate frequency in the breed.6 Xoloitzcuintli Club USA: www.xoloworld.com
Genetic Tests
Tests of Genotype: None
Miscellaneous
• Breed name synonyms: Mexican Hairless, Tepeizeuintli, Xolo
• Registries: UKC, CKC, KCGB (Kennel Club of Great Britain), AKC
-provisional, NKC
487
Yorkshire Terrier
and are known not to tolerate temperature extremes well. They are
considered of moderate trainability.
489
Cutaneous Plasmacytoma: Eight of 63 dogs diagnosed with • AKC rank (year 2008): 2 (41,914 dogs registered).
cutaneous or mucocutaneous plasmacytoma were Yorkshire terriers. • Internet resources: Yorkshire Terrier Club of America:
Prognosis was good with removal.40 www.ytca.org
Yorkshire Terrier Club Foundation: http://yorkiefoundation.org
Dermatophytosis (M. Canis): Ringworm. Increased incidence The Yorkshire Terrier Club (UK):
found in the breed. In one study, it was possibly secondary to www.the-yorkshire-terrier-club.co.uk
immunosuppression from infection with leishmaniasis, ehrlichiosis, The Canadian Yorkshire Terrier Association: www.cyta.ca
or with diabetes mellitus.41,42
References
Isolated Case Studies 1. Esteve-Ratsch B, Kneissl S, Gabler C. Comparative evaluation of the
Epitheliotropic Cutaneous (T-Cell) Lymphoma (Mycosis ventricles in the Yorkshire Terrier and the German Shepherd dog using
Fungoides): Case report of a 7 year old male Yorkshire Terrier with low-field MRI. Vet Radiol Ultrasound. 2001 Sep-Oct;42(5):410-3.
chronic skin and oral lesions.43 2. Lamb CR, Wikeley H, Boswood A, et. al.: Use of breed-specific ranges for
the vertebral heart scale as an aid to the radiographic diagnosis of cardiac
Renal Cortical Hypoplasia: Case report of a young Yorkshire terrier disease in dogs. Vet Rec. 2001 Jun 9;148(23):707-11.
with congenital malformation of the kidneys causing juvenile renal 3. OFA Website breed statistics: www.offa.org Last accessed July 1, 2010.
disease and kidney failure.44 4. Dorn CR: Canine breed-specific risks of frequently diagnosed diseases at
veterinary teaching hospitals. Monograph. AKC Canine Health Foundation.
Dermoid Sinus and Spinal Malformations: Case report on one 2000.
5. LaFond E, Breur GJ, Austin CC: Breed susceptibility for developmental
young Yorkshire terrier.45
orthopedic diseases in dogs. J Am Anim Hosp Assoc. 2002 Sep-Oct;38(5):467-77.
6. Yorkshire Terrier Club Foundation, Inc.: 2006 Health Survey Data Report.
Hypertrophic Cardiomyopathy (HCM): One case report of a 14
2007.
year old Yorkshire terrier with a cardiac murmur and syncope due to 7. Longbottom GM. A case of tracheal collapse in the dog. Vet Rec. 1977 Jul
outflow obstruction, and one case report of occult HCM in a 6 year 16;101(3):54-5.
old female Yorkshire Terrier that died under anesthesia.46,47 8. Vroom MW and Slappendel RJ: Transient juvenile hypoglycaemia in a
Yorkshire terrier and in a Chihuahua. Vet Q. 1987 Apr;9(2):172-6.
Persistent Right Aortic Arch: A 5-year-old neutered male 9. van Toor AJ, van der Linde-Sipman JS, van den Ingh TS, et. al.:
Yorkshire terrier first presented with regurgitation at 3 months of Experimental induction of fasting hypoglycaemia and fatty liver syndrome
age, and was maintained on a modified diet and motility enhancing in three Yorkshire terrier pups. Vet Q. 1991 Jan;13(1):16-23.
drugs. Megaesophagus was diagnosed at 2 years of age, and 10. Bonagura J: Chronic Valvular Heart Disease in Dogs. Proceedings World
vascular ring anomaly was diagnosed at 4 years of age. Surgery was Small Animal Veterinary Association World Congress, 2001.
performed at 5 years of age.48 11. Winkler JT, Bohling MW, Tillson DM, et. al.: Portosystemic Shunts:
Diagnosis, Prognosis, and Treatment of 64 Cases (1993-2001). J Am Anim
Lung Lobe Torsion: Case report of a 9 year old female Yorkshire Hosp Assoc Mar-Apr’03; 39[2]:169-185.
Terrier with lung lobe torsion. Treatment was surgical removal.49 12. Tobias KM And Rohrbach BW: Association of Breed with the Diagnosis
of Congenital Portosystemic Shunts in Dogs: 2,400 Cases (1980-2002). J
Color Dilution Alopecia, Hypotrichosis, Patent Ductus Am Vet Med Assoc Dec 1’03;223[11]:1636-1639.
Arteriosus, Retained Primary Teeth, Shaker Syndrome, and von 13. Tobias KM: Determination of Inheritance of Single Congenital
Portosystemic Shunts in Yorkshire Terriers. J Am Anim Hosp Assoc
Willebrand’s Disease are reported.50
Jul-Aug’03;39[4]:385-389.
14. Ocular Disorders Presumed to be Inherited in Purebred Dogs. American
Genetic Tests College of Veterinary Ophthalmologists. ACVO, 2007.
Tests of Genotype: None 15. Westermeyer HD, Ward DA & Abrams K: Breed predisposition to
congenital alacrima in dogs. Vet Ophthalmol. 2009 Jan-Feb;12(1):1-5.
Tests of Phenotype: CHIC Certification: CERF eye examination 16. Herrera HD and Weichsler, N: Severe, Unilateral, and Non-Responsive
(at 1, 3, and 6 years) and patella evaluation. Optional tests include Keratoconjunctivitis Sicca in Eleven Young Yorkshire Terriers. Proceedings
hip radiograph (for Legg-Perthes or hip dysplasia), thyroid profile WSAVA 2002 Congress. 2002.
including autoantibodies (at 1, 3, and 6 years), blood donation to the 17. Herrera HD, Weichsler N, Gómez JR, et. al.: Severe, unilateral,
unresponsive keratoconjunctivitis sicca in 16 juvenile Yorkshire Terriers. Vet
Cornell DNA bank, or to the CHIC DNA repository. (See CHIC website;
Ophthalmol. 2007 Sep-Oct;10(5):285-8.
www.caninehealthinfo.org). 18. Park SA, Yi NY, Jeong MB, Kim WT, et. al.: Clinical manifestations of
cataracts in small breed dogs. Vet Ophthalmol. 2009 Jul-Aug;12(4):205-10.
Recommend paired fasted and feeding serum bile acid and/ 19. Lee YM, Kang BT, Jung DI, et. al.: A case of adrenal gland dependent
or ammonium levels for PSS, cardiac examination and elbow hyperadrenocorticism with mitotane therapy in a Yorkshire terrier dog. J
radiographs. Vet Sci. 2005 Dec;6(4):363-6.
20. Houston DM & Moore AE: Canine and feline urolithiasis: examination of
Miscellaneous over 50 000 urolith submissions to the Canadian veterinary urolith centre
from 1998 to 2008. Can Vet J. 2009 Dec;50(12):1263-8.
• Breed name synonyms: Yorkie, Broken-haired Scotch terrier
21. Rogers KD, Jones B, Roberts L, et. al.: Composition of uroliths in small
(historical)
domestic animals in the United Kingdom. Vet J. 2011 May;188(2):228-30.
• Registries: CKC, AKC, UKC, KCGB (Kennel Club of Great Britain), 22. Lekcharoensuk C, Lulich JP, Osborne CA, et. al.: Patient and
ANKC (Australian National Kennel Club), NKC (National Kennel Club) environmental factors associated with calcium oxalate urolithiasis in dogs.
490
J Am Vet Med Assoc. 2000 Aug 15;217(4):515-9. cardiomyopathy in an aged dog. J Vet Med Sci. 2003 Jun;65(6):753-6.
23. Ling GV, Ruby AL, Johnson DL, et. al.: Renal Calculi in Dogs and Cats: 47. Pang D, Rondenay Y, Hélie P, et. al.: Sudden cardiac death associated
Prevalence, Mineral Type, Breed, Age, and Gender Interrelationships with occult hypertrophic cardiomyopathy in a dog under anesthesia. Can
(1981-1993). J Vet Intern Med. Jan/Feb’98;12[1]:11-21. Vet J. 2005 Dec;46(12):1122-5.
24. Nachreiner RF, Refsal KR, Graham PA, et. al.: Prevalence of 48. Loughin CA & Marino DJ: Delayed primary surgical treatment in a
serum thyroid hormone autoantibodies in dogs with clinical signs of dog with a persistent right aortic arch. J Am Anim Hosp Assoc. 2008
hypothyroidism. J Am Vet Med Assoc 2002 Feb 15;220(4):466-71. Sep-Oct;44(5):258-61.
25. Nachreiner R & Refsal K: Personal communication, Diagnostic Center 49. Choi J, & Yoon J: Lung lobe torsion in a Yorkshire terrier. J Small Anim
for Population and Animal Health, Michigan State University. April, 2007. Pract. 2006 Sep;47(9):557.
26. Davison LJ, Herrtage ME, Catchpole B: Study of 253 dogs in the United 50. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. L
Kingdom with diabetes mellitus. Vet Rec 2005 Apr 9; 156[15]:467-71. Ackerman. p. 244, AAHA Press, 1999.
27. Short AD, Saleh NM, Catchpole B, et. al.: CTLA4 promoter 51. The Complete Dog Book, 20th Ed. The American Kennel Club. Howell
polymorphisms are associated with canine diabetes mellitus. Tissue Book House, NY 2006. p. 521-523.
Antigens. 2010 Mar;75(3):242-52.
28. Melzer KJ and Sellon RK: Canine Intestinal Lymphangiectasia. Compend
Contin Educ Pract Vet. Dec’02;24[12]:953-961.
29. Kimmel SE, Waddell LS, Michel KE: Hypomagnesemia and hypocalcemia
associated with protein-losing enteropathy in Yorkshire terriers: five cases
(1992-1998). J Am Vet Med Assoc. 2000 Sep 1;217(5):703-6.
30. Lecoindre P, Chevallier M & Guerret S: Protein-losing enteropathy of
non neoplastic origin in the dog: a retrospective study of 34 cases. Schweiz
Arch Tierheilkd. 2010 Mar;152(3):141-6.
31. Stades FC: Hereditary retinal dysplasia (RD) in a family of Yorkshire
terriers. Tijdschr. Diergeneesk. 1978;103:1087.
32. Walde I: Retinal and corneal dysplasias in the Yorkshire terrier and other
dog breeds in Austria. Tierarztl Prax. 1997 Jan;25(1):62-7.
33. Ducote JM, Johnson KE, Dewey CW, et. al.: Computed tomography
of necrotizing meningoencephalitis in 3 Yorkshire Terriers. Vet Radiol
Ultrasound. 1999 Nov-Dec;40(6):617-21.
34. Lotti D, Capucchio MT, Gaidolfi E, et. al.: Necrotizing encephalitis in
a Yorkshire Terrier: clinical, imaging, and pathologic findings. Vet Radiol
Ultrasound. 1999 Nov-Dec;40(6):622-6.
35. Kuwamura M, Adachi T, Yamate J, et. al.: Necrotising encephalitis in the
Yorkshire terrier: a case report and literature review. J Small Anim Pract.
2002 Oct;43(10):459-63.
36. Lezmi S, Toussaint Y, Prata D, et. al.: Severe necrotizing encephalitis in a
Yorkshire terrier: topographic and immunohistochemical study. J Vet Med A
Physiol Pathol Clin Med. 2007 May;54(4):186-90.
37. von Praun F, Matiasek K, Grevel V, et. al.: Magnetic resonance imaging
and pathologic findings associated with necrotizing encephalitis in two
Yorkshire terriers. Vet Radiol Ultrasound. 2006 May-Jun;47(3):260-4.
38. Baiker K, Hofmann S, Fischer A, et. al.: Leigh-like subacute necrotising
encephalopathy in Yorkshire Terriers: neuropathological characterisation,
respiratory chain activities and mitochondrial DNA. Acta Neuropathol. 2009
Nov;118(5):697-709.
39. Pedersen NC, Vernau K, Dickinson P, et. al.: DLA Association in Various
Toy Breeds with Immune Mediated Encephalopathies. Proceedings, 4th
Tufts’ Canine and Feline Breeding and Genetics Conference. 2009.
40. Cangul IT, Wijnen M, Van Garderen E, et. al.: Clinico-pathological
aspects of canine cutaneous and mucocutaneous plasmacytomas. J Vet
Med A Physiol Pathol Clin Med. 2002 Aug;49(6):307-12.
41. Cerundolo R: Generalized Microsporum canis dermatophytosis in six
Yorkshire terrier dogs. Vet Dermatol. 2004 Jun;15(3):181-7.
42. Sparkes AH, Gruffydd-Jones TJ, Shaw SE, et. al.: Epidemiological and
diagnostic features of canine and feline dermatophytosis in the United
Kingdom from 1956 to 1991. Vet Rec. 1993 Jul 17;133(3):57-61.
43. Bhang DH, Choi US, Kim MK, et. al.: Epitheliotropic cutaneous
lymphoma (mycosis fungoides) in a dog. J Vet Sci. 2006 Mar;7(1):97-9.
44. Klopfer U, Nobel TA, Kaminski R: A nephropathy similar to renal
cortical hypoplasia in a Yorkshire Terrier. Vet Med Small Anim Clin. 1978
Mar;73(3):327-30.
45. Fatone G, Brunetti A, Lamagna F, et. al.: Dermoid sinus and spinal
malformations in a Yorkshire terrier: diagnosis and follow-up. J Small Anim
Pract. 1995 Apr;36(4):178-80.
46. Washizu M, Takemura N, Machida N, et. al.: Hypertrophic
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Section 3 Cat Breeds
Introduction
As a practitioner, one sees many fascinating breeds of cats pass through the doors, but their rarity compared with the general domestic
shorthair and longhair cat population makes it difficult for veterinarians to stay up-to-date and be fully informed about all cat breeds.
The breeds themselves are evolving quickly, as they are under perpetual development. Breeders select for characteristics that evolve quite
quickly as standards are updated or expanded, and the set of new provisional or now extinct breeds also changes.
Accessing relevant information not only about the abnormalities that may afflict each breed, but about what is normal for that breed can
be a time consuming task since literature about cat breed-related problems is sparse, and very widely dispersed. Many reports are found
in journals outside the normal spectrum of practitioner subscription journals. Reviews in clinical practice journals tend to be tables of
conditions, with limited depth of coverage of the conditions.
The scope of this resource is to provide only breed-related information—not general medicine and surgery, or treatment and does not cover
detailed coat color genetics. Resources are provided in the appendix and reference lists for those wishing to access detailed material.
Note that different cat registries have disparate standards, and geographic variation within these standards occurs. Generic breed
descriptions in the chapters have therefore been loosely based on the CFA standard, with detailed comparisons between registries being
absent due to space constraints. Due to the fact that if a reader is in a part of the world where other registry standards predominate,
referring to the local registry standard is recommended. Variations between registry standards are very complex, and can be significant,
even to the point of different breed names, different categories and varieties being recognized, different conformation accepted, and
different details of coat color, texture, and pattern distribution preferred.
Likewise, as far as specific breed origins, many different “stories” can be found in published reports. The summaries supplied herein are
aggregated from many sources, relaying what could to be the most widely accepted “theory”. The interpretation of history may be flawed,
and in many cases, it appears a lack of accurate historical documentation exists. This means that for some breed origins, we will never likely
know the “real” story. New genetic tools are also changing the way we look at breed origins, and as new information accrues, it is likely
some of the stories will give way to the new evidence.
The scope of this book encompasses the clinical signs and anticipated age of onset, progression, prognosis and cursory discussion of
particularly helpful diagnostic tests. Where the scope of the tests is outside the standard minimum database, or selection or interpretation
of those tests is non-standard, we have noted such.
Unfortunately for the cat world, support for research is sparse except when animal models of human disease apply. There is a dearth of
studies reported since the 1980s, though recently with private funding bodies like the Winn Feline Foundation and American Association
of Feline Practitioners supporting important projects, a new surge in research is now occurring. Advances in genetic technology provide
new tools such as gene sequencing, with linkage and gene testing. These have inspired a new generation of researchers and provided new
power for carrier detection. Still, when compared with dogs, there is very little available in the literature. Big holes are especially obvious in
the rare breeds.
A weakness of reporting in the primary literature is the inconsistent definition of breed names. For example, Domestic Shorthair is
sometimes used interchangeably with American Shorthair and British Shorthair if registration is not relayed in the signalment portion of
the study. Since American Shorthair breed cats used to be called Domestic shorthair, older reports may actually refer to registered cats.
If a study does not include “pedigreed” or “registered” in the content of the report, these were excluded from the present data gathering
since the purebred and domestic population gene pool is now different because registries have been closed for quite a while. Some older
references that dealt with American Shorthair (formerly Domestic Shorthair) will have thus been passed over. Breeds where color groups
or hair coats have become breeds of their own in some registries also complicate study assignment to a breed. Scottish Fold/Highland Fold,
Persian/Himalayan, Manx/Cymric are some examples.
Few formal breed-wide surveys have been done in cats, though recent efforts to gather breeder data into a larger database in the field have
been carried out. Keeping data secure and protecting identity is often necessary for wide survey acceptance. Statistical significance which
can be useful for management of breeding stock is still rarely generated. Breeder surveys are generally not statistically rigorous, and in
evidence-based medicine not as high a level of significance, so results should be considered “getting a finger on the pulse” of a problem,
rather than providing hard and fast data.
493
Another point to note is that much data from research colonies has been reported, with efforts at extrapolation; these populations are
closed and do not necessarily reflect the wider picture in a breed. Establishing breed “normals” has just begun.
Many disorders have been documented in purebred or DSH/DLH cats. Some, like polycystic kidney disease in Persian and Persian-related
cats, account for a major proportion of genetic disorders in the general registered cat population, others are only found in rare case
reports. Rare conditions are often found in early literature, and may seemed to have apparently dropped out of existence since the report,
but perhaps have undergone an insidious silent spread if not widely recognized.
If the veterinarian does not know about these rare cases, inevitably, the condition will not be widely recognized and diagnosed. The decision
to place rare reports in our chapters was based on the need for the practitioner to be aware of their possible existence and to provide
sources for research about these rarely reported conditions. Inclusion of these does not implicate it as a “breed problem” per se.
Lack of reported disorders in a chapter does not imply that those problems are not found in the breed, it just reflects the lack of reports—or
the fact that is not a particularly breed-specific disorder. Conversely, a plethora of reports in a chapter does not necessarily correlate with
an unhealthy breed, or a high prevalence of reported conditions, but may just reflect the reality that a breed is popular, therefore populous,
and more literature reports are thus generated.
Many conditions are not breed specific and thus not covered in detail in this reference. Readers are referred to general feline and internal
medicine texts to garner more information on those conditions.
The proportion of purebreds in the cat population is still lower than in dogs (cats are ratio of about 1 registered: 5 unregistered), so overall
in practice one still sees more infectious and trauma cases than genetic disorders in cats. Nevertheless, newer studies are starting to point
to genetically determined susceptibility to certain immune and infectious conditions (autoimmunity, FIP susceptibility, certain cancers) so
inherited “disorders” are in fact, much more pervasive than was previously thought.
It remains difficult in some conditions to distinguish between congenital and inherited, versus environmental or acquired (nature versus
nurture) etiologies. Thus, dividing these conditions by cause is somewhat arbitrary, and some breed conditions may need to be moved from
the Disease Predispositions to the Inherited Diseases section or vice versa as further research elucidates these problems.
It is important to know about inherited disorders since many breeds of cats are genetically closed and suffer from reduced genetic diversity.
It is important to identify and correctly manage these disorders in order to preserve genetic diversity without perpetuating harmful genetic
conditions, and each veterinarian needs to understand and embrace proper genetic counseling.
Breeding closely to embed desirable genetic constitution can also co-select for rare mutations or polygenic traits that can be amplified
within a line or a breed. Removal of undesirable genetic traits must be a gradual process so that strong genetic lines are not lost or
compromised. Long-term commitment by breeders and the health care team is needed to properly manage such disorders from a
population medicine point of view.
Newer advances in molecular biology allow linkage marker identification, definitive gene sequencing, and PCR-based genetic testing that
can identify carriers at any age with non-invasive tests. These new advances are helping breeders and veterinarians make informed choices.
This technology is a double edged sword though, and these powerful aids to selection must be applied intelligently. See the section from Dr.
Bell on genetic counseling to review appropriate management recommendations for breeders.
Not every cat breed is included in the first edition, and as the book is updated, adjustments and additions will need to be made in order
to keep the listing current. Readers are encouraged to send comments to help us update the cat breed section. Use the contact address
provided in the book preface. Chapters are in alphabetical order.
494
Abyssinian
Eyes: The large almond eyes are fairly wide set; may be green or
gold in the CFA-approved colors. There are dark rims set within a
lighter spectacle.
495
Typical age of presentation is 1-5 years old; the female to male ratio of function peripherally in later stage disease.10 Retina blood flow was
is 1.4:1, and first evidence of renal amyloid deposits in the kidney found to be severely compromised in a study of cats with late stage
can be found at 9-24 months of age. An autosomal dominance PRA.11 Antibodies against both green- and blue-sensitive cones were
inheritance with variable penetrance was proposed. In some cats, used to establish that early reduction of both of these cone types
by one year later renal failure may be evident while in others, occurs, while the inner retina is mostly preserved. Late in disease, the
deposition of amyloid is slow and they may live a clinically normal ERG is not recordable and the retina is markedly thinned.12
full lifespan. A surgical biopsy of both renal medulla and cortex is
most likely to be diagnostic. Apart from routine H&E, a Congo red Recent data using electron microscopy proves that the arterial walls
stain is performed to highlight amyloid.2 of vessels in the iris are abnormal even though innervation is normal.
The ciliary processes were also shorter and more compact than in
In a summary of generalized AA amyloidosis in various cat breeds normal cats.13
(especially Siamese and Oriental cats 1987-1994), amyloidosis was
reported to be a familial trait in the Abyssinian.3 A closed colony was studied to further elucidate the correlation with
phenotype and genotype. The rdAc allele was found in European and
In a study of cats (1983-1997; Netherlands), 3.1% of 258 Australian cats with moderate frequency.14
Abyssinian referrals were diagnosed with AA-amyloidosis. Affected
cats were quite inbred. In 25% of the Abyssinian cats with Dominant Abyssinian Rod-cone Dysplasia (Rdy): A second type
amyloidosis, inflammatory conditions were present concurrently of retinal condition has been described in Abyssinians which has
(e.g., rhinitis, FIP).4 an autosomal dominant mode of inheritance.7 Visual deficits are
congenital, and horizontal nystagmus may also be noted. At four
The amyloidosis [apo-lipoprotein—serum amyloid A (AA)] propensity weeks of age mydriasis is noted, and significant visual deficits or
is still not clearly elucidated as a solely genetic problem; sequencing blindness occur by 12-16 weeks of age. By two weeks of age, early
of the proteins shows amino acid shifts common to different breeds retinal changes are occurring and the rods and cones are equally
and this may mean that in addition to the presence of amyloid affected. Progressive loss occurs from central retina towards the
associated genes, other factors such as chronic inflammation or periphery.15 This condition has only been reported in the UK. This is a
certain infections are involved in the genesis of phenotypic clinically true dysplasia as rods and cones never fully develop.
significant amyloidosis. There may be three genes involved.5
A single mutation was identified as a single base pair deletion on
Recessive Hereditary Rod-Cone Degeneration rdAc/Progressive the Exon 4 of the CRX peptide gene in the cat, which interferes with
Retinal Atrophy [PRA]: Age of onset is usually early adulthood formation of the key protein.16
(1.5-2 y), with slow progression to generalized retinal atrophy by
middle age. A plasma lipid abnormality was found in conjunction Arterial Thromboembolism: In one study of 127 affected cats,
with the eye problem—a reduced plasma level of docosahexanoic Abyssinian cats were one of three breeds overrepresented with
acid, an omega-3 fatty acid was documented. This fatty acid is the arterial thromboembolism.17
major fatty acid in outer segments of retina rods.6 This condition is
similar to retinitis pigmentosa in humans.7 Blood Type B: There may be geographic variation since in a small
study of cats in Hungary, none of the cats tested were of B blood
It was determined that an autosomal recessive pattern of type.18
inheritance was occurring. In an early report of Swedish cats,
indirect binocular ophthalmoscopic examination proved that of Prevalence of B blood type in the USA was 20% in one report.19 In
205 cats assessed over 2 years old, 68 had bilateral disease (34%), another study of blood type distribution in the USA, 230 Abyssinian
while 45% were affected in one or both eyes. At 1.5-2 years of cats had a prevalence of 13.5% blood type B,20 and in a summary of
age, the first ophthalmoscopic changes were noted, and peripheral studies 16% pooled prevalence of type B was reported.21
tapetal fundus was discolored brown to grey, along with retinal
In Australia, all PK cats tested (n=36) were determined to be type A.22
vessel attenuation. By about three years of age, tapetum color had
(See below for more about PK deficiency).
changed to gray. Late stage, there was tapetal hyper-reflectivity,
and severe vessel attenuation was noted; PLR was reduced or Neonatal Isoerythrolysis (NI): The reported proportion of matings
absent. Latest age of onset was at four years of age.8 at risk for NI is 0.12.23
It was reported that when homozygous for the trait, affected Pyruvate Kinase Deficiency and Increased Osmotic Fragility of
kittens had an abnormal ERG as early as eight weeks of age; the RBCs: The pyruvate kinase enzyme (PK) is involved in the anaerobic
cat retina is considered fully developed at about 10 weeks of age. glycolytic pathway of erythrocytes. Lack of the enzyme function
Ophthalmoscopic examination in those cats can remain normal results in energy depletion, and premature red cell destruction. Cats
until almost two years of age.9 This study also confirmed an early with this condition may experience a range of severity of anemia,
drop in the levels of inter-photoreceptor retinoid-binding protein with some experiencing recurrent severe hemolytic anemia and
(IRBP) starting at four to six weeks of age in homozygous kittens. splenomegaly.
This protein also binds fatty acids at the retina.
In one study, osmotic fragility occurred in the absence of PK
The even distribution of retinal pathology during early phases changes deficiency. Reported onset of anemia ranged from 6 months to
to retention of function preferentially in the central retina, with loss 5 years of age (mean 23 months) and typical PCV ranged from
496
15%-25% (as low as 5%). Hepatic enzymes were elevated in some Feline Dilated Cardiomyopathy (FDC): Breed disposition was
of the cats. Macrocytic anemia with reticulocytosis occurred. reported for FDC; the hypertrophic form is rarely reported in this
Macrocytosis persisted when the anemia resolved. Osmotic fragility breed.31 Average age of onset is 7 years. Case rates have dropped
tests indicated much higher fragility than normal. Some of the 18 since diet supplementation with taurine began but is still seen.
affected cats with this primary erythrocyte fragility were closely Previously, mortality for FDC was about 85%, but with taurine
related (both Somali, Abyssinian) and an autosomal recessive mode supplementation mortality is currently in the 30%-50% range.
of inheritance was postulated.24 Cats don’t typically cough as in the dog; heart rate may range from
bradycardic to tachycardia, and both ventricles are affected. Pleural
In another study of Abyssinian and Somali cats aged 1-10 years, effusion, cold extremities, weakness and azotemia are typical.
chronic intermittent hypochromic regenerative hemolytic anemia and Affected cats are prone to arterial thromboembolism. Systolic
mild splenomegaly were reported. Pyruvate kinase activity ranged heart murmur or diastolic gallop can often be heard, and 61%
from 6%-20% of normal. Since parents were less severely affected, have arrhythmias, usually ventricular. Echocardiography is the best
it was postulated to be an autosomal recessive condition—now modality for definitive diagnosis.32
confirmed. Osmotic fragility was normal to mildly increased.25
Medial Patellar Luxation (MPL)/Hip Dysplasia (HD): In one study
In a case report, a one year old male Abby cat presented with it was noted that of 69 Abyssinian cats, 26 (38%) had abnormal
splenomegaly, mild exercise intolerance and severe regenerative patella seating with easily induced luxation; a possible dominant
hemolytic anemia (Coomb’s negative). Splenectomy produced (but polygenic) inheritance was suggested. Minimum age was 6
partial remission at 1.5 years of age; proband PK enzyme activity months; average age of the study group of cats was 4.3 years.
was 15% of normal and the proband queen’s PK enzyme activity This study group represented several US and European lines in the
was 50% of normal.26 breed; diagnosis was by manual palpation to displace the patella.33
Affected Somali and Abyssinian cats usually have a normal lifespan, In a mixed breed study looking at medial patellar luxation and
unlike dogs with this condition (see Beagles, Basenji, Westie, hip dysplasia at the University of Pennsylvania (1998) of 78
Dachshund). Dogs tend to develop liver failure and osteosclerosis non-randomly selected cats over six months of age (average age
while cats do not. Enzyme analysis and molecular genetic testing are 2.5 yr), Abyssinians were afflicted with MPL more frequently and
available at the Deubler Laboratory—see below under Genetic Testing. severely than the average cat. Cats with MPL in the pooled group
(including the Abyssinian) were three times as likely to have HD
Anemia may be noted in cats as young as six months, and has been as those without MPL. Only 11 of the 78 cats had clinical signs of
found in senior cats (12 yrs old) that were clinically normal. pelvic limb abnormalities so many cats are not being diagnosed in
clinical practices. Norberg angle (NA) and distraction index (DI) in
A recent study showed not all cats between 1-11 years of age
combination with OFA criterion were used to assess the cats. They
developed clinical signs, though a mortality rate of about 25%
found 80% of Abyssinian cats (8/10) had MPL and of these, 7/8
(presumed to be due to PK) occurred in the study group. In a little
had bilateral MPL. And 33% (3/10) had HD, while 33% (3/10) had
over half of the cats (median age 1.7 y), lethargy, diarrhea, poor
concurrent HD/MPL. A positive correlation between joint laxity and
appetite, and weight loss, pale mucous membranes and icterus were
HD was identified.34,35,36,37
most commonly noted. Symptomatic cats had variable lab findings
with increased bilirubin, globulins, liver enzymes and reticulocytes. FIP Susceptibility: An American Study found that Abyssinian cats
The authors say “As PK-deficient cats can be asymptomatic testing were significantly over-represented for a diagnosis of FIP when
for PK deficiency before breeding is strongly recommended.”27 they analyzed data for a 16 year period at a veterinary teaching
hospital.38
Disease Predispositions
Renal Failure: Renal failure rate for Abyssinian cats was identified
to be more than double the baseline rate in a study of cats seen
Rare and Isolated Reports
Congenital Hypothyroidism: Primary dyshormonogenesis has
at veterinary colleges between 1980-1990 (189,371 cases in the been diagnosed in a group of related Abyssinians that had early
Purdue University Veterinary Medical Database), at an odds ratio for onset disproportionate dwarfism, goiter, constipation and retained
risk of 2.42:1 (22 of 771 cats, prevalence 2.85%).28 kitten features. It was reported to be inherited as an autosomal
recessive disorder. This trait results in thyroid peroxidase deficiency.
Cervical Neck Lesions: Increased risk was reported. Abyssinians
By four weeks of age kittens were stunted, by six to nine months
were one of two breeds (the other being Siamese) most commonly
of age still immature, and by adulthood, variable expression was
affected by feline odontoclastic resorptive lesions (FORLs).29
noted. Deciduous teeth were shed late and epiphyseal plate closure
Gingivitis: Anecdotal evidence for increased prevalence. was delayed. Both TSH and TRH tests were abnormal, and the t-T4
and T3, and f-T4 low.39 This was proposed to be an under-diag-
Psychogenic Alopecia, Hyperesthesia: Anecdotal reports of nosed cause of fading kittens. If detected early and treated with
increased prevalence. appropriate thyroid hormone supplementation, effects may be
reduced or ameliorated.40
Urinary Tract Infection (UTI): In a study of 22,908 cats with feline
lower urinary tract disorders, Abyssinian cats were overrepresented
for UTI.30
497
Myasthenia Gravis (MG) and Thymoma-associated identify cats at risk for progression. A study comparing homozygous
Neuromuscular Disorder: Can be a congenital (Siamese) or affected and heterozygous at risk cats confirmed that cats with the
acquired condition (Aby, Somali). One study reported that compared inherited condition will show the following changes:
with mixed-breed cats, relative risk for acquired MG is highest Decreased a-wave amplitude
in Abyssinian (and Somali) cats; relative risk also increased Increased b-wave implicit times
after three years of age. The MG is associated with dysphagia, Abnormal ERG waveforms
megaesophagus, weakness, or weakness with a cranial mediastinal b-wave:a-wave ratios high
mass.41 Acetylcholine receptor antibodies produced within/by the A graphic representation of results can distinguish between
thymoma and in muscle cross reacted. Clinically, voice changes, genotypes, even before funduscopic changes are evident.45
tremor, ventroflexion of the neck and gait abnormalities were
noted. Myasthenia gravis signs are typical of the acquired idiopathic Another study showed that short ERG protocol is more efficient
form.42 Acetylcholine receptor antibody titers of > 0.3 nmol/L are than a long one in the identification of affected cats. A study using
diagnostic for acquired MG. Some afflicted cats were noted to have 12 parameters was adequate to discriminate rod-cone dystrophic
been treated for hyperthyroidism with methimazole for 2-4 months cats from normal cats.46
prior to the diagnosis of MG in one report. The study did not
attribute any causative effect though.41 Anti-acetylcholine receptor antibodies (serum) for MG: Send to
Comparative Neuromuscular Laboratory, att: Diane Shelton, UCSC
Mycobacterium avium Susceptiblity: In North America and http://vetneuromuscular.ucsd.edu/
Australia, of a case series of 12 cats under 6 years old, 10/12
were Abyssinian, and 1/12 was Somali, a closely related breed. No genetic tests are yet available for rdAc or Rdy eye diseases.
Clinical signs include weight loss, lower respiratory tract infection,
and enlarged lymph nodes, with slow re-growing hair. A familial Miscellaneous
immune-compromise was suspected in certain lines. They were • Breed name synonyms: Aby, Ticked Cat, Egyptian Cat, informal
FeLV-FIV negative cats but developed disseminated infection. name “Bunny Cat”
• Registries: FIFé, TICA, CFA, ACFA, CFF, CCA, NZCF, WCF, ACF, GCCF
Long term treatment with clarithromycin combined with another • Breed resources: CFA Abyssinian Breed Council:
agent such as rifampicin and a fluoroquinolone, or doxycycline was www.abyssinianbc.org
somewhat effective. It was proposed that there are certain lines of The Abyssinian Cat Club of America: http://www.abyworld.com/
Somali and Abyssinian cats that are predisposed due to a familial Abyssinian Cat Association (UK): www.theabycat.com
immunodeficiency.43
500
American Curl
body is well muscled and the legs are moderate in length. Paws are
moderately small and round.
Note that kittens are born with straight ears and they start curling
at about 4-7 days of age. The curl does not set fully until about 16
weeks of age or even much later. There is still considerable regional
variation in type due to continued outcrossing to domestic cats.
Grooming: The American Curl cat has low grooming needs, and is a
low shedding cat.
Good longevity.
Eyes: Most eye colors accepted. The eyes are a modified round shape. Craniofacial Deformity: Some lines of the breed carry the gene
for this condition (best known in the Burmese cat: see that chapter
Points of Conformation: Though not the largest of the cat breeds, for details) though frequency is dropping due to careful breeding
the American Shorthair is particularly noted for sturdy bone and management. These cat families tend to have a more extreme
muscling. Overall, their conformation is moderate in every way facial feature set, as with the Contemporary Burmese. This is an
(mesomorphic). The face is broad with prominent cheeks. The head autosomal recessive disorder.6
is slightly longer when compared to the British Shorthair. Ears are
medium sized and moderately wide set, with a rounded tip. Nasal dermoids are sometimes present in some cats; these are also
seen in Burmese cats carrying this gene. Eyelid colobomas and cleft
The tail is medium in length and thick, tapering to a blunt tip. Paws lips have also been seen in the ASH. A shallow longitudinal furrow
are round. The nose is medium in length and in profile, is slightly of tissue, or color change running along the nose has been found
concave. in almost 90% of American Shorthair carrier cats, and may be a
phenotypic marker of a carrier, though sensitivity and specificity of
Grooming: Moderate grooming needs are met by a light brushing this finding is not 100% so pedigree analysis should also be used.7
about two times a week. A bit more care is needed while shedding.
502
breeding programs. In screening programs carried out at the burmese.htm. Accessed Nov 2004.
University of California, Davis in 2002, American Shorthair cat 8. Lyons LA. The Lyons Den Website. Feline Genome Project: Polycystic
were found positive in two small test groups: In clinic I: 6 of 40 Kidney Disease. Available at: http:faculty.vetmed.ucdavis.edu/faculty/
American Shorthair cats were positive, and in the second clinic, 2 of lalyons/Sites/pkd.htm. Accessed Nov 6, 2004.
9. Washizu T, Washizu M, Zhang C, et al. A suspected case of ornithine
8 American Shorthair cats tested positive by ultrasound screening
transcarbamylase deficiency in a cat. J Vet Med Sci 2004;Jun;66(6):701-703.
of healthy cats from catteries. A genetic test is available.8
10. Strain GM. Hereditary deafness in dogs and cats: Causes, prevalence,
and current research. Proceedings. Tuft’s Canine and Feline Breeding and
Ornithine Transcarbamylase Deficiency: One case report
Genetics Conference. Oct 2-4, 2003 Available at: http://www.vin.com/
describes an 18 month old American Shorthair cat presented tuffs/2003. Accessed Nov 19, 2004.
with stunted growth and postprandial depression. Elevated bile
acids and ammonia were noted. Urea cycle enzyme deficiency is
of sex linked dominant inheritance in humans, but of unknown
mechanism in cats. Diagnosis is by urinary metabolite identification;
a portosystemic shunt was ruled out.9
Genetic Tests
Though there are no published recommendations for screening this
breed for HCM using echocardiography, one may consider screening
breeding stock until further information is available.
Direct genetic test for PKD is available from the UC-Davis VGL.
Miscellaneous
• Breed name synonyms: Domestic Shorthair (historical name in
use until 1960s), ASH, DASH
• Registries: ACFA, TICA, CFA, CFF, CCA, WCF
• Breed resources: National American Shorthair Club (CFA):
781 Progress Street
Macon, GA 31201
http://www.ashclub.org/
References
1. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
2. Meurs KM. Inherited heart disease in the cat. Proceedings. Tuft’s Canine
and Feline Breeding and Genetics Conference Oct 2-4, 2003 Available at
VIN: www.vin.com/tufts/2003. Accessed Nov 19, 2004.
3. Meurs K, Kittleson MD, Towbin J, Ware W. Familial systolic anterior
motion of the mitral valve and or hypertrophic cardiomyopathy is
apparently inherited as an autosomal dominant trait in a family of
American Shorthair cats. Proceedings. 15th Annual ACVIM Veterinary
Medical Forum, Lake Buena Vista FL [abstr] 1997;685.
4. Meurs KM, Kittleson MD, Towbin JA, Ware WA. Familial systolic
anterior motion of the mitral valve and/or hypertrophic cardiomyopathy
is apparently inherited as an autosomal dominant trait in a family of
American shorthair cats. J Vet Intern Med 1997;11:138 (abstract)
5. Kittleson MD, Meurs KM, Kittleson JA, et al. Heritable characteristics,
phenotypic expression, and natural history of hypertrophic cardiomyopathy
in Maine Coon cats. In: First International Feline Genetic Disease
Conference Proceedings (abstr), Feline Practice Supplement, 1999;7. Titled:
Hypertrophic cardiomyopathy in Maine Coon cats. Notes of the lecture
available at: www.winnfelinehealth.org/reports/cardiomyopathy.html
Accessed Aug 6, 2004.
6. Erdman C, Lyons LA. Facial Development Study Update, (Aug 2003-Aug
2004). Notes. University of California (Davis) Feline Genetics Extravaganza II
Aug 28-29, 2004.
7. Lyons LA. The Lyon’s Den. Feline Genome Project: Cranio-facial Defect.
Accessed at http://faculty.vetmed.ucdavis.edu/faculty/lalyons/Sites/
503
Balinese
The body coat color and points of the Balinese usually becomes
darker as the cat ages. Intermediate (medium) length coats result
from outcross mating. These shorter haired cats are termed
variants. This type of coat is short and plush, somewhat in between
the shorthair and semi-longhair. These variants are not shown.
Javanese refers to semi-longhaired Siamese (e.g., Balinese) with Recognized Behavior Issues and Traits
lynx (tabby) and tortie point patterns instead of classic Siamese Reported breed characteristics include: Highly intelligent, friendly,
solid points (lilac, seal etc). The Javanese as a separate breed was though some individuals may be aloof. The Balinese are curious,
accepted by CFA in 1979—in all other registries Javanese cats playful and often less vocal, a bit softer voiced, and a bit less active
are part of the Balinese breed. Overseas the Javanese name is than the Siamese cats. They are also highly social, and need plenty
synonymous with Oriental Longhair. of human contact and mental stimulation; may follow favored
people around the house. Balinese cats are content to be lap cats in
Traditional (Applehead) Balinese cats are of a type derived from between burst of activity. Climbing trees or perches are important
the Traditional (Applehead) Siamese. They are of heavier build with for these athletic cats; they love being up high. Good with children
a much rounder face and head conformation, smaller ears, and and dogs; may even curl up and sleep with a favored dog and
longer haircoat over the body (>2”) including ruff, pantaloons, and let themselves be groomed by that dog. If left alone all day, may
ear tufting. Most registries do not have a separate partition for benefit from another cat in the household. Not suited to an outdoor
this subtype. In the many registries, they are registered but are not lifestyle.
generally show cats.
Falling somewhere in between the Traditional Balinese and Modern Normal Breed Variations
Balinese type is another intermediate type termed “Classic”. Need to watch calorie intakes as can become obese more easily
than some other breeds
The name “Balinese” is thought to derive from these cats appearing
as graceful as Balinese dancers. Drug Sensitivities
None reported in the literature
Outcrossing to Siamese cats is still allowed in the CFA registry.
Genetic Tests
None commercially available
Miscellaneous
• Breed name synonyms: Javanese (the name applies to
non-Siamese type points such as cream, tabby, tortie and red).
In TICA and other non-CFA registries, the Balinese and Javanese
are the same breed. In Europe, they may be classed as Oriental
Longhairs.
• Other breed synonyms include: Bali, Longhaired Siamese,
Lao-Tsun Cat.
• Registries: FIFé, TICA, CFA, ACFA, CFF, NZCF, CCA, WCF, GCCF, ACF
• Breed resources: Traditional and Classic Cat International
(including Applehead Siamese, Traditional Balinese):
http://www.tccat.org/
Balinese Cat Society (UK): http://www.rantipole.demon.co.uk/bcs
505
Bengal
an elongated modified wedge. Muzzle is broad, whisker pads are
pronounced. Ears are short, wide set and rounded tips. The nose
is broad and has a slight puff in profile. Limbs are long with good
bone/ heavy muscling. The muscular body is long. Tail is thick and
tapers. Paws are large and rounded.
A five generation breeding history is necessary for registry as a Normal Breed Variations
Bengal, and within that pedigree a maximum of one Asian leopard Reduced fertility in early filial generations: F1 males are usually
cat may be present. Bengals with greater than four generations of sterile, and F2 and F3 males have reduced fertility.
inter-Bengal breeding are referred to as SBT (stud book tradition)
Bengal cats. Earlier filial (F) generations are technically still referred Bengal Kitten Information Project1 An Internet-based
to as Leopard cat crosses or hybrids, and are not typically sold for breeder survey was carried out to establish normal baselines for
the pet market, though some placid fourth filial generation cats reproduction.
(F4s) may be sold to experienced cat owners. The F1 cats (F4 or later 55 reporting breeders, 176 litters, 701 kittens,
crossed back with wild cat) are referred to as foundation cats. Some July 2003 to June 2004.
states have restrictions in place against F1 and F2 cats. The TICA Average litter size 4.0
registry was the first to accept this breed but stipulated at that time Stillbirth rate 6%
that show cats be at least F4s. C sections 3%
Average birth weight: Male 94 g female 92 g
Congenital defects included: flat-chested, cleft palate.
Physical Characteristics
Weight: female 10-15 lb (4.5-6.75 kg), male 10-22 lb (4.5-9.5 kg) Blood Type: In a small study done in the UK, 4 of 8 cats tested as
part of a survey were blood type AB, and the other four were type A.2
Coat: The short, dense, soft coat is usually brown tabby, blue
tabby and snow tabby, with marbled or spotted patterns with an A group has been working to map over 500 genetic markers in
autosomal dominant inheritance pattern. Marbling is a swirling Bengal cats. Study announced in 1998.3
of color produced by combination of the wild type rosette with
domestic classic tabby. The spotted pattern is most common.
Hair texture is silky. Spots should be very distinct and large, and
Drug Sensitivities
None reported in the literature
a necklet or necklets should be present on the throat, with a
“jawstrap” extending between the mandibles. Tail is spotted or
ringed and the tip is black. In marbled cats, the marking color is Inherited Diseases
enhanced by a darker outline color to the spots (rosettes). Belly Flat-chested Kittens: Similar to the flat-chested condition
must be spotted. Colors accepted may vary with the registry. Glitter in Burmese (see Burmese chapter), whereby reduced chest
refers to a high gloss gold or pearl sheen, and is not required, but is dorso-ventral dimension occurs. This trait is seen with some
desirable. Kitten coats may not mature until 6 months of age. frequency in Bengal cats and is seen in F1 kittens, so it is not the
result of inbreeding (Pers. Comm., Dr. Solveig Pflueger). Signs may
Eyes: Variable colors; gold, hazel, green, and blue; large, wide set. include poor weight gain, exaggerated cranial thoracic vertebral
kyphosis, vomiting, dyspnea, cyanosis, exercise intolerance and
Points of Conformation: This large cat has a fairly small head with cough, and a ridge along the costo-chondral junction of the ribs.
506
As kittens mature, and the rib cage calcification completes, clinical
signs abate in many of those kittens that were less severely affected
Miscellaneous
• Breed name synonyms: Leopardettes (historical), Bengel,
and thus not euthanized in the neonatal period. Though recognized Spotted Cat
by breeders, the flat-chested kittens have not been reported in the • Registries: FIFé, TICA, ACFA, CFF, GCCF, ACF, WCF, CCA, NZCF
literature. Signs are often first noted at 7-10 days of age. • Breed resources: International Bengal Cat Society Inc.:
http://www.tibcs.com/whatis.aspx
Pyruvate Kinase (PK) Deficiency: Autosomal recessive disease
The Bengal Cat Club (UK; GCCF):
causing hemolytic anemia. See under Abyssinian. A genetic test is
http://www.bengalcatclub.co.uk/
available.
The International Bengal Breeder’s Association Inc.:
http://www.webring.org/hub?ring=theinternation18
Disease Predispositions
FIP Susceptibility: An American study found that Bengal cats
were significantly over-represented for a diagnosis of FIP when
References
1. Little S. Bengal Kitten Information Project, Pers. Comm. March 2009.
they analyzed data for a 16 year period at a veterinary teaching 2. Knottenbelt CM, Addie DD, Day MJ, Mackin AJ. Determination of
hospital.4 the prevalence of feline blood types in the UK. J of Small Anim Pract
1999;40:115-118.
Rare and Isolated Reports 3. Lyons LA, Raymond MM, O’Brien SJ. The feline genome project: The role
Ulcerative Nasal Dermatitis: Of 48 Bengal cats seen in a Sweden of the genetic map of the cat in fancy cat breeding. First International
Feline Genetic Disease Conference Proceedings (abstr), Feline Practice
clinic between 1999 and 2003, six cats had fissured, crusted and
Supplement, 1999;20.
ulcerated erosive changes to the nasal planum. Age of onset
4. Pesteanu-Somogyi LD, Radzai C, Pressler BM. Prevalence of feline
was between 4 months and 1 year. Cause of the condition was infectious peritonitis in specific cat breeds. J Feline Med Surg. Vol
not elucidated. It was proposed to be an immune-mediated 8(1):ppp1-5. 2006.
mechanism.5 5. Bergvall K. A novel ulcerative nasal dermatitis of Bengal cats. Vet
Dermatol 2004;15(Suppl. 1):20-40.
Bengal Idiopathic Polyradiculoneuropathy: A case report 6. . Granger N, Stalin CE, Brown TB, Jeffery NDIdiopathic polyradiculoneu-
detailed a motor function loss in a 16-month-old NM. The rapid ropathy in a Bengal cat: electrophysiological findings and 1 year follow-up.
progression of dysfunction began in pelvic limbs then spread J Feline Med Surg. 2008 Dec;10(6):603-7.
to the thoracic limbs. The etiology was not determined. Studies 7. Pettigrew R, Kent, M, Berry WL, Shelton AJ. Muscle and Nerve Biopsies in
confirmed a ventral motor root (primarily axonal) neuropathy. Cyclic 138 Cats: Diagnosis and Outcome.
tetraparesis occurred over a year interval. Prognosis for the disease Online August 4th, 2010 at: http://www.vin.com/proceedings/Proceedings.pl
is considered good.6 x?CID=WSAVA2002&Category=1319&PID=9729&O=Generic
8. Feline Advisory Board Website. Accessed May 2010 at: http://www.
In a case retrospective study, Bengals represented 8.7% of the fabcats.org/breeders/inherited_disorders/bengal.php
cases, with average age of presentation one and a half years of
age. Abnormal EMGs, motor neuron velocities and action potential
amplitudes were identified by the researchers. Axonal degeneration
and demyelination were found, sometimes alone, sometimes
together. To diagnose, they recommend both nerve and muscle
biopsies. Weakness is the usual clinical complaint, with mostly
lower motor neuron signs, though a small proportion had upper
motor neuron function changes, megacolon, and less commonly,
laryngeal paresis or normal neurologic examination.Over 50% of
the cats had resolution but a small number recrudesced.7
Genetic Tests
Since at least in one very small sample, some cats have the rare
blood type AB, it may be prudent to screen breeding stock, and prior
to transfusion to check for the B allele until further information is
available about geographic and breed distribution of the blood types.
507
Birman
Roman-nosed, ears are small and wide set. Nose is medium in
length, forehead. The tail is full and moderate in size and length,
and the body of these cats is long. Limbs are heavily boned
and medium in length giving these cats a somewhat stocky
conformation. Paws are large and round.
Physical Characteristics Marked reduction in genetic diversity was identified in this breed
Weight: 10-18 lb (4.5-8 kg) when compared to random bred cats in a study of 20 domestic and
2 wild cat breeds.1
Coat: Kittens are born white and the coat does not usually finish its
development until maturity, though pigmentation begins to develop Birman Kitten Information Project:2 An Internet-based
well before weaning. The medium-long single coat is full like the breeder survey was carried out to establish normal baselines for
Persian coat, but shorter and silkier in texture. Championship reproduction. Report: 59 reporting breeders, with 204 litters, 735
CFA colors are the same as for Siamese breed cats. The gauntlet kittens. Sept 2003-Aug 2004
markings (or laces) consist of white extensions of the mittens Average litter size 3.6
running up the plantar surface of the metatarsals. This pattern Stillbirth rate 7%
is an autosomal recessive trait. Ideally, the laces are one-half to C-sections rate 9%
three-quarters of the height up to the tarsus. Average birth weight: Male 98 g female 93 g
Congenital defects:, seen in 8.3% of litters and included:
Mittens do not extend above the point where the paw meets the epibulbar dermoids, syndactyly (an autosomal dominant trait
vertical limb on the forelimb. A mask covers most of the face. The with variable expressivity leading to a split paw), cleft palate,
main coat is light in color and over the back and sides ideally looks umbilical hernia and open abdomen.
as if misted with a gold, termed golden mist; this overlay is often
absent in kittens. Type B Blood: The prevalence was reported to be 60% in a very
small study in Denmark.3 In an American report, 38 of 216 tested
Eyes: Large, wide set, sapphire blue. Deeper blue is better. were type B blood (17.5%).4
Points of Conformation: The face has a distinctive Siamese Elsewhere, 18%5 and 16%6 type B cats were reported.
look, but the heavier boning and round full face distinguishes
them. The face is more of a rounded-wedge. The profile is slightly There are some rare type AB cats in this breed. In a group of 24 cats
508
surveyed in the UK, 8% were AB in this group while 29% were B, Corneal Sequestration: Black body or cornea nigrum is often
63% type A.7 bilateral and Birman cats are over-represented. Usually in central
cornea; it is a brown to black pigmented lesion; often surrounded
Drug Sensitivities by a loose collarette of poorly adherent corneal epithelium. Defect
None reported in the literature may extend into the middle or deep stroma—or even to Descemet’s
membrane. Sloughing and corneal healing may take 2-6 months;
surgical debridement is another option. Epiphora, yellow-brown
Inherited Diseases ocular discharge and blepharospasm may be seen.12 This condition is
Azotemia: Birman cats were reported in a small British prospective corneal stromal necrosis and topical glucocorticoids are contraindi-
survey (n=106) of healthy cats to have a higher than expected cated; some cases may be linked to feline herpesvirus infection;
prevalence of azotemia, indicated by increased BUN and/or if suspected, do PCR on the black body tissue. Recurrences or
creatinine. They found 82% of cats less than 6 months old had involvement of the second eye in previously unilateral cases may
creatinine levels above the feline laboratory reference range, and occur.13
in adults of average age 4 years, 35% had elevated levels. The
reason for the high frequency of azotemia in apparently healthy FIP Susceptibility: Pedigree analysis indicated a heritability of
cats was not discovered. Though renal disease was not tested for by 0.521 after correction for inbreeding in one cattery. It was proposed
additional means, a serial blood test 18 months later for BUN/Cr did to be a polygenic inheritance for susceptibility to development
not confirm significant progression of azotemia except in two cats of clinical FIP. Nine of 11 deaths occurred in cats related to one
that succumbed to renal failure. It was suggested by the authors tom—so it was correlated with relatedness. Macrophage viral
that “one should consider renal dysfunction when undertaking permissiveness may be the underlying functional defect.14
anesthesia, surgery or treatment” in this breed and test accordingly.8
An American study found that Birman cats were significantly
Inherited Defect of Neutrophil Granulation: The condition was over-represented for a diagnosis of FIP when they analyzed data for
reported to be an autosomal recessive trait. A total of 46% of the cats a 16 year period at a veterinary teaching hospital.15
in the study population (n=78) were affected. The dark eosinophilic
cytoplasmic granules were functionally normal, but under the Respiratory Disease Propensity: There is anecdotal evidence of
microscope they had noticeably increased dye affinity, so if this more than expected prevalence in some catteries.
should be noted during diagnostic evaluation, it should be interpreted
that the neutrophils are still functional (incidental finding).9 Rare and Isolated Reports
Cataracts: Congenital (present at birth), juvenile (newborn to
Neonatal Isoerythrolysis (NI): Prevalence of Type B blood type
six years of age) forms have been reported with variable rate of
leads to a higher potential incidence of neonatal isoerythrolysis
progression.16 Most cases have been noted in a Swedish family of
(NI) due to cold acting agglutinins. All B type cats have circulating
cats, where onset of lens opacity was noted in 2-5 year old cats.
anti-A antibodies and even primiparous queens can carry these.
Progressive worsening occurred and the problem was bilateral.
Type B queens bred to type A toms can result in fatal red cell
These were considered to be primary cataracts and type of opacity
lysis in AA or AB blood type offspring with undetected NI. Kittens
varied. Two of the 6 observed cats had cataracts that normalized.12
with NI can be distinguished from other fading kittens because of
pigmenturia; anemia and icterus will also be present; not all kittens Peripheral and Central Distal Axonopathy: In a report, three
at risk for NI will develop overt clinical symptoms. The proportion of female littermates and a kitten from a previous litter with same
matings at risk for NI was reported to be 0.145.4 The proportion of parents were similarly affected. Onset as early as 10 days, to 8-10
matings at risk for NI was reported as 0.13.5 weeks of age, and signs included tendency to fall due to posterior
ataxia and weakness, and slowly progressive gait abnormalities such
Breeders should be advised not to allow offspring resulting from
as hypermetria and plantigrade stance. Histologic changes included
mating where blood types are unknown to nurse on the queen
foamy axonal degeneration, myelinopathy, and both central and
for the first 18 hours. Breeders should be made aware of the
peripheral nervous system distribution was noted. Sciatic nerves
importance of testing since in that same recent survey, it was
were degraded, but spinal nerve roots were not. Two kittens were
reported that 52% of breeders had carried out at least one breeding
reported elsewhere with primarily cerebellar lesions. A sex-linked
without typing the tom and queen. Foster nurse young kittens with
recessive gene with progressive penetrance was postulated.17
an A type queen or use milk replacer if blood types are unknown.
Epibulbar Dermoid: Lateral limbus is reported to be the usual
In one case report involving two litters, tail tip necrosis was
location, and dermoids may be unilateral or bilateral. May or may
identified.10 High neonatal mortality or tail tip necrosis should
not be hair covered. May encompass bulbar conjunctiva, eyelid
trigger tests for possible presence of NI.
margin and skin and may be associated with internal malformations
so ophthalmoscopic evaluation should be thorough (include
Disease Predispositions ophthalmoscope, biomicroscopy).12 First reported in Birman cats in
Arterial Thromboembolism (ATE): Birman cats were 1985; mode of inheritance uncertain.16
overrepresented (odds ratio 10.52) in a population of 127 arterial
thromboembolism (ATE) cats in a study done at the University of Eyelid Agenesis (frequently limited to upper and lateral eyelids):
Minnesota Veterinary Medical Teaching Hospital from 1992-2001. these cats may have concurrent iris, lens and optic nerve colobomas.
Most cats had left atrial enlargement.11 This is the most common congenital eyelid defect in cats.18
509
Congenital Hypotrichosis and Thymic Aplasia: A condition 8. Gunn-Moore DA, Dodkin SJ, Sparkes AH. J Fel Med Surg Letter to the
where thymic aplasia of kittens and lack of haircoat occurred Editor. 2002;4:165-66.
simultaneously; reflects both ectodermal and entodermal defect. 9. Hirsch VM, Cunningham TA. Hereditary anomaly of neutrophil
granulation in Birman cats. Am J Vet Res 1984;45(10):2170-2174.
In reported cases, death occurred by 13 weeks and some kittens 10. Bridle KH, Littlewood JD. Tail tip necrosis in two litters of Birman kittens.
were born dead, some euthanized because of immune-compromised J Small Anim Pract 1998;39:88-89.
11. Smith SA, Tobias AH, Jacob KA, et al. Arterial thromboembolism in cats:
state. By pedigree analysis it was considered to be an autosomal
Acute crisis in 127 cases (1992-2001) and long-term management with
recessive inheritance. The defect resulted in an overall reduced low-dose aspirin in 24 cases. J Vet Intern Med 2003;17:73-83
number of hair follicles; those that were present were hypoplastic 12. Narfström K. Hereditary and congenital ocular disease in the cat. J Fel
with hairs generally in telogen, other lymph tissues such as Peyer’s Med Surg 1999;1:135-141
patches, spleen and nodes were hypoplastic. This group consisted 13. Glaze MB. Feline corneal diseases: Part II. Proceedings. The 70th Annual
of nine related kittens; all affected cats had a common great-great AAHA Conference. 2003;1:367-368
grandsire.19,20 14. Foley JE, Pedersen NC. The inheritance of susceptibility to feline
infectious peritonitis in purebred catteries. Fel Pract 1996;24(1):14-22.
Miscellaneous Reported Conditions: 15. Pesteanu-Somogyi LD, Radzai C, Pressler BM. Prevalence of feline
Congenital portosystemic shunts: anecdotal, hepatic infectious peritonitis in specific cat breeds. J Feline Med Surg. Vol
encephalopathy, signs starting at 10-12 weeks of age. 8(1):ppp1-5. 2006.
16. Hoskins JD. Congenital defects in cats. Compend Contin Educ Pract Vet
Factor IX deficiency. 1995;17(3):385-405.
17. Moreau PM, Vallat JM, Hugon J, et al. Peripheral and central distal
Pelger-Huet Anomaly: Neutrophil dysmaturity, likely autosomal axonopathy of suspected inherited origin in Birman cats. ACTA Neuropathol
dominant. Heterozygotes clinically normal.21 1991;82:143-146.
18. Narfström K. Hereditary eye diseases. First International Feline Genetic
Disease Conference Philadelphia June, 1998 Proceedings (abstr) in: Feline
Genetic Tests Practice Supplement, 1999;13.
Blood typing before transfusions or breeding is recommended. If 19. Casal ML, Straumann U, Sigg C, et al. Congenital hypotrichosis with
kitten tail tip necrosis or neonatal mortality due to “fading kitten” thymic aplasia in nine Birman kittens. JAAHA 1994;30:600-602.
like syndrome occurs, test after the fact. 20. Casal ML, Arnold S, Straumann U et al. Congenital hypotrichosis with
thymic aplasia in Birman kittens. First International Feline Genetic Disease
Renal function test: screening of BUN and creatinine pre-op Conference Philadelphia June, 1998 Proceedings (abstr) in: Feline Practice
routinely for all cats is recommended. Supplement, 1999;33-34.
21. Feline Advisory Beaureau Website Accessed May 2010 at: http://www.
fabcats.org/breeders/inherited_disorders/birman.php
Miscellaneous
• Breed name synonyms: Sacred Temple Cat of Burma, Temple Cat,
Mitted Cat
• Registries: TICA, CFA, ACFA, CFF, FIFé (Sacred Birman; SBI), NZCF,
CCA, WCF, GCCF, ACF
• Breed resources: National Birman Fanciers:
http://www.nationalbirmanfanciers.com/
Sacred Cat of Burma Fanciers: http://www.scbf.com/
North American Birman Fanciers (ACFA):
http://www.birman.org/newsletters/nabf.html
References
1. Lipinski MJ, Young AE, Lyons LA. Genetic diversity and population
dynamics of domestic cat breeds. Proceedings. Tuft’s Canine and Feline
Breeding and Genetics Conference Oct 2-4, 2003 Available at VIN: www.vin.
com/tufts/2003. Accessed Nov 19, 2004.
2. Little, S. Birman Kitten Information Project, Pers. Comm. March 2009.
3. Jensen AL, Olesen AB, Arnberg J. Distribution of feline blood
types detected in the Copenhagen area of Denmark. Acta Vet Scand
1994;35:121-124.
4. Giger U, Bucheler J, Patterson DF. Frequency and inheritance of A and B
blood types in feline breeds of the United States. J Hered 1991;82:15-20.
5. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
6. Giger U, Casal M, Niggemeier A. The fading kitten syndrome and neonatal
isoerythrolysis. Proceedings. The 15th Annual ACVIM Medical Forum, Lake
Buena Vista FL 1997;308-310.
7. Knottenbelt CM, Addie DD, Day MJ, et al. Determination of the prevalence
of feline blood types in the UK. J of Small Anim Pract 40:115-118, 1999.
510
Bombay
Recognized Behavior Issues and Traits
Reported breed characteristics include: Calm, friendly; gregarious,
love climbing and jumping, playful as youngsters, placid as mature
cats, the Bombay cats are lap cats, curious, thrive on human
companionship and are very intelligent. Bombay cats are generally
easy to leash train. Like to fetch ball and play other games and
love the company of children. Get along with other pets well,
particularly dogs. Not particularly vocal; and when they vocalize,
this is a quiet voiced cat. Good for indoor lifestyle.
Coat: The Bombay has a very high gloss jet black close-lying short Disease Predispositions
single haircoat. Though generally breeding true, the odd mating will See American Shorthair and Burmese chapters since Bombay cats
produce some sable kittens due to residual pointing gene from the may share some disorders with the progenitor breeds, though
Burmese origins. Kittens may not be fully black but will generally Bombay cats are generally very healthy cats; likely due to hybrid
darken as they mature. Black is dominant and sable is the recessive vigor.
gene. Some light tabby markings in kittens can sometimes be seen
but will fade.
Genetic Tests
Eyes: Large round golden to copper eyes—darker is preferred No tests available commercially
(overseas, the accepted colors include yellow and green).
Miscellaneous
Points of Conformation: Conformation is quite similar to the • Breed name synonyms: Patent Leather Cat, Black Burmese, Black
Burmese cat, though the Bombay is a bit heavier built with longer Leopard Cat, Asian Shorthair, Asian Selfs, nickname: “Patent
limbs, and the rounded head is proportionately larger and both head leather kid with the copper penny eyes”
and body longer due to American Shorthair influence. The angle of • Registries: TICA, ACFA, CFA, CFF, ACF, WCF, CCA
change in the nose profile is also less pronounced in Bombay cats • Breed resources: The Bombay and Asian Self Breed Club (UK):
than in Burmese. The tail is fine, moderate in length and tapers. The http://www.bombayandasianselfbreedclub.org/
whisker pads are prominent. The muzzle is short-medium, ears are International Bombay Society:
medium-small with rounded tips. The feet are small and round. Nose Suzanne Zwecker, Secretary 5782 Dalton Drive
and pad leather is black. Canandaigua, NY 14425
Grooming: Minimal grooming is required for the Bombay cat. One
can just use hands or chamois to maintain shine.
511
References
1. Erdman C, Lyons L. Facial Development Study Update (Aug 2003-Aug
2004) In: Notes, University of California (Davis) Feline Genetics
Extravaganza II Aug 28-29, 2004.
2. Cat Fancy October 2008 Black Magic. E. Jordan. Pp 22-25.
512
British Shorthair
every few days. When bathing, avoid blow drying. More frequent
grooming needed while shedding.
Russian Blues have green eyes, they are less cobby, the coat is more
open, and they are smaller cats than the British Blue.
Disease Predispositions
Transfusion Reactions: Increased risk should be considered in this
Grooming: Low grooming needs; one can just hand groom quickly population due to prevalence of type B blood. Before transfusion,
513
blood typing will help identify cats at risk. Direct genetic test for PKD is available from UC-Davis VGL.
HCM screening recommendations not set for this breed, but until
further information is available, may consider echo screening for
breeding animals.4
514
Burmese
the face (mask), tail, feet and ears. The mask and points should be
minimal in mature cats. Burmese sable points are recessive (cb cb).
Young sable cats will darken as they mature.
Eyes: They possess large yellow or gold eyes, round in shape. In CFA,
green eyes penalize and blue eyes disqualify. The FIFé registry allows
green eyes.
The CFA accepted the Burmese breed in 1936, disallowed them for Normal Breed Variations
a while, and again reinstated them in the early 1950s, with full Epiphora: Secondary to face conformation rather than due to any
championship status by 1957. Only sable coloring was accepted by unusual anatomic defects in the lower punctum.
CFA until the late 1980s, at which time the accepted color spectrum
Blood Type: Prevalence 100% A type was reported in American
was expanded to four colors. Malayans were separately registered
cats.1
from 1979-1984.
There may be some differences in geographic distribution of blood
Burmese cats have played a role in development of other breeds
types; in a very small survey in the UK, of 10 cats tested, one was
incuding the Burmilla (Chinchilla Persian X Platinum Burmese),
type B blood.2
Tiffany (Longhaired Burmese), Bombay (Black Shorthair X), and
Tonkinese (Siamese X). Good longevity
In a recent study in Australia over 5 years, in 12,576 cats of all Can be unilateral or bilateral but is most often unilateral; is a
breeds, prevalence was 7.4:1000 cats and 22.4:1000 for Burmese corneal stromal necrosis. Topical glucocorticoids are contraindi-
cats.21 cated; some cases may be linked to feline herpesvirus infection.
If virus is suspected, a PCR on excised black body tissue may
Flat-Chested Kittens: A series of young Burmese kittens in the U.K. be helpful. Recurrences or involvement of the second eye in a
was reported to have an increased risk of a flat-chested condition previously unilateral lesion may occur. In early phases, an amber
in the pediatric phase. Dorso-ventrally flat-chested kittens were colored corneal stromal opacity may be noted. It gradually develops
usually born with normal phenotype, and then developed a form of distinct raised borders; and the surrounding cornea is cloudy
chest deformity somewhat similar to pectus excavatum by about with neovascularization; chemosis, blepharospasm, mucopurulent
nine days of age. About 3%-4% of Burmese kittens were affected. ocular discharge and hyperemic conjunctivae may also be noted.
The condition ranges in severity from mild and transient—to a The surface of sequestrum does not stain with flourescein dye but
severe form, sometimes overlapping with concurrent pectus. does retain Rose Bengal stain. Exophthalmic/brachycephalic head
conformation is thought to play a role in susceptibility. May recur
Signs include poor weight gain, cranial thoracic vertebral kyphosis, months or years later, or in a unilateral case the second eye may
vomiting, dyspnea, cyanosis, exercise intolerance and cough. become affected.27, 28
Though recognized by breeders, flat-chested kittens have not been
widely reported in the literature. Litter viability was 76% in one Feline Dilated Cardiomyopathy (DCM): Increased breed
study of affected litters. In cats in this UK study group, both queens predisposition to DCM and decreased risk of hypertrophic
and kittens had higher levels of whole blood taurine than typical cardiomyopathy is reported in Burmese cats.29 Case levels have
reference cat levels. dropped since dietary supplementation with taurine began.
Previously, mortality for DCM was about 85% and with taurine
Kitten’s levels in turn were significantly higher than the queens. supplementation the mortality is 30%-50%. Feline signs are not
Taurine has a negative effect on skeletal muscle contractility typically a cough as in the dog; heart rate may be bradycardic to
(hyperpolarization and anticholinergic effect) and this muscle tachycardia and both ventricles are affected. Affected cats are
weakness may contribute to the condition. Often as kittens mature prone to arterial thromboembolism. Systolic heart murmur, or
and the rib cage calcification completes, the clinical signs abate in diastolic gallop can often be heard, and 61% have arrhythmias,
many that were less severe and thus not euthanized in the neonatal usually ventricular.30
period. The paper did not elucidate further an established link
between hypertaurinemia and the flat-chested condition.22 Propensity to FeLV Infection: Endogenous feline leukemia
(enFeLVs) were studied in a single specimen of Burmese, Egyptian
Presence of a dorsal spinal curvature, prominent horizontal rib Mau and Persian breed cats to determine how many loci proviruses
ridge, and minimal dorsal deviation of sternum into the thoracic were typically inserted. This may indicate genetic propensity for
cavity in flat-chested kittens distinguish this condition from pectus leukemia genesis in these cats when exposed to the exogenous
excavatum.23 feline leukemia virus.
Calcium Oxalate Urolithiasis: This is one of the breeds identified They found provirus on 12/18 autosomes, with an average 19
as having a higher risk of developing this type of stone;24, 25 autosomal copies per cat. One specific locus contained both
Burmese cats were also reported to have lower risk of magnesium homologues in all 3 cats. They were also found on both X and Y
ammonium phosphate (struvite) uroliths.24 chromosomes.31
Wool Sucking: Onset is usually after weaning, this condition also
affects other Oriental breeds. Target is commonly a blanket, sweater, Rare and Isolated Reports
socks; often the behavior terminates at sexual maturity, but some Primary Glaucoma: Primary glaucoma is rare in cats when
cases may have late onset or continue signs late into life. In one compared with dogs and humans. Findings in narrow angle
report 28% of fabric eating cats were Burmese breed in a group glaucoma may include a moderately mydriatic pupil, reduced
of 152 affected cats. Wool sucking is a stereotypic oral movement PLR, episcleral blood vessel congestion and buphthalmos. In a
and though many cats begin by selecting wool as a substrate, many study of a small group of affected cats (1996-2001), closed or
narrow irido-corneal angles, with reduced number and size of
517
pectinate ligaments, and increased IOP were identified. Tapetal An American study did not find that Burmese cats were over-repre-
hyper-reflectivity, attenuated retinal vasculature and sometimes sented for diagnosis of FIP when they analyzed data for a 16 year
optic disc cupping occurred. This condition is still very rarely period at a veterinary teaching hospital.44
reported, but an early indication is that this breed may be
somewhat predisposed to narrow angle glaucoma. With early GM2 Gangliosidosis: See the Korat chapter for more detailed
diagnosis and appropriate therapeutic intervention, vision may information about this condition. A GM2 gangliosidosis lysosomal
be optimized. Routine screening of this breed may be deemed an storage disease with beta-subunit of hexosaminidase enzyme
appropriate wellness strategy.32 was reported in European Burmese cats. This condition is fatal.
Accumulation was noted in brain tissue.45
In a study of 1100 cases of feline glaucoma from 1992-2006,
researchers found 8 cases of primary glaucoma, and of these eight, A group of European breeders have formed the DEG or Data
six were domestic cats and two were Burmese cats—no other Exchange Group to share testing information. The mutation is a
purebreds were identified in that sample.33 deletion (cytosine in HEXB).46
Transient Opacity-Aqueous Humor: Suspected triglyceride rich Medial Patellar Luxation: A very small study case reported that
material accumulated in Burmese cats less than one year old that of eight clinically normal Burmese cats assessed as part of a
had no other discernable health problems. Spontaneous recovery larger study, two had abnormal patella seating with easily induced
occurred within a day, a few recrudesced (2/6 cats).34 Four additional luxation. Compared with non pedigreed cats where the rate was
cases were reported in that same year. Two were littermates.35 It is two abnormal cats out of 31 cats, they were overrepresented.47
not known whether this represented isolated cases of reaction to a
foreign stimulant. Lipid aqueous humor changes are reported to be Genetic Tests
associated with hyperlipidemia according to a recent report.36 Burmese coat genes are the least extreme of the ts-tyrosinase
partial albinism allele series. The mutation has been identified in the
A 2009 report proved that Burmese cats of the Australian strain code for tyrosinase enzyme.48
have reduced triglyceride clearance when compared to domestic
or other pedigreed cats. Resting levels were normal. This study New research shows that the c(b) allele of the albino locus gene
may shed light on altered fat metabolism in this genetic pool of are variants on the D1 chromosome specifying tyrosinase.and the
Burmese.37 chocolate (b) and cinnamon (b(9l)) a second allele at the B (brown)
locus are nucleotide variants of TYRP1 (chromosome D4).49
Severe Transient Hyperlipidemia and Anemia: In a study group
of 12 litters of kittens of weaning age this condition was described; The mutations are reported to most likely to be identical by descent
one of the litters was Burmese. A genetic defect in lipid metabolism rather than multiple mutation events occurring at the same site in
was suspected.38 another study.50
Endocardial Fibroelastosis: Reports in the older literature (1982) Glaucoma Screening: Ophthalmoscopic exam, gonioscopy, and
described a very rare condition where the endocardium was tonometry are recommended for breeding stock.
markedly thickened in a series of offspring from one Burmese
queen and tom. This was thought to be an inherited disorder, Renal Function: Screen for renal function (minimum of Creatinine/
characterized by diffuse fibrous and elastic thickening of the BUN and urinalysis) in cats eight years and older since a breed
endocardium; the left side being dilated and hypertrophied propensity to renal failure was identified.16
concurrently; tachycardia, CHF, gallop or systolic murmur and
terminal cyanosis and dyspnea were noted with onset at 3 weeks to Scott-Ritchey Research Center web site at http://www.vetmed.
4 months of age.39, 40 auburn.edu/srrc and UC-Davis VGL for Gangliosidosis GM2 testing in
European Burmese
Persistent Atrial Standstill: Bradycardia non responsive to medical
management and a pacemaker may be needed.8 Miscellaneous
• Breed name synonyms: Historically, dilutes were registered in
Synovial Osteochondromatosis: Burmese cats are overrepresented,
CFA as Malayan cats—they are now accepted as Burmese in
and this condition can be confused with benign periarticular
separate class
ossification, perhaps resulting in underreporting.41
• Other Synonyms: Burm, Thai Copper Cats, Asian Shorthair
FIP Susceptibility: Feline leukocyte antigen class II is important for • Registries: FIFé, TICA, CFA, ACFA, GCCF, ACF, WCF, NZCF, CCA
control of immune response, and is represented by a set of genes, • Breed resources: United Burmese Cat Fanciers:
and polymorphism may play a role in susceptibility; further studies http://unitedburmese.com/
are needed. Burmese cats may be particularly susceptible to FIP. It The Burmese Cat Club: http://www.burmesecatclub.com/
was noted in this small study sample that related cats of this breed The Burmese Cat Society: http://www.burmesecatsociety.org.uk/
had fewer alleles compared to other breeds.42 National Alliance of Burmese Breeders (CFA):
http://www.burmesecat.org/
Another study in Australia confirmed that the Burmese breed cats
were over-represented and that they were more likely to develop
dry FIP versus effusive FIP.43
518
References Pract Vet 1989;11(1):24-32.
28. Glaze MB. Feline corneal diseases: Part II. Proceedings. The 70th Annual
1. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
AAHA Conference. 2003;1:367-368.
Philadelphia: WB Saunders Co, 2000;396-399.
29. Fox PR. Feline cardiomyopathy (Part I). Hypertrophic cardiomyopathy.
2. Knottenbelt CM, Addie DD, Day MJ, et al. Determination of the prevalence
Proceedings. The 19th Annual ACVIM Veterinary Medical Forum, Denver CO
of feline blood types in the UK. J Small Anim Pract 1999;40:115-118.
2001:1129.
3. Little, S. Birman Kitten Information Project, Pers. Comm. March 2009.
30. Atkins CE. Feline dilated cardiomyopathy. Winter 2004 AAFP Meeting.
4. Lyons LA. The Lyon’s Den. Cranio-facial Deformity. Available at: http://
Proceedings [abstr] in: AAFP Newsletter August 2004 22(2):29-30.
faculty.vetmed.ucdavis.edu/faculty/lalyons/Sites/burmese.htm Accessed Nov
31. Roca AL, Nash WG, Menninger JC, Murphy WJ, O’Brien SJ. Insertional
15, 2004.
polymorphisms of endogenous feline leukemia viruses. J Virol. 2005
5. Erdman C, Lyons LA. Facial Development Study Update (Aug 2003-Aug
Apr;79(7):3979-86.
2004) In: Notes, University of California (Davis) Feline Genetics
32. Hampson ECGM, Smith R, Bernays ME. Primary glaucoma in Burmese
Extravaganza II Aug 28-29, 2004.
cats. Aust Vet J 2002;80(11):672-680.
6. Sponenberg DP, Graf-Webster E. Hereditary meningoencephalocele in
33. Jacobi S, Dubielzig RR Feline primary open angle glaucoma. Vet
Burmese cats. J Hered 1986;77(1):60.
Ophthalmol. 2008 May-Jun;11(3):162-5.
7. Noden DM, Evans HE. Inherited homeotic midfacial malformations in
34. Gunn-Moore DA, Crispin SM. Unusual ocular condition in Burmese cats.
Burmese cats. J Craniofac Genet Dev Biol Suppl 1986;2:249-266.
Vet Rec 1998;142(12):376.
8. Hoskins JD. Congenital defects in cats. Compend Contin Educ Pract Vet
35. Eason P. Unusual ocular condition in Burmese cats. Vet Rec
1995;17(3):385-405.
1998;142(19):524.
9. Narfström K. Hereditary eye diseases. First International Feline Genetic
36. Hardman C, et al. Proceedings. American College of Veterinary
Disease Conference Philadelphia June, 1998 Proceedings (abstr) in: Feline
Ophthalmologists, 1999.
Practice Supplement, 1999:13.
37. Kluger EK, Hardman C, Govendir M, Baral RM, Sullivan DR, Snow
10. Narfström K. Hereditary and congenital ocular disease in the cat. J Fel
D, Malik R Triglyceride response following an oral fat tolerance test in
Med Surg 1999;1:135-141.
Burmese cats, other pedigree cats and domestic crossbred cats. J Feline Med
11. Edwards CM, Belford CJ. Hypokalemic polymyopathy in Burmese cats.
Surg. 2009 Feb;11(2):82-90
Aust Vet Practit 1995;25(2):58-60.
38. Gunn-Moore DA, Watson TDG, Dodkin SJ, et al. Transient
12. Gaschen F, Jaggy A, Jones B. Congenital diseases of feline muscle and
hyperlipidaemia and anaemia in kittens. Vet Rec 1997;140:355-359.
neuromuscular junction. J Fel Med Surg 2004;6:355-366.
39. Zook BC, Paasch LH. Endocardial fibroelastosis in Burmese cats. Am J
13. Gruffydd-Jones TJ, Sparkes AH, Caney SA, et al. Hypokalemic Episodic
Pathol 1982;106(3):435-438.
weakness in Burmese kittens. First International Feline Genetic Disease
40. Rozengurt N. Endocardial fibroelastosis in common domestic cats in the
Conference Philadelphia June 1998 Proceedings (abstr) in: Feline Practice
UK. J Comp Path 1994;110:295-301.
Supplement, 1999;29.
41. Allan GS. Radiographic features of feline joint disease. Vet Clin North
14. Blaxter A, Lievesley P, Gruffydd-Jones T, et al. Periodic muscle weakness
Am: Sm Anim Pract 2000;30(2):281-301.
in Burmese kittens. Vet Rec 1986;118(22):619-620.
42. Addie DD, Kennedy LJ, Ryvar R, et al. Feline leucocyte antigen class II
15. Taboada J. Ventroflexion of the neck in cats. Proceedings. The 12th
polymorphism and susceptibility to feline infectious peritonitis. J Fel Med
ACVIM Veterinary Medical Forum, San Francisco CA 1994:385-386.
Surg 2004;6:59-62.
16. Lulich JP, O’Brien TD, Osborne CA, et al. Feline Renal Failure: Questions,
43. Norris JM, Bosward KL, White JD, et al Clinicopathological findings
answers, questions. Compend Contin Educ Pract Vet 1992;14(2):127-152.
associated with feline infectious peritonitis in Sydney, Australia: 42 cases
17. Panciera DL, Thomas CB, Eicker SW, et al. Epizootiologic patterns of
(1990-2002). Aust Vet J. 2005 Nov;83(11):666-73.
diabetes mellitus in cats: 333 cases (1980-1986). J Am Vet Med Assoc
44. Pesteanu-Somogyi LD, Radzai C, Pressler BM. J Prevalence of feline
1990;197(11):1504-1508.
infectious peritonitis in specific cat breeds. Feline Med Surg. 2006
18. Rand J. Current understanding of feline diabetes: Part 1: Pathogenesis. J
Feb;8(1):1-5.
Fel Med Surg 1999;1(3):143-153.
45. Bradbury AM, Morrison NE, Hwang M, Cox NR, Baker HJ, Martin DR
19. Rand JS, Bobbermien LM, Hendrikz JK, et al. Over representation of
Neurodegenerative lysosomal storage disease in European Burmese cats with
Burmese cats with diabetes mellitus. Aust Vet J 1997;75(6):402-405.
hexosaminidase beta-subunit deficiency. Mol Genet Metab. 2009 Feb 20.
20. Rand JS, Fleeman LM, Farrow HA, et al. Canine and feline diabetes
46. Feline Advisory Beaureau Website at: http://www.fabcats.org/breeders/
mellitus: Nature or nurture? J Nutr 2004;134:2072S-2080S.
inherited_disorders/burmese.php
21. Lederer R, Rand JS, Jonsson NN, Hughes IP, Morton JM Frequency
47. Engvall E, Bushnell N. Patellar luxation in Abyssinian cats. Fel Pract
of feline diabetes mellitus and breed predisposition in domestic cats in
1990;18(4):20-22.
Australia. Vet J. 2009 Feb;179(2):254-8.
48. Lyons LA, Imes DL, Grahn RA. Investigation of albinism in domestic cats.
22. Sturgess CP, Waters L, Gruffydd-Jones TJ, et al. Investigation of
Proceedings. The 2nd International Conference Advances in Canine and
the association between whole blood and tissue taurine levels and the
Feline Genomics. Utrecht Netherlands Oct 2004. Poster #18.
development of thoracic deformities in neonatal Burmese kittens. Vet Rec
49. Schmidt-Kuntzel A, Eizirik E, O’Brien SJ, et al. Tyrosinase and tyrosinase
1997;141:566-570.
related protein 1 alleles specify domestic cat coat color phenotypes of the
23. Little S. Breed Specific Reproduction Projects. In: Notes, University of
albino and brown loci. J Hered 2005 Jul-Aug;96(4):289-301.
California (Davis) Feline Genetics Extravaganza I July, 2003.
50. Lyons LA, Imes DL, Rah HC, et al Tyrosinase mutations associated with
24. Thumchai R, Lulich J, Osborne CA, et al. Epizootiologic evaluation
Siamese and Burmese patterns in the domestic cat (Felis catus). Anim
of urolithiasis in cats: 3,498 cases (1982-1992). J Am Vet Med Assoc
Genet. 2005 Apr;36(2):119-26.
1996;208(4):547-551.
25. Houston DM, Moore AEP, Favrin MG, Hoff B. Feline urethral plugs
and bladder uroliths: A review of 5484 submissions 1998-2003. Can Vet J Recommended Reading
2003;Dec;44(12):974-977. Glaze MB Congenital and hereditary ocular abnormalities in cats. Clin Tech
26. Neilson J. Anxieties, phobias and compulsive disorders. Proceedings. Small Anim Pract. 2005 May;20(2):74-82.
AAFP Fall Conference. 2002;125-139.
27. Pentlarge VW. Corneal sequestration in cats. Compend Contin Educ
519
Chartreux
Grooming: Grooming needs are minimal; a quick rub with a
chamois or work through with fingers generally suffices. Heavy
seasonal shedding occurs so more frequent attention is needed
while changing the coat.
In those times they were valued for their pelts and also as ratters. Strong hunting instinct so caution around pocket pets.
First specimens arrived in America in the 1970s, and the CFA
registry granted them championship status in 1987. In this breed, Drug Sensitivities
a naming convention results in all registered cats in any particular None reported in the literature
year having a name starting with the letter that has been assigned
to that year. This breed almost became extinct following World Inherited Diseases
War II, and outcrossing to Blue Persian and Blue British Shorthair None reported in the literature
was reportedly done overseas to regenerate the gene pool. No
outcrossing is allowed currently. Some European registries may
use the term Chartreux to apply to a Blue British Shorthair or
Disease Predispositions
Overrepresented breed in a very small breed sample identifying risk
European Shorthair with blue coloring, but they are distinct breeds. of developing magnesium ammonium phosphate (MAP, struvite)
Pronounced “Shart-rooh”, or in some areas, “shart-row”. uroliths.1
Drug Sensitivities
Increased tendency for post-vaccinal reactions (fever, lethargy) via
anecdotal evidence only
Inherited Diseases
Corneal Sequestrum: Black body or cornea nigrum is often
bilateral in Colorpoint cats. Usually in central cornea; brown to
black pigmented lesion; often surrounded by a loose collarette of
poorly adherent corneal epithelium. Lesion may extend into shallow
The Breed History or deep stroma, or even to Descemet’s Membrane. Sloughing and
Siamese cats were crossed with other breeds such as the American corneal healing may take 2-6 months; surgical debridement is
Shorthair and Abyssinian to develop new non-Siamese colors such another option.1
as solid red point, solid cream point, red-lynx point and chocolate-
tortie point. There are other additional point colors and patterns (16
in all). CFA registration occurred in 1974. Only Siamese outcrossing Disease Predispositions
is allowed (book closes in 2019 for CFA). Many of Siamese conditions apply (see Siamese Pointed Cat chapter)
though due to hybridization, the gene pool is broader and overall,
the Colorpoint Shorthair cats are considered healthy and hardy.
Physical Characteristics
Weight: Female 6-8 lb (2.5-3.5 kg), male 8-12 (3.5-5.5 kg) Anecdotal reports of heart problems in some lines
Coat: Glossy coat is very short with fine hair texture and lies close. Gingivitis and periodontal disease/periodontitis: anecdotal evidence
Body of the coat is off-white in color with subtle shading which of increased breed propensity
tends to darken as the cats age. The pointing and coat type are
exactly the same as the Siamese; just the colors differ. Leather and
paw pad pigmentation should be in sync with the coat coloring.
Genetic Tests
None commercially available
Eyes: Almond shaped medium sized eyes are close set, though
greater than one eye width apart. Eyes are colored sapphire blue. Miscellaneous
• Breed name synonyms: none
Points of Conformation: Siamese in conformation, though a • Registries: CFA, CCA (in other registries such as GCCF, they are a
slightly more muscular build is evident due to early outcrossing color class of Siamese)
with American Shorthair. Head is long, a tapered wedge, with • Breed resources: For clubs, contact the CFA at:
no stop and a straight profile. Ears are large and pointed, and 1805 Atlantic Avenue, Manasquan NJ 08736-0805
their outer margin follows the wedge of the face in a straight
continuation. Nose is long and straight. Body and limbs are lithe.
Feet are oval and small. Neck is long and slim. Tail is long, fine, and
References
1. Narfström K. Hereditary and congenital ocular disease in the cat. J Fel
tapers to a point. Med Surg 1999;1:135-141.
Grooming: Coat is low maintenance except for periodic light brush
or bath.
521
Cornish Rex
Grooming: Does not mat. Minimal grooming is needed and this
should be done with a chamois or fingers only. They do shed, but
hairs are small.
Coat: The Cornish Rex comes in many colors and patterns Inherited Diseases
Bi-colored is the most popular in the registry and show ring; Neonatal Isoerythrolysis (NI): Published data support a high risk
smokes are also fairly common. The short coat is very soft and of complications if parent blood type is not tested prior to breeding.
wavy, curly or rippled. There is a spectrum of hair length, thickness The proportion of matings reported at risk is 0.23.2
and curl. Longer coat is not as wavy (plush), shorter coat is “nappy”
(termed suede). This mutation leaves only undercoat—there are All B type cats have circulating anti-A antibodies and even
no guard hairs. Uniform tight soft hairs lie close, organizing into primiparous queens can carry these. Breeding type B queens to type
“washboard” rows of wavy hairs much like the old-fashioned marcel A toms can result in fatal red cell lysis in blood type A offspring
hairstyle. Whiskers are curly. with undetected NI. Kittens with NI can be distinguished from other
fading kittens because pigmenturia; anemia and icterus will also
Born curly coated, these cats go straight haired until about 16 be present; not all kittens at risk for NI will develop overt clinical
weeks of age when they begin to curl, with coat quality finishing symptoms.3 Use a foster A type queen for the fist 18 hours or milk
development at sexual maturity. Any bare areas apart from temples replacer if confirmed case of NI.
and ears are a serious show fault.
Eyes: Oval eyes, medium to large, many colors accepted. Disease Predispositions
Transfusion Reactions: Due to increased frequency of B blood
Points of Conformation: English standard varies from the type, an increased risk of transfusion reactions is expected.
American standard. Small to medium cats, they possess a “racy”
body, with a long wedge or “egg”-shaped small head, narrow Dystocia: A survey of 2,928 litters that included multiple cat breeds
muzzle, with hollow-cheeked look, very large high set ears lacking was carried out to ascertain prevalence of dystocia and over-repre-
furnishings, with rounded tips. Brows are also crinkled. Chin is well sentation of Cornish Rex cats was found, though only 16 Cornish
developed, profile is lightly Roman nosed, whisker break is evident, rex litters were analyzed. Average dystocia rate in the study group
and neck is long. Legs are long, with small oval feet. It is normal for was 5.8% of litters, with a low rate in a mixed breed colony of 0.4%,
them to stand with an arched back, creating a tucked-up abdomen and for comparison, a rate of 12.5% in Cornish Rex.4
appearance. The tail is long and slender, tapering to a point.
522
Hypertrophic Cardiomyopathy: The most common cardiac tufts/2003. Accessed Nov 19, 2004.
condition in all breeds of cats (10% prevalence), possibly inherited 7. Norris JM, Bosward KL, White JD, Baral RM, Catt MJ, Malik R.
in the Rex breeds.5 Clinicopathological findings associated with feline infectious
peritonitis in Sydney, Australia: 42 cases (1990-2002). Aust Vet J. 2005
Hereditary Deafness: Is associated with the dominant gene for Nov;83(11):666-73.
white cat (W); may be found in white cats of this breed.6 8. Pesteanu-Somogyi LD, Radzai C, Pressler BM. Prevalence of feline
infectious peritonitis in specific cat breeds. J Feline Med Surg. 2006
FIP Susceptibility: A study in Australia confirmed that the Cornish Feb;8(1):1-5.
9. Engvall E, Bushnell N. Patellar luxation in Abyssinian cats. Fel Pract
Rex breed cats were over-represented.7
1990;18(4):20-22
10. Robinson R. Genetic aspects of umbilical hernia incidence in cats and
An American study found that Rex cats were significantly
dogs. Vet Rec 1977;Jan1;100(1):9-10.
over-represented for a diagnosis of FIP when they analyzed data for 11. Hoskins JD. Congenital defects in cats. Compend Contin Educ Pract Vet
a 16 year period at a veterinary teaching hospital.8 1995;17(3):385-405.
Genetic Tests
Though not specifically reported in the literature, blood typing prior
to mating or transfusions would be prudent.
Miscellaneous
• Breed name synonyms: Curly-coat cat, Crex, Rexed cat.
• Registries: FIFé, TICA, CFA, ACFA, CFF, GCCF, ACF, WCF, NZCF, CCA
• Breed resources: The Rex Cat Club (GCCF-U.K.):
http://www.sam.luxford-watts.zen.co.uk/home.html
Cornish Rex Society: In the U.K.:
http://www.cornish-rex.co.uk/
In the U.S.:
http://www.flickoff.com/wavelink.htm
(Cornish) Rex Breeders United (CFA):
446 Itasca Ct NW
Rochester MN 55901
CFA Cornish Rex Breed Council: http://www.cornishrexbc.org
References
1. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
2. Giger U, Casal M, Niggemeier A. The fading kitten syndrome and neonatal
isoerythrolysis. Proceedings. The 15th Annual ACVIM Medical Forum, Lake
Buena Vista FL 1997;308-310.
3. Giger U, Bucheler J, Patterson DF. Frequency and inheritance of A and B
blood types in feline breeds of the United States. J Hered 1991;82:15-20.
4. Gunn-Moore DA, Thrusfield MV. Feline dystocia: prevalence, and
association with cranial conformation and breed. Vet Rec 1995;136:350- 353.
5. Little S. Selected inherited diseases of the cat, in Proceedings.
International Ragdoll Congress Oct, 2004; Pers. Comm.
6. Strain GM. Hereditary deafness in dogs and cats: causes, prevalence,
and current research. Proceedings. Tuft’s Canine and Feline Breeding
and Genetics Conference. Oct 2-4, 2003 Available at: http://www.vin.com/
523
Devon Rex
pads are evident. Other features include a moderately short nose,
very large rounded ears which are set low, lending the cats an elfin
look. The neck is fine. The tail is long and slender. Legs are long,
straight and medium in bone. Paws are small and oval.
Clinical cases presented with signs such as hematoma and Cervical Ventroflexion: In a study carried out in Great Britain,
conjunctival hemorrhage, post-operative bleeding, sudden death primary muscle weakness was diagnosed in young cats, with
due to intra-thoracic hemorrhage, and it was reported that some marked neck ventroflexion and normal Creatine Kinase and muscle
had untested relatives (such as littermates) affected or that biopsies. No therapy was found to be helpful.13
had died. The screening of cats revealed PT and APTT tests were
substantially prolonged.5 Hypotrichosis: Thin hair regresses to baldness at 2 weeks old.
May re-grow by 6-10 weeks of age, but loss occurs again at
Multiple Vitamin K-dependent blood coagulation factor deficiency sexual maturity leaving cats permanently bald.14 It is thought to
was found in another report of two littermates with bleeding be an autosomal recessive mode of inheritance. Hair follicles are
tendency. An underlying mutation in the vitamin K-dependent hypoplastic and hairs are in telogen.
γ-glutamylcarboxylase enzyme was identified as the reason for
the bleeding disorder; this enzyme plays an important role in Hereditary Deafness: Is associated with the dominant gene for
reconstituting Vitamin K in the liver cycle.6 white cat (W); may be found in white cats of this breed.15
A report in a British Devon Rex cat indicated that the same Neonatal Isoerythrolysis (NI): High prevalence of B blood type
coagulation factor deficiency combination was again present. makes this a concern in this breed; typed parents are now the
Another cat with the same grandmother also died of post-operative standard for breeders. Published proportion of matings at risk for
hemorrhage. The cats responded to oral/subcutaneous vitamin K NI is 0.24 for this breed.16 Also given as 0.246.1 All B type cats have
administration and transfusion.7 circulating anti-A antibodies and even primiparous queens can
carry these. Type B queens bred to type A toms can result in fatal
A likely autosomal recessive inheritance was reported. Age of onset red cell lysis in A blood type offspring with undetected NI. Kittens
is generally before one year of age.8 with NI can be distinguished from other fading kittens because of
pigmenturia; anemia and icterus will also be present; not all kittens
It is important to note that not all reported afflicted cats had at risk for NI will develop overt clinical symptoms.1
clinically evident bleeding episodes. The prevalence of this defect
is unknown in the breed, so testing Devon Rex cats by coagulation
profile before surgery might be prudent until further data is available.
Disease Predispositions
Transfusion Reactions: Due to high prevalence of blood type B,
Devon Rex Hereditary Myopathy (Breeder Synonym: Spasticity): natural allo-antibodies markedly increase the risk of transfusion
A neuromuscular disease leading to muscle weakness, and is similar reactions so donors and recipients should be blood typed.
to limb girdle muscular dystrophy in humans. First reported in
Toe and Skin Fold Greasiness, Paronychia: Seborrheic dermatitis
1974, this condition presents as an unusual gait (high stepping),
caused by M. Pachydermatis is more common in the breed (90%
significant neck ventroflexion, head bobbing, limping, abnormal
samples positive in a cross sectional survey comparing Cornish and
mastication due to pharyngeal muscle weakness, megaesophagus,
Devon Rex cats with DSH cats).17
difficulty drinking (nose may be inserted underwater), dorsal
scapula protrusion, shaking, and collapse. Aspiration pneumonia or In a study the previous year, the same researchers isolated M. sloffiae
sudden death due to choke is a possible consequence of difficulty from claw folds of seborrheic cats.18
with prehension of food and water. Neck ventroflexion may worsen
during micturition and defecation and while walking, and signs may Another study by the same authors that year explored the use of
wax and wane in intensity over days to weeks.9 Blood count, serum itraconazole to treat this seborrhea in a 21 day pulse treatment.19
biochemistry including CK and electrolytes are all within normal
ranges. Histology is best performed on proximal limb and cervical Hypertrophic Cardiomyopathy (HCM): The most common cardiac
muscles, and magnitude of changes is correlated with age and condition in cats (10% prevalence). Suspected to be inherited in the
severity of clinical signs at time of biopsy. breed, and cats with HCM should be removed from the breeding
pool.20
Age at onset of signs varies but signs are often noted by breeders
at 4-7 weeks, though some are delayed to about 13 weeks of Medial Patellar Luxation (MPL) and Hip Dysplasia (HD):
age (range of onset 4-20 weeks).8, 10 Though afflicted cats usually Historically, a proposed genetic predisposition to patellar luxation
worsen, as an adult some may adapt to the disability. In a survey was reported, with hip dysplasia prevalence also increased in this
of cats from the UK, Australia, and New Zealand an autosomal breed.21 In 1985, it was one author’s early finding that prevalence of
recessive monogenic pattern of inheritance was proposed to MPL was apparently much greater in the Devon Rex.22
explain the trait.8 A recent report indicates that dystroglycan
(DAG1) may be the gene causing this problem, and the researchers A nonrandom group of 78 cats of different breeds including 25
have attempted to sequence the mutation; apparently the same Devon Rex cats were assessed. About 32% of this group of cats
mutation is present in Sphynx Spasticity.11 and 40% (10 of 25) of Devons had HD using OFA-like criteria and a
positive correlation between joint laxity, DJD and HD was identified.
525
The majority of cats were not clinically lame, but diagnostic imaging paroxysmal supraventricular tachycardia (SVT) and was diagnosed
tests showed pathologic changes. using an implantable loop recorder, and treated with sotalol.31
The Devon Rex cats were affected more severely and with higher Swimmer Syndrome: After several weeks, a 3-week old showed
frequency than the average cat. In the pooled all-breed group with response to bandaging and physiotherapy. Euthanasia is the usual
MPL in the study group, those with MPL were three times more veterinary recommendation for this condition.32
likely to have concurrent hip dysplasia than those without MPL.23, 24,
25, 26
Genetic Tests
Coagulation profile and blood typing before surgery, transfusion, or
In the 1999 study done at University of Pennsylvania joint laxity
in breeding animals is recommended.
measures included Norberg angle (NA), distraction index (DI)] as
well as OFA criterion. Some degree of MPL was found in 58% of Though no program is recommended in the literature, screening
pooled cats and concurrent MPL and HP in 24%. Of the 25 Devon breeding animals for HD and MPL using radiography and orthopedic
Rex cats, 16 had MPL (64%); eight Devon Rex cats had both HD and examination may be helpful to manage these conditions in the breed.
MPL (32%).26
Both HD and PL are more common than was previously presumed. Miscellaneous
Medial patellar luxation is thought to be congenital and can be • Breed name synonyms: Curly-coated cat, Devon, Rexed cat,
unilateral or bilateral. Higher prevalence of MPL is suggestive of a nickname: Poodle cat
hereditary basis. • Registries: FIFé, TICA, CFA, ACFA, CFF, CCA, NZCF, WCF, ACF, GCCF
• Breed resources: Devon Rex Breed Club:
Dystocia: A report summarizing a survey of 2,928 litters that http://www.devonrexbreedclub.com/
included multiple cat breeds was analyzed to ascertain prevalence The Rex Cat Club (GCCF-U.K.):
of dystocia, and over-representation of Devon Rex cats was found http://www.sam.luxford-watts.zen.co.uk/home.html
(22 Devon litters analyzed). Average dystocia rate in the study Rex Breeders United:
group was 5.8% of litters, with a low in mixed breed cat colony of 446 Itasca Ct NW
0.4%, to a high of 18.2% in the Devon Rex study group.27 Rochester MN 55901
526
Devon Rex cats. Neuromuscul Disord. 2008 Dec;18(12):942-52
13. Taboada J. Ventroflexion of the neck in cats. Proceedings. 12th Annual
American College of Veterinary Internal Medicine Forum, San Francisco CA
1994;385-386.
14. Hoskins JD. Congenital defects in cats. Compend Contin Educ Pract Vet
1995;17(3):385-405.
15. Strain GM. Hereditary deafness in dogs and cats: causes, prevalence,
and current research. Proceedings. Tuft’s Canine and Feline Breeding and
Genetics Conference. Oct 2-4, 2003. Available at: http://www.vin.com/
tufts/2003. Accessed Nov 19, 2004.
16. Giger U, Casal M, Niggemeier A. The fading kitten syndrome and
neonatal isoerythrolysis. Proceedings. The 15th Annual ACVIM Medical
Forum, Lake Buena Vista FL 1997;308-310.
17. Bond R, Stevens K, Perrins N, Ahman S Carriage of Malassezia spp.
yeasts in Cornish Rex, Devon Rex and Domestic short-haired cats: a
cross-sectional survey. Vet Dermatol. 2008 Oct; 19(5):299-304.
18. Ahman S, Perrins N, Bond R Carriage of Malassezia spp. yeasts
in healthy and seborrhoeic Devon Rex cats. Med Mycol. 2007
Aug;45(5):449-55.
19. Ahman S, Perrins N, Bond R. Treatment of Malassezia pachydermatis-
associated seborrhoeic dermatitis in Devon Rex cats with itraconazole--a
pilot study Vet Dermatol. 2007 Jun;18(3):171-4.
20. Meurs KM. Inherited heart disease in the cat. Proceedings. Tuft’s Canine
and Feline Breeding and Genetics Conference Oct 2-4, 2003 Available at
VIN: www.vin.com/tufts/2003. Accessed Nov 19, 2004.
21. Little S. Selected inherited diseases of the cat, in Proceedings.
International Ragdoll Congress Oct, 2004. Available at: www.catvet.
homestead.com/Inherited_Diseases_2004.pdf, Accessed Nov 23, 2004.
22. Prior JE. Luxating patellae in Devon Rex cats. Vet Rec 1985;
Au;17;117(7):154-155.
23. Lagenbach A, Giger U, Green P, et al. Relationship between
degenerative joint disease and hip joint laxity by use of distraction index
and Norberg angle measurement in a group of cats. J Am Vet Med Assoc
1998;213(10):1439-1443.
24. Smith GK Lagenbach A, Giger U, et al. Patellar luxation and hip dysplasia
in a group of cats. First International Feline Genetic Disease Conference
Philadelphia June 1998 Proceedings (abstr) in: Feline Practice Supplement,
1999;23.
25. Little S. Feline hip dysplasia. Notes. Winn Feline Foundation Website.
Available at: www.winnfelinehealth.org/hip-dysplasia.html Accessed Sep
29, 2004.
26. Smith GK, Langenbach A, Green PA, et al. Evaluation of the association
between medial patellar luxation and hip dysplasia in cats. J Am Vet Med
Assoc 1999;215(1):40-45.
27. Gunn-Moore DA, Thrusfield MV. Feline dystocia: prevalence, and
association with cranial conformation and breed. Vet Rec 1995;136:350-
353.
28. Beatty JA, Barrs VR, Martin PA, et al. Spontaneous hepatic rupture in six
cats with systemic amyloidosis. J Small Anim Pract 2002;43:355-363.
29. Noli C, Colombo S, Abramos F, et al. Papular eosinophilic/mastocytic
dermatitis (Feline Urticaria Pigmentosa) in Devon Rex cats: A distinct
disease entity or a histopathological reaction pattern? Vet Dermatol
2004;15:253-259.
30. Pesteanu-Somogyi LD, Radzai C, Pressler BM. Prevalence of feline
infectious peritonitis in specific cat breeds. J Feline Med Surg. 2006
Feb;8(1):1-5.
31. Ferasin L. Recurrent syncope associated with paroxysmal
supraventricular tachycardia in a Devon Rex cat diagnosed by implantable
loop recorder. J Feline Med Surg. 2009 Feb;11(2):149-52.
32. Verhoeven G, de Rooster H, Risselada M, Wiemer P, Scheire L, van Bree
H. Swimmer syndrome in a Devon rex kitten and an English bulldog puppy.
J Small Anim Pract. 2006 Oct;47(10):615-9.
527
Egyptian Mau
are noted in the breed standards. Hair texture varies between coat
colors but is silky and lustrous in general.
It is thought that they were domesticated from spotted African Recognized Behavior Issues and Traits
Wild Cats, Felis libyca subsp. ocreata. Egyptians used to hold cats in Reported breed characteristics include: Variable personalities are
special regard, and frequently mummified them. At one cemetery present in the breed, from those demanding attention to aloof
site, 300,000 cat mummies were interred. Bastet, daughter of cats but overall, are considered well balanced. They are vigorously
Ra was the Egyptian goddess of fertility and in statuary, was playful, and are lively and friendly with family in general. They
represented with a cat head. chortle and talk softly. Tend to bond closely with one family
member and be fiercely loyal. Can be taught tricks and many will
Egyptian Mau spotted cats came from Cairo to America in 1956 leash train. Like to jump and sit in high places, so a perch or cat
via Italy. The breed was accepted by CFF in 1968 and accorded tree should be provided. Need time to explore new environments, so
championship status by CFA in 1977. The FIFé approved them in it is best to gradually introduce new people and places.
1992. In the UK, Shorthair Oriental Spotted Tabbies were called
“Maus” for a while and this has caused some confusion regarding
the two breeds. No outcrossing is currently allowed. The progenitor Normal Breed Variations
female for the North American lines was a silver cat named Baba. Are the fastest domestic cat runners checked so far—clocked at 30
mph (48 km/hr).
Physical Characteristics Deciduous teeth can be delayed in shedding.
Weight: 5-12 lb (2-5.5 kg), males larger than females
May shake their tail when happy; appears as if spraying but no
Coat: The original coat was the spotted pattern in bronze (dark urine produced.
brown-black spots on bronze agouti), but now silver (charcoal spots
on silver agouti) or smoke (black spots over silver-charcoal body Slightly longer average gestation period—queens often go up to 70
hairs and white undercoat) are also accepted. Black and blue kittens days.
occur and can be registered but are pet quality. Agouti hairs have at
least two bands of color striping. Hair is short-medium in length. Best to limit feeding.
Good sharp contrast between spots and background is highly Some cats like water, but this does not necessarily translate into
valued. Spots of the silver and bronze coats can be any size or enjoying baths.
shape but should not form any tabby pattern. Bronze cats may
have a pattern limited to the topline though. Some tabby markings Kitten Internet Information Project:1
are seen in the Smokes. Forehead pattern is in an M-shape, which 52 litters
had significance in ancient times, as it reminded the Egyptians of 192 kittens
their sacred scarab. Dark lines extend between the ears back to the 3.7 kittens/litter
neck. These lines are termed frown marks. Mascara marking lines 6% stillbirths
the eyes. A dorsal stripe goes down the topline extending to the tail 10% C-sections
base. Other specific coat markings such as tail and limb banding Female average birth weight: 101 g, male 107 g
528
Drug Sensitivities 3. Kelly DF, Gaskell CJ. Spongy degeneration of the central nervous system
in kittens. Acta Neuropathol (Berl) 1976;35:151-158.
None reported in literature
Inherited Diseases
None reported in the literature
Disease Predispositions
Feline leukemia Virus: Endogenous feline leukemia (enFeLVs) were
studied in a single specimen of Burmese, Egyptian Mau and Persian
breed cats to determine how many loci and where proviruses were
typically inserted. This may indicate genetic propensity for leukemia
genesis in these cats when exposed to the exogenous feline
leukemia virus. They found provirus on 12/18 autosomes, with an
average 19 autosomal copies per cat. One specific locus contained
both homologues in all 3 cats. They were also found on both X and
Y chromosomes.2
Genetic Tests
No commercially available tests
Miscellaneous
• Breed name synonyms: Mau, Egyptian Cat, Spotted Cat
• Registries: FIFé, TICA, CFA, ACFA, NZCF, CCA, WCF, GCCF
• Breed resources: Egyptian Mau Breeders and Fanciers Club
(CFA): http://www.geocities.com/Petsburgh/2369/
Global Egyptian Mau Society: http://www.egyptianmau.org/
The Egyptian Mau Club (UK):
http://www.egyptianmaus.co.uk/
National Egyptian Mau Council (CFA):
http://www.egyptianmaubc.org/records.html
References
1. Little, S. Pers. Comm. 2009
2. Roca AL, Nash WG, Menninger JC, Murphy WJ, O’Brien SJ. Insertional
polymorphisms of endogenous feline leukemia viruses. J Virol. 2005
Apr;79(7):3979-86
529
Exotic/Exotic Shorthair
Drug Sensitivities
None reported in the literature
Inherited Diseases
See Persian chapter for more information about shared traits.
Grooming: Coat care consists of a brief daily grooming session. Jaw and teeth anatomical abnormalities: (asymmetric jaw,
There is a much reduced matting tendency when compared with crowded teeth)
Persians. May need to cleanse away tears/debris at the medial
Dystocia: Increased dystocia due to large domed skulls.
canthus on an “as need” basis.
Transfusion Reactions: Due to high prevalence of blood type B,
Recognized Behavior Issues and Traits natural allo-antibodies markedly increase the risk of transfusion
Reported breed characteristics include: Playful, friendly, curious, reactions so donors and recipients should be blood typed).
quiet and affectionate. Excellent compatibility with children and
other pets. These cats are a bit livelier than the typical Persian cats, Calcium Oxalate Urolithiasis: In a case control study outlining risk
but share the small voice of the Persian. Many enjoy being lap cats. of development of uroliths, Exotics were found to be at increased
Not demanding of attention. risk of forming calcium oxalate uroliths.7
Miscellaneous
• Breed name synonyms: Shorthaired Persian, Zot
• Registries: FIFé (Exotic), TICA (Exotic Shorthair), CCA, NZCF
(Exotic) CFA, ACFA (Exotic Shorthair), CFF, WCF (Exotic Shorthair),
ACF (Exotic Shorthair), GCCF (Exotic)
• Breed resources: Exotic Cat Club (GCCF):
http://www.exotic-cat-club.org/
Exotic Shorthair Cat Society (U.K):
http://www.exoticcatsociety.co.uk/
Exotic CFA Breed Council:
http://www.exoticbc.org/
United Silver and Golden Fanciers Online (Silver/golden
Persians and exotics):
http://www.unitedsilverandgoldenfanciers.com/
References
1. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
2. Barthez PY, Rivier P, Begon D. Prevalence of polycystic kidney disease in
Persian and Persian-related cats in France. J Fel Med Surg 2003;5(6):345-347.
3. Beck C, Lavelle RB. Feline polycystic kidney disease in Persian and
other cats: a prospective study using ultrasonography. Aust Vet J
2001;79(3):181-4.
4. Barrs VR, Gunew M, Foster SF, et al. Prevalence of autosomal dominant
kidney disease in Persian cats and related breeds in Sydney and Brisbane.
Aust Vet J 2001;79:257-259.
5. Lyons LA. The Lyon’s Den. Feline Genome Project: Polycystic Kidney
Disease. Available at: http://faculty.vetmed.ucdavis.edu/faculty/lalyons/
Sites/pkd.htm Accessed Nov 6, 2004.
6. Giger U, Bucheler J, Patterson DF. Frequency and inheritance of A and B
blood types in feline breeds of the United States. J Hered 1991;82:15-20.
7. Lekcharoensuk C, Lulich JP, Osborne CA, et al. Association between
patient-related factors and risk of calcium oxalate and magnesium
ammonium phosphate urolithiasis in cats. J Am Vet Med Assoc
2000;Aug15;217(4):520-525.
8. Strain GM. Hereditary deafness in dogs and cats: causes, prevalence,
and current research. Proceedings. Tuft’s Canine and Feline Breeding and
Genetics Conference. Oct 2-4, 2003. Available at: http://www.vin.com/
tufts/2003. Accessed Nov 19, 2004.
531
Havana Brown
Physical Characteristics
Weight: Females 6-8 lb (2.5-3.5 kg), males 8-10 lb (3.5-4.5 kg)
Eyes: Oval eyes are medium in size, and are any shade of green with
a darker richer color preferred.
The Breed History
In Britain around the year 1951, a cross between a seal point Points of Conformation: The head is long and there is a distinct
Siamese and a black part-Siamese shorthair cat produced a solid stop and distinct pinch behind the whisker pad, with a so-called
brown offspring named Elmtower Bronze Idol, the first cat in “corn-cob” or “hour glass” muzzle—this is a breed distinguishing
the GCCF registry for the breed. Brown colored cats had already feature. Ears are large with rounded tips, tipping forward, and also
arrived from Europe much earlier (reported to be in the 1890s in a lightly haired and furnished. They possess a lithe medium length
London cat show; perhaps the oldest being Granny Grumps). These body, medium size and length of neck, long legs, and a medium
chocolate solid foreign-type cats were called Chestnut Brown thickness, tapering long tail. A foreign type, the Havana Brown is
Foreign for a while. At some point, Russian Blues were reported to not as tubular as Siamese or Oriental breed cats. Paws are small,
be introduced into the breed during outcrossing. compact and oval shaped.
The name Havana may originate from the rabbit breed that has Grooming: Little grooming needed. Quick weekly brush with rubber
the same coloring, or perhaps they are so-named because they brush, chamois or soft cloth is fine.
are brown like Havana cigars. The word brown was added to the
Havana name when the breed was imported to the USA in 1956.
American Havana Browns generally derive from one champion sire,
Recognized Behavior Issues and Traits
Reported breed characteristics include: Very intelligent, affectionate,
Quinn’s Brown Satin of Sidlo. need close human contact, playful, these high activity cats love to
jump up high, and are quiet voiced and very adaptable. Possessing a
Roofspringer Mahogany Quinn was the foundation female in
dog-like personality, Havana Browns may be trained to fetch and be
America, and Sildo’s mother.
leash trained. The Havana may bond closely with a favorite person.
These cats were recognized first as the Chestnut Foreign Shorthair They prefer a tranquil home, and sometimes can be a bit standoffish
by GCCF in 1958 and the name was changed to Havana in 1970. In towards people they do not know.
some registries, Havana is the preferred breed name since lilac color
is now also accepted. Normal Breed Variations
Caloric intake may need to be limited to prevent obesity.
In the CFA the Havana Brown (as it is now called in America)
was accepted for championship status in 1964. There is only very Very low genetic diversity was found in a study carried out at the
limited outcrossing (pre-approval required) allowed in CFA and University of California, Davis. Cats from 13 different catteries
none allowed in TICA. For a while (1974) CFA cut off outcrossing, and different breeds were assessed at multiple microsatellite DNA
but breeders petitioned the organization to help them diversify the markers. Final assessment was that this breed had one third of the
gene pool in the late 1990s. genetic diversity of random bred cats in this sample of 56 cats.1, 2, 3
Havana and Korat were assigned moderate genetic diversity (0,53)
The British version, the Havana or Chestnut Brown Foreign cat is in this study.
more like a Chestnut Oriental Shorthair cat of CFA in breed standard
for conformation; the American cat is more moderate in build. Kitten Internet Information Project:4
21 litters
This is a very rare breed; in 1998, 1000 cats in total were registered, 83 kittens
with 130 in the breeding pool at only 12 active CFA catteries, and in 3.9 kittens/litter
1997 only 36 cats were registered in the CFA. 11% stillborn
24% C-sections
As a note aside, Havana and Serval (African Wildcat) hybridization Average female birth weight 86 g, average male birth weight 95 g.
has lead to a newer breed, Savannah.
532
Drug Sensitivities
Nothing reported in the literature
Inherited Diseases
Hemophilia: Has been reported in this breed with low prevalence;
an X-linked recessive trait so males express the trait; only rarely
seen in females when homozygous for this recessive gene.4
Disease Predispositions
Calcium Oxalate Urolithiasis: According to a case-control study5
it was reported that Havana Brown cats are at increased risk of
forming calcium oxalate uroliths.6
Genetic Tests
If suspect hemophilia, run coagulation profile and specific factor
assays (Hemophilia A: Factor VIII, Hemophilia B: Factor IX).
Miscellaneous
• Breed name synonyms: Havana, Chestnut Brown Foreign Cat,
Swiss Mountain Cat (historical)
• Registries: TICA (as Havana--both lilac and brown colors
accepted), CFA, ACFA, GCCF (in Oriental, as Havana)
• Breed resources: Havana Brown Breed Council (CFA):
www.havanabrownbc.org
• Havana Brown Fanciers (CFA NW USA):
http://www.havanabrownfanciers.net/
• Havana and Oriental Lilac Cat Club (GCCF):
http://www.havanaandorientallilaccc.co.uk
References
1. Lipinski MJ, Young AE, Lyons LA. Genetic diversity and population
dynamics of domestic cat breeds. Proceedings. Tuft’s Canine and Feline
Breeding and Genetics Conference Oct 2-4, 2003 Available at VIN: www.vin.
com/tufts/2003. Accessed Nov 19, 2004.
2. Lyons LA. The Lyon’s Den Website. Breed Diversity and Cat Domestication
Project. Available at: http://faculty.vetmed.ucdavis.edu/faculty/lalyons/
Sites.... Accessed November 23, 2004.
3. Menotti-Raymond M, David VA, Pflueger SM, Lindblad-Toh K, Wade CM,
O’Brien SJ, Johnson WE. Patterns of molecular genetic variation among cat
breeds. Genomics. 2008 Jan;91(1):1-11.
4. Little, S. Pers. Comm. 2009.
5. Brooks MB. Feline hereditary coagulopathies. First International Feline
Genetic Disease Conference Philadelphia June, 1998 Proceedings (abstr) in:
Feline Practice Supplement, 1999;6,17,20.
6. Lekcharoensuk C, Lulich JP, Osborne CA, Koehler LA, Urlich LK, Carpenter
KA, Swanson LL. Association between patient-related factors and risk of
calcium oxalate and magnesium ammonium phosphate urolithiasis in cats.
J Am Vet Med Assoc 2000;Aug15;217(4):520-525.
7. Scott DW. Feline dermatology 1986 to 1988: Looking through to the
1990s through the eyes of many counselors. JAAHA 1990;26:515-532.
533
Highland Fold
back up to a straight position. The tail is medium long, tapering
with a rounded tip. Legs are medium-short, and paws are round. A
tail that is short, of reduced flexibility or kinked disqualifies.
Genetic Tests
Blood typing before breeding or transfusions is advisable due to
prevalence of B blood type in the breed.
Miscellaneous
• Breed name synonyms: Fold, Longhaired Scottish Fold,
Lop-eared cat or Lop (historical), nickname: Foldie.
• Registries: TICA (Scottish Fold Longhair and Scottish fold
separated), CFA, ACFA (Scottish Fold is a separate breed from
Highland Fold), CFF, ACF (Scottish fold Longhair, Scottish Fold),
CCA (Longhair and Shorthair are divisions within the Scottish
Fold) -not accepted in GCCF
• Breed resources: The Longhair Clan—Longhair Scottish Fold
Breed Club (CFF): Jean Viel III 49 Hancock St., Salem, MA 01970
• Scottish Fold Fanciers: http://www.ziplink.net/users/days/SFF.html
References
1. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
2. Giger, U, Bucheler J, Patterson DF. Frequency and inheritance of A and B
blood types in feline breeds of the United States. J Hered 1991;82(1):15-20.
3. Strain GM. Hereditary deafness in dogs and cats: causes, prevalence,
and current research. Proceedings. Tuft’s Canine and Feline Breeding and
Genetics Conference. Oct 2-4, 2003. Available at: http://www.vin.com/
tufts/2003. Accessed Nov 19, 2004.
4. Lekcharoensuk C, Lulich JP, Osborne CA, et al. Association between
patient-related factors and risk of calcium oxalate and magnesium
ammonium phosphate urolithiasis in cats. J Am Vet Med Assoc
2000;Aug15;217(4):520-525.
535
Himalayan
Tears need to be cleansed from the medial canthus regularly to
prevent dermatitis and tear staining.
Neonatal Isoerythrolysis (NI): Death usually at 12-24 hours Blood type prior to breeding or transfusion.
of age; it was noted that queens were all primiparous, with
retro-placental hemorrhage in late pregnancy being the proposed Radiographs hips to screen for hip dysplasia.
immune stimulator.18 One report gives the proportion of matings at
537
Miscellaneous neonatal isoerythrolysis. Proceedings. The 15th Annual ACVIM Medical
Forum, Lake Buena Vista FL 1997;308-310.
• Breed name synonyms: Colorpoint Longhair (Britain), Pointed 20. Chaitman J, van der Woerdt A, Bartick TE. Multiple eyelid cysts
Persian, Himmy, Persian Colorpoint, Persian-Himalayan, Khmer resembling apocrine hidrocystomas in three Persian cats and one
(historical) Himalayan cat. Vet Pathol 1999;36:474-476
• Registries: FIFé (within Persian), TICA (separate breed), AACE 21. French TW, Fox LE, Randolph JF, et al. A bleeding disorder (von
(separate breed) CFA (division within Persian), ACFA (separate Willebrand’s disease) in a Himalayan cat. J Am Vet Med Assoc
breed), CFF, (division of Persian), GCCF (Colorpoint Longhair, 1987;190(4):437-439.
subset of Persian), ACF (in Persian), WCF (provisional Persian/ 22. Counts DF, Byers PH, Holbrook KA, et al. Dermatosparaxis in a
Himalayan), NZCF (within Persian), CCA (separate breed from Himalayan cat: I. Biochemical studies of dermal collagen. J Invest Dermatol
Persian) 1980;74:96-99.
• Breed resources: Atlantic Himalayan Club: 23. Collier LL, Leathers CW, Counts DF. A clinical description of
www.himalayan.org/links.htm Dermatosparaxis in a Himalayan cat. Fel Pract 1980;10(5):25-36.
Colorpoint Cat Club (GCCF): 24. Plotnick A, Brunt JE, Reitz B. Cutaneous asthenia in a cat. Fel Pract
http://www.thecolourpointcatclub.co.uk/ 1992;20(4):9-12.
Colorpoint Society of Great Britain (GCCF): 25. Bradley WA. Fibrodysplasia ossificans in a Himalayan cat. Aust Vet
http://www.colourpointsocietygreatbritain.co.uk/ Practit 1992;22(4):154-158.
Persian Cat CFA Breed Council: www.persianbc.org 26. Bassett JR. Hypocalcemia and hyperphosphatemia due to primary
hypoparathoidism in a six-month-old kitten. JAAHA 1998;34:503-507.
27. Pesteanu-Somogyi LD, Radzai C, Pressler BM. Prevalence of feline
References infectious peritonitis in specific cat breed. J Feline Med Surg. Vol 8(1):pp1-5.
1. Giger U, Bucheler J, Patterson DF. Frequency and inheritance of A and B 2006.
blood types in feline breeds of the United States. J Hered 1991;82:15-20.
2. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
3. Lyons LA. The Lyon’s Den. Feline Genome Project: Polycystic Kidney
Disease. Available at: http://faculty.vetmed.ucdavis.edu/faculty/lalyons/
Sites/pkd.htm Accessed Nov 6, 2004.
4. Narfström K. Hereditary and congenital ocular disease. J Fel Med Surg
1999;1:135-141.
5. Hoskins JD. Congenital defects in cats. Compend Contin Educ Pract Vet
1995;17(3):385-405.
6. Rubin LF. Hereditary cataract in Himalayan cats. Fel Pract
1986;16(1):14-15.
7. Pentlarge VW. Corneal sequestration in cats. Compend Contin Educ Pract
Vet 1989;11(1):24-32.
8. Glaze MB. Feline corneal diseases: Part II. Proceedings. The 70th Annual
AAHA Conference. 2003;1:367-368.
9. Adamama-Moraitou KK, Patsikas MN, Koutinas AF. Feline lower airway
disease: a retrospective study of 22 naturally occurring cases from Greece.
J Fel Med Surg 2004;6:227-233.
10. La Croix NC, van der Woerdt A, Olivero DK. Nonhealing corneal ulcers in
cats: 29 cases (1991-1999). J Am Vet Med Assoc 2001;18(5):733-735.
11. Thumchai R, Lulich J, Osborne CA, et al. Epizootiologic evaluation
of urolithiasis in cats: 3,498 cases (1982-1992). J Am Vet Med Assoc
1996;208(4):547-551.
12. Lekcharoensuk C, Osborne CA, Lulich JP. Epidemiologic study of
risk factors for lower urinary tract diseases in cats. J Am Vet Med Assoc
2001;218(9):1429-1435.
13. Lekcharoensuk C, Lulich JP, Osborne CA, Koehler LA, Urlich LK, Carpenter
KA, Swanson LL. Association between patient-related factors and risk of
calcium oxalate and magnesium ammonium phosphate urolithiasis in cats.
J Am Vet Med Assoc 2000;Aug15;217(4):520-525.
14. Keller GG, Reed AL, Lattimer JC, et al. Hip dysplasia: A feline population
study. Veterinary Radiology & Ultrasound 1999;40(4):460-464.
15. DeManuelle T. Feline dermatopathies: Newly described disorders.
Proceedings. 70th Annual AAHA Conference Proceedings 1:93-95, 2003.
16. Levy JK. Congenital Portosystemic vascular shunts in cats: 98 cases.
First International Feline Genetic Disease Conference Philadelphia June,
1998 Proceedings (poster abstr) in: Feline Practice Supplement, 1999:30.
17. Jones BR. Inherited hyperchylomicronaemia in the cat. J of Small Anim
Pract 1993;34:493-499.
18. Jonsson NN, Pullen C, Watson ADJ. Neonatal isoerythrolysis in
Himalayan kittens. Austr Vet J 1990;67(11):416.
19. Giger U, Casal M, Niggemeier A. The fading kitten syndrome and
538
Japanese Bobtail
Grooming: The Japanese Bobtail cat has low grooming
requirements and low shedding tendency. This is a somewhat water
resistant coat. Longhair cats require a bit more grooming, but have
low matting tendency. Not recommended to blow dry this coat in
Shorthairs.
539
Miscellaneous
• Breed name synonyms: JBT, Bobtail, Mi-ke, Neko, Maneki Neko,
Jibit
• Registries: FIFé (SH only), TICA (LH, SH variety separate in
Japanese bobtail breed group), CFA (LH and SH variety in
SH division), ACFA (LH and SH separate breeds), CCA, CFF, NZCF,
WCF, ACF
• Breed resources: Breeders of Bobtails Society (BOBS):
Lynne Berge,
1069 Gridley Street, Bay Shore NY 28621
Japanese Bobtail Breeders’ Society: http://www.jbbs.org/
Shorthair Japanese Bobtail Club (CFA):
http://www.japanesebobtails.com/clubs.html
References
1. Lipinski MJ, Froenicke L, Baysac KC, Billings NC, Leutenegger CM, Levy
AM, Longeri M, Niini T, Ozpinar H, Slater MR, Pedersen NC, Lyons LA
The ascent of cat breeds: genetic evaluations of breeds and worldwide
random-bred populations.
Genomics. 2008 Jan;91(1):12-21
2. Giger U. Frequency and inheritance of A and B Blood types in feline
breeds in the United States. J Hered 1991;82:15-20.
3. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co. 2000;396-399.
540
Korat
Recognized Behavior Issues and Traits
Reported breed characteristics include: Gentle, affectionate.
Considered sensitive to noise and handling, they should be exposed
to various sounds and people/handling from a young age. Korats may
resist being held up in the air or stretched/restrained. Playful, good
with children, form a strong bond with their owners. High activity
cats, territorial, may like to be a bit of a boss. May shadow people
around the home, some like to play fetch and are quiet voiced around
home, but vocal in strange environments such as a show ring.
Miscellaneous
• Breed name synonyms: Blue Cat, Temple Cat, Thai Cat, Si-Sawat
Cat.
• Registries: FIFé, TICA, CFA, ACFA, CCA, WCF, ACF, GCCF.
• Breed resources: Korat Cat Fanciers Association:
http://www.koratworld.com/
FiFe Korat breed council: http://www.fifekoratbc.com
Si-Sawat (Korat) Society: http://www.si-sawat.org/
542
LaPerm
Points of Conformation: The La Perm is a semi-foreign cat in type,
though they are still presumed to be of Domestic Shorthair cat in
origin. Neck is fine, body is medium; they possess a medium-sized
rounded modified wedge head that is carried quite erect. The ears
are medium sized with well-developed furnishings, ideally including
lynx tipping in longhairs. The tail is tapering, and is long. They have
compact rounded feet.
Coat is double, with the undercoat being dense, and the outer hairs References
curly and soft in texture. When stroked, it feels springy; hair texture 1. Jordan, E. Breed Profile: LaPerm Pp 22-25. Cat Fancy September 2008
is variable between cats. Eyebrow and whisker pad hairs are curly.
Seasons may affect coat density and length.
Eyes: Eyes are large, and not necessarily coat related in color.
543
Maine Coon
Recognized Behavior Issues and Traits
Reported breed characteristics include: Sometimes called the
“Gentle Giant” Maine Coon cats are adaptable, and require regular
exercise and branches or ledges for climbing and jumping. Playful,
and keeping kitten attitude until late in life, these cats like to play
fetch. Most will leash train. Agile, powerful, calm, intelligent, good
with children and dogs, these cats vocalize with a chirping trill, and
the meow is very soft. Some enjoy swimming, and Maine Coon cats
enjoy human companionship, and make very good companions. Not
considered a lap cat.
The Breed History
A hardy hunter, this is the only North American longhair cat. Normal Breed Variations
Originating in Maine, this breed is now designated as the State Cat They are slow to mature (~3-4 years), and puberty finishes late.
of Maine. Perhaps resulting from crosses between domestic cats
and Angora and other longhaired imported cats, their large size They have excellent tolerance to harsh cold climates.
and a luxurious haircoat are breed hallmarks. It is possible that
They normally have have small litters with just two to three kittens
Pilgrims brought longhaired cats with them that were the progenitor
but are noted for good mothering.
cats, and natural selection resulting from harsh winters favored
a long dense coat. Some also credit the origins of the coat type They tend to gain weight easily.
to outcrossing with imported longhaired Siberian Forest Cats or
Norwegian Forest Cats. A valued working farm cat, the Maine Coon Blood type B: Prevalence of 3% type B cats was reported.1
was used extensively for rodent control. They are one of the first
American breeds (first records date to the 1860s), and also one of the The long hair phenotype in cats is a recessive characteristic so how
largest domestic cats anywhere. Very popular, they usually rank near it is distributed in the different longhaired breeds, and coded for is
the top in CFA. Championship status in CFA was awarded in1976. No of interest. Mutation (AM412646:c.194C>A) is responsible for long
outcrossing is allowed. hair in Persian and Maine Coon. Mutation 3 AM412646:c.474delT) is
only present in Maine Coon cats.2
Physical Characteristics
Weight: Range 10-22 lb (4.5-10 kg) Females smaller and more Drug Sensitivities
refined than the males. None reported in the literature
Coat: Glossy haircoat is longer over the body than on the head
and shoulders and longer on stomach and the legs. Ruff is present,
Inherited Diseases
Hypertrophic Cardiomyopathy (HCM): The most common cardiac
especially in males. The Maine Coon is double-coated and fur is
condition in cats (10% prevalence); in Maine Coon the inheritance
thick, shaggy, but soft in texture and waterproof. Most colors and
is consistent with an autosomal dominant gene with high
patterns are accepted though brown tabby is the best known.
penetrance. In cats, this heart condition is often associated with
Chocolate, lavender, cinnamon, pointed and agouti are not accepted.
arterial systemic thromboembolism and congestive heart failure;
Eyes: Eyes are large, and all colors are accepted. Blue and odd eyes specific changes occurring in this breed include papillary muscle
are found in the white cats. hypertrophy, left atrial dilatation, left ventricular wall thickening
and mitral valve systolic anterior motion. In cats, pulmonary edema
Points of Conformation: Powerful musculature characterizes these is not necessarily perihilar as in dogs.
large cats that are also endowed with a large wedge shaped head.
The tapering tail is very long and this thick hairy tail, with rings in Offspring from crossing affected to unaffected cats developed
tabbies may have given rise to the Coon part of the breed name. The clinical signs between 1-2 years of age, with severe disease by
Maine Coon possesses a profile with the medium-length nose that 2-4 years old. If both parents were affected, offspring became
is slightly concave. Well haired ears are large, with pointed tips and symptomatic at about 3 months of age, and severe disease was
lynx tufts. Paws are round and well haired. Tail is long and tapering established by 6-18 months of age. Sudden death and heart failure
from a broad base. are terminal sequelae. A sarcomere gene mutation leading to
coronary arteriosclerosis and interstitial fibrosis with sarcomere
Grooming: Though the Maine Coon coat does not tend to mat, myofibrillar disarray was postulated to be the pathophysiologic
regular grooming is needed. Preferably a quick daily session, but mechanism of failure. This condition closely mimics light chain
many find once weekly brushing will suffice. mutations in man.3
544
In man, a number of myosin mutations have been identified, so Spinal Muscle Atrophy (SMA): Autosomal recessive genetic
some HCM cats may be testing negative because their mutation is disease causing tremor, proximal muscle weakness, and muscle
yet unidentified. atrophy beginning at ~4 mo of age. Apparent loss of function
is rapid initially, but progresses slowly after 7-8 mo of age, and
In one earlier report, myomesin (M band sarcomeric protein) was variably disabled cats lived for at least 8 y. Electromyography
found to be reduced or absent within the myocardium of cats with and microscopic examination of muscle and nerve biopsies are
familial HCM and increased anomalous β-myosin heavy chain consistent with denervation atrophy as a result of a central lesion.
protein was also found.4 Affected cats were used to propagate A genetic test is available.14
a colony for characterization, and echocardiogram serial studies
confirmed 55% of the offspring were affected.5
Disease Predispositions
The newest research has now elucidated the genetic defect to Hip Dysplasia (HD) +/-Patellar Luxation (PL): Hip dysplasia is
be myosin-binding protein C (MYBPC3-A31P). A survey of cats more common in cats than was previously thought and almost
from many geographic areas confirmed the dominant mutation is all cats are clinically normal—clinical signs do not correlate with
widespread in the breed, with a worldwide rate of 34%, with 90% radiographic changes. A few reports suggest a predilection in
being heterozygous.6 females in cats, unlike dogs where no sex predilection exists and a
polygenic mode of inheritance is proposed.15
A prospective ultrasound screening of a group including
homozygotes and heterozygotes for the mutation demonstrated In one report in a non random group of 78 cats, 45% of Maine
regional diastolic dysfunction but left ventricular hypertrophy was Coon cats had PL and 18% had concurrent HD/PL; overall, the
also found in wild type cats.7 pooled group of cats were three times more likely to have these
conditions concurrently than either alone.16
Once severe HCM is established, progression to terminal endpoints
occurs within a few months to several years at the most.8 Typical In a University of Missouri Veterinary Medical Teaching Hospital
clinical signs of feline heart disease can be seen but significant study, in 684 cats representing 12 breeds and non-registered
disease can be present in the absence of any clinical signs.9 domestic cats, domestic cats had hip dysplasia prevalence of
5.8%, pooled purebred cats had 12.3% prevalence, and an overall
Serum cardiac troponin 1 levels (cTnI), a sensitive and specific frequency of HD of 6.6% was found in the entire study group.
marker of myocardial damage may be elevated according to early Unlike dogs, minimal remodeling of the femoral neck was noted.
studies and may be useful in future, though further studies are Shallow remodeled acetabulum, with the cranio-dorsal acetabular
needed. Levels increased to a peak 12-48 hours after an episode of margin most significantly affected was reported as the primary
damage, and stayed elevated for 8 days.10 lesion instead in cats. Reported OFA database survey results
(1974-1995) for 284 Maine Coon cats between 12 and 23 months
Overall, left ventricular outflow obstruction, left ventricular diastolic of age showed 21% were positive for HD according to OFA protocol
dysfunction, left ventricular wall (less commonly asymmetric septal) standards.17,18
hypertrophy and interstitial fibrosis and ischemia lead to typical
heart failure.11 In another non random group of 121 Maine Coon cats, using the
Norberg Angle (NA) and Distraction Index (DI) it was determined
Papillary muscle hypertrophy is another finding.6 Average age of 50.4% of Maine Coon cats had HD using OFA guidelines, 85% of
onset is 6-1/2 years, and more cases are seen in males. It has been these cats had bilateral changes; 57% had concurrent degenerative
postulated that growth hormone excess may have a role in some joint disease. Mean DI for affected cats was 0.64, while the mean
cases. Prognosis for asymptomatic cats is good (5-10 year survival), NA was 80 degrees. The DI in normal cats averaged 0.55, and NA 92
poor for those with arterial thromboembolism (6 months) and degrees. If these were dogs, the affected cat scores would be typical
moderate survival time of 18 months is typical (with appropriate of dog breeds with high prevalence of HD such as Newfoundland
management) for heart failure.12 and Saint Bernard.19 It was notable that most cats are clinically
normal. Owner complaints may include reduced height of jumping,
Report recommendations include: investigate all murmurs in kittens walking tucked under, and not running as much.20
over four months old, screen breeding stock annually during their
breeding career using auscultation and echocardiography starting Thought to be a polygenic trait, it is assumed to be moderately
at age 2 for males, and 3 for females; ECG, thoracic radiographs to highly heritable. It is not yet known if limited feeding/weight
and blood pressure determination may also be recommended if control has a role as in dogs, but larger framed cats more
signs suggestive of clinical heart disease such as heart murmur are commonly have hip dysplasia. Until further studies are done, it
present. It is very important to note disease may be present without might be prudent to avoid overfeeding young growing cats.20,21,22
a murmur.
Renal Failure: The renal failure rate for Maine Coon cats was more
If it is suspected that the cat has died of heart disease, it is than double the baseline rate in a study of cats from 23 veterinary
recommended to conduct a necropsy. Average heart weight at post colleges from 1980-1990 (189,371 cases from Purdue University
mortem is 20 g for moderately affected cats, and 30 g for severely Veterinary Medical Database) at an odds ratio for risk of 2.44:1.23
affected patients; myofibrillar disarray is a hallmark histologic
lesion.13
545
Rare and Isolated Reports were to recheck breeding cats annually for HD since some may
develop radiographic signs only later in life.12
Glycogenosis Type IV (GSD IV) Mimicking Disorder: Though GSD
IV is a condition of Norwegian Forest cats, a very similar condition
Renal Function: Screening for renal function using serum creatinine
has been noted in a report of 7 Maine Coon cats. It was thought to
and urinalysis in cats 8 years or older is recommended since a breed
be an autosomal recessive disorder leading to the neuromuscular
propensity to renal failure was found.23 Microalbuminuria and Urine
disease in that small group of cats. Muscle atrophy, gait deficits,
P:C ratio may also be used for early screening.
rear weakness and reluctance to jump were signs noted by about 4
months of age. Progression to dsyphagia, and rear limb paraplegia HCM Monitoring: Yearly auscultation by a veterinarian to check
occurred over a year. Elevated creatine phosphokinase enzymes and for murmurs/arrhythmias is a minimum in normal cats. Breeding
nervous tissue conduction abnormalities were not evident; iodine cats should be checked annually by echocardiogram since some
stain did not reveal abnormal glycogen accumulation but histology may develop HCM later in life. Monitor starting at age 2 for males,
of nervous tissue was abnormal.29 and 3 for females; ECG, thoracic radiographs and blood pressure
determination may also be recommended if signs suggestive
Flat-chested Kittens: Flat-chested Kittens: Similar to the
of clinical heart disease such as heart murmur/arrhythmia are
flat-chested condition in Burmese (see Burmese Chapter), whereby
present.12, 13
reduced dorso-ventral chest dimension occurs. This trait is only
seen in some lines. (Dr. Solveig Pflueger, Pers. Comm.) Signs may Normal M-mode echo parameters reported for Maine Coon cats
include poor weight gain, exaggerated cranial thoracic vertebral differ somewhat from the typical domestic cat, so these means
kyphosis, vomiting, dyspnea, cyanosis, exercise intolerance and should be used for reference when screening healthy cats and are
cough, and a ridge along the costo-chondral junction of the ribs. provided in this report.28
As kittens mature and the rib cage calcification completes, clinical
signs abate in many of those kittens that were less severely affected HCM Genetic testing is available at NC State-Meurs Lab.
and thus not euthanized in the neonatal period. Though recognized
by breeders, the flat-chested kittens have not been reported in the Direct genetic test for SMA is available from MSU-Fyfe Lab.
literature. Generally, it is first noted at 7-10 days of age.
547
Manx
Grooming: Daily grooming is needed to prevent build-up of
undercoat, may need to blow dry after bath in longhairs due to
thick double coat.
Eyes: Eyes are large and round; color conforms to coat. Reduced tail length, and especially reduced lower spine length
are correlated with abnormalities of the sacrocaudal area leading
Points of Conformation: The Manx is of medium size and cobby to deleterious effects in addition to the breed specific trait of
(stocky) conformation; features tend to roundness. A large, rounded taillessness being selected for. Heritability for the gene was reported
head, with full cheeks is the standard. Ears are small-medium, to be 0.4.1 There is a progression of severity of abnormalities as
round tipped, and angled outward (so-called “cradle” set). The nose the gene expression becomes fuller. Since homozygosity of alleles
is broad, medium length, and straight in profile. Neck is short. They at the Manx tailless gene locus appears to be lethal in utero, an
possess round feet. Spine forms a gradual upward arch. informed breeding program will produce kittens with tails of all
lengths. The heterozygote may be semi-lethal; there is an excess
Recognized Behavior Issues and Traits of females in viable Manx gene carriers; the sex ratio change is not
well characterized.2 Abnormalities of fetuses as young as 5 weeks
Reported breed characteristics include: Gentle sweet cats, playful,
love close contact with people, adapt well to other pets. Gait tends gestation include gross malformation of the CNS.3
to be rolling behind; a hop somewhat like a rabbit in rumpies.
Associated M gene abnormalities include:
Easygoing, some learn to open door knobs, many like water, and
Myelodysplasia/Anury/Spinal Dysraphism: The lower spinal
willingly leash train. Some say that Manx have dog-like traits, such column does not form normally. The spectrum includes:
as toy burying. Some cats are like one-man dogs and follow a • vertebral defects (missing or irregular vertebrae) in lumbar and
favored person around the house and may act like “watchdog” cats sacral area;
in the home. Good hunters. Quiet voiced and often use a trilling • taillessness, an absence of caudal vertebrae (SYN: anury) –this
vocalization. Good with children if raised with them; they like a is the characteristic being selected for;
quiet home. • neuronal defect (myelodysplasia), leading to cavitation of
548
dorsal white matter and tract degeneration which may begin as Tail Arthritis: Some cats with stumpy or longy tails left undocked
high as the mid-lumbar cord;3 may develop arthritis later in life if the caudal vertebrae malformed
• neural tube and notochord defect leading to incomplete - anecdotal.
early embryologic closure, with sacral and caudal dysgenesis
or partial agenesis (spinal dysraphism). Resulting in: Spina
Bifida, Hydromyelia, Myelocele, Tethered Cord, and
Rare and Isolated Reports
Corneal Dystrophy: An inherited condition resulting from local
Syringomyelia; these occur with low frequency in live born kittens. metabolic defects. This is an autosomal recessive trait. Signs are
often noted at about 16 weeks of age and progress from anterior
Vesicourethral Dysfunction: Those with incontinence problems
stromal edema to diffuse bullous keratopathy.9 Stromal dystrophy
tend to be euthanized early. A published case report outlined
may lead to epithelial rupture at a young age; Descemet’s
detailed status of a cat afflicted with detrusor muscle atonia,
membrane is also abnormal.10 This is usually a bilateral condition.11
pelvic floor EMG deficits, proximal urethra malfunction and
total lack of adrenergic enervation of the bladder and proximal
urethra.4 According to that report, 50% of rumpy cats have urinary Genetic Tests
incontinence and sacral cord abnormalities. Bladder may be grossly None commercially available
distended with neurogenic dysfunction.3
Miscellaneous
In a case control study of 285,000 records of cats with and without • Breed name synonyms: Tailless Cat, Cymric (for longhaired in
urinary tract disease, the Manx was reported to be at increased risk some registries), Man’s Cat, Isle of Man Cat
for congenital urinary tract defects and urinary incontinence.5 • Registries: FIFé, TICA, CFA, ACFA, GCCF (short haired), ACF,
WCF (provisional), NZCF, CCA, CFF. In some registries, longhairs or
Gait Abnormalities: Ataxia progressing to paraplegia; sometimes semi-longhairs are called Cymric (TICA), in others they are termed
kittens bunny hop. Bunny hopping is strongly associated with longhaired Manx (CFA).
syringomyelia, and plantigrade posture while walking or standing can • Breed resources: The American Manx Club:
occur.3 Gait deficits may be of neurogenic origin, or alternatively, be a http://www.americanmanxclub.com
mild lameness associated with pelvic bony malformation. Club foot is The International Manx & Cymric Society (ACFA):
sometimes also present. Gait changes are not present in all cats. 254 S. Douglas
Bradley IL 60915
Colon Dysfunction: Constipation/obstipation; neurogenic. Not
Cymric Cat Club (CFA):
present in all cats. Hyaline degeneration of the smooth muscle
PO Box 917
layers is evident and reduced ganglion cell numbers in Meissner’s
Snohomish WA 98291
plexus noted; grossly a megacolon, with associated abdominal
The Breed Club Europe Manx and Cymric:
distention and fecal perineal staining in afflicted cats. Some cats
http://www.raskatt.com/emc/emc.html
may also have mild rectal prolapse.3
Disease Predispositions
None reported in the literature
Genetic Tests
None commercially available
Miscellaneous
• Breed name synonyms: Munchie, Munchk, nicknames
“Dachshund Cat”, “Basset Cat”
• Registries: TICA (Munchkin and Munchkin Longhair), AACE
• Breed resources: Munchkin Breed Club:
http://www.munchkin.net/
References
1. Little S. Dr. Little’s Website. Munchkin Kitten Information Project. Pers.
Comm. March, 2009
2. Sturgess CP, Waters L, Gruffydd-Jones TJ, et al. Investigation of the
association between whole blood and tissue taurine levels and the
development of thoracic deformities in neonatal Burmese kittens. Vet Rec
1997;141:566-570.
551
Norwegian Forest Cat
Grooming: Grooming generally consists of a quick brush every few
days and they do not tend to mat like some of the longhair breeds.
They may need daily grooming while shedding.
552
Variable expression of the condition occurs, with two main age affected kittens at birth, muscle glycogen stores are depleted—no
ranges of onset: at birth, or at late juvenile phase, with presentation other abnormalities are found here. Detailed report of histologic
ranging from normal appearing stillborn kittens, collapse in changes can be found in this reference.12
neonates (hypoglycemia, cardiopulmonary collapse), and in the
late phase form, with progressive neuromuscular and cardiac Neonatal Isoerythrolysis (NI): Proportion of matings at risk for NI
degeneration in between 5 and 7 months of age, or a sudden was reported to be 0.06.3
cardiac decompensation in cats about 9 months to 1 year of age.
In the neonate, this condition might be confused with fading kitten Disease Predispositions
syndrome.7 Hypertrophic Cardiomyopathy (HCM) is of increased prevalence, but
not proven to be inherited.
Sequencing of the exon deletion producing the disorder was carried
out and by 1999 testing for carriers had begun, with subsequent
efforts by breeders to eliminate the mutant allele in breeding stock. Genetic Tests
Glycogenosis Type IV DNA Test
Clinical signs may initially include muscle tremors and a creatine
kinase spike typically occurs with onset at 5 months of age. By 8 Josephine Deubler Genetic Testing Laboratory (PennGen)
months of age, severe tremors, hyperthermia, poor stamina and University of Pennsylvania Veterinary Hospital. Minimum of 1-2 ml
muscle wasting noted. Mild ataxia (some describe it as “bunny EDTA blood should be sent immediately (not frozen); cooling the
hopping”, and difficulties with prehension and deglutition noted. sample is not essential. Should be processed within 48 hours. Test
Abnormal EEG, EMG and ECG, and progressively, abnormal request form, service fees and other information available online
echocardiograms noted. Progressive neurological signs (tetraplegia), at: http://w3.vet.upenn.edu/research/centers/penngen/services/
and tonic-clonic seizures and hypoglycemia preceded euthanasia.8 deublerlab/gsd4.html. This is a direct test not a linkage test and can
identify carriers.
As the disease progresses, histologic studies have shown that
muscle fibers are replaced by fibrosis; this contracture can lead The lab will do concurrent blood typing on that sample. One can
to permanent flexion of digits and carpi, and extension of the also submit two buccal swabs.
tibiotarsal and femorotibial joints.9 According to this same author,
pedigree analysis indicates that this gene originated in 2 cats Miscellaneous
imported to the US from Norway and Germany, but that these two • Breed name synonyms: “Wegie”; an American Nickname, Forest
cats were not found by pedigree analysis to be related, though the Cat, National Cat of Norway, Norwegian Cat, NFC, Norst Skogkatt
mutation is the same. (Nordic for Norwegian forest cat), Skaukatt, Skoggkatt, Wegrie,
Norwegische Waldkatze (German), Chat des Bois Novegien
Branching enzyme activity was confirmed to be very low in an (French).
inbred family of NFC, and a breeding colony to further study this • Registries: FIFé, TICA, CFA, ACFA, CFF, GCCF, ACF, WCF, NZCF
condition was established. Activity was less than 1/10th normal in (Norwegian), CCA .
liver and muscle, and less severely reduced in parents of that cat.10 • Breed resources: CFA Norwegian Forest Cat Breed Council:
http://www.nfcbc.org/
Three related cats were closely studied and clinical signs had Norwegian Forest Cat Club (UK): http://www.nfcc.co.uk/
progressed to tetraplegia, generalized muscle atrophy and Norwegian Forest Cat Fanciers’ Association:
contracted tendons by 8 months old. One cat died suddenly http://www.forestcats.net/
before any clinical signs were noted, and another cat succumbed National Norwegian Forest Cat Club:
to left sided heart failure at 13 months old. Nervous, cardiac and 17 Ashwood Rd.
skeletal tissues were primarily affected by storage products, with Trenton NJ 08610
degenerative changes noted on histology.11 The Viking Cat Club: http://www.vikingcatclub.co.uk/
GBE activity is 25-75% of normal in unaffected carriers, and is
5% of normal activity (in liver, muscle) in affected cats. In the References
late juvenile onset version of the condition, progression takes 1. Drögemüller C, Rüfenacht S, Wichert B, Leeb T Mutations within the
10-15 weeks, and the concurrent hyperthermia is still poorly FGF5 gene are associated with hair length in cats. Anim Genet. 2007
Jun;38(3):218-21. (A)
understood. Perhaps endogenous pyrogens are released during
2. Giger U, Bucheler J, Patterson DF. Frequency and inheritance of A and B
tissue degeneration, or ongoing general tremors may generate heat. blood types in feline breeds of the United States. J Hered 1991;82:15-20.
Echocardiographs confirm that fibrosis of the subendocardium 3. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
occurs (focal hyperechoic areas noted), and there is left ventricular Philadelphia: WB Saunders Co, 2000;396-399.
hypertrophy. Mild elevation of alanine aminotransferase activity 4. Giger U, Casal M, Niggemeier A. The fading kitten syndrome and neonatal
may reflect hepatopathy but only small amounts of abnormal isoerythrolysis. Proceedings. The 15th Annual ACVIM Medical Forum, Lake
storage products are found in hepatocytes in histopathology Buena Vista FL 1997;308-310.
preparations. Cranial nerve function is normal with the exception 5. Little S. Dr. Susan Little’s Website. Norwegian Forest Cat Kitten
of a reduced swallowing reflex. For diagnosis of the perinatal onset Information Project, Pers. Comm. March, 2009.
form, note that abnormal glycogen can be found in ventricular 6. Gaschen F, Jaggy A, Jones B. Congenital diseases of feline muscle and
myocytes and in many CNS neurons at that age. In both normal and neuromuscular junction. J Fel Med Surg 2004;6:355-366.
7. Fyfe JC. Glycogen storage disease Type IV in Norwegian Forest Cats:
553
Molecular detection of carriers. In: First International Feline Genetic Disease
Conference 1998. Proceedings (abstr), Feline Practice Supplement, 1999;10.
8. Coates JR, Paxton R, Cox NR, et al. A case presentation and discussion
of Type IV glycogen storage disease in a Norwegian Forest Cat. Progress in
Veterinary Neurology 1996;7(1):5-11.
9. Fyfe JC. Glycogenosis Type IV of Norwegian Forest Cats. Proceedings.
17th Annual Meeting of the American College of Veterinary Internal
Medicine. 1999:281.
10. Fyfe JC, Giger U, Van Winkle TJ, et al. Glycogen storage disease type
IV: Inherited deficiency of branching enzyme activity in cats. Pediatr Res
1992;Dec;32(6):719-725.
11. Fyfe JC, Giger U, Van Winkle T, et al. Familial glycogen storage disease
(Type IV GSD IV). Proceedings. 8th Annual Meeting of the American College
of Veterinary Internal Medicine Veterinary Medical Forum. Washington, DC
1990:1129.
12. Fyfe JC, Van Winkle TJ, Haskins ME, et al. Animal model of human
disease: Glycogen Storage Disease Type IV. Comp Path Bullet XXVI
1994;(3):3-6.
554
Ocicat
Recognized Behavior Issues and Traits
Reported breed characteristics include: Affectionate, curious, active,
playful; some can be lap cats. Need human companionship, devoted
but not clinging, easy to train; can leash train, fetch, and are
adaptable in new environments. They are good with children and
other pets, and also with strangers. Sociable; they behave a bit like a
dog. Ocicats like to talk but are less vocal than Siamese.
555
Oriental
in longhairs, is well plumed. The paws are small, compact and oval.
Eyes: Eyes are medium sized, and almond in shape. Cross-eyed cats In a retrospective case study of 7,159 sick and healthy cats at a
are penalized.Eyes may be green, though in white and bi-color cats Veterinary Medical Teaching Hospital in Australia over a decade, 60
in America, they may also be odd-eyed, green or blue, and in the cats had LSA. As a percent of all types of LSA, Siamese and Orientals
UK, white cats are accepted with blue eyes only. when pooled accounted for 33.3% of the cases, though they made
up only 2% of the hospital population. Mediastinal form was most
Points of Conformation: Medium sized cats, the limbs are long. common (86% were Siamese) and all were FeLV negative.4
The conformation is a classic foreign Oriental tubular cat. The head
is a tapering-wedge shape with a long nose; on profile head and This condition has been reported from Australia, Europe and the
nose are completely flat with no break. No whisker pad pinch. The USA. A recent study report describes pedigree analysis of two
flared ears are large with pointed tips, and the neck is long and families that also seems to confirm that this is indeed an AR trait.5
slender. Tail is long and thin; almost whip like, and tapers to a point;
556
A study is underway with candidate genes BCL2 and MYC being
subjected to mapping of genetic markers surrounding them.5,6
Genetic Tests
None commercially available
Miscellaneous
• Breed name synonyms: OSH, POSH, Oriental Shorthair, Oriental
Longhair, Solid Siamese, Foreign. Historical: Chestnut Foreign
Shorthair; Lavender Foreign Shorthair; White Foreign Shorthair.
• Registries: FIFé (Oriental LH, Oriental SH), TICA (Oriental SH,
Oriental LH), CFA, ACFA (Oriental LH, Oriental SH), CFF, CCA, NZCF,
WCF (in with Siamese), ACF (Oriental SH, Oriental LH), GCCF (just
oriental LH)
• Breed resources: CFA Oriental Breed Council:
www.orientalbc.org
Oriental Shorthairs of America:
http://home.comcast.net/~OSA_club/index.htm
References
1. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
2. Lekcharoensuk C, Lulich JP, Osborne CA, et al. Association between
patient-related factors and risk of calcium oxalate and magnesium
ammonium phosphate urolithiasis in cats. J Am Vet Med Assoc
2000;Aug15;217(4):520-525.
3. Lorimer HE. Hereditary lymphosarcoma in Oriental shorthair cats. First
International Feline Genetic Disease Conference Philadelphia June, 1998
Proceedings (abstr) in: Feline Practice Supplement, 1999:29.
4. Court EA, Watson ADJ, Peaston AE. Retrospective study of 60 cases of
feline lymphosarcoma. Aust Vet J 1997;75(6):424-427.
5. Geary LA, Lyons LA. Lymphosarcoma in Siamese/Oriental Shorthair
breeds. Notes. University of California (Davis) Feline Genetics Extravaganza
II Aug 28-29, 2004.
6. Lyons LA, Geary LA. Lymphosarcoma in Siamese/OSH populations.
Proceedings of the 2nd International Conference Advances in Canine and
Feline Genomics. Oct 2004 Utrecht Netherlands. Poster #30.
7. Strain GM. Hereditary deafness in dogs and cats: causes, prevalence,
and current research. Proceedings. Tuft’s Canine and Feline Breeding and
Genetics Conference. Oct 2-4, 2003 Available at: http://www.vin.com/
tufts/2003. Accessed Nov 19, 2004.
8. Gunn-Moore DA, Watson TDG, Dodkin SJ, et al. Transient hyperlipidaemia
and anaemia in kittens. Vet Rec 1997;140:355-359.
557
Persian
Recognized Behavior Issues and Traits
Reported breed characteristics include: Gentle, easygoing, placid,
affectionate, quiet voiced, adaptable, playful, not big jumpers and
climbers, get along well with children and other cats, and best as
indoor cats. Himalayan cats are considered on average a bit more
active than Persian cats due to infusion of Siamese blood.
Signs of the condition are variable in age of onset and degree of Congenital Portosystemic Vascular Shunts: Persian and
expression/rate of progression. Even within closely related families, Himalayan together accounted for 16% of cases out of 98 cats
expression can be significantly different. Multiple cysts may be in one report. Signs were noted by 6 months of age; a single
found in both medulla and cortex. Smooth and round, and of extrahepatic portocaval anomaly was the most common type of
variable size, these hypoechoic structures can be easily visualized defect seen.20
with ultrasound using a 7.5 MHz transducer (10 MHz in kittens). By
ultrasound evaluation, it was determined that in some kittens as Neonatal Isoerythrolysis (NI): Prevalence of B blood type makes
young as 7 weeks old, cysts were already present. Many cats have NI a concern in this breed. All B type cats have circulating anti-A
good longevity, while about one quarter of seriously affected cats antibodies and even primiparous queens carry these. Type B queens
die before 5 years of age. Those living a full lifespan may harbor bred to type A toms can result in fatal red cell lysis in A blood type
a few small cysts, so normal health does not preclude presence of offspring with undetected NI. Kittens with NI can be distinguished
cystic condition.7 from other fading kittens because of pigmenturia; anemia and
icterus will also be present; not all kittens at risk for NI will develop
Age of onset of clinically significant renal disease ranges from 3-10 overt clinical symptoms.2 The proportion of matings at risk for NI
years, with a mean of 7 years of age. Concurrent tubulo-interstitial was reported to be 0.12.21
nephritis of variable severity and distribution occurs. Neither the
brachycephalic head conformation nor longhair genes segregate FIP Susceptibility: Pedigree analysis indicated a high heritability
with the PKD gene. No increased probability of hypertension was (> 0.54) in a selection of catteries, with perhaps a polygenic trait
reported associated with ADPKD.8 controlling susceptibility to development of clinical FIP. There was
no correlation between FIP death and inbreeding.22
Another study reported increased mean arterial pressure (MAP) and
aldosterone:renin ratio in Persians over 4 years of age with PKD.9 FeLV Susceptibility: Feline leukocyte antigen (FLA), important for
control of immune response, is represented by a set of genes and
Note that absence of cysts at 6 months of age is strongly correlated polymorphism here may play a role in susceptibility.23
with a low risk of development of cysts in the future.10 Note that
cysts may also be found in the liver and pancreas in some cats.5 In a
study in the Netherlands, of 27 affected cats, 68% had cystic changes
Disease Predispositions
Corneal Sequestration (SYN: Black body or cornea nigrum):
in the liver or congenital hepatic fibrosis, and pancreatic cysts or In early phases, an amber colored corneal stromal opacity may be
pancreatic fibrosis.11 One report mentions associated peritoneoperi- noted. It gradually develops distinct raised borders; the surrounding
cardial hernias.12 That same report suggests that for screening cornea is cloudy and neovascularized; chemosis, blepharospasm,
purposes, the cutoff for positive PKD status be set at three or more mucopurulent ocular discharge, and hyperemic conjunctivae may
cysts found in two kidneys by US evaluation. Cysts range in size from also be noted. Surface of sequestrum does not stain with fluorescein
1 mm to over 1 cm, and as they grow, pressure on the surrounding dye but does retain rose bengal stain. Exophthalmic conformation is
tissues leads to dysfunction—renomegaly and renodynia may occur. thought to play a role in susceptibility.24 It is central or paracentral in
Late stage, the surface of the kidney may become irregular.13 Cysts distribution, and Persian cats are over-represented. When matured,
derive from both distal and proximal nephron.14 Persian cat ADPKD this is a brown to black pigmented lesion; often surrounded by
strongly resembles ADPKD in humans.15 a loose collarette of poorly adherent corneal epithelium. Lesions
may extend into shallow or deep stroma, or even to Descemet’s
Feline Hypertrophic Cardiomyopathy (HCM): The pattern
membrane. Sloughing and corneal healing may take 2-6 months;
of inheritance is unclear in this breed. Left ventricular outflow
surgical debridement is an option.44 Most often they are unilateral,
obstruction, left ventricular (LV) diastolic dysfunction, LV wall/
but can be bilateral; it is a corneal stromal necrosis.
septum hypertrophy, myocardial hypertrophy, interstitial fibrosis
and ischemia lead to typical signs of heart failure; also may see Topical glucocorticoids are contraindicated; some cases may be
aortic thromboembolism. Dyspnea and crackles, arrhythmias, and associated with feline herpesvirus infection; if suspected, do a
murmurs are typical findings.16 Persian cats are overrepresented PCR test for the virus on excised black body tissue. Recurrence, or
so perhaps there is a genetic influence. Average age of onset is involvement of the second eye in previously unilateral cases may
6.5 years. Over 75% of cases are in males, usually sudden death occur.25 Mean age of affected Persians is 5 1/2 years.26
or acute left sided heart failure is the terminal event. Concurrent
pulmonary edema is distributed in a patchy pattern diffusely Non-healing Corneal Ulcers: In a retrospective study of cats with
through the lung field (not necessarily perihilar, as is typical in refractory ulcers, the Persian was found to be overrepresented.
dogs), and they are not usually hypothermic. Histologic examination These indolent ulcers involve only the superficial epithelium and
shows one quarter of cats have myofiber disarray. Growth hormone unless complicated, do not extend into the stroma. During extended
excess may play a role in this condition.17 treatment regimens averaging 5 weeks, the same cats were also
predisposed to corneal sequestration.27
In a study of a partially inbred colony of cats with Persian ancestry,
plasma atrial natriuretic factor was elevated; an autosomal Cervical Neck Lesions: Increased risk for Persian cats was reported.
dominant inheritance was suspected.18 Of cats with in one study, 47% afflicted were Persians.28
559
Lower Urinary Tract Disease: Increased risk of calcium oxalate Hereditary Deafness: Is associated with the dominant gene for
urolithiasis was reported.29 A retrospective study (3,498 urolithiasis white cat (W); may be found in white cats of this breed.41
cases) found increased risk for calcium oxalate (CaOx) uroliths but
reduced risk for forming Magnesium Ammonium Phosphate (MAP Hip Dysplasia (HD): This condition is much more prevalent
or struvite) crystals.30 Persian cats were found to be 3.2 times more than was previously thought. In a 1998 report, in a nonrandom
likely to develop CaOx stones, and 1.4 times as likely to develop group of 78 cats of different breeds, 32% of this pooled group
MAP as cats of other breeds in another report.31 of cats, and 60% of Persians had HD using OFA-like criteria. A
positive correlation with joint laxity and HD was identified.42 A
In a retrospective analysis of 22,908 LUTD cases (1980-1997), study (1991-1995) found that based on VD hip radiographs, (684
Persian cats were reported to be at increased risk of congenital Cats, 12 breeds) HD prevalence was 5.8% in unregistered versus
defects as well.32 A new type of uroliths was reported, consisting 12.3% in purebred cats. Persian cats had a 15.8% rate (3/19).
of Mg, K, and inorganic pyrophosphate; a possible dysfunction of Classic radiographic signs were found to be different than in dogs,
the pyrophosphate-hydrolyzing alkaline phosphatase enzyme was with minimal remodeling of the femoral neck. Instead, shallow
proposed (perhaps a genetic defect) as a reason for the novel stone acetabulum and remodeling of the cranio-dorsal acetabular rim
structure.33 were noted.43
560
Eyelid agenesis: Most commonly seen in the temporal upper another case, unilocular cysts in a senior Persian were reported and
palpebral.44 were characterized as cystadenomas.58
Cataracts: Congenital or juvenile cataracts have been reported.44 Progressive Retinal Atrophy PRA: Kittens are 2-3 weeks of age at
onset, autosomal recessive. By about 4 months of age, they have
Heterochromia Iridis: Variations in iris and retinal pigment severe photoreceptor loss.59
epithelium and choroid may occur.44
Miscellaneous: Dermatophytosis, Otitis Externa, Umbilical Hernia,
Retinal Degeneration: Begins as foci of hyperreflective tapetum, Peritoneopericardial hernia, Portosystemic Shunt, Cryptorchidism,
then coalesce to become generalized; leading to blindness.44 In one Lymphocytic Cholangitis, Hemophilia A.60
report, two litters from the same parents developed visual deficits,
and fundus abnormalities on ophthalmoscope exams were noted
by a few months of age. Diffuse outer segment degeneration
Genetic Tests
Mannosidosis Genetic (Direct) Test
occured.49
Josephine Deubler Genetic Testing Laboratory, (PennGen) at the
A recent report strongly suggests this is an autosomal recessive rod University of Pennsylvania Veterinary Hospital offers testing.
cone dysplasia. By 3 weeks of age in offspring of homozygous cross
Minimum of 1-2 ml EDTA blood processed within 48 hours. Is
with heterozygous parents, pupillary light reflexes were abnormal,
not necessary to cool; and do avoid freezing. Test request form
by 6 weeks the tapetum hyperreflective, and by 15 weeks of age, the
is available online. Can do concurrent blood typing on the same
retinal degeneration was advanced; all were blind by 16 weeks old.50
sample. Can also submit a pair of buccal swabs for testing. http://
Hyperlipoproteinemia/Hyperlipidemia: Pattern is familial. High research.vet.upenn.edu/SubmitaSample/tabid/554/Default.aspx
circulating triglycerides and hyperchylomicronemia occur. Signs
PKD: Direct genetic test is available at UC-Davis VGL and the
may include: iridocyclitis, lipemia retinalis (pink or creamy retinal
Animal Health Trust.
vasculature), xanthomata (lipid granulomas of skin), and lipid
aqueous humour. Nerves may become impinged due to xanthomata, Ultrasound screening of kidneys should be done with transducer
leading to paresis or paralysis.51 of 7.5 MHz for adults, 10 MHz for kittens. In older cats, cysts are
larger and thus easier to detect. Typical findings are spherical
Anterior chamber contents may have a creamy or white appearance
cysts with smooth sharp outline, anechoic internally, with through
when hyperchylomicronemia is present, and opalescence when
transmission of larger cysts.9 Recommend scan breeding stock at
hypertriglyceridemia alone is present. Arcus lipoids cornea and lipid
10 months of age in 2 planes; both kidneys, and again at 2 years
keratopathy can also be seen with hyperlipoproteinemia.52 Uveitis
old if early US is equivocal (single cyst or a few in one kidney only),
has also been described.
or if negative since may not pick up PKD at 10 months of age if
Concurrent atherosclerosis of abdominal vessels, aorta and very small cysts or no changes. In some patients, renomegaly may
coronary vessels also occurred. Deficiency of lipoprotein lipase be visible on routine radiographs. Because of prevalence, breeding
enzyme is thought to be the underlying defect responsible for the PKD positive cats to negative cats may be necessary for a while to
hyperlipoproteinemias.53 prevent gene pool diversity loss.61
In another report of kittens with severe hypertriglyceridemia, Blood type before transfusions or mating are recommended.
anemia was also evident.54
Miscellaneous
Dystrophic Epidermolysis Bullosa: This is a collagen VII defect • Breed name synonyms: Himalayan, Himalayan-Persian, Longhair,
leading to reduced anchoring fibrils, so trauma leads to formation Longhaired Exotic, Khmer (historical, Europe), British Longhair
of blisters that progress to ulcers; an easily torn off skin is the • Registries: FIFé, TICA (separate from Himalayan here), CFA, *ACFA
result. Sloughing of foot pads and oral mucosa occurs in addition (separate from Himalayan), *CFF (separate from Himalayan here;
to loss of hairy skin.55 chocolate and lavender are known as Kashmir). GCCF (division
includes colourpoint, exotic SH), ACF (includes colourpoints), WCF
Primary Hereditary Seborrhea Oleosa: First signs are noted at (provisional Persian/Himalayan category), NZCF (colourpoints in
only 2-3 days of age and are severe and quickly progressive, with here), CCA (Himalayan separate)
no coat color predilection. Greasy, scaly skin and a rancid odor are *CFF and ACFA distinguish between Peke-faced and standard
present. Orthokeratotic hyperkeratosis is found on biopsy. A primary Persian.
keratinization defect is thought to be the underlying condition. To • Breed resources: The Atlantic Himalayan Club:
date, no effective treatment options have been reported.56 http://www.himalayan.org/links.htm
CFA Persian Breed Council: www.persianbc.org
Multiple eyelid cysts: Histology is similar to apocrine The Feline PKD Homepage: www.felinepkd.com/
hidrocystomas of humans. In one report, these were described as United Silver and Golden Fanciers Online:
multilocular cysts; PAS+, diastase resistant granules were seen http://www.unitedsilverandgoldenfanciers.com/
in the cytoplasm of affected cells. Blepharospasm, epiphora and
masses/color changes of eyelids were the chief complaints.57 In
561
References 2004;Jul-Aug;7(4):213-227.
27. La Croix NC, van der Woerdt A, Olivero DK. Nonhealing corneal ulcers in
1. Giger U, Griot-Wenk M, Bucheler J, et al. Geographical variation
cats: 29 cases (1991-1999). J Am Vet Med Assoc 2001;18(5) :733-735.
of the feline blood type frequencies in the United States. Fel Pract
28. van Wessum R, Harvey, CE, Hennet P. Feline dental resorptive
1991;19(6):21-27.
lesions-prevalence patterns. Vet Clin North Am: Sm Anim Pract
2. Giger U, Bucheler J, Patterson DF. Frequency and inheritance of A and B
1992;22:1405-1416.
blood types in feline breeds of the United States. J Hered 1991;82:15-20.
29. Houston DM, Moore AEP, Favrin MG, Hoff B. Feline urethral plugs
3. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
and bladder uroliths: A review of 5484 submissions 1998-2003. Can Vet J
Philadelphia: WB Saunders Co, 2000;396-399.
2003;Dec;44(12):974-977.
4. Knottenbelt CM Addie DD Day MJ Mackin AJ. Determination of
30. Thumchai R, Lulich J, Osborne CA, et al. Epizootiologic evaluation
the prevalence of feline blood types in the UK. J Small Anim Pract
of urolithiasis in cats: 3,498 cases (1982-1992). J Am Vet Med Assoc
1999;40:115-118.
1996;208(4):547-551.
5. Lyons LA, Biller DS, Erdman CA, et al.. Feline polycystic kidney disease
31. Lekcharoensuk C, Lulich JP, Osborne CA, Koehler LA, Urlich LK, Carpenter
mutation identified in PKD1. J Am Soc Nephrol 2004;15:2548-2555.
KA, Swanson LL. Association between patient-related factors and risk of
6. Drögemüller C, Rüfenacht S, Wichert B, Leeb T. Mutation within the
calcium oxalate and magnesium ammonium phosphate urolithiasis in cats.
FGF5 gene are associated with hair length in cats. Animal Genet 2007
J Am Vet Med Assoc 2000;Aug15;217(4):520-525.
JUN;38(3):218-221.
32. Lekcharoensuk C, Osborne CA, Lulich JP. Epidemiologic study of
7. Cooper KC, Piveral P. Autosomal dominant polycystic disease in Persian
risk factors for lower urinary tract diseases in cats. J Am Vet Med Assoc
cats. Fel Pract 2000;28(2):20-21.
2001;218(9):1429-1435.
8. DiBartola SP. Autosomal dominant polycystic kidney disease. Proceedings.
33. Frank A, Norrestam R, Sjodin A. A new urolith in four cats and one
18th Annual ACVIM Forum. Seattle WA 2000:438-440.
dog: composition and crystal structure. J Biol Inorg Chem 2002;Apr;7(4-
9. Pedersen KM, Pedersen HD, Häggström, J, et al. Increased mean arterial
5):437-44.
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35. Richardson EF, Mullen H. Cryptorchidism in cats. Compend Contin Educ
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13. Lyons LA, Biller DS. Autosomal dominant polycystic disease in Persian
38. Bond R, Curtis CF, Ferguson EA, et al. An idiopathic facial dermatitis of
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39. Takle GL, Hnilica KA. Eight emerging feline dermatoses. Vet Med May
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14. Eaton KA, Biller DS, DiBartola SP, et al. Autosomal dominant polycystic
40. Schwartz S. Separation anxiety syndrome in cats. 136 cases (1991-2000).
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15. Biller DS, DiBartola SP, Eaton KA, et al. Inheritance of polycystic kidney
41. Strain GM. Hereditary deafness in dogs and cats: causes, prevalence,
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17. Atkins CE. Feline hypertrophic cardiomyopathy. Winter 2004 AAFP
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18. Martin L, VandeWoude S, Boon D, et al. Left ventricular hypertrophy
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44. Narfström K. Hereditary and congenital ocular disease in the cat. J Fel
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21. Giger U, Casal M, Niggemeier A. The fading kitten syndrome and
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46. Alroy J, Freden GO, Goyal V, Raghavan SS, Schunk KL. Morphology
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23. Addie DD, Kennedy LJ, Ryvar R, et al. Feline leucocyte antigen class II
47. Berg T, Tollersrud OK, Walkley SU, et al. Purification of feline lysosomal
polymorphism and susceptibility to feline infectious peritonitis. J Fel Med
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48. Aguirre G, Ray J, Haskins M. Ocular manifestations of inherited
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AAHA Conference. 2003;1:367-368.
ACVO, Oct 26-30, 1994:28-29.
26. Featherstone HJ, Sansom J. Feline corneal sequestra: a
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review of 64 cases (80 eyes) from 1993 to 2000. Vet Ophthalmol
Educ Pract Vet 1982;4(2):152-164.
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50. Rah HC, Maggs DJ, Blankenship T, et al. Characterization of early onset
of retinal degeneration in Persian cats. Proceedings. Tuft’s Canine and Feline
Breeding and Genetics Conference. Oct 2-4, 2003. Available at: http://www.
vin.com/tufts/2003. Accessed Nov 19, 2004.
51. Jones BR. Inherited hyperchylomicronaemia in the cat. J Small Anim
Pract 1993;34:493-499.
52. Crispin SM. Ocular manifestations of hyperlipoproteinaemia. J Small
Anim Pract 1993;34:500-506.
53. Wisselink MA, Koeman JP, Wensing TH, et al. Hyperlipoproteinaemia
associated with atherosclerosis and Cutaneous Xanthomatosis in a cat. Vet
Q 1994;16(4):199-202.
54. Gunn-Moore DA, Watson TDG, Dodkin SJ, Blaxter AC, Crispin SM,
Gruffydd-Jones TJ. Transient hyperlipidaemia and anaemia in kittens. Vet
Rec 1997;140:355-359.
55. Olivry T, Dunston SM, Markinkovich MP. Reduced anchoring fibril
formation and collagen VII immunoreactivity in feline dystrophic
epidermolysis bullosa. Vet Pathol 1999;36:616-618.
56. DeManuelle T. Feline dermatopathies: Newly described disorders.
Proceedings. 70th Annual AAHA Conference Proceedings 2003;1:93-95.
57. Chaitman J, van der Woerdt A, Bartick TE. Multiple eyelid cysts
resembling apocrine hidrocystomas in three Persian cats and one
Himalayan cat. Vet Pathol 1999;36:474-476
58. Cantaloube B, Raymond-Letron I, Regnier A. Multiple eyelid
apocrine hidrocystomas in two Persian cats. Vet Ophthalmol
2004;Mar-Apr;7(2):121-125.
59. Rah H, Maggs DJ, Blankenship TN, Narfstrom K, Lyons LA. Early-onset
autosomal recessive progressive retinal atrophy in Persian cats. Invest
Ophthalmol Vis Sci. 2005;46(5):1742-7.
60. Feline Advisory Beaureau accessed online August 2010 at: http://www.
fabcats.org/breeders/inherited_disorders/persian.php
61. Little S. Selected inherited diseases of the cat, in Proceedings.
International Ragdoll Congress Oct, 2004. Pers. Comm., 2005.
Recommended Reading
Glaze MB Congenital and hereditary ocular abnormalities in cats. Clin Tech
Small Anim Pract. 2005 May;20(2):74-82.
563
Pixiebob
Grooming: Low grooming needs for this breed, low tendency to mat.
564
Ragdoll
Bi-color: (inverted moderately symmetrical V mask on forehead,
in white, that includes whisker pads and extends contiguously
under chin, chest, along underside). White feet are mitted due to
the gloving gene. The color of the point of the ears determines the
assigned coat color. This pattern may be shown in CFA.
Renal Failure: Renal failure rate for Russian Blue cats was more
Physical Characteristics than double the baseline in a study of cats from 23 veterinary
Weight: 8-12 lb (3.5-5.5 kg) college records between 1980-90 (189,371 cases, Purdue University
Veterinary Medical Database), at an odds ratio of 2.17:1.3
Coat: The very dense, short haircoat is plush and double with
a glossy finish and silky texture. The only accepted color is a
distinctive blue coat (a type of grey) with silver tipping of the guard Genetic Tests
hairs—a lighter shade of base color is preferred. The silvery sheen is None commercially available
highly desirable. No white is allowed in the coat. Kittens sometimes
have a faint tabby marking pattern but this usually fades with time. Miscellaneous
Nose leather is grey, and pads lavender to mauve. • Breed name synonyms: Archangel Cat, Foreign Blue, Maltese Cat,
Spanish blue, Russian, Blue Cat
Eyes: Oval wide-set eyes are vivid green, though in kittens they • Registries: FIFé, TICA, CFA, ACFA, CFF, CCA, WCF, GCCF (as Russian)
start out a yellow color. The Australia (ACF) and New Zealand (NZCF) registries call this breed
“the Russian” and also accept blue, black and white coated cats.
Points of Conformation: A medium sized cat, the body is lithe and • Breed resources: Russian Blue Breeders’ Association (GCCF):
long. The head is a medium wedge, and has a blunt muzzle without http://www.russianblue.org.uk/
a break producing a flat profile, nose is straight and long. The large
Russian Blue Fanciers (CFA):
ears are wide set with little hair cover and slightly rounded tips.
http://www.russianblue.info/RBF/rbf.htm
Neck is long and tail is fine and tapers, round feet are compact and
small. Coat color, texture and eye color do not usually reach their
zenith until at least 2 years of age. References
1. Lipinski MJ, Young AE, Lyons LA. Genetic diversity and population
Grooming: Low shedding and low grooming needs; gentle dynamics of domestic cat breeds. Proceedings. Tuft’s Canine and Feline
Breeding and Genetics Conference Oct 2-4, 2003 Available at VIN: www.vin.
occasional attention is sufficient.
com/tufts/2003. Accessed Nov 19, 2004.
2. Lekcharoensuk C, Osborne CA, Lulich JP. Epidemiologic study of risk
Recognized Behavior Issues and Traits factors for lower urinary tract diseases in cats. J Am Vet Med Assoc
Reported breed characteristics include: These athletic cats love to 2001;May1;218(9):429-435.
jump and climb, and are very playful. The Russian Blue cats are 3. Lulich JP, O’Brien TD, Osborne CA, Polzin DJ. Feline Renal Failure:
not big talkers, and have a soft voice. They are intelligent; may Questions, answers, questions. Compend Contin Educ Pract Vet
1992;14(2):127-152.
learn to open doors. They form a strong bond with their human
567
Scottish Fold
ears stay folded; some pop back up to a straight position. Tail is
medium long, flexible, bushy and tapering with a rounded tip. Folds
have muscular and stocky conformation.
About one half of the offspring will have straight ears in a Fold X
straight mating; these cats are termed Scottish Fold Variants, and
are important for breeding not showing.
Grooming: The Scottish Fold has low grooming needs, just weekly
brushing is required, though more frequent care may be needed
during shedding. One should monitor ear health.
The Breed History
Originating from Pertshire in Tayside Scotland, the first Folds Recognized Behavior Issues and Traits
were reported in 1961. The progenitor white cat had two folded Reported breed characteristics include: These are moderately active
kittens that were then crossed to British Shorthair and British Isles cats. They possess placid dispositions, and have low vocalizing
domestic shorthair cats to establish the breed. Later, crosses to tendency, with small chirping voice. They enjoy close human
American Shorthair cats were carried out. contact, may shadow their owners, and be a lap cat. A quirk is that
they may sit up in “Prairie dog stance” and when getting a better
First cats were exported to America in 1971. The GCCF in Britain view, “sitting Buddha”. The Scottish Fold cats are adaptable, and do
discontinued registry of the breed in 1973 due to the effects of the well in both quiet and noisy/busy households. Good with other pets,
gene on cartilage elsewhere in the body. The CFA granted provisional excellent hunters.
status in 1977 and accepted the Scottish Fold for championship
status later. Breeders are still allowed to outcross to American and
British Shorthairs, and in some registries, Exotic Shorthairs. Normal Breed Variations
Small litters are the norm.
The longhaired Scottish Fold, resulting from Persian-type
outcrossing is a separate breed called the Highland Fold in some Need to watch caloric input; tend to obesity.
registries, and in other registries is a division termed Scottish Fold
B Blood Type: Prevalence of 19% blood type B was reported.1 Four
Longhair.
of 27 cats (~15%) tested had B blood type in another report.2
570
Selkirk Rex
moderate shedding tendency. Rough grooming may break hairs or
straighten curls.
Coat: The shorthair coat is soft, wavy and plush, curled with a
Miscellaneous
• Breed name synonyms: Rexed cat, Rex Cat, Curly-coated cat.
wavy tail; the longhair coat is thick but with loose curl ringlets, like Informal name: “cat in sheep’s clothing”
a lamb’s; the main difference in the two coats is that the longhair • Registries: TICA (Longhair, Shorthair), CFA, ACFA (Longhair,
is less plush, has a longer ruff, and the tail hairs are longer and Shorthair), CFF, ACF, GCCF, NZCF
plumed. • Breed resources: The Rex Cat Club (GCCF-U.K.):
http://www.sam.luxford-watts.zen.co.uk/home.html
Homozygotes are more sparsely coated and have tighter curls (the
breed standard is closest to the heterozygote cat). Whiskers are
curly and short and may break off. Coat colors include pointed,
smoke, shaded, solids. Coats are curled at birth, but then they go
straighter and remain that way until sexual maturity. The final adult
coat matures at 18-24 months of age. The Selkirk Rex coat is a bit
fuller than the Devon or Cornish Rex cat, with some guard hairs.
They do not tend to molt like the young Devon and Cornish cats.
Climate and seasons may affect the coat.
571
Siamese Pointed
Cat or Siamese
The Tonkinese is quite close in body type to the Applehead.
Grooming: The Siamese cat has low grooming needs. Just a quick
wipe with hand or chamois is needed.
New research shows that the c(b) allele of the albino locus gene Three distinct phenotypes from two separate distinct mutations
are variants on the D1 chromosome specifying tyrosinase and the (L476P, D520N) were reported in a study. The L476P homozygote
chocolate (b) and cinnamon (b(9l)) a second allele at the B (brown) cats have coarse facial features (broad face, short nose, small ears),
locus are nucleotide variants of TYRP1 (chromosome D4).8 dwarfism, degenerative joint disease (DJD), widespread leukocyte
and other cellular lysosomal inclusions, and dermatan sulfaturia.
The mutations are reported to most likely to be identical by descent The two other genotypes (D520N homozygous, and L476P/D520N)
rather than multiple mutation events occurring at the same site in have normal growth and appearance but internal changes. The
another study.9 L476P/D520N is the mildest in expression.17 Skeletal disorders such
as DJD are primary endpoints of the MPS VI trait.
Familial AA Amyloidosis: Systemic amyloidosis is an inherited
disorder leading to amyloid deposition in various organs and In a screening study of three continents, the mutation D520N was
tissues, including liver and kidney. The liver is commonly the found in 11.4% of the open Siamese cat population from 5 of 6
significant organ involved in Siamese cats (compare with countries. It was concluded that the genotypes D520N/D520N and
amyloidosis in Abyssinians where significant signs are mostly D520N/L476P are likely widely distributed in the general population.
renal). Cats 1-5 years of age are typically affected. Considered to These cats will be normal except for an increase in DJD, particularly
be familial, Siamese cats account for ~95% of reported cases of AA at the caudal aspect of the proximal humeral epiphysis, and mild
amyloidosis. Spontaneous hepatic rupture associated with hepatic changes in the femorotibial joints may also occur. Radiographic
amyloid deposition can occur.10 hallmarks of the condition include: generalized osteopenia, severe
vertebral epiphyseal dysplasia, coarse trabeculae and irregular
In a case report, two cats from one cattery with amyloidosis were subchondral bone development. Facial dysmorphia and stunted
described. This condition led to spontaneous liver hemorrhage growth are evident starting at about 8 weeks of age in severe
in one cat, and chronic renal failure in another, so signs vary genotype kittens. Hind limb paresis or paralysis may develop due
depending on which organ is most affected.11 to compression of the spinal cord. A stiff gait and reduced activity
may be noted. Mild basophilic granulation in neutrophils routinely
In one report (1987-1994), 6.2% of Siamese/Oriental cats presented
prepared for blood films can be useful as a screening test. Definitive
for post mortem were affected by generalized AA amyloidosis. The
diagnosis requires specialized testing available at the University of
amyloid fibril protein (AA) amino acid sequence is different than
Pennsylvania, or one can run the urine dermatan sulfate test.18
that found in the Abyssinian form of this condition. Clinical signs
of amyloidosis include anorexia, vomiting, stomatitis, anemia, In North America, at least seven families have produced clinical
emaciation, painful distended abdomen and diarrhea. Post mortem cases of MPS VI. Presence of atypical DJD or other skeletal disease
changes may include pale friable engorged liver and spleen, and in Siamese should place MPS VI on the differential list.
573
This trait can affect the eyes also. Corneal opacification occurs; Pancreatitis: In a retrospective case study (40 cases) Siamese cats
frosted appearance of the eyes may be noted by 11 weeks of age, were overrepresented (15% of the cases). Necrosis and suppurative
progressing until one year of age; marked pathology occurs in the inflammation were two distinct forms. Hypokalemia occurred in
RPE, but is not visualized clinically.19 about half of the cats, and normal lipase and amylase were found. In
a previous report, 39% of pancreatitis cases were Siamese breed.41
In man this disease is termed Maroteaux-Lamy Syndrome.
Dsytocia: A survey of 2,928 litters (multiple cat breeds) was carried
Progressive Retinal Atrophy (rdAc): Autosomal recessive genetic out to ascertain prevalence of dystocia, and an over-representation
disease causing blindness. Found at a gene frequency of 33% in the of Siamese cats was found. A total of 571 Siamese litters were
breed. See under Abyssinian. A genetic test is available. analyzed. The average rate in a mixed breed colony for dystocia was
0.4% of litters. A rate of 10% was found in Siamese cats.42
Disease Predispositions
Wool Sucking: Onset is usually after weaning, also affects Siamese Cervical Neck Lesions: Increased risk was reported in a survey where
crosses. Target is commonly a blanket, or knitted clothing. Compulsive Siamese were one of two breeds (the other being Abyssinian) most
behavior often ends at sexual maturity, but some cases may have late commonly affected by Feline Odontoclastic Resorptive Lesions.43
onset or continue signs late into life. A study found 55% of fabric
Gingivitis and Periodontal Disease: Anecdotal evidence of
eating cats were Siamese in a group of 152 affected cats. Behavior
increased prevalence.
is characterized by compulsive stereotypic oral movement. Though
many cats begin with substrate of wool, many add other types of Slipped Capital Femoral Epiphysis: Siamese breed cats were 23%
fabric, and even non-fabric substrates (plastics). Early weaned cats are of affected cats (3/13) in a survey, though they made up only 5%
over-represented but there is no clear causal relationship.32 of the population (of 13,250). Average body weight in the pooled
study group was 5.6 kg, significantly over the normal average for
Separation Anxiety Syndrome: Of a study group of 136 cats with
cats. A physeal dysplasia was characterized by diffusely widened
SAS symptoms, Siamese accounted for 6 % of the cats. In this
physis with disorganized cartilage. Though this condition is typically
breed, most commonly the females defecated, and males expressed
associated with trauma in dogs, in this set of cases there was no
excessive vocalization.33
history of any trauma. It is likely the growth plate cannot handle
Floppy Pinnae: With a middle adulthood age of onset, normal normal shear stresses due to the dysplasia. This condition affected
ears become floppy ears (just the upper portion of the pinna). cats 4.5-24 months of age. A genetic etiology is suspected. Insulin
This condition can resolve without treatment.22 One theory is that levels or insulin receptor resistance in obesity was proposed to play
flopping is due to relapsing polychondritis, which requires a biopsy a role in physeal dysplasia.44
for diagnosis.34,35
Medial Patellar Luxation (MPL): A study reported that of 12
Corneal Sequestration (Synonym: Black body or cornea Siamese cats assessed as part of a larger study, five had abnormal
nigrum): Siamese cats are over-represented. Usually in central patella seating with easily induced luxation. Compared with the rate
or paracentral cornea; brown to black pigmented lesion; often of affected cats in non-pedigreed (2/31), Siamese had an increased
surrounded by a loose collarette of poorly adherent corneal MPL prevalence in this particular study.45
epithelium. Stromal necrosis may extend into shallow or deep
Hip Dysplasia (HD) may be associated with luxating patellas.46
stroma, or even to Descemet’s membrane. Sloughing and corneal
healing may take 2-6 months; surgical debridement is another In another report, Siamese cats had a frequency of 7.1% hip
option. Material may be tear concretion mixed with stroma and dysplasia.47
inflammatory cells.36
Adenocarcinoma (small intestine): Breed associated risk
Progressive Retinal Atrophy (PRA): A breed predilection for diffuse was reported to be eight times that for other cat breeds.48
bilateral PRA was reported. First changes include attenuation of In a population where 7.8% of cats in the group were of
retinal blood vessels, retinal thinning in the area centralis (tapetal Siamese breed, 71% of the cases were diagnosed in Siamese
glow), then generalized tapetal hyperreflectivity, and progressing to cats.36 In 100 previously published cases 42% were Siamese
ghosted or absent dorsal vessels with attenuated optic disc. Vision breed. In retrospective case study at MSU (1975-1985) for GI
loss occurs late in the process and night vision is retained. Client adenocarcinoma in cats, 6/11 cases were Siamese. In this report
complaints include the cat bumping into things, reluctance to jump, tubular adenocarcinoma case survival time was an average of 11
and mydriasis.37,38 months, while mucinous and undifferentiated type had average
survival times of 4 months. Overall, a survival time of 5 months
Open Angle Glaucoma: A chronic primary glaucoma that may
with metastasis, and 10 months for patients without metastases
have Siamese breed predilection. Affected cats gradually progress in
was the reported average.49
severity of clinical signs, and may develop luxation of lens.6
Lymphosarcoma (LSA): In a retrospective case study of 7,159
Hyperthyroidism: Reduced risk for this breed was reported.39
admissions over a decade, 60 cats had LSA; Siamese cats were
Siamese cats were almost 10x less likely to develop hyperthyroidism
predisposed. Young Siamese and Orientals when pooled accounted
(Odds Ratio 9.6) than non-Siamese.40
for 33.3% of LSA cases, though they made up only 2% of the
hospital population. Mediastinal LSA (thymus, mediastinal lymph
574
nodes) was most common in Siamese cats, and 86% of mediastinal Congenital Hydrocephalus: A genetic basis for Siamese cats
cases were diagnosed in Siamese, with mean age 2 years. All with this trait was proposed. The hydrocephalus leads to dilated
were FeLV negative. Breed lines diagnosed with early onset LSA ventricles, with resulting pressure necrosis of the nervous tissue
had origins in Europe and Australia.50 A recent report describes surrounding them. Clinically, domed skulls, lateral strabismus
analysis of two families that supports the hypothesis that this is an (setting sun sign), vision defects, and spastic gait problems result.
autosomal recessive trait, and homozygous in affected patients.51 Aggression, dullness, circling, and seizures may also be seen.20
Feline Dilated Cardiomyopathy (DCM): Siamese cats may be Neuroaxonal Dystrophy: A degenerative neurologic condition
predisposed. Incidence has dropped since dietary supplementation in two littermates has been described. The condition resulted in
with taurine began, but cases still occur. Average age of onset is 7 swollen distal ends/pre-terminal segments of the axons in the
years. Previously, mortality for DCM was ~85%, but with taurine central nervous system. This is an autosomal recessive condition.
supplementation the mortality is in ~30%-50% range. Feline Ataxia starts at about 2 weeks of age; head tremor occurs first,
clinical signs are not typically a cough as in the dog; heart rate then hypermetria and rear limb paralysis. In these 2 kittens, coat
may range from bradycardia to tachycardia. Systolic heart murmur pigmentation was normal.22
or diastolic gallop can often be heard, and 61% have arrhythmias,
usually ventricular. Echocardiography is the best modality for Hypomyelination of the Central Nervous System (Congenital
definitive diagnosis.52 Tremors): Two littermates were reported to be affected by early onset
tremors, seizures and ataxia. A third kitten died at three days of age.
Renal Failure: Rate for Siamese was identified to be more than By four weeks of age, the surviving littermates had tremors with
double baseline in a study (1980-1990, 189,371 cases. Purdue frenzied biting episodes when active; normal at rest. Peripheral myelin
Veterinary Medical Database) at an odds ratio for risk of 2.6:1, with was normal, while CNS myelin was abnormal/reduced. The unusual
prevalence of 2.8%.53 frenzied biting behavior has not been reported in other species with
this condition and is thought to be associated with paresthesia
Lower Urinary Tract Disease: Higher than expected rates of cystine secondary to inappropriate responses of hypo-myelinated nerves.23
urolithiasis reported in a small study group (3/18 were Siamese).54
Oxalate uroliths have been reported to be the most common type Inherited Hyperchylomicronemia: Presenting signs include
of stones in Siamese cats (especially males), and urate and cystine weakness, loss of appetite and severe anemia by 4 weeks of age.
stones also more common than expected.55 This defect in lipoprotein lipase enzyme activation was seen in two
related litters. The clinically normal parents and related kittens had
Myasthenia Gravis: The congenital form seen in the breed is not reduced enzyme activity also. This is suspected to be an autosomal
associated with antibodies against the acetylcholine receptor (as in recessive inheritance.24
Abyssinian and Somali cats). Same symptoms as the acquired form
are seen.56 Fasting hyperchylomicronemia, hypertriglyceridemia, lipemia
retinalis, splenomegaly, and xanthomata of skin, and liver and
Feline Bronchial Asthma: (Synonyms: allergic bronchitis, chronic kidney, and sometimes anemia are also described. Xanthomata (fat
bronchitis, feline lower airway disease). Siamese breed cats are granulomas) in the vicinity of the nerves lead to nerve compression
overrepresented—in a retrospective study, of 22 cats with lower and subsequent dysfunction such as rear limb paresis (with
airway disease, Siamese made up 55% of afflicted cats. Cough was plantigrade stance) and cranial nerve dysfunction. If the levels of
seen in most but not all cats. Radiographs were normal in 23% lipid and lipoproteins are high, the blood may take on the gross
of affected cats. These authors summarize earlier findings that appearance of cream of tomato soup.25
indicate Siamese and Himalayan cats are at higher risk, perhaps
due to genetic susceptibility. Siamese may have a more prolonged A transient hyperlipidemia and anemia was described in three
clinical course, and a relapsing tendency.57 litters of Siamese kittens. Severe hypertriglyceridemia and anemia
were noted around the time of weaning, and 3 of 4 siblings and 1
Rare and Isolated Reports of 5 half siblings from the litters were affected. Marked elevation
Sphingomyelinosis: (Feline Neimann-Pick Disease): An of chylomicrons and VLDL were identified. Anorexia, ataxia, and
autosomal recessive polyneuropathy resulting from the reduction lethargy were predominant clinical signs.26
of the enzyme sphingomyelinase. This results in a storage disease
Hemophilia B (Christmas Disease, Factor IX Deficiency):
characterized by accumulation of cholesterol, gangliosides and
A sex-linked recessive hemorrhagic disorder with resulting
sphingomyelin. Head and fine generalized tremors, stunted
hemarthrosis, excessive post-surgical hemorrhage, gingival
growth, progressive lower motor neuron tetraparesis, hypermetria
hemorrhage and spontaneous hematoma formation. Females are
and ataxia begin at about 8-20 weeks of age. Signs are slowly
asymptomatic carriers, males are affected.16
progressive over months. Anisocoria and blindness are usually
present by 5 months of age. Head tremors lead to dysphagia. Late GM1-Gangliosidosis: A beta-galactosidase deficiency.16 Recent
stage signs include plantigrade/palmigrade stance, weakness, and studies show the same mutation is responsible for this condition in
hepatosplenomegaly. Onset of polyneuropathy is usually before both Korat and Siamese cats.27
1 year of age.20 Diagnosis is by nerve biopsy, lysosomal enzyme
and lipid testing in skin, liver and or brain tissue, and EMG (slow Ceroid Lipofuscinosis: This is a lysosomal storage disease, with
conduction velocity).21 lipofuscin accumulation. Signs may include seizures and weakness.
575
An autosomal recessive inheritance has been postulated.14,28 peripheral vestibular disease, juvenile ataxia, aortic stenosis.62
576
spontaneous liver haemorrhage and chronic renal failure. J Small Anim 40. Scarlett JM, Moise NS, Rayl J. Feline hyperthyroidism—a descriptive and
Pract 39:442-447, 1998. case-control study. Prev Vet Med 1988;6:295-309.
12. van der Linde-Sipman JS, Niewold TA, Tooten PCJ, et al. Generalized 41. Hill RC, van Winkle TJ. Acute necrotizing pancreatitis and acute
AA-amyloidosis in Siamese and Oriental cats. Vet Immunol Immunopathol suppurative pancreatitis in the cat: A retrospective study of 40 cases
1997;56(1-2):1-10. (1976-1989). JVIM 1993;7:25-33.
13. Gruys E, Van de Stadt M, Blok JJ, et al. Feline Amyloidosis. First 42. Gunn-Moore DA, Thrusfield MV. Feline dystocia: prevalence, and
International Feline Genetic Disease Conference Proceedings (abstr), in: association with cranial conformation and breed. Vet Rec 1995;136:350-
Feline Practice Supplement, 1999:15. 353.
14. van Rossum M, van Asten FJAM, Rofina J, et al. Analysis of cDNA 43. van Wessum R, Harvey, CE, Hennet P. Feline dental resorptive
sequences of feline SAAs. Amyloid: J Protein Folding Disord 2004;11:38-43. lesions-prevalence patterns. Vet Clin North Am: Sm Anim Pract
15. Yogalingam G, Litjens T, Bielicki J, et al. Feline Mucopolysaccharidosis 1992;22:1405-1416.
Type VI. J Biol Chem 1996;271(44):27259-27265. 44. Craig LE. Physeal dysplasia with slipped capital femoral epiphysis in 13
16. Hoskins JD. Congenital defects in cats. Compend Contin Educ Pract Vet cats. Vet Pathol 2001;38:92-92.
1995;17(3):385-405. 45. Engvall E, Bushnell N. Patellar luxation in Abyssinian cats. Fel Pract
17. Crawley AC, Yogalingam G, Muller VJ, et al. Two mutations within a 1990;18(4):20-22.
feline Mucopolysaccharidosis type VI colony cause three different clinical 46. Keller GG, Reed AL, Lattimer JC, Corley EA. Hip dysplasia: A feline
phenotypes. J Clin Invest 1998;101:109-119. population study. Veterinary Radiology & Ultrasound 1999;40(4):460-464.
18. Crawley AC, Muntz FH, Haskins ME, et al. Prevalence of Mucopolysac- 47. Gardner CH, Hicks SL, Puette JR, et al. What is your diagnosis? J Am Vet
charidosis Type VI mutations in Siamese cats. J Vet Int Med 2003;17:495- Med Assoc 2003;223(6):783-784.
498. 48. Birchard SJ. Nonlymphoid intestinal neoplasia in 32 dogs and 14 cats.
19. Aguirre G, Ray J, Haskins M. Ocular manifestations of inherited JAAHA 1986;22:533-537.
metabolic diseases in cats. Proceedings. The 25th Annual Meeting of the 49. Cribb AE. Feline gastrointestinal adenocarcinoma: A review and
ACVO, Oct 26-30, 1994:28-29. retrospective study. Can Vet J 1988;29:709-712.
20. Shell LG. A review of feline neuromuscular diseases, Seizures in the cat 50. Court EA, Watson ADJ, Peaston AE. Retrospective study of 60 cases of
In: Symposium: Feline neurologic diseases. Vet Med Jun 1998;542-574. feline lymphosarcoma. Aust Vet J 1997;75(6):424-427.
21. Cuddon PA. Feline neuromuscular disease. Fel Pract 1994;22(2):7-13. 51. Lyons LA, Geary LA. Lymphosarcoma in Siamese/OSH populations.
22. Rodréguez F, Espinosa de los Monteros A, Morales M, et al. Neuroaxonal 2nd International Conference Advances in Canine and Feline Genomics.
dystrophy in two Siamese kittens. Vet Rec 1996;138:548-549. Proceedings. Poster #30.
23. Stoffregen DA, Huxtable CR, Cummings JF, et al. Hypomyelination of 52. Atkins CE. Feline dilated cardiomyopathy. Winter 2004 AAFP Meeting.
the central nervous system of two Siamese kitten littermates. Vet Pathol Proceedings [abstr] in: AAFP Newsletter August 2004 22(2):29-30.
1993;30:388-391. 53. Lulich JP, O’Brien TD, Osborne CA, et al. Feline Renal Failure: Questions,
24. Watson TDG, Gaffney D, Mooney CT, et al. Inherited hyperchylomi- answers, questions. Compend Contin Educ Pract Vet 1992;14(2):127-152.
cronaemia in the cat: Lipoprotein lipase function and gene structure. J 54. Osborne C, Lulich J, Sanderson S, et al. Feline cystine urolithiasis-18
Small Anim Pract 1992;33:207-212. cases. First International Feline Genetic Disease Conference Philadelphia
25. Jones BR. Inherited hyperchylomicronaemia in the cat. J of Small Anim June, 1998 Proceedings (abstr) in: Fel Pract Suppl, 1999:31-32.
Pract 1993;34:493-499. 55. Houston DM, Moore AEP, Favrin MG, et al. Feline urethral plugs and
26. Gunn-Moore DA, Watson TDG, Dodkin SJ, et al. Transient bladder uroliths: A review of 5484 submissions 1998-2003. Can Vet J
hyperlipidaemia and anaemia in kittens. Vet Rec 1997;140:355-359. 2003;Dec;44(12):974-977.
27. Baker HJ. The molecular basis of feline GM1 and GM2 gangliosidoses. 56. Bagley RS. Diseases of the peripheral nervous system, neuromuscular
First International Feline Genetic Disease Conference Philadelphia June, junction and muscle; Evaluation of weakness. Proceedings. AAFP Fall
1998 Proceedings (abstr) in: Fel Pract Suppl 1999:11. meeting. 1998:31-33.
28. Giger U, Haskin ME. Inherited disorders. In: August, JR ed. 2nd ed. 57. Adamama-Moraitou KK, Patsikas MN, Koutinas AF. Feline lower airway
Consultations in Feline Medicine Philadelphia: WB Saunders. 1994:183-191. disease: a retrospective study of 22 naturally occurring cases from Greece.
29. Haynes JS, Wade PR. Hepatopathy associated with excessive hepatic J Fel Med Surg 2004;6:227-233.
copper in Siamese cats. Vet Pathol 1995;32:427-429. 58. Rozengurt N. Endocardial fibroelastosis in common domestic cats in the
30. Gaschen FP. Feline myopathies. Proceedings. NAVC 2002 16:437-438. UK. J Comp Path 1994;110:295-301.
31. Watson ADJ. Feline precursor porphyria, characterized by persistent 59. Itoh N, Itoh S, Kawara S, et al. Persistent atrial standstill in a Siamese
delta aminolevulinic aciduria. J Small Anim Pract 1990;31:393-397. cat. Fel Pract 1994;22(4):14-17.
32. Neilson J. Anxieties, phobias and compulsive disorders. Proceedings. 60. Chastian CB, Turk MAM, O’Brian D. Benign Cutaneous mastocytomas in
AAFP Fall Conference. 2002:125-139. two litters of Siamese kittens. J Am Vet Med Assoc 1988;193(8):959-960.
33. Schwartz S. Separation anxiety syndrome in cats. 136 cases 61. Scott DW. Feline dermatology 1986-1988: Looking to the 1990s through
(1991-2000). J Am Vet Med Assoc 2002;220(7):1028-1033. the eyes of many counselors. J Am Anim Hosp Assoc 1990;26:515-523.
34. Pearson T. Floppy pinnae in Siamese cats. Letter to the Editor. Vet Rec 62. Feline Advisory Beaureau Website accessed at: http://www.fabcats.org/
1998;143(16):456. breeders/inherited_disorders/siamese.php
35. Rest JR. Floppy pinnae in Siamese cats. Letter to the Editor. Vet Rec
1998;143(20):568.
36. Narfström K. Hereditary and congenital ocular disease. J Fel Med Surg Recommended Reading
1999;1:135-141. Glaze MB Congenital and hereditary ocular abnormalities in cats. Clin Tech
37. Giuliano EA, van der Woerdt, A. Feline retinal degeneration: Clinical Small Anim Pract. 2005 May;20(2):74-82
experience and new findings (1994-1997). J Am Anim Hosp Assoc Miller MS, Tilley LP, et al. In: Kirk RW, Bonagura JD, eds. Current Veterinary
1999;35:511-514. Therapy XI. Philadelphia: WB Saunders Co. 1992:786-791.
38. Carlile JL. Feline Retinal atrophy. Vet Rec 1981;108:311. Tilley LP, Liu SK. Persistent Atrial Standstill in the dog and cat. Proceedings.
39. Kass PH, Peterson ME, Levy J, et al. Evaluation of environmental, The Annual ACVIM Veterinary Medical Forum NY (abstr) 1983:43.
nutritional, and host factors in cats with hyperthyroidism. JVIM
1999;13:323-329.
577
Siberian Forest Cat
cats and children. Soft voiced. They are good climbers, excellent
jumpers, and are suited for indoor-outdoor and outdoor lifestyles.
These cats can also live in apartment if proper climbing and
entertainment equipment is provided.
1/3rd of the American cats tested are low allergen protein (FeL d1)
which makes these cats suitable for some allergy sufferers.2
The Breed History
This is an ancient indigenous street cat from Russia. Controlled Drug Sensitivities
breeding towards a uniform breed standard began only in the None reported in the literature
1900s. This is the National Cat of Russia. Early records of a cat
meeting this description trace back to 1000 AD. No outcrosses Inherited Diseases
are allowed. First specimens arrived in the United States in 1990, None reported in the literature
but the Siberian Forest Cat breed is still very rare in the USA. TICA
accepted them in 1998. The CFA had accepted this breed in the
Miscellaneous Class in 2000 and they achieved championship status
Disease Predispositions
None reported in the literature
in 2006.
578
Singapura
Recognized Behavior Issues and Traits
Reported breed characteristics include: A playful, friendly, curious
and intelligent cat with a strong need for close human contact. They
possess a soft quiet voice with low tendency to vocalization and are
gentle lap cats. Some can open doorknobs; are quite trainable, and
most remain playful until late in their lifespan. They get along well
with other cats—an unusual observation is that some stud cats get
along well and sleep together peacefully.
Coat: Haircoat is dense and very short and lies close to the body.
Hair has a fine texture. Sepia brown agouti is the sole acceptable
Miscellaneous
• Breed name synonyms: Pura, National Cat of Singapore,
color and it is ivory body color with warm dark brown ticking Singapore, Sing, drain cat, river cat
(genetically a sable ticked tabby). Each hair has banding with a • Registries: TICA, CFA, ACFA, ACF, GCCF, WCF (provisional), CCA
minimum of two dark bands; light next to body and a dark tipped • Breed resources: Singapura Fancier’s Society: CFA, 1805 Atlantic
extremity. Tail tip and upper topline aspect are darker. Barring Avenue, Manasquan NJ 08736
pattern may be present inside the legs and lightly on the face. The International Singapura Alliance (CFA):
Mascara eyeliner, and dark lines from inner canthus to nose http://singapura-alliance.org/pageID_5906292.html
(cheetah lines) and nose liner marks are present. Lighter non-agouti United Singapura Society and Founders’ International
color coat is evident on the chest and underside. Singapuras (CFA): 82 W Catalina Dr. Oak View CA 93022
Independent Singapura Fanciers:
Eyes: Coloring of the eyes includes green, yellow or hazel. Eyes are
http://sh1.webring.com/people/fs/singapuracats/
very large in size and almond-rounded in shape.
Progressive Singapura Cat Club (UK):
Points of Conformation: This is the smallest domestic cat; a http://www.singapuracatclub.co.uk/
moderately built cat. Head is rounded with blunt nose and broad
muzzle, with well-defined whisker pads and prominent chin. Ears
are large and wide set, lightly pointed, with little hair covering.
Neck is short and thick. Small oval feet are present. Tail is short to
medium in length, and blunt tipped but slender.
The head is a rounded wedge shape, large ears are placed wide set
and set well back, with interior furnishings and slightly rounded tips.
The coat doesn’t finish maturing until about 18 months of age so Pyruvate Kinase (PK) Deficiency and Increased Osmotic Fragility
ticking evaluation is compromised until then. of Red Blood Cells (RBCs): Autosomal recessive. The PK enzyme is
involved in anaerobic glycolytic pathway of erythrocytes. Reduced
Eyes: Eyes are hazel, green or amber colored. Almond shaped eyes activity of the enzyme results in energy depletion and premature
are large and slanting. red cell destruction. Cats with this condition may experience
recurrent severe hemolytic anemia and splenomegaly.
Points of Conformation: Medium-large sized cat, lithe and
semi-foreign build, and the back is long. “Fox-like” is a frequent
580
In one report of 18 Somali and Abyssinian cats, osmotic fragility Transfusion Reactions: B blood type similarly results in increased
occurred in the absence of PK deficiency. Onset of anemia in one risk of transfusion reactions so donors and recipients should be
report ranged from 6 months to 5 years of age (mean 23 months) typed ahead of a transfusion.
and PCV ranged from 15%-25% (some as low as 5%). Hepatic
enzymes were elevated in some cats. Macrocytosis that persisted
when anemia resolved was noted. It was suggested that this
Rare and Isolated Cases
Retinal Dysplasia (RD): Abnormal retinal development can affect
condition may have a heredity basis since affected cats were closely focal, multifocal or diffuse areas of the retina. Retina degeneration
related (affecting both Somali and Abyssinian).5 and subsequent scarring interferes with vision. In Sweden, a
suspected hereditary form of RD (multifocal) was seen in related
In another study of both Abyssinian and Somali cats aged 1-10
Somali cats.12
years old, chronic intermittent macrocytic regenerative hemolytic
anemia and mild splenomegaly was reported. Pyruvate kinase Malignant Histiocytosis: A case report described a multisystem
activity ranged from 6%-20% of the normal activity. Osmotic histiocytosis, including neurologic signs, inappetence, and vomiting.
fragility of RBCs was normal to slightly increased.6 Other cases have occurred, but this is a variant of the condition.13
Affected Somali and Abyssinian cats usually have a normal lifespan Thymoma-associated Neuromuscular Disorder: Can occur as a
unlike dogs with this condition (seen in Beagles, Basenji, West primary condition (no antibodies—see Siamese) or an acquired form
Highland White Terrier, Dachshund). Dogs tend to develop liver for which Abyssinian and possibly Somali cats are predisposed;
failure and osteosclerosis while cats do not. Enzyme analysis and Acetylcholine receptor antibodies produced within/by the tumor
molecular genetic tests are available.7 and in muscle cross react resulting in voice changes, myasthenia
gravis, tremor, ventroflexion of the neck and gait abnormalities
Anemia may be noted in cats as young as 6 months old, and has
–myasthenia gravis signs are as for the idiopathic form.14
been found in senior cats (12 yr) that were clinically normal.
Myasthenia Gravis (MG, acquired): Highest relative risk for
A case was described in which the index cat developed a 100%
acquired MG compared with a baseline of mixed breed cats was
bilirubin cholelith which was thought to be due to chronic
reported for Abyssinians and related Somali cats, with relative risk
hemolysis. (link to reference A on the reference page.8
increasing after 3 years of age. The MG was commonly associated
A recent study showed high variability in age of onset and with cranial mediastinal mass (not always).15 See Abyssinian
severity of clinical signs so testing before breeding was strongly chapter for more information. See above also: Thymoma-associated
recommended.9 Neuromuscular Disorder.
In Australia, 24 cats were tested for the gene and the mutant allele Genetic Tests
frequency was 0.29.10 Pyruvate kinase deficiency
Amyloidosis: See Abyssinian chapter for details Direct test is available from PennGen.
Neonatal Isoerythrolysis (NI): The prevalence of B blood type can Minimum of 1-2 ml purple top EDTA blood and should be sent
lead to increased incidence, and the proportion of matings reported immediately (don’t freeze). Test within 48 hrs of sampling.
to be at risk for NI is 0.14.11
The lab can do concurrent blood typing on that sample. They can
All B type cats have circulating anti-A antibodies and even also use 2 buccal swabs.
primiparous queens can carry these. Type B queens bred to type A
toms can result in fatal red cell lysis in A blood type offspring with Direct genetic tests for rdAc PRA and Rdy are available from
undetected NI. Kittens with NI can be distinguished from other UC-Davis VGL.
fading kittens because of pigmenturia; anemia and icterus will also
be present; not all kittens at risk for NI will develop overt clinical Blood typing done before mating and transfusions
symptoms.1
581
Grand Somali Society:
238 Church St
Poughkeepsie NY 12601
CFA Somali Breed Council: http://www.somalibc.org
References
1. Giger, U, Bucheler J, Patterson DF. Frequency and inheritance of A and B
Blood types in feline breeds in the United States. J Hered 1991;82:15-20.
2. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
3. Knottenbelt CM, Addie DD, Day MJ, et al. Determination of the prevalence
of feline blood types in the UK. J of Small Anim Pract 1999;40:115-118.
4. Drögemüller C, Rüfenacht S, Wichert B, Leeb T. Mutation within the
FGF5 gene are associated with hair length in cats. Animal Genet 2007
JUN;38(3):218-221.
5. Kohn B, Goldschmidt MH, Hohenhaus AE, et al. Anemia, splenomegaly,
and increased osmotic fragility of erythrocytes in Abyssinian and Somali
cats. J Am Vet Med Assoc 2000;217(10):1483-1491.
6. Giger U, Rajpurohit Y, Skelly B, et al. Erythrocyte pyruvate kinase
deficiency in cats. In: First International Feline Genetic Disease Conference
Proceedings (abstr), Feline Practice Supplement, 1999:8.
7. Deubler Lab Website. Available at: http://research.vet.upenn.edu/
SubmitaSample/tabid/554/Default.aspx
8. van Geffen C, Savary-Bataille K, Chiers K, Giger U, Daminet S. Bilirubin
cholelithiasis and haemosiderosis in an anaemic pyruvate kinase-deficient
Somali cat. J Small Anim Pract. 2008 Sep;49(9):479-82. Need full text article
still
9. Kohn B, Fumi C. Clinical course of pyruvate kinase deficiency in
Abyssinian and Somali cats J Feline Med Surg. 2008 Apr;10(2):145-53.
10. Barrs, V.R., Giger, U., Wilson, B., Chan, C.T.T., Lingard, A.E., Tran, L., Seng,
A., Canfield, P.J., Beattya, J.A. Erythrocytic pyruvate kinase deficiency
and AB blood types in Australian Abyssinian and Somali cats. Aust Vet J.
2009;87(1):39-44
11. Giger U, Casal M, Niggemeier A. The fading kitten syndrome and
neonatal isoerythrolysis. Proceedings. The 15th Annual ACVIM Medical
Forum, Lake Buena Vista FL 1997:308-310.
12. Narfström K. Hereditary and congenital ocular disease. J Fel Med Surg
1999;1:135-141.
13. Reed N, Begara-McGorum IM, Else RW, Gunn-Moore DA. Unusual
histiocytic disease in a Somali cat. J Feline Med Surg. 2006 Apr;8(2):129-34.
14. Bagley RS. Diseases of the peripheral nervous system, neuromuscular
junction and muscle; Evaluation of weakness. Proceedings. AAFP Fall
meeting. 1998:31-33.
15. Shelton GD, Ho M, Kass PH. Risk factors for acquired myasthenia gravis in
cats: 105 cases (1986-1998). J Am Vet Med Assoc 2000;Jan1;216(1):55-57.
582
Sphynx/Sphinx
Eyes: Lemon-gold eyes, slanted and large. Other colors are
uncommon but accepted.
Physical Characteristics Females may cycle less frequently than other queens; kittens may
Weight: females 6-8 lb (2.7-3.6 kg), males 8-12 lb (3.6-5.4 kg) be born with some hair along the spine, which disappears
Coat: This cat breed is not truly hairless as many believe. There is Blood Type B: Frequency of B blood type was reported to be 17%.1
a fine down cover described as “peach fuzz” or suede. Hairs must
Sphynx Kitten Information Project:2 An Internet based survey was
be less than 1/8th“ long, and sometimes small short tufts of hair
carried out to determine breed reproduction normal parameters
are found on tail tip, scrotum, brow, bridge of nose, back of ears, or
April 2002-March 2003.
outside of paws. All colors and patterns are accepted.
Survey involved 18 breeders, 50 litters (mostly from Canada, US),
Heterozygotes have more down than do homozygotes. May or may
201 kittens:
not have whiskers or brows. If present, whiskers may be short or
Average litter size 4
break off easily.
Stillbirth rate 5%
Dystocia < 1%, of those 7% required C-section
583
Average birth weight: Male 96 g female 95 g Sphynx Cat Association:
Congenital deformities (2.5% of litters) included: cleft palate, http://www.hoosierkitties.com/breed/sphinx.htm
umbilical hernias. CFA Sphynx Breed Council: www.sphynxbc.org/
Genetic Tests
Blood typing before breeding and transfusions
Miscellaneous
• Breed name synonyms: Hairless Cat (historical), Bald Cat, Sphinx,
Canadian Hairless
• Registries: TICA, CCA, CFA, ACFA, CFF, NZCF, CCA, FIFé, ACF
• Breed resources: International Sphynx Society (CFA):
www.classytouch.net
International Sphynx Breeders and Fanciers Association:
HC66, Box 70035
Pinetop AZ 85935
584
Tonkinese
In the Natural mink the body is a light brown. This is intermediate
between the light body of Siamese, and the dark body of the
Burmese. Coat tends to darken further with age. Allow up to 16
months for dilute coats to fully develop.
Coat: They possess a short thick coat of fine silky glossy hairs that Normal Breed Variations
lay close to the body. A small cowlick is usually present on the Watch calorie intake due to tendency to obesity
chest. A small number of colors are accepted: Platinum (termed
Lilac in Siamese), Blue, Natural (termed Brown outside North A prevalence of 100% blood type A was reported.3
America), and Champagne (Chocolate in Siamese). The Natural
or Brown color is the same as the Sable Burmese or Seal Point
Siamese. Other colors are accepted in some registries.
Drug Sensitivities
None reported in the literature
Three Patterns can be Registered:
1. Mink: Ideal show type. Delineation between points and body Inherited Diseases
color should be visible but not be sharp. (cb cs). Note that cb and cs See Siamese and Burmese chapters—share many of their conditions
are co-dominant which results in this intermediate phenotype.1 but generally quite hardy and healthy; likely due to hybrid vigor.
2. Pointed: Sharp transition of points; as in Siamese cats (cs cs).
3. Solid: Very weak transition to points; only slight lightening on Disease Predispositions
the body, as in Burmese cats (cb cb). Medial Patellar Luxation: A study in 1990 noted that of 22
Tonkinese cats assessed as part of a larger study, 4 had increased
Latter two types are pet quality (AOV registered), and occasional patella mobility/less secure seating. Minimum age in the overall
honeys or fawns are also AOV. mixed breed study group was 6 months; average age of the cats
was 3.6 years. Compared with non pedigreed cats in this study
Tonkinese points are autosomal recessive inheritance. These
group with a rate of 2:31 cats affected, this breed had a greater
patterns reflect three types of partial temperature sensitive (ts)
laxity rate.4
oculocutaneous albinism, there is a spectrum of mutation effects at
one locus.2
585
Genetic Tests
No tests available commercially but now that the mutations of
the tyrosinase gene leading to the ts-albinism (pointing) have
been identified, checking for carriers of pointing alleles will follow,
reducing the number of test crosses needed by breeders.1
Miscellaneous
• Breed name synonyms: Tonk, Tonkanese, Golden Siamese
(historical), Old-fashioned Siamese, Pointed Burmese
• Registries: CCA, TICA, CFA, ACFA, CFF, GCCF, ACF, NZCF, CCA
• Breed resources: Tonkinese Breed Association:
Website: http://www.tonkinesebreedassociation.org/
Tonkinese Cat Club (GCCF): http://www.tonkinesecatclub.co.uk/
References
1. Imes DL, Young AE, Grahn RA, Lyons LA. Get to the point: Identifying
albinism mutations in cats. Proceedings. Tuft’s Canine and Feline Breeding
and Genetics Conference Oct 2-4, 2003 Available at VIN: www.vin.com/
tufts/2003. Accessed Nov 19, 2004.
2. Lyons LA, Imes DL, Grahn RA. Investigation of albinism in domestic cats.
Proceedings. 2nd International Conference Advances in Canine and Feline
Genomics. Oct 2004. Utrecht Netherlands. Poster #18.
3. Giger U. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy XIII.
Philadelphia: WB Saunders Co, 2000;396-399.
4. Engvall E, Bushnell N. Patellar luxation in Abyssinian cats. Fel Pract
1990;18(4):20-22.
586
Turkish Angora
intelligent, curious, possess good hunting instincts, love to jump,
and are able to jump very high. They like close human contact and
some will shadow their owners. They like a regular routine and are
noted to have a strong personality.
Drug Sensitivities
None reported in the literature
The Breed History
This ancient longhair breed originated in Turkey. First written records Inherited Diseases
date to the 1800s. These graceful, tall, slender cats almost became Neonatal Isoerythrolysis (NI): Increased risk of NI is present due
extinct in the early 1900s due to extensive crossing with Persians. to considerable prevalence of blood type B. Authors recommend
typing cats before breeding; even the first breeding since
In Turkey a special breeding program was maintained to preserve primiparous females’ offspring can be affected.1
the original cat type. Only the Turkish cats originating from that
breeding program in the Ankara zoo have been accepted into the Congenital Deafness: Sometimes seen in white coat with
modern registry. In 1963, the first pair was brought to America. First blue-eyed and odd-eyed pigmentation.2
CFA registrations occurred in the year 1970. Note that in Britain,
Angora cats are registered (GCCF) but are not the same breed as the Disease Predispositions
Turkish Angora, but are in fact closer in breeding and type to the Transfusion Reactions: High risk of reactions due to presence of
Oriental longhair in the US. No outcrossing is allowed in CFA. type B blood type in this breed, and blood typing should be done
before transfusions according to the authors.1
Physical Characteristics
Weight: Females 5-9 lb (2.3-4 kg), males 6-11 lb (2.5-5 kg) Genetic Tests
Blood typing before breeding and transfusions
Coat: Many colors are accepted, but not Oriental shades such as
lavender, chocolate or the Himalayan pointed pattern. Single layer
coat is medium long, glossy and silky, lying close to the body, and
Miscellaneous
• Breed name synonyms: Turk, Angora, Turkish Longhair, Ankara
hairs have a slight wave. White is the most common color. The full cats (historical syn)
features of the coat are not developed until 18 to 24 months of • Registries: FIFé, TICA, CFA, ACFA, CFF, WCF, CCA
age. Longer hair is present on ruff and britches and the tail is a full • Breed resources: Turkish Angora Fanciers International:
bottle brush-plume tail. http://turkishangora.org/
The Turkish Cat Society (UK): www.turkishcatsociety.co.uk
Variation occurs between registries in accepted coloring. This
applies to shading and silver (genetics: inhibitor gene plus agouti
gene) which is not allowed in CFA but is allowed in TICA and FIFé. References
1. Arikan S, Duru SY, Gurkan M, Agaoglu ZT, Giger U. Blood type A and B
Eyes: The large eyes are almond shaped and colors include green, frequencies in Turkish Van and Angora cats in Turkey. J Vet Med A Physiol
Pathol Clin Med. 2003;Aug;50(6):303-306.
copper, gold, green-gold, blue and odd-eyed.
2. Strain GM. Hereditary deafness in dogs and cats: causes, prevalence,
and current research. Proceedings. Tuft’s Canine and Feline Breeding and
Points of Conformation: These are small-medium sized cats, lithe,
Genetics Conference. Oct 2-4, 2003, Available at: http://www.vin.com/
with long bodies, are fine boned, and possess a fine wedge shaped
tufts/2003. Accessed Nov 19, 2004.
head. Nose is medium in length and straight with no break, ears are
large, tufted, and close set. Tail is long and tapering, and paws are
compact, small and round. Toe tufting is preferred.
587
Turkish Van
Coat texture is very soft (like cashmere) and plush; it is a
semi-longhaired single silky coat. Coat lies flat, with britches and
feathers on belly, feet and legs. Length and fullness of coat depends
on the season. This is a water resistant coat.
In Turkey, indigenous people often refer to “van” cats as all white Recognized Behavior Issues and Traits
cats with odd-eyes; perhaps a description more in line with what Reported breed characteristics include: Highly intelligent—the
the fancy organizations have labeled the Turkish Angora. The CFA hallmark of the breed is their love of swimming, though not all
accepted this breed in Miscellaneous Class in 1988, provisional in individuals are water-loving. Gait of the male cats can appear to
1993, and for Championship status in 1994. The GCCF and FIFé both swing due to the wide pelvis. They are active cats, friendly and
recognized the breed in 1969. independently minded, vocal and love climbing but not jumping; they
like to keep their feet on the ground. Good for leash training and love
Physical Characteristics to play fetch. Some can open cupboard doors. Can be startled with
Weight: Breed standard specifies both weight and length. certain sounds; some don’t travel well and may resist carrying. Not
Males- > 28” height, > 10 lb to 19 lb (4.5-8.5 kg) considered lap cats. Vans are often described as “dog like”.
Females > 25” height, > 8 lb (3.5 kg)
Coat: The most common color is van, a chalk white body with dark
Normal Breed Variations
Litter average size 4 kittens
orange-red (auburn) tail and lighter red-orange colored blazed These are slow maturing cats (~3-5 years)
marking over the skull. Sometimes head markings extend up onto
the ears (considered ideal). Ideally, a white blaze should extend up Blood Type: In a survey of 85 cats in Turkey, 60% were B blood
the middle of the forehead. The tail is faintly ringed in orange or type.1 In a recent survey of 78 Van cats in Turkey, naturally
cream cats, but not in blue or tortie cats. The other color markings occurring alloantibody titers were measured; in this study 57.7% of
are combined with a white body in a van pattern. Some registries the cats were type B (n=45 cats). In this subset, all the B type cats
(CFA) allow for up to 20% of the body to be the colored hairs (in had grossly evident agglutinating anti-A antibodies in plasma. Type
“thumbprints”). Cream is a dilute of the orange color. A cats (n=33) were also checked and 78% had anti-B antibody in
their plasma; of these 18% had microscopic agglutination only.2
Point restricted or Oriental colors (lilac, chocolate) are not
accepted in any registries. Van is piebald spotting genetically (SS),
a dominant gene with incomplete penetrance. Different grading Drug Sensitivities
systems have been published to describe the differing degrees of None reported in the literature
white, with grades 2-9 having some variation of the piebald; with
ideal Van markings being around 8-9 on the scales. If there is more Inherited Diseases
than 20% color on body, or lacking van color on head or tail it will Neonatal Isoerythrolysis (NI): Increased risk due to high
be a pet quality cat. prevalence of B blood type; Neonatal isoerythrolysis occurs when
A or AB type kittens of a B type queen are allowed to nurse in the
588
immediate postnatal period. Authors recommended typing male
and female cats before breeding, even the first breeding, since a
primiparous females’ offspring can be affected.1,2
Disease Predispositions
Transfusion Reactions: High risk of reactions due to presence of
type B blood type in this breed, so blood typing should be done
before transfusions according to the authors.1 Where there was an
A type donor and B type recipient, if not typed, the recipient had a
8.9% probability of an acute severe reaction, while another 77.8%
could be expected to have acute mild reactions, with the balance
having premature red cell destruction post-transfusion.
Genetic Tests
Blood typing should be performed before transfusion or breeding
due to high prevalence of blood type B.
Miscellaneous
• Breed name synonyms: Van cat, Swimming Cat, Water Cat,
Turk, National Cat of Turkey, Turkey, White Ringtail (historical SYN),
Russian Longhair, White Russian
• Registries: FIFé, TICA, CFA, ACFA, GCCF, ACF, WCF, NZCF
• Breed resources: Vantastix Turkish Van Breed Club:
www.vantastixcatclub.com
Classic Turkish Van Cat Association: http://www.vantasia.org/
Turkish Van Cat Club (UK):
http://www.turkishvancatclub.co.uk/index1.htm
References
1. Arikan S, Duru SY, Gurkan M, Agaoglu ZT, Giger U. Blood type A and B
frequencies in Turkish Van and Angora cats in Turkey. J Vet Med A Physiol
Pathol Clin Med. 2003; Aug; 50(6):303-306.
2. Arikan S, Akkan HA. Titres of naturally occurring alloantibodies against
feline blood group antigens in Turkish Van cats. J Small Anim Pract 2004;
Jun;45(6):289-292.
589
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Appendix A
Available Genetic Tests for Breed Specific Canine and Feline Genetic Disorders
Disorder Breeds Type of Test Test Facility
AB Blood Groups Cats Direct UC-Davis VGL
Benign Familial Juvenile Epilepsy Lagotto Romagnolo Direct Canigen
Black Hair Follicular Dysplasia Large Munsterlander Direct HealthGene
Bobtail (Canine Brachyury) Australian Shepherd Direct ANTAGENE
Australian Stumpy Tail Cattle Dog Genoscoper
Austrian Pinscher Animal Health Trust (some
Bourbonnais Pointer breeds)
Brazilian Terrier
Brittany Spaniel
Croatian Sheepdog
Danish/Swedish Farmdog
Jack Russel Terrier
Karelian Bear Dog
Mudi
Polish Lowland Sheeplog
Pyrenean Shepherd
Savoy Sheepdog
Schipperke
Spanish Waterdog
Swedish Vallhund
Canine Leukocyte Adhesion Irish Red and White Setter Direct Optigen
Deficiency (CLAD) Irish Setter Animal Health Trust
Cardiomyopathy, Boxer Direct North Carolina State University
Arrhythmogenic Right - Meurs Lab
Ventricular (ARVC)
Cardiomyopathy, Dilated (DCM) Doberman Pinscher Direct North Carolina State University
- Meurs Lab
Cardiomyopathy, Juvenile Portuguese Water Dog Direct PennGen
Cataract, Juvenile (Early Onset Boston Terrier Direct Animal Health Trust
Hereditary Cataract – EHD) French Bulldog VetGen
Staffordshire Bull Terrier
Cataract Australian Shepherd Direct – Susceptibility Gene Animal Health Trust
Cerebellar Ataxia Spinone Italiano Linkage Animal Health Trust
Cerebellar Ataxia Finnish Hound Direct Genoscoper
Cerebellar Ataxia (NCL-A) American Staffordshire Terrier Direct ANTAGENE
Optigen
Ceroid lipofuscinosis Border Collie Direct Animal Health Trust
Optigen
Ceroid lipofuscinosis American Bulldog Direct OFA (Am. Bulldogs and Tibetan
Dachshund Terrier)
English Setter U Missouri (Dachshund and
Tibetan Terrier English Setter)
Chondrodysplasia Norwegian Elkhound Direct Genoscoper
591
Disorder Breeds Type of Test Test Facility
Coat Color and Nose Color Afghan Hound Direct HealthGene
Variation Australian Shepherd
Belgian Shepherd
Border Collie
Briard
Brittany
Cardigan Welsh Corgi
Chinese Shar Pei
Collie (Rough, Smooth)
Cocker Spaniel
Curly-Coated Retriever
Dachshund
Dalmatian
Doberman Pinscher
English Cocker Spaniel
English Setter
English Springer Spaniel
Field Spaniel
Flat-coated Retriever
French Bulldog
German Shepherd
German Longhaired Pointer
German Shorthaired Pointer
German Wirehaired Pointer
Great Dane
Greyhound
Groenendael
Japanese Chin
Labrador Retriever
Laekenois
Large Munsterlander
Lowchen
Malinois
Miniature Schnauzer
Newfoundland
Pointer
Pomeranian
Poodle
Portuguese Water Dog
Pudelpointer
Pug
Shetland Sheepdog
Staffordshire Bull Terrier
Tervuren
Whippet
Wirehaired Pointing Griffon
Coat Color Gene Variations Most Dog Breeds – see VetGen Direct VetGen
website
Coat Color Genes - Cats Most Cats Direct UC-Davis VGL
Coat Length (FGF5) Alaskan Malamute Direct Animal Health Trust
Border Collie UC-Davis VGL
Cats (all breeds)
German Shepherd
Pembroke Welsh Corgi
Weimeraner
Cobalamin Malabsorption Australian Shepherd Direct PennGen
(Methylmalonic Aciduria) Giant Schnauzer
592
Disorder Breeds Type of Test Test Facility
Cobalamin Malabsorption Basset Hound Phenotypic PennGen
(Methylmalonic Aciduria) Beagle
Border Collie
DSH
Komodor
Shar Pei
Collie Eye Anomaly Australian Shepherd Direct Optigen
(Choroidal Hypoplasia) Border Collie
Boykin Spaniel
Lancashire Heeler
Nova Scotia Duck Tolling Retriever
Rough Coated Collie
Shetland Sheepdog
Smooth Coated Collie
Whippet, Longhair
Cone (Retinal) Degeneration Alaskan Malamute Direct Optigen
Australian Shepherd
German Shorthaired Pointer
Congenital Hypothyroidism with Rat Terrier Direct Michigan State University – Fyfe
Goiter (CHG) Toy Fox Terrier Lab.
PennGen
Congenital Keratoconjunti- Cavalier King Charles Spaniel Direct Animal Health Trust
vitis Sicca and Ichthyosiform
Dermatitis
Congenital Cavalier King Charles Spaniel Direct Auburn Univ. – Boudreaux Lab
Macrothrombocytopenia
Congenital Stationary Night Briard Direct Optigen
Blindness (RPE65-CSNB) Animal Health Trust
Copper Toxicosis Bedlington Terrier Direct VetGen
Animal Health Trust
Cyclic Neutropenia Smooth Coated Collie Direct HealthGene
(Grey Collie Syndrome) Rough Coated Collie
Cystinuria Newfoundland Direct Optigen (Newf only)
Labrador Retriever PennGen
VetGen (Newf only)
Degenerative Myelopathy (DM) American Eskimo Dog Direct - Susceptibility Gene OFA
American Water Spaniel
Bernese Mountain Dog
Borzoi
Boxer
Canaan Dog
Cardigan Welsh Corgi
Chesapeake Bay Retriever
Collie
French Bulldog
German Shepherd Dog
Irish Setter
Kerry Blue Terrier
Kuvasz
Mixed-breed/Other breeds
Pembroke Welsh Corgis
Poodle, Standard
Pug
Rhodesian Ridgeback
593
Disorder Breeds Type of Test Test Facility
Encephalitis, Pug Dog (PDE) Pug Direct – Susceptibility Gene UC-Davis
Episodic Falling Cavalier King Charles Spaniel Direct Animal Health Trust
Exercise Induced Collapse (EIC, Boykin Spaniel Direct UMinn VDL
Dynamin 1 Mutation) Chesapeake Bay Retriever
Curly Coated Retriever
German Wirehaired Pointer
Labrador Retriever
Pembroke Welsh Corgi
Factor VII Deficiency Alaskan Klee Kai Direct PennGen
Beagle Animal Health Trust (Beagle and
Scottish Deerhound Scottish Deerhound)
Facor IX Deficiency Airdale Terrier Direct Cornell Univ. Comparative Coag.
(Hemophilia B) Bull Terrier Lab (GWP)
German Wirehaired Pointer HealthGene (Others)
Labrador Retreiver
Lhasa Apso
Factor XI Deficiency Kerry Blue Terrier Direct PennGen
Fanconi Syndrome Basenji Linkage OFA
Fanconi Syndrome Basenji Phenotypic PennGen
Norwegian Elkhound
Fucosidosis English Springer Spaniel Direct PennGen
Animal Health Trust
Glanzmann’s Thrombasthenia Great Pyrenees Direct Auburn Univ. – Boudreaux Lab.
(Type I) Otterhound
Globoid cell leukodystrophy Cairn terrier Direct Jefferson Medical Coll.
West Highland White Terrier
Glycogenosis (GSD) Type IIIa Curly Coated Retriever Direct Michigan State University – Fyfe
Lab.
Glycogenosis (GSD) Type IV Norwegian Forest Cat Direct PennGen
GM1-Gangliosidosis Portuguese Water Dog Direct New York University
Neurogenetics Lab
GM1 (GLB1) and GM2 (HEXB) Korat Direct UC-Davis VGL
Gangliosidosis
GM2-Gangliosidosis Burmese Direct UC-Davis VGL (Burmese)
Japanese Chin OFA (Japanese Chin)
Hypersarcosinemia Portuguese Water Dog Phenotypic PennGen
Hyperuricosuria (SLC2A9) American Staffordshire Terrier Direct UC-Davis VGL
Australian Shepherd Animal Health Trust
Bulldog
Black Russian Terrier
Dalmatian
German Shepherd Dog
Giant Schnauzer
Jack/Parson Russel Terrier
Large Munsterlander
Labrador Retriever
Pomeranian
Weimaraner
Hypertrophic Cardiomyopathy Maine Coon Cat Direct North Carolina State University
Ragdoll - Meurs Lab
UC-Davis VGL (Ragdoll)
594
Disorder Breeds Type of Test Test Facility
Ichthyosis Golden Retriever Direct Antagene (Goldens)
Norfolk Terrier Optigen (Goldens)
Venta Lab-MSU 517-355-6463
x1552 (Norfolks)
Improper Coat (IC13) Portuguese Water Dog Direct Optigen
Ivermectin Sensitivity Australian Shepherd Direct Washington State U – Pharm
(MDR1) Collie Lab
German Shepherd Dog
Old English Sheepdog
Shetland Sheepdog
Other breeds
L-2-HGA (L-2-hydroxyglutaric Staffordshire Bull Terrier Direct Animal Health Trust
aciduria)
Mannosidosis DSH Direct PennGen
Persian
Merle Gene (SILV) Australian Shepherds Direct (GenMark has been bought by
Beauceron Sheepdog Idexx, who will be offering again
Border Collie in the future)
Cardigan Welsh Corgi
Catahoula Leopard Dog
Chihuahua
Cocker Spaniel
Collie
Dachshund
Great Danes
Norwegian Hound
Pitt Bull
Pomeranian
Pyrenean Shepherd
Shetland Sheepdogs
Mitochondrial Myopathy Cocker Spaniel Phenotypic PennGen
Old English Sheepdog
Mucolipidosis II (I-Cell Disease) DSH Direct PennGen
Mucopolysaccharidosis (MPS) DSH Direct PennGen
German Shepherd Dog
Miniature Pinscher
Miniature and Toy Poodle
Miniature Schnauzer
Plotthound
Schipperke
Siamese
Wirehaired Dachshund
Mucopolysaccharidosis (MPS) Cardigan Welsh Corgi Phenotypic PennGen
Pembroke Welsh Corgi
Rottweiler
Musladin-Lueke Syndrome Beagle Direct UC-Davis VGL
Muscular Myopathy Labrador Retriever Direct Alfort School of Veterinary
(Centronuclear myopathy) Medicine, France
Animal Health Trust
Myostatin Mutation (Gross Whippet Direct DDC Veterinary
Muscle Hypertrophy, Bully
Whippets)
595
Disorder Breeds Type of Test Test Facility
Myotonia Congenita Miniature Schnauzer Direct Optigen
PennGen
Myotonia Hereditaria Australian Cattle Dog Direct U-Guelph AHL
Narcolepsy Dachshund Direct Optigen
Doberman Pinscher
Labrador Retriever
Neonatal Ataxia Coton de Tulear Direct Antagene
Univ. Missouri
Neonatal Encephalopathy Standard Poodle Direct OFA
Nephropathy (Hereditary N., English Cocker Spaniel Direct Optigen
Familial N.)
Oculoskeletal Dysplasia (OSD)/ Labrador Retriever Direct Optigen
Retinal Dysplasia (RD) Samoyed
Perianal Fistula/Anal German Shepherd Direct Susceptibility Gene Genoscoper
Furunculosis
Persistent Muellerian Duct Miniature Schnauzer Direct Cornell:Meyers-Wallen Lab
Syndrome
Phosphofructokinase Deficiency American Cocker Spaniel Direct Optigen
(PFK) English Springer Spaniel PennGen
Whippet (VetGen only) VetGen
Animal Health Trust (ESS)
Polycystic Kidney Disease (PKD) American Shorthair Direct UC-Davis – VGL
British Shorthair Animal Health Trust
Himalayan
Persian
Scottish Fold
Polyneuropathy (Leonberger Leonberger Direct UMinn VDL
Polyneuropathy) U Bern
Polyneuropathy (NDRG1) Greyhound Direct Optigen
Primary Hyperoxaluria Tibetan Spaniel Phenotypic PenGen
Primary Hyperparathyroidism Keeshond Linkage Cornell – Goldstein Lab
Primary Lens Luxation (PLL) Australian Cattle Dog Direct Animal Health Trust
Chinese Crested OFA
Jack Russell Terrier
Lakeland Terrier
Lancashire Heeler
Miniature Bull Terrier
Parson Russell Terrier
Patterdale Terrier
Rat Terrier
Sealyham Terrier
Tenterfield Terrier
Tibetan Terrier
Toy Fox Terrier
Volpino Italiano
Welsh Terrier
Wire Fox Terrier
Progressive Retinal Atrophy Papillon Direct Genoscoper
Progressive Retinal Atrophy Dachshund, Miniature Direct Animal Health Trust
(cord1) Longhaired and Smooth haired Susceptibility Gene U-Missouri
English Springer Spaniel
Progressive Retinal Atropy (crd2) American Pit Bull Terrier Direct Optigen
596
Disorder Breeds Type of Test Test Facility
Progressive Retinal Atrophy Glen of Imaal Terrier Direct Optigen
(crd3)
Progressive Retinal Atrophy - Bullmastiff Direct Optigen
Dominant (English) Mastiff
Progressive Retinal Atrophy Golden Retriever Direct Animal Health Trust
(GR-PRA1) Optigen
Progressive Retinal Atrophy American Cocker Spaniel Direct Optigen
(prcd) American Eskimo Dog
Australian Cattle Dog
Australian Shepherd
Chesapeake Bay Retriever
Chinese Crested
Cockapoo
English Cocker Spaniel
Entelbucher Mountain Dog
Finnish Lapphund
Golden Retriever
Goldendoodle
Kuvasz
Labradoodle
Labrador Retriever
Lapponian Herder
Norwegian Elkhound
Nova Scotia Duck Trolling Retriever
Poodle; Miniature & Toy
Portuguese Water Dog
Silky Terrier
Spanish Water Dog
Stumpy Tail Cattle Dog
Swedish Lapphund
Yorkshire Terrier
Progressive Retinal Atrophy Irish Red and White Setter Direct Optigen
(rcd1) Irish Setter Animal Health Trust
VetGen (Irish Setter)
Progressive Retinal Atrophy Sloughi Direct Optigen
(rcd1a) Animal Health Trust
Progressive Retinal Atrophy Collie – Smooth and Rough Direct Optigen
(rcd2)
Progressive Retinal Atrophy Cardigan Welsh Corgi Direct Michigan State Univ. -
(rcd3) Peterson-Jones Lab.
Optigen
VetGen
Progressive Retinal Atrophy Gordon Setter Direct Animal Health Trust
(rcd4) Irish Setter
Progressive Retinal Atrophy Abyssinian Direct UC-Davis VGL
(rdAc) Ocicat
Siamese
Somali
Progressive Retinal Atrophy Abyssinian Direct UC-Davis VGL
(Rdy) Somali
Progressive Retinal Atrophy – Miniature Schnauzer Direct Optigen
Type A
Progressive Retinal Atrophy – Samoyed Direct Optigen
X-Linked Siberian Husky
597
Disorder Breeds Type of Test Test Facility
Pyruvate Dehydrogenase Clumber Spaniel Direct U-Missouri
Phosphatase Deficiency Sussex Spaniel Animal Health Trust
(PDH or PDP1)
Pyruvate Kinase Deficiency (PK) Abyssinian Direct Optigen (Basenji)
American Eskimo Dog PennGen (All)
Basenji VetGen (Basenji)
Beagle Animal Health Truist (Westies)
Bengal UC-Davis VGL (Cats)
Cairn Terrier
Chihuahua
Dachshund
DSH
Somali
West Highland White Terrier
Renal Dysplasia Lhasa Apso Direct Susceptibility Gene DOGenes
Shih Tzu
Soft Coated Wheaton Terrier
Retinal Dysplasia – Canine Australian Shepherd Direct Optigen
Multi-focal Retinopathy (CMR) Bullmastiff
Cane Corso
Coton de Tulear
Dogue de Bordeaux
Great Pyrenees
Lapponian Herder
Mastiff (English and French)
Perro de Presa Canario
Severe Combined Bassett Hound Direct PennGen
Immunodeficiency (SCID) Cardigan Welsh Corgi
Pembroke Welsh Corgi
Spinal Muscular Atrophy Maine Coon Cat Direct Michigan State University – Fyfe
Lab.
Thrombopathia Bassett Hound Direct Auburn Univ. – Boudreaux Lab.
Landseer
Spitz
Trapped Neutrophil Syndrome Border Collie Linkage Optigen
(TNS) Univ. New South Wales
Von Willebrand’s Disease – Type I Bernese Mountain Dog Direct VetGen
Coton de Tulear
Doberman Pinscher
Drentsche Patrijshound
German Pinscher
Kerry Blue Terrier
Manchester Terrier
Papillion
Pembroke Welsh Corgi
Poodle
Von Willebrand’s Disease – Type I Irish Red and White Setters Direct Animal Health Trust
Von Willebrand’s Disease – Type II Collie Direct VetGen
Deutsch Drahthaar
German Shorthaired Pointer
German Wirehaired Pointer
Pointer
Von Willebrand’s Disease – Type III Kooikerhondje Direct VetGen
Scottish Terrier
Shetland Sheepdog
598
Appendix B
Genetic Testing Centers
Alfort School of Veterinary Medicine - CNM DDC Veterinary
7 avenue du General de Gaulle 225 Corporate Court
F-94704 Maisons-Alfort Fairfield, OH 45014
CEDEX – FRANCE 800-625-0874
http://www.labradorcnm.com/ www.vetdnacenter.com/canine-bully-test-whippets.html
ANTAGENE Genoscoper
Immeuble Le Meltem Karvaamokuja 3
2 allée des Séquoias FI-00380 Helsinki Finland
69578 Limonest cedex – France +358 9 737 823, +358 44 5747 434
Tél: +33 (0)4 37 49 90 03 http://www.genoscoper.com/in_english2/
Fax: +33 (0)4 37 49 04 89
www.antagene.com HealthGene
2175 Keele St.
Auburn University – Boudreaux Lab Toronto, ON M6M 3Z4 Canada
Mary Boudreaux, DVM 877-371-1551
Dept of Pathobiology http://www.healthgene.com/
166 Greene Hall
College of Veterinary Medicine Jefferson Medical College
Auburn University, AL 36849 Dr. David Wenger
(334) 844-2692 Dept of Neurology
http://www.vetmed.auburn.edu/faculty/pathobiology-faculty/ Jefferson Medical College
boudreaux 1020 Locust St, 394
Philadelphia, PA 19107
Cornell University Goldstein Molecular and Genetics Laboratory 215-955-1666
Richard E. Goldstein, DVM David.wenger@mail.tju.edu
NYSCVM – Cornell University
Ithaca, New York 14853-6401 Michigan State University – Peterson-Jones Lab
Phone: 607-253-4480 Dr Petersen-Jones - Corgi Test.
Fax: 607-253-3534 Michigan State University,
http://www.vet.cornell.edu/labs/goldstein/ D-208 Veterinary Medical Center,
East Lansing, MI 48824-1314
Cornell University – Meyers-Wallen Lab 517-353-3278
Vicki Meyers-Wallen, VMD, PhD http://www.cardigancorgis.com/documents/Acrobat/membersPRA-
Baker Institute – Cornell University SubmissionForm.pdf
Ithaca, New York 14853
Phone 607-256-5683 Michigan State University – Fyfe Lab
Fax: 607-256-5608 Dr. John C. Fyfe
http://bakerinstitute.vet.cornell.edu/faculty/page.php?id=206 Laboratory of Comparative Medical Genetics
2209 Biomedical Physical Sciences Bldg
Cornell Univ. Comparative Coagulation Lab Michigan State University
Animal Health Diagnostic Center East Lansing, MI 48824-4320
NYSCVM – Cornell University 517-355-6463x1559
Ithaca, New York 14853-6401 http://mmg.msu.edu/92.html
607-275-0622
http://www.diaglab.vet.cornell.edu/coag/test/hemopwh.asp
599
New York University Neurogenetics Laboratory U-Guelph Animal Health Laboratory
Dr. Bai Jin Zeng University of Guelph
NYU Medical Center P.O. Box 3650, 95 Stone Road West
New York, NY 10016 Guelph, Ontario
212-263-2943 N1H 8J7 CANADA
http://www.pwdca.org/health/tests/information/GM1TestInstruc- 519-824-4120 ext 54502
tions.html www.labservices.uoguelph.ca/units/ahl/
North Carolina State University – Meurs Lab Univ. Minnesota Veterinary Diagnostic Laboratory
ATTN: Veterinary Cardiac Genetics Laboratory College of Veterinary Medicine, University of Minnesota
Research Building 460 1333 Gortner Ave
4700 Hillsborough Street St. Paul, MN 55108
Raleigh, NC 27606 612-625-8787
Tel: 919-513-8279 http://www.vdl.umn.edu/ourservices/canineneuromuscular
http://www.cvm.ncsu.edu/vhc/csds/vcgl/
University of Missouri - Animal Molecular Genetics Lab
OptiGen Univ of MO College of Vet Medicine
Cornell Business & Technology Park 320 Connaway Hall
767 Warren Road, Suite 300 Columbia, MO 65211
Ithaca, NY 14850 http://www.caninegeneticdiseases.net/
Phone: 607-257-0301
Fax: 607-257-0353 University of New South Wales – Wilton Lab
http://www.optigen.com/ Dr. Alan Wilton
School of Biotechnology and Biomolecular Sciences
Orthopedic Foundation for Animals University of New South Wales
2300 E Nifong Boulevard New South Wales 2052, Australia
Columbia, Missouri, 65201-3806 E-mail: a.wilton@unsw.edu.au
Phone: (573) 442-0418
Fax: (573) 875-5073 VetGen
www.offa.org 3728 Plaza Drive, Suite One
Ann Arbor, MI 48108
PennGen Laboratories 800-483-8436
3850 Spruce Street www.vetgen.com
Philadelphia, PA 19104-6010
215-898-8894 Washington State University – Pharm Lab
www.vet.upenn.edu/penngen Veterinary Clinical Pharmacology Lab (WSU-VCPL)
PO Box 2280
Texas A&M Comparative Dermatology Lab Pullman, WA 99165-2280
Texas A&M College of Vet Med Phone/FAX: 509-335-3745
442 University Drive www.vetmed.wsu.edu/depts-VCPL/
College Station, TX 77845
979-845-2651
compderm-NFT@cvm.tamu.edu
University of Bern
Institute of Genetics
PO-Box 8466
CH-3001 Bern, Switzerland
Tel +41 (0) 31 631 2322 Fax +41 (0) 31 631 2640
www.vetsuisse.unibe.ch/genetic/content/service/dog/index_eng.html
600
Appendix C: Part I
Quick Reference to Conditions by Breed: Breed Specific Conditions in Dogs
This list is not exhaustive or complete, but recognizes the published conditions as presented in the breed chapters.
Subject Condition Breed-Dog
Behavioral Aggression Bedlington Terrier
Cairn Terrier
Chinese Shar Pei
Chow Chow
Cocker Spaniel
Dalmatian
English Cocker Spaniel
English Springer Spaniel
German Shepherd Dog
Portuguese Water Dog
Rottweiler
Scottish Terrier
Silky Terrier
West Highland White Terrier
Aggression, Dog To Dog German Shorthaired Pointer
Anxiety Dalmatian
Vizsla
Flank Sucking Doberman Pinscher
Fly Catching Behavior Cavalier King Charles Spaniel
Nervousness Pointer
Noise Phobia German Shorthaired Pointer
Separation Anxiety Border Collie
Spinning/Tail Chasing Bull Terrier
Miniature Bull Terrier
Cardiovascular 2nd and 3rd Degree Heart Block Cocker Spaniel
Acepromazine Collapse Boxer
Aortic Stenosis Dogue De Bordeaux
German Shepherd Dog
Glen of Imaal Terrier
Golden Retriever
Aortic Thromboembolism Cavalier King Charles Spaniel
Arrhythmias German Shepherd Dog
Greyhound
Atherosclerosis Doberman Pinscher
Miniature Schnauzer
Atrial Septal Defect Boxer
Poodle
Atrial Stenosis Bull Terrier
Atrioventricular (AV) Block Afghan Hound
Chow Chow
English Springer Spaniel
German Wirehaired Pointer
Labrador Retriever
Atrioventricular Valve Dysplasia Mastiff
Cardiomyopathy, Arrhythmogenic Boxer
601
Subject Condition Breed-Dog
Cardiomyopathy, Dilated Airedale Terrier
Borzoi
Cocker Spaniel
Doberman Pinscher
English Cocker Spaniel
Great Dane
Irish Wolfhound
Leonberger
Newfoundland
Poodle
Saint Bernard
Scottish Deerhound
Standard Schnauzer
Cardiomyopathy, Juvenile Dilated Manchester Terrier
Portuguese Water Dog
Chronic Myxomatous Valvular Endocarditis Yorkshire Terrier
Conotruncal Defect Beagle
Border Terrier
Keeshond
Heart Murmur Airedale Terrier
Bedlington Terrier
Border Terrier
Brussel’s Griffon
Cairn Terrier
Greyhound
Vizsla
Hypotension, Physiologic Mild Irish Wolfhound
Left Ventricular Outflow Obstruction Bull Terrier
Miniature Bull Terrier
Mitral Valve Stenosis Bull Terrier
Mitral Valvular Disease American Water Spaniel
Cavalier King Charles Spaniel
Dachshund
Great Dane
Greyhound
Japanese Chin
Miniature Schnauzer
Norfolk Terrier
Pekingese
Pomeranian
Poodle
Saluki
West Highland White Terrier
Yorkshire Terrier
Patent Ductus Arteriosis (PDA) American Water Spaniel
Bichon Frisé
German Shepherd Dog
Maltese
Pembroke Welsh Corgi
Pomeranian
Poodle
Pyrenean Shepherd
Shetland Sheepdog
602
Subject Condition Breed-Dog
Pericardial Effusion, Idiopathic Golden Retriever
Portosystemic (Liver) Shunt Australian Cattle Dog
Bernese Mountain Dog
Bichon Frisé
Border Collie
Cairn Terrier
Chihuahua
Dandie Dinmont Terrier
Havanese
Irish Wolfhound
Lhasa Apso
Maltese
Miniature Pinscher
Miniature Schnauzer
Norfolk Terrier
Norwich Terrier
Old English Sheepdog
Papillon
Parson Russell Terrier
Pekingese
Pug
Scottish Deerhound
Shih Tzu
Silky Terrier
Standard Schnauzer
Tibetan Spaniel
West Highland White Terrier
Yorkshire Terrier
Pulmonic Stenosis American Water Spaniel
Beagle
Boxer
Bulldog
Chihuahua
Chow Chow
French Bulldog
Mastiff
Miniature Schnauzer
Nova Scotia Duck Tolling Retriever
Parson Russell Terrier
Samoyed
Smooth Fox Terrier
Wire Fox Terrier
Sick Sinus Syndrome Cocker Spaniel
English Springer Spaniel
Miniature Schnauzer
West Highland White Terrier
Subaortic Stenosis Black Russian Terrier
Bouvier Des Flandres
Boxer
Curly Coated Retriever
Newfoundland
Rottweiler
Tricuspid Valve Dysplasia Borzoi
Curly Coated Retriever
Labrador Retriever
603
Subject Condition Breed-Dog
Vascular Ring Anomaly/ Persistant Right Boston Terrier
Aortic Arch (PRAA) German Pinscher
German Shepherd Dog
Vasculitis, Necrotizing Boxer
Ventricular Septal Defect Bloodhound
Shiba Inu
Dermatological Acrodermatitis, Lethal Bull Terrier
Actinic Keratosis American Staffordshire Terrier
Bull Terrier
Dalmatian
Alopecia X Chow Chow
Finnish Spitz
Keeshond
Pomeranian
Poodle
Samoyed
Siberian Husky
Alopecia, Endocrine American Eskimo Dog
Chesapeake Bay Retriever
Alopecia, Focal Silky Terrier
Alopecia, Seasonal Flank Affenpinscher
Airedale Terrier
Bearded Collie
Boxer
Manchester Terrier
Wirehaired Pointing Griffon
Anal Gland Disease Manchester Terrier
Pekingese
Scottish Deerhound
Atopic/Allergic Dermatitis Akita
Airedale Terrier
Australian Terrier
Bedlington Terrier
Bernese Mountain Dog
Bichon Frisé
Boston Terrier
Bouvier Des Flandres
Boxer
Briard
Brussel’s Griffon
Bull Terrier
Cairn Terrier
Cavalier King Charles Spaniel
Chesapeake Bay Retriever
Chinese Shar Pei
Chinook
Clumber Spaniel
Cocker Spaniel
Collie
Dalmatian
English Cocker Spaniel
English Setter
Field Spaniel
French Bulldog
604
Subject Condition Breed-Dog
Glen of Imaal Terrier
German Shepherd Dog
German Shorthaired Pointer
Golden Retriever
Great Dane
Great Pyrenees
Greyhound
Ibizan Hound
Irish Setter
Keeshond
Kerry Blue Terrier
Labrador Retriever
Lhasa Apso
Mastiff
Newfoundland
Norwegian Elkhound
Norwich Terrier
Old English Sheepdog
Otterhound
Petit Bassett Griffon Vendéen
Portuguese Water Dog
Pug
Rhodesian Ridgeback
Rottweiler
Scottish Deerhound
Scottish Terrier
Sealyham Terrier
Shiba Inu
Silky Terrier
Soft Coated Wheaten Terrier
Spinone Italiano
Sussex Spaniel
Tibetan Spaniel
Tibetan Terrier
Toy Fox Terrier
Vizsla
Welsh Terrier
West Highland White Terrier
Wirehaired Pointing Griffon
Whippet
Yorkshire Terrier
Black Hair Follicular Dysplasia Saluki
Schipperke
Bullous Pemphigus Great Dane
Calcinosis Circumscripta German Shepherd Dog
Labrador Retriever
Rottweiler
Color Dilution Alopecia Dachshund
Doberman Pinscher
German Pinscher
Italian Greyhound
Miniature Pinscher
Whippet
Comedomes Chinese Crested
Miniature Schnauzer
Xoloitzcuinti
605
Subject Condition Breed-Dog
Cutaneous And Renal Glomerular Greyhound
Vasculopathy (CRGV)
Cutaneous Lupus Erythematosus (Nasal Brittany
Solar Dermatitis) Collie
German Shorthaired Pointer
Shetland Sheepdog
Cutaneous Mucinosis Chinese Shar Pei
Cutaneous Vasculopathy German Shepherd Dog
Demodicosis Afghan Hound
Basenji
Boxer
Bull Terrier
Bulldog
Cane Corso
Chinese Shar Pei
Collie
Dalmatian
Doberman Pinscher
French Bulldog
German Shorthaired Pointer
Great Dane
Italian Greyhound
Manchester Terrier
Miniature Pinscher
Old English Sheepdog
Pointer
Rottweiler
Schipperke
Scottish Terrier
Staffordshire Bull Terrier
Tibetan Spaniel
Vizsla
Whippet
Wire Fox Terrier
Dermatomyositis Beauceron
Collie
Shetland Sheepdog
Yorkshire Terrier
Dermoid Sinus Rhodesian Ridgeback
Digital Keratoma (Corns) Greyhound
Discoid Lupus Erythematosus (DLE) German Shepherd Dog
Epidermolysis Bullosa Beauceron
Follicular Dysplasia Boxer
Doberman Pinscher
Irish Water Spaniel
Portuguese Water Dog
Weimaraner
Hepatocutaneous Syndrome (Superficial Scottish Terrier
Necrolytic Dermatitis) Shetland Sheepdog
West Highland White Terrier
Hyperkeratosis, Digital Irish Terrier
606
Subject Condition Breed-Dog
Ichthyosis Cavalier King Charles Spaniel
Golden Retriever
Norfolk Terrier
Parson Russell Terrier
Lawn Chemical Hypersensitivity Xoloitzcuinti
Lichenoid-Psoriasiform Dermatosis English Springer Spaniel
Shetland Sheepdog
Malassezia Pachydermatis Parson Russell Terrier
West Highland White Terrier
Mucocutaneous Pyoderma German Shepherd Dog
Nasal Parakeratosis Labrador Retriever
Otitis Externa Boykin Spaniel
Brittany
Cane Corso
Chinese Shar Pei
Clumber Spaniel
Cocker Spaniel
English Springer Spaniel
Golden Retriever
Great Pyrenees
Greyhound
Poodle
Portuguese Water Dog
Spinone Italiano
Wirehaired Pointing Griffon
Otitis Media Cavalier King Charles Spaniel
Palmar Hyperkeratosis Dogue De Bordeaux
Pattern Baldness Chihuahua
Curly Coated Retriever
Greyhound
Whippet
Pemphigus Foliaceus Akita
Bearded Collie
Chinese Shar Pei
Chow Chow
Collie
English Springer Spaniel
Finnish Spitz
Newfoundland
Schipperke
Perianal Fistula/Furunculosis German Shepherd Dog
Leonberger
Pigmented Plaques Pug
Pilomatricoma Soft-Coated Wheaten Terrier
Pododermatitis/Interdigital Cysts Bulldog
Sebaceous Adenitis Akita
Chow Chow
English Springer Spaniel
Lhasa Apso
Old English Sheepdog
Poodle
Samoyed
Vizsla
607
Subject Condition Breed-Dog
Sebaceous Cysts Bouvier Des Flandres
Cavalier King Charles Spaniel
Golden Retriever
Gordon Setter
Kerry Blue Terrier
Norwegian Elkhound
Otterhound
Portuguese Water Dog
Rottweiler
Sebaceous Gland Hyperplasia Border Terrier
Seborrheic Dermatitis Airedale Terrier
Basset Hound
Cairn Terrier
Chinese Shar Pei
Cocker Spaniel
English Springer Spaniel
Golden Retriever
Irish Setter
Spiculosis Kerry Blue Terrier
Sunburn Xoloitzcuinti
Superficial Suppurative Necrolytic Miniature Schnauzer
Dermatitis
Symmetrical Lupoid Onchodystrophy (SLO) Bearded Collie
English Setter
Giant Schnauzer
Gordon Setter
Greyhound
Systemic Lupus Erythematosus (SLE) German Shepherd Dog
Nova Scotia Duck Tolling Retriever
Uveodermatologic (VKH-Like) Syndrome Akita
Old English Sheepdog
Samoyed
Shetland Sheepdog
Siberian Husky
Vit A-Responsive Dermatosis Cocker Spaniel
Zinc Responsive Dermatosis Alaskan Malamute
Siberian Husky
Endocrine/Metabolic Ceroid Lipofuscinosis American Staffordshire Terrier
Australian Cattle Dog
Border Collie
Cocker Spaniel
Dachshund
Dalmatian
English Setter
Miniature Schnauzer
Polish Lowland Sheepdog
Saluki
Tibetan Terrier
Cobolamin Deficiency Chinese Shar Pei
Cobalamin Malabsorption Border Collie
Giant Schnauzer
608
Subject Condition Breed-Dog
Copper Storage Disease Bedlington Terrier
Skye Terrier
West Highland White Terrier
Copper Toxicosis Dalmatian
Doberman Pinscher
Diabetes Mellitus Australian Terrier
Beagle
Bichon Frisé
Border Collie
Border Terrier
Cairn Terrier
Cavalier King Charles Spaniel
Collie
Finnish Spitz
Keeshond
Labrador Retriever
Manchester Terrier
Miniature Pinscher
Miniature Schnauzer
Norwegian Elkhound
Poodle
Pug
Puli
Samoyed
Schipperke
Silky Terrier
Standard Schnauzer
Tibetan Terrier
West Highland White Terrier
Yorkshire Terrier
Eosinophilic Diseases Cavalier King Charles Spaniel
Siberian Husky
Fucosidosis English Springer Spaniel
Globoid Cell Leukodsytrophy Cairn Terrier
West Highland White Terrier
Glucocerebrosidosis Silky Terrier
Glycogenosis Type IIIa Curly Coated Retriever
GM1-Gangliosidosis English Springer Spaniel
Portuguese Water Dog
Shiba Inu
GM2-Gangliosidosis Japanese Chin
Hyperadrenocorticism (Cushing’s Disease) Australian Terrier
Bedlington Terrier
Boston Terrier
Cairn Terrier
Dachshund
Dandie Dinmont Terrier
Miniature Schnauzer
Poodle
West Highland White Terrier
Yorkshire Terrier
Silky Terrier
Standard Schnauzer
Hyperlipoproteinemia/Hyperlipidemia Miniature Schnauzer
Shetland Sheepdog
609
Subject Condition Breed-Dog
Hyperparathyroidism, Primary Keeshond
Hyperuricosuria American Staffordshire Terrier
Australian Shepherd
Black Russian Terrier
Bulldog
Dalmatian
German Shepherd Dog
Giant Schnauzer
Jack Russell Terrier
Labrador Retriever
Parson Russell Terrier
Pomeranian
Weimaraner
Hypoadrenocorticism (Addison’s Disease) American Eskimo Dog
Bearded Collie
Great Dane
Great Pyrenees
Leonberger
Nova Scotia Duck Tolling Retriever
Poodle
Portuguese Water Dog
Rottweiler
Soft Coated Wheaten Terrier
West Highland White Terrier
Hypoglycemia Yorkshire Terrier
Hypothyroidism, Autoimmune All Breeds
Hypothyroidism, Congenital Giant Schnauzer
Hypothyroidism, Congenital With Goiter Toy Fox Terrier
IgA Deficiency German Shepherd Dog
Irish Setter
Immunodeficiency, Inherited Cavalier King Charles Spaniel
Weimaraner
L-2 Hydroxyglutaric Aciduria Staffordshire Bull Terrier
Malignant Hyperthermia Greyhound
MDR1 Mutation (Drug & Ivermectin Australian Shepherd
Sensitivity) Border Collie
Collie
German Shepherd Dog
Old English Sheepdog
Shetland Sheepdog
Metabolic Vitamin E Deficiency English Cocker Spaniel
Mitochondrial Myopathy (Pyruvate Clumber Spaniel
Dehydrogenase) Sussex Spaniel
Mucopolysaccharidosis I Plott Hound
Mucopolysaccharidosis IIIa Dachshund
Mucopolysaccharidosis IIIB Schipperke
Mucopolysaccharidosis VI Cardigan Welsh Corgi
Miniature Pinscher
Miniature Poodle
Miniature Schnauzer
Mucopolysaccharidosis VII German Shepherd Dog
610
Subject Condition Breed-Dog
Phosphofructokinase (PFK) Deficiency English Springer Spaniel
Pituitary Dwarfism German Shepherd Dog
Primary Immunodeficiency Chinese Shar Pei
Pyruvate Kinase Deficiency American Eskimo Dog
Basenji
Beagle
Cairn Terrier
Dachshund
West Highland White Terrier
Severe Combined Immunodeficiency (SCID) Parson Russell Terrier
Severe Combined Immunodeficiency (SCID) Basset Hound
-X Linked
Spectrin Deficiency Golden Retriever
Sulfonamide Hypersensitivity Doberman Pinscher
Miniature Schnauzer
Samoyed
Xanthomatosis (Dalmatian Bronzing) Dalmatian
Gastrointestinal Atrophic Gastritis Norwegian Lundehund
Colitis Chinook
Kerry Blue Terrier
Colorectal Polyp Collie
Cricopharyngeal Dysfunction/Achalasia Golden Retriever
Esophageal Achalasia Miniature Schnauzer
Exocrine Pancreatic Insufficiency Bedlington Terrier
Cavalier King Charles Spaniel
Chow Chow
Collie
German Shepherd Dog
Weimaraner
Gallbladder Disease Shetland Sheepdog
Gastic Dilitation/Volvulus (GDV) Akita
Airedale Terrier
Bernese Mountain Dog
Beauceron
Bloodhound
Borzoi
Bouvier Des Flandres
Briard
Bullmastiff
Cane Corso
Chesapeake Bay Retriever
Chinese Shar Pei
Chow Chow
Collie
Curly Coated Retriever
Doberman Pinscher
Dogue De Bordeaux
Flat-Coated Retriever
German Shepherd Dog
German Shorthaired Pointer
Giant Schnauzer
Golden Retriever
611
Subject Condition Breed-Dog
Gordon Setter
Great Dane
Great Pyrenees
Irish Red and White Setter
Irish Setter
Irish Wolfhound
Komondor
Leonberger
Mastiff
Neopolitan Mastiff
Newfoundland
Old English Sheepdog
Poodle
Rottweiler
Saint Bernard
Samoyed
Scottish Deerhound
Spinone Italiano
Sussex Spaniel
Weimaraner
Gluten Enteropathy (Sensitivity) Irish Setter
Hepatitis Cairn Terrier
English Cocker Spaniel
English Springer Spaniel
Labrador Retriever
Histiocytic Ulcerative Colitis Boxer
French Bulldog
Immunoproliferative Enteropathy Basenji
Inflammatory Bowel Disease (IBD) Clumber Spaniel
German Shepherd Dog
Greyhound
Norwegian Lundehund
Portuguese Water Dog
Rottweiler
West Highland White Terrier
Irritable Bowel Syndrome Norwegian Elkhound
Megaesophagus Chinese Shar Pei
German Shepherd Dog
Golden Retriever
Great Dane
Irish Setter
Miniature Schnauzer
Wire Fox Terrier
Pancreatitis Airedale Terrier
Australian Terrier
Boxer
Cavalier King Charles Spaniel
Collie
Miniature Schnauzer
Standard Schnauzer
Protein Losing Enteropathy (PLE) Maltese
Norwegian Lundehund
Rottweiler
Soft Coated Wheaten Terrier
Yorkshire Terrier
612
Subject Condition Breed-Dog
Xanthogranulomatous Inflammation of the American Staffordshire Terrier
Small Bowel
Vacuolar Hepatopathy Scottish Terrier
Villous Atrophy Bouvier Des Flandres
Hematological Auto-Immune Hemolytic Anemia (AIHA/ Airedale Terrier
IMHA) Bichon Frisé
Cairn Terrier
Cocker Spaniel
Collie
English Springer Spaniel
Finnish Spitz
Labrador Retriever
Maltese
Miniature Pinscher
Miniature Schnauzer
Old English Sheepdog
Parson Russell Terrier
Saluki
Shetland Sheepdog
Vizsla
C3 Compliment Deficiency Brittany
Cyclic Neutropenia Collie
Dalmatian RBC Type Dalmatian
Factor I Deficiency Vizsla
Factor VII Deficiency Beagle
Scottish Deerhound
Factor XI Deficiency Kerry Blue Terrier
Glanzmann’s Thrombasthenia Great Pyrenees
Otterhound
Hemophagocytic Syndrome Tibetan Terrier
Hemophilia A (Factor VIII) German Shepherd Dog
Golden Retriever
Hemophilia B (Factor IX) Airedale Terrier
Black & Tan Coonhound
French Bulldog
German Wirehaired Pointer
Lhasa Apso
Rhodesian Ridgeback
Hypereosinophilia Rottweiler
Hyperkalemia, Benign Shiba Inu
Hyperphosphatasemia, Benign Scottish Terrier
Siberian Husky
Immune-Mediated Thrombocytopenia (ITP) Airedale Terrier
Old English Sheepdog
Leukemia Golden Retriever
Leukocyte Adhesion Deficiency (CLAD) Irish Red And White Setter
Irish Setter
Leukopenia, Physiologic Belgian Tervuren
Microcytosis, Benign Shiba Inu
Platelet ADP Deficiency Cocker Spaniel
613
Subject Condition Breed-Dog
Platelet Procoagulant Deficiency German Shepherd Dog
Stomatocytosis Miniature Schnauzer
Standard Schnauzer
Thrombocytopenia, Physiologic Cavalier King Charles Spaniel
Thrombopathy, Hereditary Basset Hound
Trapped Neutrophil Syndrome (TNS) Border Collie
von Willebrand’s Disease Airedale Terrier
Basset Hound
Bernese Mountain Dog
Chesapeake Bay Retriever
Collie
Doberman Pinscher
German Pinscher
German Shepherd Dog
German Shorthaired Pointer
German Wirehaired Pointer
Golden Retriever
Irish Red And White Setter
Kerry Blue Terrier
Manchester Terrier
Papillon
Pembroke Welsh Corgi
Pointer
Poodle
Scottish Terrier
Shetland Sheepdog
Toy Fox Terrier
Musculoskeletal Atlantoaxial Subluxation Japanese Chin
Atlanto-Occipital Subluxation Pekingese
Pomeranian
Calvarial Hyperostotic Syndrome Bullmastiff
Central Tarsal Bone Fracture Greyhound
Centro-Nuclear Myopathy Labrador Retriever
Cervical Vertebral Arthrosis Scottish Deerhound
Chondrodysplasia Norwegian Elkhound
Chondrodystrophy (Dwarfism) Beagle
Cranial Cruciate Ligament (ACL) Rupture Akita
Australian Terrier
Bernese Mountain Dog
Boxer
Chesapeake Bay Retriever
Chow Chow
Dogue De Bordeaux
German Shepherd Dog
Giant Schnauzer
Golden Retriever
Greyhound
Labrador Retriever
Leonberger
Mastiff
Neopolitan Mastiff
Newfoundland
Rottweiler
Saint Bernard
614
Subject Condition Breed-Dog
Craniomandibular Osteopathy (CMO) Cairn Terrier
Scottish Terrier
West Highland White Terrier
Disikospondylitis Airedale Terrier
Great Dane
Distal Tibial Valgus Deformity Shetland Sheepdog
Dwarfism, Hypochondroplastic Irish Setter
Elbow Dysplasia All Breeds
Eosinophilic Myositis Belgian Sheepdog
Episodic Myokymia Jack Russell Terrier
Exercise Induced Collapse (EIC) Boykin Spaniel
Chesapeake Bay Retriever
Curly Coated Retriever
Labrador Retriever
Gross Muscle Hypertrophy (Bully Whippets) Whippet
Hemivertebra Boston Terrier
French Bulldog
German Shorthaired Pointer
Pug
Hemivertebra, Kinked Tail Cairn Terrier
Scottish Terrier
Hip Dysplasia All Breeds
Humeral Condyle Dysplasia Cocker Spaniel
Hypertrophic Osteodystrophy (HOD) German Shepherd Dog
Golden Retriever
Great Dane
Irish Setter
Kuvasz
Labrador Retriever
Weimaraner
Incomplete Ossification Of The Humeral Brittany
Condyle
Inflammatory Myopathy Boxer
Newfoundland
Lateral Luxation Of The Superficial Digital Shetland Sheepdog
Flexor Tendon
Leg Fractures Italian Greyhound
Legg-Calve-Perthes Disease Affenpinscher
American Eskimo Dog
Australian Shepherd
Australian Terrier
Border Terrier
Cairn Terrier
Cavalier King Charles Spaniel
Chihuahua
Chinese Crested
Dachshund
Lakeland Terrier
Lhasa Apso
Löwchen
Maltese
615
Subject Condition Breed-Dog
Manchester Terrier
Miniature Pinscher
Miniature Schnauzer
Parson Russell Terrier
Pekingese
Poodle
Pug
Schipperke
Shih Tzu
Silky Terrier
Smooth Fox Terrier
Toy Fox Terrier
West Highland White Terrier
Wire Fox Terrier
Xoloitzcuinti
Yorkshire Terrier
Lumbosacral Transitional Vertebrae Great Pyrenees
Metacarpal Sesamoid Disease Rottweiler
Muscular Dystrophy Bouvier Des Flandres
Cavalier King Charles Spaniel
Irish Terrier
Myasthenia Gravis, Acquired Akita
Chihuahua
German Shepherd Dog
German Shorthaired Pointer
Golden Retriever
Newfoundland
Scottish Terrier
Myasthenia Gravis, Congenital Dachshund
English Springer Spaniel
Parson Russell Terrier
Smooth Fox Terrier
Myopathy, Inherited Great Dane
Myotonia Congenita Chow Chow
Miniature Schnauzer
Occipital Bone Hypoplasia (Chiari-Like Brussels Griffon
Malformation) Cavalier King Charles Spaniel
Osteoarthritis Bernese Mountain Dog
Bouvier Des Flandres
Great Pyrenees
Greyhound
Rottweiler
Vizsla
Osteochondritis Dessicans (OCD) Bernese Mountain Dog
Border Collie
Bouvier Des Flandres
Boxer
Bulldog
Chesapeake Bay Retriever
English Setter
German Shepherd Dog
German Shorthaired Pointer
German Wirehaired Pointer
Golden Retriever
Great Dane
616
Subject Condition Breed-Dog
Great Pyrenees
Irish Wolfhound
Kuvasz
Labrador Retriever
Leonberger
Mastiff
Newfoundland
Old English Sheepdog
Rottweiler
Saint Bernard
Tibetan Mastiff
Osteochondrodysplasia/Chondrodysplasia Alaskan Malamute
Great Pyrenees
Havanese
Osteogenesis Imperfecta Dachshund
Panosteitis Bernese Mountain Dog
German Shepherd Dog
Golden Retriever
Great Dane
Great Pyrenees
Leonberger
Mastiff
Rottweiler
Tibetan Mastiff
Patella Luxation All Breeds
Polyarthritis, Juvenile-Onset Akita
Polymyositis Vizsla
Sesamoid Disease Greyhound
Shoulder Instability Poodle
Skeletal Dysplasia Nova Scotia Duck Tolling Retriever
Spinal Muscle Atrophy Brittany
Spondylosis Deformans Boxer
Temporomandibular Joint (TMJ) Dysplasia Basset Hound
Cavalier King Charles Spaniel
Tibial Tuberosity Avulsion Staffordshire Bull Terrier
Neurological Axonal Dystrophy Ibizan Hound
Axonopathy Boxer
Canine Epileptoid Cramping Syndrome Border Terrier
(Spike’s Disease)
Canine Multiple System Degeneration Chinese Crested
(CMSD) Kerry Blue Terrier
Cerebellar Abiotrophy Airedale Terrier
American Staffordshire Terrier
Border Collie
Gordon Setter
Harrier
Old English Sheepdog
Scottish Terrier
Spinone Italiano
Cerebellar Ataxia, X-Linked Pointer
617
Subject Condition Breed-Dog
Cervical Spondylomyelopathy/Vertebral Bernese Mountain Dog
Instability (Wobbler Syndrome) Borzoi
Dalmatian
Doberman Pinscher
Great Dane
Mastiff
Rottweiler
Weimaraner
Congenital Hydrocephalus w/Cerebellar Bullmastiff
Ataxia
Coonhound Paralysis (Polyradicuoneuritis) Black and Tan Coonhound
Bluetick Coonhound
Redbone Coonhound
Deafness, Congenital American Eskimo Dog
American Foxhound
Australian Cattle Dog
Australian Shepherd
Australian Terrier
Beagle
Bedlington Terrier
Border Collie
Boston Terrier
Bull Terrier
Cavalier King Charles Spaniel
Chinese Crested
Cocker Spaniel
Dachshund
Dalmatian
Doberman Pinscher
English Cocker Spaniel
English Foxhound
English Setter
Great Pyrenees
Havanese
Ibizan Hound
Icelandic Sheepdog
Italian Greyhound
Kuvasz
Löwchen
Maltese
Manchester Terrier
Miniature Bull Terrier
Norwich Terrier
Nova Scotia Duck Tolling Retriever
Old English Sheepdog
Papillon
Parson Russell Terrier
Pointer
Puli
Sealyham Terrier
Smooth Fox Terrier
Tibetan Terrier
Toy Fox Terrier
Whippet
Deafness, Juvenile Rhodesian Ridgeback
618
Subject Condition Breed-Dog
Degenerative Myelopathy (DM) American Eskimo Dog
American Water Spaniel
Bernese Mountain Dog
Bloodhound
Borzoi
Boxer
Canaan Dog
Cardigan Welsh Corgi
Chesapeake Bay Retriever
Collie
French Bulldog
German Shepherd Dog
Irish Setter
Kerry Blue Terrier
Kuvasz
Old English Sheepdog
Pembroke Welsh Corgi
Poodle
Pug
Rhodesian Ridgeback
Distal Juvenile Myelopathy Rottweiler
Dysmyelinogenesis Welsh Springer Spaniel
Encephalopathy, Neonatal Gordon Setter
Poodle
Episodic Collapse Cavalier King Charles Spaniel
Hepatocerebellar Degeneration Bernese Mountain Dog
Hereditary Ataxia Parson Russell Terrier
Smooth Fox Terrier
Hereditary Quadriplegia And Ambylopia Irish Setter
Hereditary Sensory Neuropathy Pointer
Horner’s Syndrome, Idiopathic Collie
Golden Retriever
Hydrocephalus Chihuahua
Maltese
Pomeranian
Hypertrophic Neuropathy Tibetan Mastiff
Hypomyelination/Dysmyelination Bernese Mountain Dog
Chow Chow
English Springer Spaniel
Idiopathic Epilepsy/Inherited Seizures Airedale Terrier
American Eskimo Dog
American Water Spaniel
Australian Shepherd
Australian Terrier
Beagle
Bedlington Terrier
Belgian Sheepdog
Belgian Tervuren
Bernese Mountain Dog
Border Collie
Boxer
Brittany
Brussel’s Griffon
619
Subject Condition Breed-Dog
Canaan Dog
Cane Corso
Cavalier King Charles Spaniel
Chesapeake Bay Retriever
Chinook
Collie
Dalmatian
Dogue De Bordeaux
English Cocker Spaniel
English Springer Spaniel
Field Spaniel
Flat-Coated Retriever
Finnish Spitz
German Shepherd Dog
German Shorthaired Pointer
Giant Schnauzer
Golden Retriever
Great Pyrenees
Greyhound
Ibizan Hound
Irish Setter
Irish Water Spaniel
Irish Wolfhound
Italian Greyhound
Keeshond
Labrador Retriever
Mastiff
Miniature Pinscher
Norwegian Elkhound
Norwich Terrier
Nova Scotia Duck Tolling Retriever
Otterhound
Papillon
Petit Bassett Griffon Vendéen
Poodle
Portuguese Water Dog
Pyrenean Shepherd
Rottweiler
Saint Bernard
Schipperke
Scottish Terrier
Shetland Sheepdog
Siberian Husky
Silky Terrier
Spinone Italiano
Standard Schnauzer
Tibetan Mastiff
Tibetan Terrier
Vizsla
Welsh Terrier
Wirehaired Pointing Griffon
Intervertebral Disc Disease (IVDD) Basset Hound
Beagle
Cardigan Welsh Corgi
Cavalier King Charles Spaniel
Clumber Spaniel
Dachshund
French Bulldog
620
Subject Condition Breed-Dog
Greyhound
Lhasa Apso
Pekingese
Pembroke Welsh Corgi
Rottweiler
Shih Tzu
Tibetan Spaniel
Juvenile Polyarteritis (Pain Syndrome) Beagle
Petit Bassett Griffon Vendéen
Laryngeal Paralysis, Aquired Afghan Hound
Irish Setter
Labrador Retriever
Newfoundland
Laryngeal Paralysis, Congenital Bouvier Des Flandres
Staffordshire Bull Terrier
Leukodystrophy, Spinal Cord Bullmastiff
Leukoencephalomyelopathy Rottweiler
Lissencephaly Lhasa Apso
Lumbosacral Stenosis/Cauda Equina Belgian Malinois
Syndrome German Shepherd Dog
Greyhound
Meningoencephalitis Greyhound
Myoclonic Epilepsy Basset Hound
Beagle
Dachshund
Narcolepsy Dachshund
Doberman Pinscher
Labrador Retriever
Necrotizing Meningitis Bernese Mountain Dog
Necrotizing Meningoencephalitis Chihuahua
French Bulldog
Maltese
Pekingese
Pomeranian
Pug
Yorkshire Terrier
Necrotizing Myelopathy (Afghan Afghan Hound
Myelopathy)
Neuroaxonal Dystrophy Papillon
Parson Russell Terrier
Rottweiler
Peripheral Neuropathy Doberman Pinscher
Polioencephalomyopathy (Spongiform Australian Cattle Dog
Leukoencephalomyelopathy) Shetland Sheepdog
Polymicrogyria Poodle
Polyneuropathy Alaskan Malamute
Bouvier Des Flandres
Dalmatian
Great Pyrenees
Greyhound
Leonberger
Progressive Neuronopathy Cairn Terrier
621
Subject Condition Breed-Dog
Rosenthal Fiber Encephalopathy Bernese Mountain Dog
Scottie Cramp Scottish Terrier
Seizures, Fly Biting Partial Great Pyrenees
Sensorimotor Axonopathy Golden Retriever
Spina Bifida Bulldog
Spinal Dysraphism/ Myelodysplasia Weimaraner
Spinal Muscle Atrophy Pointer
Spinal Subarachnoid Cysts Rottweiler
Spinocerebellar Degeneration Brittany
Steroid Responsive Meningitis/Arteritis Nova Scotia Duck Tolling Retriever
Pembroke Welsh Corgi
Syringomyelia Brussel’s Griffon
Cavalier King Charles Spaniel
English Toy Spaniel
Vestibular Disease Tibetan Terrier
White Shaker Syndrome Maltese
West Highland White Terrier
Oncology/Cancer Adenocarcinoma, Nasal Collie
Bladder and Urethral Tumors Beagle
Choroid Plexus Brain Tumor Golden Retriever
Cutaneous Plasmocytoma Yorkshire Terrier
Gastric Carcinoma Belgian Sheepdog
Belgian Tervuren
Chow Chow
Collie
Norwegian Lundehund
Staffordshire Bull Terrier
Glial Tumors Boston Terrier
Hemangioma, Synovial Belgian Sheepdog
Hemangiosarcoma Airedale Terrier
German Shepherd Dog
Golden Retriever
Greyhound
Italian Greyhound
Portuguese Water Dog
Saluki
Vizsla
Whippet
Histiocytic Sarcoma Rottweiler
Histiocytoma, Cutaneous Dachshund
Histiocytosis, Malignant Bernese Mountain Dog
Flat-Coated Retriever
Golden Retriever
Labrador Retriever
Intracutaneous Cornifying Epithelioma Norwegian Elkhound
Iridociliary Epitheiial Tumors Labrador Retriever
Lingual Fibrosarcoma Golden Retriever
Liver Cancer Standard Schnauzer
622
Subject Condition Breed-Dog
Lymphosarcoma Airedale Terrier
Bernese Mountain Dog
Briard
Dogue De Bordeaux
Golden Retriever
Gordon Setter
Greyhound
Labrador Retriever
Old English Sheepdog
Portuguese Water Dog
Rottweiler
Vizsla
West Highland White Terrier
Mammary Cancer Borzoi
Brittany
English Setter
English Springer Spaniel
German Shorthaired Pointer
Mammary Gland Osteoma Poodle
Mast Cell Tumor Airedale Terrier
Australian Terrier
Bernese Mountain Dog
Boxer
Chinese Shar Pei
German Shorthaired Pointer
Golden Retriever
Maltese
Norwegian Elkhound
Pug
Rhodesian Ridgeback
Staffordshire Bull Terrier
Vizsla
Weimaraner
Melanoma Cocker Spaniel
Gordon Setter
Melanoma, Limbal Golden Retriever
Labrador Retriever
Melanoma, Lingual Chinese Shar Pei
Chow Chow
Meningioma Boxer
Golden Retriever
Multifocal Renal Cystadenocarcinoma And German Shepherd Dog
Nodular Dermatofibrosis
Oral Cancer Boxer
German Shorthaired Pointer
Golden Retriever
Osteosarcoma Airedale Terrier
Boxer
Golden Retriever
Great Dane
Great Pyrenees
Greyhound
Irish Setter
Irish Wolfhound
623
Subject Condition Breed-Dog
Leonberger
Mastiff
Newfoundland
Old English Sheepdog
Rottweiler
Saint Bernard
Scottish Deerhound
Plasma Cell Tumor Cocker Spaniel
Prostate Carcinoma Bouvier Des Flandres
Sertoli Cell Tumor Cairn Terrier
Pekingese
Soft Tissue Sarcoma Rhodesian Ridgeback
Squamous Cell Carcinoma, Digit Bouvier Des Flandres
Briard
Giant Schnauzer
Labrador Retriever
Poodle
Squamous Cell Carcinoma, Lingual Labrador Retriever
Poodle
Samoyed
Synovial Myxoma Doberman Pinscher
T Cell Lymphoma (Mycosis Fungoides) Boxer
Testicular Tumors Maltese
Thyroid Cancer Golden Retriever
Siberian Husky
Transitional Cell Carcinoma Airedale Terrier
Scottish Terrier
West Highland White Terrier
Uveal Spindle Cell Tumor Siberian Husky
Ophthalmological Blindness, Congenital Doberman Pinscher
Cataracts All Breeds
Chorioretinopathy Borzoi
Choroidal Hypoplasia Bearded Collie
Chronic Superficial Keratitis (Pannus) Australian Shepherd
Belgian Malinois
Belgian Sheepdog
Belgian Tervuren
Bloodhound
Bulldog
Chinese Shar Pei
Chow Chow
Dachshund
German Shepherd Dog
Greyhound
Irish Red And White Setter
Pekingese
Pug
Shih Tzu
Siberian Husky
Collie Eye Anomaly/Choroidal Hypoplasia/ Australian Shepherd
Coloboma (CEA/CH) Border Collie
Collie
624
Subject Condition Breed-Dog
Nova Scotia Duck Tolling Retriever
Pyrenean Shepherd
Shetland Sheepdog
Cone Degeneration Alaskan Malamute
Australian Shepherd
German Shorthaired Pointer
Corneal Dystrophy Affenpinscher
Afghan Hound
Airedale Terrier
Alaskan Malamute
Basenji
Beagle
Bearded Collie
Bedlington Terrier
Bichon Frisé
Boston Terrier
Boykin Spaniel
Briard
Brussel’s Griffon
Cavalier King Charles Spaniel
Chow Chow
Collie
Dachshund
Dalmatian
Dandie Dinmont Terrier
Dogue De Bordeaux
English Toy Spaniel
German Pinscher
German Shepherd Dog
Great Pyrenees
Irish Wolfhound
Kuvasz
Labrador Retriever
Lhasa Apso
Mastiff
Miniature Bull Terrier
Miniature Pinscher
Norwich Terrier
Nova Scotia Duck Tolling Retriever
Pointer
Polish Lowland Sheepdog
Puli
Rottweiler
Saint Bernard
Samoyed
Scottish Terrier
Shetland Sheepdog
Shih Tzu
Siberian Husky
Standard Schnauzer
Tibetan Terrier
Weimaraner
Vizsla
Weimaraner
We lsh Springer Spaniel
Welsh Terrier
Wirehaired Pointing Griffon
Yorkshire Terrier
625
Subject Condition Breed-Dog
Corneal Epithelial Defects, Spontaneous Keeshond
Corneal Ulcer Boxer
Golden Retriever
Distichiasis Airedale Terrier
Alaskan Malamute
American Staffordshire Terrier
American Water Spaniel
Australian Shepherd
Australian Terrier
Basset Hound
Beagle
Bedlington Terrier
Bichon Frisé
Black and Tan Coonhound
Boston Terrier
Boxer
Boykin Spaniel
Brittany
Brussel’s Griffon
Bulldog
Bullmastiff
Canaan Dog
Cavalier King Charles Spaniel
Chesapeake Bay Retriever
Clumber Spaniel
Cocker Spaniel
Collie
Curly Coated Retriever
Dachshund
Dalmatian
Dandie Dinmont Terrier
Doberman Pinscher
Dogue De Bordeaux
English Cocker Spaniel
English Setter
English Toy Spaniel
Field Spaniel
Flat-Coated Retriever
French Bulldog
German Shorthaired Pointer
Glen Of Imaal Terrier
Golden Retriever
Great Dane
Great Pyrenees
Havanese
Icelandic Sheepdog
Irish Red And White Setter
Irish Setter
Irish Water Spaniel
Irish Wolfhound
Japanese Chin
Keeshond
Kerry Blue Terrier
Kuvasz
Labrador Retriever
Leonberger
Lhasa Apso
626
Subject Condition Breed-Dog
Löwchen
Maltese
Miniature Schnauzer
Neopolitan Mastiff
Norwegian Elkhound
Nova Scotia Duck Tolling Retriever
Old English Sheepdog
Papillon
Parson Russell Terrier
Pekingese
Pembroke Welsh Corgi
Pharaoh Hound
Poodle
Portuguese Water Dog
Pug
Saint Bernard
Samoyed
Schipperke
Scottish Terrier
Sealyham Terrier
Shetland Sheepdog
Shiba Inu
Shih Tzu
Soft Coated Wheaten Terrier
Swedish Vallhund
Staffordshire Bull Terrier
Standard Schnauzer
Sussex Spaniel
Tibetan Spaniel
Tibetan Terrier
Vizsla
Weimaraner
Welsh Springer Spaniel
Welsh Terrier
Yorkshire Terrier
Early Retinal Degeneration (Erd) Norwegian Elkhound
Ectopic Cilia Shih Tzu
Ectropion Basset Hound
Black and Tan Coonhound
Bloodhound
Boxer
Bulldog
Cane Corso
Chesapeake Bay Retriever
Chinese Shar Pei
Chow Chow
Clumber Spaniel
Cocker Spaniel
Dogue De Bordeaux
Gordon Setter
Great Dane
Leonberger
Mastiff
Neopolitan Mastiff
Newfoundland
Saint Bernard
Spinone Italiano
Sussex Spaniel
627
Subject Condition Breed-Dog
Entropion Akita
Bedlington Terrier
Bernese Mountain Dog
Black and Tan Coonhound
Bloodhound
Bulldog
Bullmastiff
Cane Corso
Chesapeake Bay Retriever
Chinese Shar Pei
Chow Chow
Clumber Spaniel
English Toy Spaniel
French Bulldog
German Shorthaired Pointer
Great Dane
Great Pyrenees
Icelandic Sheepdog
Irish Setter
Irish Water Spaniel
Japanese Chin
Komondor
Labrador Retriever
Leonberger
Lhasa Apso
Mastiff
Neopolitan Mastiff
Newfoundland
Pekingese
Pug
Rottweiler
Saint Bernard
Shih Tzu
Spinone Italiano
Tibetan Spaniel
Welsh Springer Spaniel
Wirehaired Pointing Griffon
Epiphora Poodle
Episcleritis Cocker Spaniel
Everted Cartilage of Third Eyelid Giant Schnauzer
Great Dane
Irish Wolfhound
Leonberger
Newfoundland
Weimaraner
Exposure Keratopathy Chow Chow
Lhasa Apso
Shih Tzu
Eyelid Cysts Newfoundland
Glaucoma, Primary Akita
Alaskan Malamute
Australian Cattle Dog
Basset Hound
Beagle
Bichon Frisé
Boston Terrier
628
Subject Condition Breed-Dog
Bouvier Des Flandres
Cairn Terrier
Chinese Shar Pei
Chow Chow
Cocker Spaniel
Dalmatian
Dandie Dinmont Terrier
English Cocker Spaniel
Entlebucher Mountain Dog
Flat-Coated Retriever
Golden Retriever
Great Dane
Lakeland Terrier
Lhasa Apso
Newfoundland
Norwegian Elkhound
Norwich Terrier
Parson Russell Terrier
Pekingese
Poodle
Samoyed
Shiba Inu
Shih Tzu
Siberian Husky
Vizsla
Welsh Springer Spaniel
Welsh Terrier
Wire Fox Terrier
Glaucoma, Secondary Australian Cattle Dog
Border Collie
Bull Terrier
Chinese Crested
English Springer Spaniel
Golden Retriever
Great Dane
Labrador Retriever
Newfoundland
Norfolk Terrier
Parson Russell Terrier
Poodle
Rhodesian Ridgeback
Smooth Fox Terrier
Goniodysplasia Bouvier Des Flandres
Vizsla
Iris Coloboma Dachshund
Dalmatian
Sussex Spaniel
Iris Cysts Golden Retriever
Great Dane
Irish Red And White Setter
Irish Wolfhound
Newfoundland
Iris Sphincter Dysplasia Dalmatian
Keratoconjunctivitis Sicca (KCS) Australian Terrier
Bedlington Terrier
Bulldog
629
Subject Condition Breed-Dog
Cavalier King Charles Spaniel
Cocker Spaniel
English Cocker Spaniel
Kerry Blue Terrier
Lhasa Apso
Pekingese
Portuguese Water Dog
Shih Tzu
West Highland White Terrier
Yorkshire Terrier
Lacrimal Gland Hypersecretion Bichon Frisé
Lens Luxation Australian Cattle Dog
Bearded Collie
Brittany
Chinese Crested
Chinese Shar Pei
Greyhound
Italian Greyhound
Japanese Chin
Lakeland Terrier
Miniature Bull Terrier
Parson Russell Terrier
Petit Bassett Griffon Vendéen
Pyrenean Shepherd
Sealyham Terrier
Tibetan Terrier
Toy Fox Terrier
Welsh Terrier
Whippet
Wire Fox Terrier
Macroblepharon Great Dane
Mastiff
Pug
Shih Tzu
Microphthalmia Australian Shepherd
Beagle
Cavalier King Charles Spaniel
Collie
Dachshund
Doberman Pinscher
Old English Sheepdog
Nystagmus Belgian Sheepdog
Optic Nerve Coloboma Basenji
Brussel’s Griffon
Norfolk Terrier
Optic Nerve Hypoplasia Bullmastiff
Dachshund
German Pinscher
Irish Wolfhound
Miniature Pinscher
Norfolk Terrier
Poodle
Shih Tzu
630
Subject Condition Breed-Dog
Pectinate Ligament Dysplasia English Springer Spaniel
Flat-Coated Retriever
Persistent Hyaloid Artery Australian Shepherd
Basset Hound
Boykin Spaniel
Brussel’s Griffon
Cairn Terrier
Dachshund
English Toy Spaniel
Irish Setter
Japanese Chin
Soft Coated Wheaten Terrier
Sussex Spaniel
Persistent Hyperplastic Primary Vitreous Bouvier Des Flandres
Staffordshire Bull Terrier
Persistent Hyperplastic Tunica Vasculosa Doberman Pinscher
Lentis German Pinscher
German Shorthaired Pointer
Japanese Chin
Persistent Pupillary Membranes (PPM) All Breeds
Photoreceptor Dysplasia, Type-A PRA Miniature Schnauzer
(Partially Dominant)
Pigmentary Keratitis Japanese Chin
Progressive Retinal Atrophy (PRA), Central Polish Lowland Sheepdog
Progressive Retinal Atrophy (PRA), Bullmastiff
Dominant Mastiff
Progressive Retinal Atrophy (PRA), Recessive Airedale Terrier
American Eskimo Dog
Australian Cattle Dog
Australian Shepherd
Basenji
Belgian Sheepdog
Belgian Tervuren
Bernese Mountain Dog
Border Collie
Borzoi
Boykin Spaniel
Briard
Brussel’s Griffon
Cardigan Welsh Corgi
Chesapeake Bay Retriever
Chinese Crested
Cocker Spaniel
Collie
Dachshund
English Cocker Spaniel
English Springer Spaniel
Entlebucher Mountain Dog
Glen Of Imaal Terrier
Golden Retriever
Gordon Setter
Harrier
Irish Red And White Setter
Irish Setter
631
Subject Condition Breed-Dog
Irish Terrier
Irish Wolfhound
Italian Greyhound
Kuvasz
Labrador Retriever
Lhasa Apso
Löwchen
Miniature Pinscher
Norfolk Terrier
Papillon
Pekingese
Pomeranian
Poodle
Portuguese Water Dog
Pyrenean Shepherd
Rottweiler
Schipperke
Shih Tzu
Standard Schnauzer
Tibetan Mastiff
Tibetan Spaniel
Tibetan Terrier
West Highland White Terrier
Yorkshire Terrier
Progressive Retinal Atrophy (PRA), Unknown Canaan Dog
Greyhound
Silky Terrier
Progressive Retinal Atrophy (PRA), X-Linked Samoyed
Siberian Husky
Prolapsed Gland Of The Nictitans (Cherry Beagle
Eye) Bloodhound
Bulldog
Cane Corso
Cocker Spaniel
Lhasa Apso
Neopolitan Mastiff
Shih Tzu
Tibetan Spaniel
Proliferative Keratoconjunctivitis Collie
Punctate Keratitis Dachshund
Retinal Degeneration, Unknown Inheritance Belgian Malinois
Black Russian Terrier
Black and Tan Coonhound
Briard
Retinal Dysplasia Akita
Affenpinscher
Airedale Terrier
Alaskan Malamute
American Staffordshire Terrier
American Water Spaniel
Australian Shepherd
Basset Hound
Beagle
Bearded Collie
Bedlington Terrier
Belgian Sheepdog
Belgian Tervuren
632
Subject Condition Breed-Dog
Black & Tan Coonhound
Bloodhound
Border Collie
Boykin Spaniel
Briard
Bull Terrier
Bulldog
Bullmastiff
Cane Corso
Cardigan Welsh Corgi
Cavalier King Charles Spaniel
Chinese Shar Pei
Chinook
Clumber Spaniel
Cocker Spaniel
Collie
Doberman Pinscher
Dogue De Bordeaux
English Cocker Spaniel
English Springer Spaniel
English Toy Spaniel
Field Spaniel
French Bulldog
German Shepherd Dog
German Shorthaired Pointer
Giant Schnauzer
Golden Retriever
Gordon Setter
Great Pyrenees
Ibizan Hound
Icelandic Sheepdog
Irish Red And White Setter
Irish Wolfhound
Labrador Retriever
Lhasa Apso
Maltese
Mastiff
Miniature Schnauzer
Miniature Schnauzer
Newfoundland
Norfolk Terrier
Old English Sheepdog
Pembroke Welsh Corgi
Petit Bassett Griffon Vendéen
Pharaoh Hound
Pointer
Puli
Rottweiler
Samoyed
Schipperke
Scottish Terrier
Sealyham Terrier
Silky Terrier
Swedish Vallhund
Standard Schnauzer
Sussex Spaniel
Welsh Springer Spaniel
West Highland White Terrier
Yorkshire Terrier
633
Subject Condition Breed-Dog
Rod Dysplasia Norwegian Elkhound
Sudden Acute Retinal Degeneration (SARDS) Dachshund
Miniature Schnauzer
Tapetal Degeneration Beagle
Uveal Cysts Labrador Retriever
Uveitis Golden Retriever
Uveitis, Cataract Resorption Induced Boston Terrier
Vitreous Degeneration Brussel’s Griffon
Bull Terrier
Chihuahua
Chinese Crested
Curly Coated Retriever
Greyhound
Havanese
Italian Greyhound
Kerry Blue Terrier
Löwchen
Miniature Bull Terrier
Miniature Pinscher
Papillon
Pomeranian
Poodle
Saluki
Schipperke
Scottish Terrier
Sealyham Terrier
Shih Tzu
Silky Terrier
Smooth Fox Terrier
Swedish Vallhund
Whippet
Oronasal Ankyloglossia, Ventral Anatolian Shepherd
Brachygnathism Chihuahua
Norwich Terrier
Cleft Palate Bernese Mountain Dog
Boston Terrier
Boxer
Brussel’s Griffon
Chihuahua
Portuguese Water Dog
Dental Problems Italian Greyhound
Gingival Hypertrophy Boxer
Hypodontia Chinese Crested
Kerry Blue Terrier
Inverted Canines Bull Terrier
Staffordshire Bull Terrier
Malocclusion German Shorthaired Pointer
Missing Teeth Airedale Terrier
Bedlington Terrier
Cairn Terrier
Chinese Crested
Kerry Blue Terrier
Manchester Terrier
634
Subject Condition Breed-Dog
Norwich Terrier
Soft Coated Wheaten Terrier
Swedish Vallhund
Tibetan Terrier
Xoloitzcuinti
Periodontal Disease Beagle
Poodle
Prognathism Chihuahua
Norwich Terrier
Retained Deciduous Teeth Tibetan Spaniel
Rostrally Displaced Mxillary Canine Teeth Shetland Sheepdog
Supernumerary Teeth Greyhound
Undershot Bedlington Terrier
Cairn Terrier
Portuguese Water Dog
Soft Coated Wheaten Terrier
Respiratory Brachycephalic Complex Boston Terrier
Bulldog
Cavalier King Charles Spaniel
French Bulldog
Lhasa Apso
Norwich Terrier
Pekingese
Pug
Shih Tzu
Staffordshire Bull Terrier
Tibetan Spaniel
Bronchiectasis Cocker Spaniel
English Springer Spaniel
Poodle
Rottweiler
Siberian Husky
Chronic Interstitial Lung Disease Staffordshire Bull Terrier
West Highland White Terrier
Chylothorax Afghan Hound
Ciliary Dyskinesia Bichon Frisé
English Springer Spaniel
Old English Sheepdog
Collapsing Trachea Chihuahua
Norwich Terrier
Pomeranian
Poodle
Schipperke
Silky Terrier
Yorkshire Terrier
Lung Lobe Torsion Afghan Hound
Pug
Pneumothorax, Spontaneous Siberian Husky
Pyothorax English Springer Spaniel
Rhinitis/Bronchopneumonia Irish Wolfhound
Systemic and Deformities Anasarca Bulldog
Clumber Spaniel
635
Subject Condition Breed-Dog
Atresia Ani Boston Terrier
Chow Chow
Finnish Spitz
German Shorthaired Pointer
Maltese
Poodle
Hiatal Hernia Bulldog
Chinese Shar Pei
French Bulldog
Hydrops Fetalis Pug
Imperforate Nasal Puncta Bedlington Terrier
Inguinal Hernia Cairn Terrier
Tibetan Spaniel
Leishmaniasis American Foxhound
Molera (Open Fontanel) Chihuahua
Musladin-Leuke Syndrome Beagle
Nasopharyngeal Dysgenesis Dachshund
Perineal Hernia Boston Terrier
Bouvier Des Flandres
Cardigan Welsh Corgi
Collie
German Shepherd Dog
Old English Sheepdog
Pekingese
Pembroke Welsh Corgi
Poodle
Recurrent Limb Edema Great Dane
Recurrent Fever of Unknown Origin (Shar Chinese Shar Pei
Pei Fever)
Splenic Torsion Great Dane
Umbilical Hernia Airedale Terrier
Bernese Mountain Dog
Bichon Frisé
Cairn Terrier
Cavalier King Charles Spaniel
Chesapeake Bay Retriever
Chihuahua
Cocker Spaniel
German Shorthaired Pointer
Great Pyrenees
Irish Setter
Leonberger
Manchester Terrier
Nova Scotia Duck Tolling Retriever
Portuguese Water Dog
Rottweiler
Shih Tzu
Tibetan Spaniel
Tibetan Terrier
Vizsla
Wirehaired Pointing Griffon
Urogenital Bladder Stones, Calcium Oxalate Cairn Terrier
Dandie Dinmont Terrier
Poodle
Standard Schnauzer
636
Subject Condition Breed-Dog
Bladder Stones, Not Categorized Australian Terrier
Bichon Frisé
Brussel’s Griffon
Keeshond
Pekingese
Portuguese Water Dog
Pug
Shih Tzu
West Highland White Terrier
Yorkshire Terrier
Bladder Stones, Silica Old English Sheepdog
Bladder Stones, Urate Black Russian Terrier
Bulldog
Dalmatian
Bladder Stones, Xanthine Cavalier King Charles Spaniel
Dachshund
Cryptorchidism/Retained Testicles Airedale Terrier
Australian Shepherd
Australian Terrier
Beagle
Bedlington Terrier
Belgian Tervuren
Bichon Frisé
Boxer
Brussel’s Griffon
Cairn Terrier
Canaan Dog
Chihuahua
Chinook
Clumber Spaniel
French Bulldog
German Shorthaired Pointer
Icelandic Sheepdog
Italian Greyhound
Manchester Terrier
Nova Scotia Duck Tolling Retriever
Old English Sheepdog
Papillon
Poodle
Portuguese Water Dog
Rottweiler
Siberian Husky
Silky Terrier
Swedish Vallhund
Tibetan Spaniel
Toy Fox Terrier
Vizsla
Wirehaired Pointing Griffon
Whippet
Xoloitzcuinti
Yorkshire Terrier
Cystinuria and Cystine Bladder Stones Australian Cattle Dog
Australian Shepherd
Basenji
Basset Hound
Cardigan Welsh Corgi
637
Subject Condition Breed-Dog
Dachshund
Irish Terrier
Labrador Retriever
Mastiff
Miniature Pinscher
Newfoundland
Pembroke Welsh Corgi
Scottish Deerhound
Silky Terrier
Smooth Fox Terrier
Staffordshire Bull Terrier
Tibetan Spaniel
Wire Fox Terrier
Dystocia Boston Terrier
Boxer
Chihuahua
Scottish Terrier
Ectopic Ureters Entlebucher Mountain Dog
Siberian Husky
Skye Terrier
Soft-Coated Wheaten Terrier
Fanconi Syndrome Basenji
Glomerulonephritis Greyhound
Gomerulonephropathy Bullmastiff
Hereditary Nephritis Bull Terrier
English Cocker Spaniel
Samoyed
Hermaphrodism German Shorthaired Pointer
Hypospadias Boston Terrier
Juvenile Nephropathy Boxer
Juvenile Renal Disease Chow Chow
Doberman Pinscher
Miniature Schnauzer
Norwegian Elkhound
Poodle
Rottweiler
Kidney Disease, Not Catergorized American Eskimo Dog
Shetland Sheepdog
Polycystic Kidney Disease Bull Terrier
Prostate Disease Doberman Pinscher
Protein Losing Nephropathy Soft Coated Wheaten Terrier
Renal Amyloidosis Beagle
Chinese Shar Pei
English Foxhound
Renal Arteriosclerosis Greyhound
Renal Dysplasia Lhasa Apso
Shih Tzu
Skye Terrier
Soft Coated Wheaten Terrier
Tibetan Terrier
West Highland White Terrier
638
Subject Condition Breed-Dog
Renal Dysplasia, Juvenile Bernese Mountain Dog
Golden Retriever
Gordon Setter
Urinary Incontinence, Hormonal Doberman Pinscher
Giant Schnauzer
Great Pyrenees
Irish Setter
Weimaraner
XX Sex Reversal Cocker Spaniel
German Shorthaired Pointer
Norwegian Elkhound
Soft-Coated Wheaten Terrier
Weimaraner
639
Appendix C: Part II
Quick Reference to Conditions by Breed Breed Specific Conditions in Cats
Subject Condition Breed-Cat
Behavior Wool Sucking Burmese
Siamese
Separation Anxiety Syndrome Persian
Siamese
B Blood type/NI/Transfusion reactions Abyssinian
Bengal
Birman
British SH
Cornish Rex
Devon Rex
Exotic/Exotic SH
Highland Fold
Himalayan
Japanese Bobtail
Norwegian Forest Cat
Persian
Ragdoll
Scottish Fold
Somali
Sphynx
Turkish Angora
Turkish Van
Cardiac/Vascular Dilated Cardiomyopathy Abyssinian
Burmese
Siamese
Congenital Portosystemic Vascular Shunts Himalayan
Persian
Hypertrophic Cardiomyopathy American SH
British SH
Cornish Rex
Devon Rex
Maine Coon
Persian
Ragdoll
PDA Persian
Endocardial Fibroelastosis Burmese
Siamese
Persistent Atrial Standstill Burmese
Siamese
Arterial Thromboembolism Abyssinian
Birman
Ragdoll
Dental/Oral/Nasal Cavity Cervical neck lesions Abyssinian
Persian
Siamese
Brachycephalic Syndrome (stenotic nares, Exotic/Exotic SH
long palate, exophthalmos, asymmetric jaw, Persian
tooth crowding, breathing problems etc)
640
Subject Condition Breed-Cat
Ears and Hearing Curl ear Floppy Pinna American Curl
Havana Brown
Siamese
Hereditary deafness (associated with White American Shorthair
haircoat gene) British Shorthair
Cornish Rex
Devon Rex
Exotic/Exotic SH
Highland Fold
Maine Coon
Manx
Oriental
Persian
Scottish Fold
Turkish Angora
Endocrine/Metabolic Systemic AA amyloidosis (renal form) Abyssinian
Includes Storage diseases Somali
Systemic AA Amyloidosis (hepatic form) Devon Rex
Siamese
Mucopolysaccharidosis VI Balinese
Siamese
Alpha Mannosidosis Persian
GM1-Gangliosidosis Korat
Siamese
GM2-Gangliosidosis Burmese
Korat
Hypokalemic Polymyopathy Burmese
Diabetes Mellitus (Type II) Burmese (Australian lines)
Congenital Hypothyroidism Abyssinian
Glycogenosis Type IV Norwegian Forest Cat
Glycogenosis Type IV Mimicking Disorder Maine Coon
Primary Hypoadrenocorticism British Shorthair
Primary Hypoparathyroidism Himalayan
Pyruvate kinase deficiency/erythrocyte Abyssinian
Fragility Bengal
Somali
Transient hyperlipidemia and anemia Burmese
Oriental
Hyperchylomicronemia Himalayan
Sphingomyelin lipidosis Balinese
(Sphingomyelinosis)-Neimann-Pick Siamese
Ornithine Transcarbamylase deficiency American Shorthair
Chediak-Higashi Syndrome Persian
Hyperlipoproteinemia/Hyperlipidemia Persian
Ceroid Lipofuscinosis Siamese
Copper Storage Disease Siamese
Gastrointestinal Hematology and Immune Inherited defect of Neutrophil Granulation Birman
Hemophilia B (Factor IX) Christmas Disease British Shorthair
Siamese
641
Subject Condition Breed-Cat
FIP Susceptibility Birman
Burmese
Persian
Multiple Vitamin-K dependent blood Devon Rex
coagulation factor deficiency
Congenital hypotrichosis and thymic aplasia Birman
Hemophilia Havana Brown
Von Willebrand’s Disease (FVIII) Himalayan
Transient hyperlipidemia and anemia Burmese
Oriental
Hyperlipoproteinemia/Hyperlipidemia Persian
Inherited Hyperchylomicronemia Siamese
Integument and Haircoat Ulcerative nasal dermatitis Bengal
Congenital hypotrichosis and thymic aplasia Birman
Hypotrichosis Cornish Rex
Devon Rex
Papular Eosinophilic/Mastocytic Devon Rex
dermatitis=Urticaria Pigmentosa Sphynx
Primary Hereditary Seborrhea Oleosa Himalayan
Persian
Dermatosparaxis (cutaneous asthenia, Himalayan
dermal fragility)
Hepatocutaneous syndrome (superficial Maine Coon
necrolytic dermatitis)
Dystrophic epidermolysis Bullosa Persian
Idiopathic Facial dermatitis Persian
Himalayan/Siamese Pointing Gene Siamese
[Imperfect (temperature sensitive)
oculocutaneous albinism]
Cutaneous Mastocytoma Siamese
Vitiligo Siamese
Alopecia Universalis Sphynx
Liver and Pancreas Pancreatitis Siamese
Hepatocutaneous syndrome Maine Coon
Musculoskeletal Hip Dysplasia Himalayan
Persian
Hereditary Myopathy (Spasticity) Devon Rex
Sphynx
Hypokalemic Polymyopathy Burmese
Osteochondrodysplasia Highland Fold
Scottish Fold
Luxating Patella Abyssinian (medial)
Burmese (medial)
Cornish Rex
Siamese (medial)
Tonkinese (medial)
Synovial Osteochondromatosis Burmese
Hip Dysplasia +/- Luxating Patella Devon Rex
Maine Coon
642
Subject Condition Breed-Cat
Fibrodysplasia Ossificans Himalayan
Muscular Dystrophy (laminin alpha 2) Maine Coon
Siamese
Chondrodysplasia Munchkin
Early Onset Osteodystrophy Scottish Fold
Slipped Capital Femoral Epiphysis Siamese
Nervous Peripheral and central distal axonopathy Birman
Hypomyelination/Dysmyelination Egyptian Mau
Siamese
Congenital hydrocephalus Siamese
Neuroaxonal Dystrophy Siamese
Congenital Myasthenia Gravis Siamese
Motor Neuron Disease/Spinal Muscle Maine Coon
Atrophy
Acquired Myasthenia Gravis Somali
Oncology Thymoma associated neuromuscular Abyssinian
disorder (incl. MG) Somali
Mediastinal LSA Oriental
Siamese
Intestinal Adenocarcinoma Siamese
Ophthalmic Recessive PRA Abyssinian
Ocicat
Persian
Siamese
Somali
Cataracts (Congenital or Juvenile) Birman
British SH
Himalayan
Persian
Epibulbar dermoids Birman
Burmese
Dominant PRA Abyssinian
Somali
Eyelid agenesis Birman
Burmese
Persian
Corneal Sequestration Birman
Burmese
Colorpoint SH
Himalayan
Persian
Siamese
Primary Glaucoma (narrow angle) Burmese
Non-healing corneal ulceration Himalayan
Persian
Transient Aqueous Humor opacity Burmese
Eyelid Cysts (hidrocystomas) Himalayan
Persian
Corneal Dystrophy Manx
Entropion Persian
643
Subject Condition Breed-Cat
Nystagmus Siamese
Convergent Strabismus Siamese
Himalayan/Siamese Pointing Gene Siamese
[Imperfect (temperature sensitive)
oculocutaneous albinism]
Glaucoma (open angle) Siamese
Retinal Degeneration Somali
Respiratory Bronchial Asthma (feline lower airway Himalayan
disease=FLAD) Siamese
Systemic and Deformities Tail mutations American Bobtail
(include tail mutants) Japanese Bobtail
Flat-chested kittens Bengal
Burmese
Maine Coon
Munchkin
Sacrocaudal Dysgenesis/Taillessness Manx
Mid-facial (Craniofacial) deformity +/-nasal American Shorthair
dermoids +/-Nares agenesis Bombay
Burmese
Twisty cat Munchkin
Urogenital Polycystic Kidney Disease American Shorthair
British Shorthair
Exotic/Exotic SH
Highland Fold
Himalayan
Persian
Scottish Fold
Predisposition to renal failure Abyssinian
Burmese
Maine Coon
Russian Blue
Siamese
Kitten and Juvenile Azotemia Birman
CaOx urolithiasis British Shorthair
Burmese
Exotic/Exotic SH
Havana Brown
Highland Fold
Himalayan
Persian
Ragdoll
Scottish Fold
Siamese
Predisposition to UTI Abyssinian
MAP urolithiasis predisposition Chartreux
Oriental
Cystine Urolithiasis Siamese
Cryptorchidism Persian
Dystocia predisposition Cornish Rex
Devon Rex
Exotic/Exotic SH
Persian
Siamese
644
Appendix D
Cat Fancy Registries and Kennel Clubs
Kennel Clubs Cat Fancy Associations
A kennel club is the repository for breeding records, generates The term cat fancy refers to the promotion, breeding and showing
registration certificates, organizes dog shows, and awards. The of cats whether as hobby or job. Cat breed associations were formed
clubs set judging standards, and whether it’s a job or a hobby, their to protect and promote purebred cats. They maintain breeding
mission is to help the owners, breeders and handlers protect and records and provide pedigrees and registration certificates, cat show
promote the breeds. coordination and standards, and awards for championships. A cat’s
registration can be moved to an association in another country, but
American Kennel Club (AKC) championships do not transfer with the cat into the new registry.
260 Madison Ave
New York, NY 10016 Cat Fanciers’ Association (CFA)
212.696.8200 1805 Atlantic Ave, PO Box 1005
http://www.akc.org/ Manasquan, NJ 08736-0805
732.528.9797
United Kennel Club (UKC) http://www.cfainc.org
100 E Kilgore Rd
Kalamazoo, MI 49002-5584 The International Cat Association (TICA)
269.343.9020 Fax: 269.343.7037 PO Box 2684
http://www.ukcdogs.com Harlingen, TX 78551
956.428.8046 Fax: 956.428.8047
National Kennel Club (NKC) http://www.tica.org
255 Indian Ridge Rd, PO Box 331
Blaine, TN 37709 Cat Fanciers’ Federation (CFF)
865.932.9680 Fax: 865.932.2572 PO Box 661
http://www.nationalkennelclub.com/ Gratis, OH 45330
937.787.9009 Fax : 937.787.4290
Kennel Club of Great Britain (KCGB) http://www.cffinc.org
1 Clarges Street
London UK W1J 8AB American Cat Fanciers’ Association (ACFA)
Tel: 0870.606.6750 Fax: 020.7518.1058 Box 1949
http://www.the-kennel-club.org.uk/ Nixa, MO 65714
417.725.1530 Fax: 417.725.1533
Canadian Kennel Club (CKC) www.acfacat.com
89 Skyway Avenue, Suite 100
Etobicoke, Ontario Canada M9W 6R4 American Association of Cat Enthusiasts (AACE)
416.675.5511 Fax: 416.675.6506 Box 213
http://www.ckc.ca/ Pine Brook, NJ 07058
973.335.6717 Fax: 973.334.5834
Australian National Kennel Council (ANKC) www.aaceinc.org
http://www.ankc.org.au/
Contact the relevant State or Territory Controlling Body listed on American Cat Association (ACA)
the website. 8101 Katherine Ave
Panorama City, CA 91402
New Zealand Kennel Club (NZKC) National Cat Fanciers’ Association (NCFA)
Prosser Street, Private Bag 50903, Porirua 6220 10215 Mt. Morris
Tel: (04) 237.4489 Fax: (04) 237.0721 Flushing MI 48433
http://www.nzkc.org.nz/
Fédération International Féline (FIFé)
c/o The General Secretary
Little Dene, Lenham Heath
Maidstone, Kent ME17 2BS UK
Tel: +44 (0)1622 850913
Fax: +44 (0)1622 850908
http://www.fifeweb.org
645
Canadian Cat Association/Association Féline Canadienne
(CCA, AFC)
289 Rutherford Road S Suite 18
Brampton, ON Canada L6W 3R9
905.459.1481 Fax: 905.459.4023
www.cca-afc.com
*(in the US)
CANADIAN CAT ASSOCIATION (CCA)
83 Kennedy Rd Unit 1806
Lookout, MO 65726
646
Appendix E
Other Resources
Cornell Feline Health Center American Society for the Prevention of Cruelty to Animals
New York State College of Veterinary Medicine (ASPCA)
Cornell University 424 92nd St
Ithaca, NY 14853 New York, NY 10128
Dr. Louis J Camuti Memorial Feline Consultation 212.876.7700
and Diagnostic Service http://www.aspca.org
800.548.8937
http://www.vet.cornell.edu/fhc/ ASPCA Animal Poison Control Center
888.426.4435
The Robert H. Winn Feline Foundation http://www.aspca.org/pet-care/poison-control/
1805 Atlantic Ave Box 1005
Manasquan NJ 08736 Humane Society of the United States
732.528.9797 2100 L St NW
http://www.winnfelinehealth.org Washington, DC 20037
202.452.1100
American Veterinary Medical Association (AVMA) http://www.hsus.org
1931 N Meacham Rd. Suite 100
Schaumburg, IL 60173 The Delta Society
800.248.2862 580 Naches Ave SW Suite 101
http://www.avma.org Renton, WA 98055
425.226.7357
http://www.deltasociety.org/
American Association of Feline Practitioners (AAFP)
390 Amwell Road Canadian Veterinary Medical Association
Suite 403 339 Booth Street
Hillsborough, NJ 08844 Ottawa ON K1R 7K1
phone: 800-874-0498 Email: admin@cvma-acmv.org
phone: 908-359-9351 http://canadianveterinarians.net/
fax: 908-292-1188
http://www.catvets.com Feline Advisory Bureau
Taeselbury
American Animal Hospital Association (AAHA) High Street
12575 W Bayaud Ave Tibbury, Wiltshire SP3 6LD
Lakewood, CO 80228 United Kingdom
303.986.2800 +44 (0) 1747 871 872
http://aahanet.org http://www.fabcats.org
Morris Animal Foundation
45 Inverness Dr
E Englewood CO 80112
Tel: 800.243.2345 or 303.790.2345
Fax: 303.790.4066
http://www.morrisanimalfoundation.org
647
Appendix F
General References for the Dog
1. AKC at http://www.akc.org/index.cfm 10. VIN www.vin.com
2. UKC http://www.ukcdogs.com/WebSite.nsf/WebPages/Home 11. University of Montreal Veterinary Medical Database
3. OFA www.offa.org www.medvet.umontreal.ca/bibio/vetjr.html
4. Canine Health Information Center www.caninehealthinfo.org 12. IVIS www.ivis.org
5. Journal of the American Animal Hospital Association www.jaaha.org 13. Canadian Guide to Dogs http://www.canadasguidetodogs.com/
6. Journal of Veterinary Internal Medicine www.acvim.org/websites/ breederinfo6.htm
acvim/index.php?p=76 14. National Kennel Club http://www.nationalkennelclub.com/
7. The Genetic Connection: A guide to health Problems in Purebred 15. The Kennel Club U.K. http://www.the-kennel-club.org.uk/services/
Dogs. Ackerman, L. AAHA Press 1999. 16. Ketring, K.L., Glaze, M.B. Atlas of Breed-Related Canine Ocular
8. Canadian Kennel Club http://www. ckc.ca Disorders. VLS Books, 1998.
9. Pub Med http://ncbi.nlm.nih.gov/PubMed accessed for research 17. The Complete Dog Book 20th Ed. The American Kennel Club.
papers. Howell Book House, NY, 2000.
648
Appendix G
Glossary of Terms
This list of terms primarily encompasses genetic definitions and containing one dominant and one recessive (Bb), they are said to be
brief descriptions of breed standard terminology. heterozygous.
Chinchilla Crossbreeding
In the cat, describes a coat of white, with very minimal tipping; The mating together of two individuals from different breeds.
compare with smoke where tipping covers a much greater portion
of the hair shaft, and shaded where pigment is in between in its
distribution.
Cryptorchidism
Retained testes, may be intra-abdominal or pre-scrotal.
Homozygous Leather
Individuals that have identical alleles in a gene pair for a particular In cats, this is the surface of the outer nose and the term is usually
characteristic. combined with a color of the nose in the breed standard; this
and paw pad color are often required to be correlated with the
appropriate coat color.
Hybrid
The crossing of two species (e.g., Bengal is breeding a domestic
cat to an Asian leopard cat). This term is also sometimes used to Line Breeding
describe crosses between two different breeds. A breeding strategy whereby mating occurs between a male and
female that are more closely related to each other than the average
(inbreeding coefficient) of the population. This is a breeding
Hyperadrenocorticism strategy that results in concentration of desirable genes due to
SYN: Cushing’s disease. Hyper-function of the adrenal gland caused crosses of vertically related individuals in a pedigree. This can result
by a pituitary or adrenal tumor. Clinical signs may include increased in concentration of undesirable recessive traits so judgment is
thirst and urination, symmetrical truncal alopecia, and abdominal important when using this technique.
distention.
652
Linkage the gametes, egg and sperm). Prophase, metaphase, anaphase and
When genes are in close proximity on the chromosome (on loci telophase are the main event sequences in mitosis. Cell division
close together), these loci are likely to be passed on to an offspring results in a full complement (2N or diploid chromosome number) in
together during meiosis, and this allows a linked marker to identify the two daughter cells. See meiosis.
the passage of a yet unidentified gene that is of importance, with
reasonable probability. Monogenic
A characteristic controlled by a single gene.
Locus (pl. loci)
A locus is the physical location of a gene on the chromosome. This Mutation
actually encompasses a pair of locations for each set of alleles on A permanent change in the base sequence of DNA. This may be the
the homologous chromosomes, but on the sex chromosomes, in the result of changing a single base to another one, the removal of part
male, loci are unpaired. of the base sequence or the addition of extra bases in the sequence.
When a mutation occurs within a gene, it may alter the genetic
Longie/Longy plan that is embedded within that gene.
Manx tail in longest conformation; most normal appearance and
used in breeding program but not shown. Necklace
Tabby markings on the neck that may be broken or unbroken.
Lynx Tufts
At the tip of the ear, the hairs follow the margins and extend Nucleotide
straight up over the tip of the ear. The building blocks of DNA consisting of nucleic acids bound to
phosphorylated deoxyribose or in RNA, to phosphorylated ribose.
Marbled
A coat pattern whereby spots have a dark margin; for example, in Nucleus
Bengal coats. A structure present within most cells which contains the DNA in the
form of chromosomes.
Marker
A component of a genetic map which uniquely identifies a locus. Odd-Eyes
Where two different colors of iris are present; usually blue or less
Mask commonly green; the other usually gold, or sometimes copper or
A pattern on the haircoat over the front of the head; darker color orange.
on the face, extends over muzzle and whisker pads, and may
continue at the top with tracings to the ears. Orange
Red/ginger X-linked coat color in cats (O). Pigment is phaeomelanin
Megaesophagus rather than wild type eumelanin.
Dilation and loss of contractility of the muscles of the esophagus.
Causes food regurgitation and secondary aspiration pneumonia. Oriental Type
Describes the body type typical of breeds such as the Siamese.
Meiosis These cats are long, tubular, lean, angular, and the head is long and
The two-stage cell division process that results in one half of the wedge-shaped with large ears, limbs long and fine, tail fine and
normal cell chromosome number; this type of cell division occurs tapering; sometimes called whip-like, minimal flank depth. Finer
in testes or ovaries to produce the gametes for reproduction. than Foreign Type and much finer than Cobby Type.
Homologous chromosome pairs separate along the cell midline
so that each offspring cell at the end of the meiosis II process has Outbreeding
1/2N chromosomes; this way when egg and sperm fuse to make The mating of two individuals who are less related than the average
the offspring, the N (normal chromosome number) is maintained (inbreeding coefficient) of the population.
through subsequent generations.
Outcrossing
Microsatellite Breeding using two individuals that are less closely related than
A special region of DNA which possesses an unusual base sequence the average population; no common ancestors in previous three
where two, three or four bases are repeated over and over again, generations.
for example CACACACA etc or GCGCGCGC etc. these microsatel-
lites have proved to be very useful markers in developing the canine Pannus, Chronic Superficial Keratitis
genetic map. Chronic corneal inflammatory process that can cause vision
problems due to corneal pigmentation.
Mitosis
This is the cell division process that occurs in body cells, (excepting
653
Parti-Color laboratory; used in DNA testing.
A coat color pattern whereby more than one color is superimposed
on a white background (e.g., calico) Prevalence
The measured number of ongoing cases (not new cases as with
Patellar Luxation incidence) for a characteristic or disease/disorder in a population;
Slipping kneecaps that can move out of their normal position either not counted over a time frame- just how many are present at a
medial or lateral. particular point in time.
Self Spectacles
Another term meaning a solid colored coat; a coat without patterns. Outside of the rims (see rims), the lighter coat color provides a
round appearance of glasses around the eyes.
Semi-Foreign
A cat with a build that is somewhat slender but not as elongated Standoff
and fine as the oriental type cat such as Siamese. Japanese Bobtail A haircoat that sits up away from the skin, rather than laying flat
is an example of semi-foreign type. and following along the curves of the body.
Shaded Torbie
A patched tabbie.
A tipping pattern with color on the hair shaft with pigment
distribution somewhere between the chinchilla (minimal) and
smoke (greater). Tortie
An abbreviation for the word tortoiseshell; see tortoiseshell.
Smoke
A haircoat produced by the silver inhibitor gene acting on the Tortoiseshell
non-agouti base coat color which results in the hair being A cat with black and orange and brown hairs admixed in a variable
grey-silver at the base of each hair, extending up onto the hair a pattern. Seen in female cats, and rarely in males if sex chromosome
variable extent, but often about 30-50% of the hair is light. Tipping numbers are abnormal.
color determines the type of smoke (blue, black, red smoke); see
shaded and chinchilla.
655
Tri-Color Wool Hairs
Term for the haircoat with three colors (e.g., calico cat (tortie and Form the soft undercoat in double coated breeds; also called down
white). hairs.
Umbilical Hernia
Congenital opening in the body wall from where the umbilical cord
was attached.
Undercoat
The short wooly or down hairs.
Urolithiasis
Mineral concretions (stones), also called calculi present in the
urinary tract, including nephroliths (kidney stones), and bladder
stones.
Usual
In some cat breeds it refers to the most common coat color and
pattern. (e.g., in the Abyssinian, the ruddy agouti coat is termed
“usual”).
Van
A coat pattern whereby the main coat color is white, the tail is
colored, and the head has colored markings also. Van pattern is
piebald spotting genetically (SS), a dominant gene with incomplete
penetrance.
The term originated with the Turkish Van cat coloration, but now
is used in a generic sense for other breeds with similar color
patterning.
Van is also the shortened synonym for the Turkish van breed.
Wedge
The term used to describe a head conformation when it is a quite
elongated triangle; the Siamese, Colorpoint Shorthair or Balinese
heads are good examples. Ear bases to outside of muzzle form
a straight line, no obvious whisker break, flat skull, and straight
profile characterize this head. Modified or rounded wedge head
conformation is a softer triangle, and examples include Birman,
Egyptian Mau, Ocicat and Abyssinian; a short wedge—the Devon
Rex. British Shorthair, Himalayan, Bombay and Burmese are breed
examples, would be described as rounded heads for comparison.
Semi-foreign type cats such as Japanese Bobtail and Norwegian
Forest cats are described as having triangular heads.
Whisker Break
The junction between whisker pad and face at the muzzle to
cheekbone area.
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