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Proceedings of the Southern European


Veterinary Conference and Congreso
Nacional AVEPA

Oct. 17-19, 2013 - Barcelona, Spain

Next Conference:

Oct. 16-18, 2014 - Barcelona, Spain

Reprinted in the IVIS website with the permission of the SEVC - AVEPA
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INFERTILITY IN THE MALE DOG

Stefano Romagnoli, DVM, MS, Ph.D, Dipl. ECAR


Department of Animal Medicine, Production and Health,
University of Padova, Agripolis, Legnaro, 35020 (PD), ITALY

stefano.romagnoli@unipd.it

When considering a male dog presented for infertility, the following steps need to be carefully
followed: a) collect a thorough history; b) perform an accurate clinical exam of the entire
reproductive system; c) evaluate one or more semen samples.

Information needed in order to collect a meaningful reproductive history - The first and
most important information to be collected is a complete list of all bitches mated, starting from
when the dog was still fertile, so as to be sure to understaqnd when the problem began.
Furthermore, clinicians should try to put together the following information:
a) If and how was fertility assessed for mated bitches
b) If and how was ovulation determined in previous breedings
c) In case some of the bitches bred did whelp, it is very important to calculate the exact
duration of pregnancy. Gestations of 57-59 days mean that the bitch had already
ovulated when she was mated, while gestations of 67-72 days mean that the bitch
ovulated 2-9 days following mating. Gestations whose lengths is shorter or longer
than the intervfal 60-66 days may be characterized by a small litter size, but this is
more likely due to poor breeding management rather than to poor male fertility.
d) If, how and when (after breeding) was pregnancy diagnosis carried out on mated
bitches
e) Whether any drugs were used which could depress testosterone production (such as
androgens, glucocorticoids, oestrogens, progestogens, cimetidine or ketoconazole)
or act on the ejaculatory process (such as xylazine or fentolamine)
f) Whether the dog has suffered from any disease, accidents, injuries or trauma which
could be relevant to reproduction.

The clinical exam - Following a complete physical exam (to rule out systemic disease directly or
indirectly affecting reproduction), scrotum, prostate and penis should be carefully inspected and
palpated. Normal testicles are freely movable within the scrotal sac, have the same shape and
consistency and their size must be average for the breed. Epididymides are palpated on the
dorso-lateral aspect of the testicle to check for the presence of nodules, keeping in mind that
palpation can only exclude the presence of macroscopic lesions. The prostate is examined using
the index finger of one hand per rectum to locate the symmetrically bilobed spongy structure,
whose caudal half can be felt with the fingertip cranial to the pelvis; the other hand should locate
the prostate abdominally and push it backward towards the rectally located index finger. Finally,
penis and prepuce are examined to rule out presence of lesions as well as to make sure that the
penis can be normally extruded from the prepuce.

Proceedings of the Southern European Veterinary Conference & Congreso Nacional AVEPA, 2013 - Barcelona, Spain
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Causes of infertility – Failure to conceive in the male dog can be due to a) failure to achieve
erection, b) failure to achieve ejaculation, c) failure to achieve copulation, or d) poor semen
quality. The most common cause of infertility in male dogs is poor semen quality; failure to
achieve copulation is fairly common, while failure to achieve ejaculation is uncommon but
reported in the dog, and failure to achieve erection is rare. Infertility in apparently normal males
who are able to ejaculate fertile semen as well as to achieve a coital tie may occasionally be
observed in the dog.

ERECTILE DYSFUNCTIONS

The erection process – As in other mammalian species, erection is orchestrated by the hormonal
cascade of the hypothalamus-pituitary-gonadal axis, always preceded by a GnRH-LH release and
allowed by a testosterone peak. Following the testosterone peak, stimulation of the pelvic nerve
causes release of one or more neurotransmitters (probably vasoactive intestinal polypeptide
and/or acetylcholine) which are responsible for an increase in arterial flow and rapid filling (within
20 seconds of pelvic nerve stimlation) of the corpus spongiosum and corpus cavernosum. The
pars longa distalis of the penis doubles in diameter and elongates, while the bulbus glandis grows
remarkably and very rapidly during this time reaching the size from a small orange in a 5-10 kg
dog to a large orange in 40-50 kg dog.

Failure to achieve erection can be due to androgen insufficiency, pain, or psychological problems.
Androgen insufficiency is rare in the dog as a cause of erectile dysfunction. Low testosterone
secretion may be due to testicular atrophy, intersex states or pituitary insufficiency. Hind limb or
spinal pain, orchitis/epididymitis or prostatitis may prevent the normal erection process from
starting or being maintained because of pain in maintaining a normal erection posture.
Psychological problems include a hard discipline imposed to the male dog since puberty (such as
beating him up whenever mounting or thrusting behaviour is exhibited), presence of a dominant
or aggressive female, or an unfriendly environment in which breeding or semen collection takes
place. Identifying such a problem require collecting a detailed history and careful observation of a
breeding attempt in order to differentiate a reproductive disease problem from an orthopedic or
psychological problem. A change of environment and/or breeding routine may be necessary in
order to obtain some success.

EJACULATORY DYSFUNCTIONS

The bladder neck plays an important role during seminal emission and seminal expulsion
preventing a retrograde flow of semen into the urinary bladder. During the ejaculatory process,
the canine bladder neck shows periods of intense contractile activity followed by phases of
relaxation: the duration of each relaxation phase decreases gradually until a continuous
contractile momentum of the dorsal segment of the bladder neck (the ventral segment of the
canine bladder neck is mainly concerned with continence and voiding) occurs towards the end of
the ejaculatory process. When the dorsal segment of the bladder neck is relaxed (during sexual
rest and in between urethral muscle peristaltic contractions early in the ejaculatory process)
semen may flow back into the urinary bladder following the least resistant pathway. If the bladder
neck contracts at ejaculation, then the urethra becomes the least resistant pathway through which
semen is propelled outside. If the bladder neck fails to contract, the least resistant pathway
becomes the bladder itself and semen ends up there, where it canbe found by looking at the urine
sediment soon after failure to ejaculate following erection and thrusting.

How to treat retrograde ejaculation

Proceedings of the Southern European Veterinary Conference & Congreso Nacional AVEPA, 2013 - Barcelona, Spain
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Sympathomimetic agents such as ephedrine, pseudoephedrine hydrochloride,


phenylpropanolamine and imipramine are generally used (alone or in combination) to treat
human retrograde ejaculation. Treatment protocols employing sympathomimetic drugs
reported in the dog include phenylpropanolamine (3 mg/kg per os twice daily) and
pseudoephedrine hydrochloride (3-5 mg/kg per os 3 times daily or 3 and 1 hour prior to
breeding/semen collection). We have observed retrograde ejaculation causing
oligozoospermia in one English Setter dog and aspermia in one German Sheperd dog
(Romagnoli and Majolino, 2008). As an example, one of these cases is briefly summarized
here. An 8-year old previously fertile English Setter dog was referred with a history of infertility
observed over the last 2 years. On the first 2 semen collections with estrous teaser bitches,
the dog showed good libido displaying pelvic thrusting, alternate stepping on the hind limbs,
anal contractions and lordosis, but produced only 0.0 and 0.1 cc of semen (the latter with 70%
progressively motile spermatozoa), respectively. A 15 ml voided urine sample collected at the
second semen evaluation showed a total count of 45 million, 70% progressively motile
spermatozoa. The dog was treated with pseudoephedrine at the dose of 5 mg/kg, 4, 1 and
0.5 hours prior to semen collection, and produced on two different occasions one week apart
0.3 and 1.0 cc of normal semen with 70% progressively motile spermatozoa, respectively; the
owner was instructed to administer pseudoephedrine at home using the above dosage prior to
natural breeding, and the dog produced a normal litter.

FAILURE to ACHIEVE a NORMAL COPULATION

In canines, a normal breeding is characterized by the coital lock (or inside tie), a phase during
which the penis is locked into the vagina due to engorgement of the bulbus glandis. The interval
between exposure to the female in heat and first attempt at mounting and intromission is highly
variable, with some males achieving a successful breeding almost immediately while others may
engage in a very elaborate and prolonged courtship (social and exploratory) behaviour before
even attempting to mount the bitch. A breeding without a coital lock is often characterized by lack
of conception, although occasionally such incomplete events may result in pregnancy. Adult
dogs may fail to achieve an inside tie because of delayed puberty, sexual overuse, pain,
psychological constraints or idiopathic poor libido. Whenever a coital lock cannot be achieved,
the female should be checked carefully as presence of vaginal stricture, vaginal prolapse or poor
breeding management may make it impossible for the male to mount her properly.

Young dogs may lack the experience necessary to perform a breeding, especially if the female
does not cooperate. Ability to ejaculate is not equivalent to ability to mount, and the use of older,
experienced female may be beneficial. Semen collection is anecdotally reported as helpful in
such cases as young studs seem to somehow “learn the trick”. Older dogs may be unable to
copulate because of a physiological decline in androgen production. In case of adult studs
undergoing frequent use, a daily routine of ejaculation does not reduce libido, although it will
reduce total number of spermatozoa because of depletion of extragonadal (epididymis, vas
deferens) reserves. Increasing ejaculation frequency up to 2-3 times daily may actually reduce
libido in a manner which is positively correlated to to frequency of ejaculation, although a sexual
rest of 2 days will allow both semen quality and libido to return to normal. Hind limb or spinal pain
(due to a joint or vertebral disc disease) or pelvic pain due to prostatitis may cause inability to
achieve the normal copulatory posture.

Persistence of the penile frenulum will prevent normal copulation in the dog. The frenulum is a
thin membrane of connective tissue joining the ventral aspect of the tip of the penis to either the

Proceedings of the Southern European Veterinary Conference & Congreso Nacional AVEPA, 2013 - Barcelona, Spain
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prepuce or the corpus of the penis. Its presence is due to the fact that dissolution of the
balanopreputial fold (an androgen-dependant process) did not occur normally. Persistence of the
penile frenulum has been reported in 24 dogs, the majority of which were cocker spaniels (almost
all from the same kennel) and four were poodles. Presenting complaints include excessive
licking, dermatitis between the rear limbs due to urine dribbling, curvature of the penis during
erection (or phallocampsis), pain at breeding, low libido. Some dogs, especially if never used as
studs, may be fully asymptomatic which explains the wide age range at first diagnosis of 3
months to 8 years. A persistent frenulum can be transected under a light plane of general
anesthesia or even local anesthesia (thin frenulums may be snipped with scissors without any
risk of haemorrhage). Once the frenulum has been removed the male will re-gain his ability
and/or desire to mount and can be used as stud, as no inheritance has been demonstrated at
least in the dog.

POOR SEMEN QUALITY

From a classification standpoint, the most important alteration of semen quality are azoospermia
(absence of spermatozoa in the ejaculate), oligozoospermia (low number of spermatozoa in the
ejaculate), asthenozoospermia (presence of a high percentage of spermatozoa which do not
show a normal progressive motility) or teratozoospermia (presence of a high percentage of
spermatozoa with morphological defects). Hematospermia refers to presence of blood, although
this is not necessarily related to infertility, and necrospermia means high number of dead
spermatozoa. Only azoospermia and oligozoospermia will be dealt with in this paper.

Poor semen quality can be due to poor quality of spermatozoa or may reflect abnormal seminal
plasma. Poor quality of spermatozoa can be due to congenital defects such as testicular
hypoplasia, the immotile cilia syndrome, chromosomal abnormalities (XXY syndrome, XX males),
mono- or bilateral cryptorchidism, anomalies of the duct system (cysts or other developmental
anomalies of the epididymis, the vas deferens or the rete testis). Hypogonadism is a poorly
characterized disease in the dog. A recent survey showed >70% of 314 cases of canine
hypogonadism as being of idiopathic etiology. A familial tendency is suspected in some breeds
(Bull Mastiff, Bernese mountain dog, Beagle, Welsh Corgi, Cocker Spaniel). Abnormal seminal
plasma may be due to prostatic disease or to inflammation of the testis or of the epididymis.

Azoospermia - Azoospermia means ejaculation of seminal fluid devoid of spermatozoa. Its


incidence in the dog is estimated to be around 35%. Dogs may fail to ejaculate the second,
sperm-rich fraction if they feel uneasy or apprehensive at the time of semen collection and/or if
there is no bitch in heat present. In such cases only the pre-sperm fraction is ejaculated, which is
prostatic fluid. Some dogs need to be trained to give semen through manual stimulation, and
this may require repeating the procedure a few times in the presence of a bitch in full heat.
Before a diagnosis of azoospermia is confirmed, semen collection should be repeated (in a
trained dog) at least 3-4 times over several days. Whenever an azoospermic sample is collected,
carnitine or alkaline phosphatase (AP) should be measured on seminal plasma. Both compounds
are secreted in the epididymis and their concentration is high in normal semen. While carnitine
assay is not often easy to obtain from a clinical chemistry laboratory, AP can be measured using
normal clinical chemistry equipment. Normal dogs with semen coming from the testicles have AP
values > 5.000, while when an incomplete sample is collected AP is < 5000 U/L but often even <
2000 U/L. Therefore, assaying AP is a good way to identify the source of the collected sample.
Seminal plasma AP is measured by laboratory equipment routinely used to measure the enzyme
in serum. Seminal plasma samples must diluted properly as AP concentrations is normally very
high (> 5.000 U/L, but often > 20.000 U/L) and therefore gets out of the normal range for a
reference serum AP assay. Laboratory technicians should be advised to centrifuge the semen
sample (some sophisticated equipments may be damaged by spermatozoa) and also to dilute the

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centrifuged sample as seminal plasma AP concentrations may be as high as 40.000 IU/L, and the
result of the undiluted sample could be so high that might be not readable. An azoospermic
semen sample with high AP comes from the testicles, while an azoospermic sample with low AP
may come from the prostate (indicating incomplete ejaculation) or its source is however posterior
to the epididymis (indicating bilateral duct outflow blockage. When AP concentrations are
equivocal, two ejaculates may be collected 1 hour apart and AP can be assayed on the second
one, which gives a higher accuracy. If possible, seminal plasma AP should be measured on the
second (spermatic) fraction, especially when the result is not clear-cut (such as with values
between 5000 and 2000 U//L) and semen collection is repeated. This is because if the prostatic
fraction is of a very high quantity a normal concentrations of seminal plasma AP can be diluted
out.

Azoospermia is more commonly diagnosed in purebred adult (3-7 years of age) dogs, although it
may also occur in crossbreds. Azoospermic dogs may have sired one or more litters previously.
In the few reports in the literature about this condition in the dog, the Labrador breed seem to be
at a somewhat higher risk than other breeds. Heritability is suspected as azoospermic related
Scottish terriers and Labrador retrievers have been reported, with 2 male offsprings of an
azoospermic Labrador retriever becoming infertile between 2 and 7 years of age (while another
male offspring was fertile until the age of 12).

Etiology - Azoospermia may be due to pre-testicular, testicular or post-testicular factors. Pre-


testicular factors include endocrine conditions such as hypopituitarism, hypothyroidism, steroid
excess (Cushing syndrome or exogenous steroid administration), or treatment with antineoplastic
drugs, inguinal or scrotal hernia. Prolonged fever may also cause spermatogenic dysfunction,
although in humans fever is responsible for a decline in semen quality but not for azoospermia.
Testicular causes of azoospermia include intersex, germinal cell aplasia, bilateral cryptorchidism,
testicular injury due to trauma, irradiation, thermal insult, orchitis, autoimmune testicular disorders
(such as spermatogenic arrest) and testicular cancer.

The following intersex condition may cause azoospermia: female pseudohermaphroditism refers
to individuals with male external genitalia and female gonads, is rather uncommon and is due to
masculinization of female fetuses in utero due to exogenous hormonal treatment of the dam in
pregnancy; 79,XXY characterized by hypoplastic testicles, lack of spermatogenesis and
underdeveloped external genitalia; presence of spermatozoa in the ejaculate of affected dogs is
poorly reported, but is thought to be rare as only 6% of humans with this conditions can be fertile;
XX sex reversal characterized by presence of male external genitalia and testicular and/or
ovarian gonadal tissue in a dog with a 78,XX karyotype, has been reported in Kerry blue terriers,
pugs, English cocker spaniels, Beagles, Weimaraners and German shorthaired pointers; affected
dogs are sterile.

Diagnosis - No specific clinical signs has been associated with azoospermia in dogs: although
often smaller and softer than usual, testicles of affected dogs may be normal in size and
consistency. Testicular degeneration and softening of both testicles is reported in dogs after
bilateral vasectomy or bilateral ligation of the cauda epididymis, which seems to suggest that an
altered consistency of testicular tissue may occur in dogs with an outflow obstruction (obstructive
azoospermia). Libido is usually normal to excellent in affected dogs.

Diagnosis of azoospermia needs to be confirmed by repeating semen collection, and


characterized by localization and type of defect present. Measurement of AP (if possible on the
second fraction instead of in total semen) is of umost importance in confirming and characterizing
the diagnosis, as its concentration is low in male dogs with bilateral outflow obstruction.
Epididymal abnormalities may or may not be palpable or even visible ultrasonographically. Fine
needle aspiration (FNA) of the testicle (and cauda epididymis) may help rule out absence of
spermatogenesis. This test can be very important to confirm outflow obstruction allowing a
treatment trial with corticosteroids. Although it is often stated that FNA does not differentiate

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between outflow obstruction and incomplete ejaculation, this is not exaclty true as incomplete
ejaculation can be suspected at the first semen collection attempt. However, a diagnosis of
azoospermia requires repeating semen collection for several times making sure that the dog is
comfortable with the procedure, which must rule out incomplete ejaculation. FNA is commonly
performed under light sedation: a 20-gauge needle attached to a 50 cc syringe is introduced at
the testicular midline and strong suction is applied several times in at least 3 or 4 different
directions until some fluid is observed to be sucked up into the butterfly needle tubing. The
needle is then withdrawn and squirted on to a glass slide, smeared out, stained as for a blood
smear and examined under light microscope under the oil immersion (100x) objective.
Obviously, extravasation of spermatozoa may lead to development of sperm granulomas, which
means that less invasive techniques should be considered in the initial diagnostic process. If an
azoospermic semen sample has high AP concentration, pre-testicular and testicular causes
should be carefully investigated. The clinical approach includes a complete physical examination,
endocrine testing (thyroid hormone testing ACTH measurement and ACTH stimulation or
dexamethasone suppression test, as well as measurement of FSH and LH), karyotype, culture of
ejaculated seminal fluid for aerobic and anaerobic bacteria and mycoplasma cytology of the
sediment of the seminal fluid following centrifugation, testicular/epididymal ultrasonography, and
Brucella canis serology.

Serum LH and FSH are normal to slightly elevated in dogs with gonadal failure. FSH
concentrations increase in dogs with testicular disease and its rise correlates with degree of
severity of spermatogenetic alteration. As spermatogenesis progressively decreases, testicles
produce less and less inhibin which results in higher and higher concentration of FSH being
released from the pituitary. Both FSH and LH are released in pulses from the pituitary, therefore
their assay requires frequent blood samplings (3 samples at 20-minute intervals) or a GnRH
stimulation test using 50-100 mcg of GnRH IV and collection of a basal (pre-GnRH) sample
followed by a second sample collected after one hour. Normal LH, FSH and testosterone
concentration in the adult dog post GnRH stimulation are approximately 30 ng/ml, 60-300 ng/ml
and 1-4 ng/ml, respectively.

Oligozoospermia – The term oligozoospermia describes an ejaculate characterized by a total


number of spermatozoa lower than normal. The total number of spermatozoa produced daily
depends on body weight and ranges in the majority of adult, healthy male dogs between 500 and
2000 millions. However, values of 300 millions or even less are still considered normal,
especially in small breeds in which a more proper unit of measure is probably 20 millions
spermatoza/kg of BW. Presence of an estrous or proestrus teaser bitch during manual semen
collection increases the total number of spermatozoa ejaculated. Daily semen collection will
cause a decrease in semen output, although normal dogs are reported to be able to produce
approximately 300-450 million sperms daily, which suggests that even when the male is under
“production stress” oligozoospermia should not occur and if it does it may be a sign of an
underlying problem. Oligozoospermic dogs may still be fertile, especially if used judiciously with
good breeding management (e.g. allowing some sexual rest and collecting semen exactly 2-4
days after ovulation). The lower total number of spermatozoa still compatible with fertility is
approximately 150 millions. Fertility has been achieved in some instances also with doses as low
as 36 millions sperms, although this should be considered an exception.

Causes of oligozoospermia include season, testicular disease (neoplasia, orchitis/epididymitis),


prostatitis, endocrine disease and the use of drugs. Semen quality declines during summer
months in the Northern emisphere (although not to a degree incompatible with fertility at least in
healthy dogs) with a decrease in total number of spermatozoa ejaculated. Sertoli cell tumor is
reported to cause decreased spermatogenesis directly in the affected testis and indirectly in the
contralateral testis due to excess androgen and estrogen secretion (altering the hypothalamus-
pituitary-gonadal axis) as well as to elevation in intrascrotal temperature. Prostatic disease is
associated with infertility because of alteration of biochemical parameters of prostatic fluid (see
paper on “Canine Prostatic Diseases”). Testicular or scrotal inflammation decrease semen
quality both in the acute phase (because of local hyperthermia, often reversible) and in the

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chronic stage (due to atrophy and fibrosis, often irreversible). Brucella spp., Escherichia coli,
mycoplasma and other aerobic flora are among the most commonly reported causes of
orchitis/epididymitis in the dog. Poor semen quality and infertility due to (familial) lymphocytic
thyroiditis is reported in Beagles and Borzois, but its incidence in the rest of the canine population
is unknown. Hypothyroidism is also a reported cause of poor semen quality and infertility.
Although the link between thyroid insufficiency and infertility has never been completely proven
(experimentally induced hypothyroidism is not characterized by infertility or reduced libido in male
dogs), male dogs with poor semen quality should undergo a complete thyroid evaluation. Several
drugs are known to affect spermatogenesis, among which glucocorticoids, anabolic steroids,
estrogens, androgens, progestogens, chemotherapeutic agents, ketoconazole, amphotericin B,
cimetidine, GnRH agonists or antagonists. Although safe dose regimens are defined only for a
few of them (e.g. progestogens) the negative effect on testicular function generally disappears at
the end of treatment.

Treament of oligozoospermia depends on etiology. If the cause is reversible or treatable, one


should keep in mind that the normal duration of the spermatogenic cycle (62 days) will influence
the outcome of therapy, i.e. no improvement can be observed for at least 2 months. In case of
Sertoli cell tumor, removal of the affected testis will lead to an improvement of semen quality, and
litters can be sired again although diffusion of the tumor to the contralateral testicle left in situ has
been reported. The same surgical option (removal of affected testis) can be performed in case of
unilateral orchitis with extensive inflammatory lesions, as these may spread to the contralateral
testis and cause permanent sterility.

TREATING THE INFERTILE MALE DOG

There are very few fertility problems of the male dogs which can be solved using specific
treatments. Chronic bacterial orchitis, epididymitis or prostatitis should be treated with long-term
(4-12 weeks) specific antibiotics. Drugs with low protein binding and high lipid solubility should be
selected such as chloramphenicol or fluoroquinolones. Determination of prostatic fluid pH (usually
neutral or slightly acidic) prior to treatment can be of help since weak base antibiotics (i.e.
erythromycin or trimethoprim-sulpha) will achieve a higher prostatic concentration. Low
testosterone (following a GnRH stimulation test) and high LH/FSH levels indicate primary
testicular failure, for which there is currently no treatment. Dogs with low testosterone and low
gonadotropins should be investigated for pituitary neoplasia. Low gonadotropic function will
result in spermatogenic dysfunction, therefore it is advisable to try to stimulate gonadal secretory
activity using hCG at 500/dog IU SC twice weekly (to cause Leydig cell function) and PMSG at 20
IU/kg SC 3 times weekly (to cause Sertoli cell function). Treatment should be continued for
approximately 3 months. Both drugs are likely to cause development of specific antibodies which
makes their prolonged use probably less and less productive with time elapsing.

Clomiphene and tamoxifen have been used with success in oligozoospermic men in non-
controlled clinical studies, while the synthetic androgen mesterolone has been used in a small
number of dogs at the dosage rate of 0.75-1.5 mg/kg. In one report a significant improvement
(from 3% to 85% progressively motile spermatozoa) was obtained treating a dog with naloxone, 1
mg IM twice daily for 14 days (naloxone stimulate release of GnRH from the hypothalamus).
Treatment of oligozoospermia in 5 dogs with GnRH agonist (1 mcg/kg SC) with or without
subsequent administration with hCG (1600 UI IM) gave favourable results in one dog and a
transient improvement in semen quality in 2 other dogs. GnRH (3.3 mcg/kg of gonadorelin
(Cystorelin, Abbott) IM once weekly for 4 months) and a GnRH agonist (1 mcg/kg once, IM) have
been tried with some anecdotal success in 2 dogs with oligozoospermia. Natural PGF2alpha
(PGF) is reported to improve semen quality in the dog giving >200% increase in sperm numbers
when administered at 100 mcg/kg SC once 15 minutes prior to semen collection; although this is
more a technique to collect a reluctant or inexperienced dog rather than a real treatment for
oligozoospermia, still a dog with poor semen quality may give a better sample when pretreated
with PGF. PGF increases epididymal contractility. Anecdotal success for treating dogs with

Proceedings of the Southern European Veterinary Conference & Congreso Nacional AVEPA, 2013 - Barcelona, Spain
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asthenozoospermia, teratozoospermia and poor semen quality is reported also for cabergoline
used at the regular anti-galactogenic dose of 5 mcg/kg per os once every other day for 3 weeks.

If present, improvement will always be slow to appear because of the 62-day spermatogenic
cycle in the dog: in one report of a dog with teratozoospermia because of posthitis and scrotal
oedema, return to fertility and to normal semen quality occurred 18 and 26 weeks after therapy
was institued, respectively. When dealing with oligozoospermic dogs or when semen quality is
unknown, semen evaluations should be planned at least one week prior to the expected day of
breeding, as gonadal reserves may take several days to be restored when spermatogenic
function is abnormal. When semen quality is below normal, ovulation must be timed very
accurately and artificial insemination performed intravaginally on day 4, 5 and 6 post-LH peak
(day 2, 3 and 4 post-ovulation) if total count is >100.000.000 spermatozoa. If this approach fails
or if total count is >20.000.000 spermatozoa, artificial insemination should be performed
intrauterine on day 5 post-LH peak.

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Ferguson JM and Renton JP: Observation on the presence of spermatozoa in canine urine. J
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Freshman JL, Amann RP et al – Clinical evaluation of infertility in dogs. Comp Cont Ed Pract Vet
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Hart BL. Normal behaviour and behavioural problems associated with sexual function, urination
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Hess M – Documented and anecdotal effects of certain pharmaceutical agents used to enhance
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Johnston SD, Root Kustrizt MV, Olson PN. Clinical approach to infertility in the male dog. In:
Canine and Feline Theriogenology. WB Saunders 2001, pp 370

Ling GV, Ruby AL – Comparison of two sample collection methods for quantitative bacteriologic
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Oettle EE. Soley JT – Sever sperm abnormalities with subsequent recovery following scrotal
oedema and posthitis in the dog. J Small An Pract 27:477-484, 1986

Olson PN, Mulnix JA, Nett TM – Concentrations of LH and FSH in the serum of sexually intact
and neutered dogs. Am J Vet Res 53:762-766, 1992
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