Angular Limb Deformities and Faulty Conformation Proper

We could spend all day talking about limb deformities and faulty conformations, but the truth is, they are of macroscopic
importance and little microscopic change is seen between the problem and normal tissues.
Each deformity can be appreciated through observation of the specimen, knowledge of anatomical standards of the breed, and
patience for its proper identification.
Some of the most common:
Flexor Laxity
Flexor Contracture
Congenital
Acquired
Pyusitis
Bowing
Deviations
Rotations
Fetlock Valgus
Carpal Valgus
Weak Heels
Contracted Foot
Flat-Foot
Pumiced Foot, Dropped Sole or Convex Sole
Ringed or Ribbed Hoof
Club Foot
Crooked Foot or Unequal Foot
Angular Limb Deformities and Faulty Conformation Proper





Polydactyly
Bruised Sole and Corns
When making a small exploratory hole in the area over the bruise, blood (pooled
blood that is dark red to purple in color) should ooze out and possibly pus too (white-
yellow viscous liquid). The blood stains the tissues reddish purple. This is a
hemorrhage into a focal area / confined space.
Micro: presence of RBCs found among tissues of the sole; possible presence of cells of
inflammatory response. The presence of blood cells and increased pressure within this
confined area may or may not disrupt tissue function.

Corns these are sole bruises brought on by shoeing. They can be unilateral in one
hoof, bilateral in one hoof, or present in more than one hoof. The blood discoloration
from the bruise has now turned from a dark red color to a green, blue, yellow color.
Bruised Sole and Corns
When making a small exploratory hole in the area
over the bruise, blood (pooled blood that is dark
red to purple in color) should ooze out and
possibly pus, too (white-yellow viscous liquid).
The blood stains the tissues.
A dry corn has not undergone any
inflammatory response. There is only color
change to the tissues.
Horizontal Section Of A Corn. The Section
Cut At About The Base Of The Papillae Of
The Sensitive Sole. A, Papillae, With Horn-
Cells Surrounding Them; B, Interpapillary Or
Intertubular Horn; C, Hollow Spaces In The
Intertubular Material Filled With Blood; D, A
Papilla And Its Surrounding Horn-Cells Filled
With Blood.
Perpendicular Section Of The Wall Of A Contracted Quarter In A
Case Of Chronic Corn. Both The Sensitive And Horny Laminae
Are Bent Backwards, And Hemorrhages Have Taken Place At The
Base Of The Sensitive Laminae. the regularly leaf-like arrangement
of the horny laminae has been largely broken up. Certain of the
laminae are altogether wanting, while others are broken in their
length and rendered incomplete.
Microscopic examination of the structures involved in such a case
reveals the fact that with the contraction is an alteration in the
normal direction of the horny and sensitive laminae. They become
bent backward, and, instead of the regular and normal arrangement,
show the distorted appearance.
A moist corn gets its name from the great presence of exudates from the inflammatory
response of the tissues. The sole is yellow, soft and moist when touched. When cut
into, the sole reveals layers that are infiltrated with exudate. This increase in fluid
causes a build up of pressure and a decrease in the function of keratin producing cells.
This, obviously, leads to the decreased production of the horn. When cut deep enough,
a cavity is reached where no new horn was produced naturally.
A suppurating corn has the inflammatory exudates and pus that can lead to cavity
production on the bones. When this happens, the pus has a sandy, gritty feel (small
pieces of eroded bone). Microscopically, there is necrosis to all affected tissues that
could soon lead to a septic arthritis.
Sandcrack (Toe, Quarter and Heel Crack)
A crack in the hoof may appear anywhere and of any length. We can divide them up in three types
based on their:
Location on the hoof wall:
1.) Toe Crack
2.) Quarter Crack
3.)Heel Crack




Length:
1)Complete
2)Incomplete
Degree:
1)Simple
2)Complex
Age:
1)Old
2)New
Origin:
1)High
2)Low
Macro: The outer hoof wall presents a vertical opening that can vary in width and
length. Depending on the severity of the situation (i.e. bacterial infection/ deep lesion)
, there may or may not be presence of a creamy white viscous liquid (pus) or foul
smell (gangrene). If the deeper structures are involved, an inflammatory process will
ensue and microscopically necrosis will be present. All of this may lead to cartilaginous
quitter.
Micro: Aside from general spacing of the tissue, the other obvious histological features
to be observed are:
Inflammatory response, necrosis, gangrene and cavities of bone all of which begin
upon antigen infection
Puncture Wounds
The hoof, although hard laterally, is made of soft tissues on the palmar surface. A sharp
object can easily puncture through the soft tissues as the weight of the horse presses down
on it. Punctures can be either 1.) Simple or Superficial or 2.) Deep
Aside from pain and lameness, we may see the object protruding from the hoof; a nail for
example. Initially there may be bleeding and bruising of the hoof. Severity of the problem
depends primarily on where the object punctures. The center areais the heart of the hoof;
enclosed there are all major structures.
If there is contamination by opportunistic organisms, there will be pus and cellular debris in
the hoof and possibly a build-up of gas. If the pressure is not released, they will burst out
of the coronary band and ooze out.
Bone Cyst in Pedal Bone
Bruised Sole & Corns
Canker
Contracted heels
Fracture of Navicular Bone
Fracture of Pedal Bone
Keratoma
Laminitis (Founder)
Navicular Disease
Pedal Osteitis

Puncture Wounds
Pyramidal Disease (Buttress Foot)
Quittor
Sandcrack (Toe,Quarter & Heel Crack)
Scratches (Greasy Heel)
Seedy Toe (Hollow Wall)
Sheared Heels
Sidebone
Thrush
Inflammatory Responses of the Keratogenous
Apparatus:
Laminitis (Founder)
Laminitis is the inflammation of the sensitive structures and tissues of the foot.
Acute active stage (the first 72hours)
Chronic changes in structure and blood supply
Inflammatory Responses of the Keratogenous
Apparatus:
Macro: Swollen limb with an
outpouring of inflammatory
exudates. When cut, the pedal
bone is observed to be pressing
down on the sole. The arrows
show the separation of the
sensitive structures filled with
exudate of red color.
Inflammatory Responses of the Keratogenous
Apparatus:
Macro: Swollen limb with an
outpouring of inflammatory
exudates. When cut, the pedal
bone is observed to be pressing
down on the sole. The arrows
show the separation of the
sensitive structures filled with
exudate of red color.
Inflammatory Responses of the Keratogenous
Apparatus:
Micro: Inflammation of the laminae, reduced
blood flow to the hoof wall, cell death and
breakdown of connection between wall and
pedal bone then occur. We can see in the
photo how the lack of irrigation of the blood
vessels eventually causes them to break down
and deteriorate leaving the primary and
secondary laminae to separate.
In the early stages, congestion is visible that
turns into exudation as the problem gets worse.
BM basement membrane
Ep epidermal cells
PEL primary epidermal lamella
PDL primary dermal lamella
PMNs polymorphonuclear leucocytes
SDL secondary dermal lamella
SEL secondary epidermal lamella
V blood vessels
TNF-a tumor necrosis factor -a
TGG- b transforming growth factor -b
E erythrocytes
MMP matrix metalloproteinase

Figure: Normal lamellae: type IV collagen (A),
laminin (B) and collagen type VII (C)
immunostaining. The basement membranes
(arrowheads) of the epidermal lamellae and
the blood vessels (V) of the dermal lamellae
are clearly immunostained as a fine dark
brown line in A and B. The blood vessels did
not immunostain in C. Nuclei of the
epidermal basal cells and dermal fibroblasts
are counterstained with haematozylin. The
basement membrane is closely adhered to
the basal cells of the lamellar epidermis and
there is no evidence of separation. Bar =100
pm. WE CAN SEE THERE IS NO
SEPARATION.
Disintegration of the basement membrane (BM) of the hoof lamellae and failure of the
BM to remain attached to the basal cells of the secondary epidermal lamellae (SEL) is
one of the earliest pathological events to occur in acute laminitis
The attenuated, distorted appearance of the BM in histochemically stained sections
examined with the light microscope, led to speculation that loss of collagen and
glycoprotein from the lamellar basement membrane was part of the mechanism
initiating collapse of the lamellar anatomy

Figure: Laminitis: type IV collagen
immunostaining. Section of the tip
of a primary epidermal lamella
(PEL) affected by grade 3 laminitis.
At the tip of the PEL the epidermal
basal cells are clumped together
and are devoid of BM. The
immunostained BM (arrowheads)
from which they have separated
has remained in its original
position in the dermis and has
retained the outline of the
secondary epidermal lamellae
(SEL). The BM of blood vessels (V)
in the primary dermal lamellae
(PDL) are also stained and serve as
positive controls. Bar =100 pm.
Inset shows laminin
immunostained BM of SEL, empty
of epidermal cells. Bar =10 Nm

Figure: Laminitis: type VII collagen
immunostaining. Section from the tip
of a primary epidermal lamella (PEL)
affected by grade 3 laminitis. The SELs
are devoid of epidermal cells. The
immunostained BM has remained in its
original position in the dermis
retaining the outline of the SEGs.
Numerous PMNs (arrowheads) have
already crossed the lamellar BM and
are within the epidermal compartments
of the SELs. The BM of dermal blood
vessels did not immunostain with type
VII collagen antibody. Bar = 50 pm.
Inset shows, at the same magnification,
laminin immunostained section cut
from the same block. The BM of the
blood vessels (V) as well as the lamellar
BM is immunostained.
Neutrophils were numerous in the dermis
surrounding the PEL tip and many had left
the dermis and were located between layers
of BM in what were once epidermal
compartments


Fig 4:.
A. At the bases of the SELs most of the BM
did not immunostain (arrowheads)
suggesting that disintegration of the BM had
occurred.
Fragments of immunostained lamellar BM
are still present in this region (arrows)
suggesting that BM lysis is incomplete at this
stage.
The SEL tips are attenuated (compare with
Fig 1) but the BM has not separated from the
basal cells.
B. The BM has disappeared from most of the
SEL epidermal cells which are now an
amorphous column of epidermal cells (Ep
Cells) on either side of the central
keratinised axis of the PEL.
Inflammatory Responses of the Keratogenous
Apparatus:
Keratoma
A non-cancerous tumor that affects the tissues of the hoof wall and sole.
Macro: Dense, hard, thickened area of the horn; shiny; bulging, white mass that pushes out between the white line
and wall and the white line is pushed toward the center of the sole. The pedal bone may shrink in severe cases
from the pressure and even absorb some of the Calcium from the tumor resulting in a radiograph that is less
white (or dense) in that area
Micro: Inflammation, proliferation of keratin producing cells that make up the horn
(wall and sole). We see a prominent lamination of Keratin (or hyperplasia). The
mass has been shown to be composed of proliferating squamous epithelium with some
orthokeratosis and parakeratosis; also present was inflammation of the corium
Inflammatory Responses of the Keratogenous
Apparatus:
Canker
It is not common, but lately climate changes (mild winters and wet springs) have caused a
rise in outbreaks of this infection. Canker or Pododermatitis Chronica Verrucosa is an
irregular disease and difficult to treat. Some have even referred to it as Hoof Cancer because
of its persistent rapid growth and odd aspect.
Macro: Affecting the frog (usually), there is hypertrophy of the keratinous cells and a growth of a gray
to white granular material from the area that is soft and cauliflower-like. It is irregular and foul smelling
from the caseous exudate and is referred to as chronic, hyperproliferative, suppurative,
pyogranulomatous pododermatitis of the frog. It is difficult to treat and can lead to severe infections all
the way to the heel. (7) The horn is no longer attached to the sensitive structures. When the tissue is
scraped away from the horn, it reveals a thin, shiny, almost transparent gray membrane over the
sensitive structures.
Micro:
Hyperplasia of the epithelium and connective tissue of the papillae of the corium; The
epithelium does not keratinize but instead degenerates to a necrotic mass that covers
the hyperplastic papillary bodies; neutrophilic inflammation; lymphocyte infiltrates in
the dermis
Inflammatory Responses of the Keratogenous
Apparatus:
Abscesses:
Abscesses may be present in different areas of the foot. Usually, two forms are seen in horses:
i.) Subsolar
ii.) Hoof Wall (Gravel)
Macro:
The abscess is an accumulation of pus (white-yellow viscous fluid; white blood cells, cell debris, and bacteria).
The bacterial invasion leads to a cascade of events in the inflammatory response.
Also visible is a separation between the sole or hoof wall and the pedal bone because, unlike soft tissues, the
hoof can not change its shape or expand to accommodate the accumulation of fluid
Inflammatory Responses of the Keratogenous
Apparatus:
Scratches (Greasy Heel, Mud Fever, Cracked Heels or Pastern Dermatitis)
This can be caused by a variety of reasons:
Bacterial Infections
Dermatophilosis
Staphylococcus
Fungal Diseases (like Ringworm)
Chorioptic Mange
Allergic reactions to Irritants
Trauma
Neoplastic Disorders
Metabolic Disorders
The specific cause can be determined through scrapings, biopsies or cultures of the lesion.
Macro: there will be a presence of
inflammation and swelling at the site; open
sores and even a foul, rotten odor may be
present. Usually it is located on the rear half of
the pasterns. The hair may be matted down
from the discharge. The skin thickens and
hardens with time; gray-white patches or
plaques that are firm and moist.
If the problem becomes a chronic issue, small
tissue masses will be seen, often described as
grapes
Micro: Depending on the antigen, our microscopic image will change.
Consistent features would be inflammation reaction and intracellular
fluid

Example: Case Study, Strongyloides infection
Inflammatory Responses of the Keratogenous
Apparatus:
Seedy Toe (Hollow Wall or White Line Disease)
This ailment affects the white line of the hoof creating a separation between the wall and sole. Some farriers
refer to this problem as Onychomycosis (or bacterial infection of the nail bed) but this is a misnomer as the
bacteria are not responsible for the problem, they are just opportunistic and take advantage of the weakened
immune system and barrier. The most common bacteria found:
Genus Scedosporium, also Pseudoallsheria, Scopulariopsis and Aspergillus.
Macro: The name Seedy Toe was given due to the
presence of the hoofs dry, crumbly texture.
An area of black discoloration may be seen in the
white line area that correlates with a Hidden
Gallery or an area inside the wall of the
hoof that is hollow because the wall and sole
have separated. Usually it can be found
higher up around the coronet.
The hoof, itself, is dry and brittle and may
even break away.
Micro: In addition to the presence of opportunistic
microorganisms, there will probably be inflammation
in the laminar dermis. Keratin degeneration is present
in the Stratum medium of the hoof wall.
Inflammatory Responses of the Keratogenous
Apparatus:
Thrush:
A degenerative disease of the frog which results in an opportunistic bacterial infection.
The cause of Thrush could be many different bacteria but one that is well-known to be
problematic is a Gram rod shaped anaerobic bacteria called Fusobacterium necrophorum.
It can be found throughout the natural environment of the horse and especially thrives in
moist environments.
Macro: The area of the frog that is affected is
humid or moist, white, crumbly and presents a
thick, foul smelling, black discharge in the lacunae;
fissures and softening of the tissue at the bottom of
them; presence of liquid (edema) and darkened
spots of different sizes (hemorrhages)
Micro: Thickening of the Stratum spinosum and Stratum germinativum with cell vacuolation and vacuolated spaces
between cells and necrobiotic nuclear changes;
loss of Stratum corneum;
mitosis present in the Stratum germinativum;
bacteria in the detritus; u
nlike Canker, the corium is not affected;
the collagenous tissue is hyalinated.
Quittor or Lateral Cartilage Necrosis
This affects the cartilage (lateral) of the pedal
bone and is a chronic bacterial infection. It
can be of 4 types:
Simple or Cutaneous
Tendinous
Subhorny
Cartilaginous
Simple or Cutaneous
Macro: affecting the coronary tissue, it begins as a small bright red spot of
inflammation that changes to a blue-black color. White yellow pus or dark, red,
foul smelling pus is present and the limb is swollen.
Micro: necrosis of the coronary tissue, inflammation of the subcutaneous tissue

Tendinous
Macro: affecting the deeper structures of the hoof
Micro: necrosis affecting the coronary tissue and tendons and ligaments
Subhorny
Macro: Green color and usually the size of a pea; Pus (white-yellow viscous fluid
or black-gray depending on which structures are affected) exudes from an open
wound around the coronet near the damaged cartilage, most often it is mixed
with blood giving it a reddish tint; presence of an abscess, swelling and skin
thickening around the coronet; fistulas filled with a spotty liquid. The liquid has
small green fragments that are consistent with pieces of the diseased cartilage.
Micro: Necrosis of the cartilage and may affect deep tissues and form an abscess.
The fistulas are filled with granulation tissue
Cartilaginous
Macro: the cartilage is affected; the heel is constantly moist from a thick,
purulent, blood stained, fetid discharge
Micro: necrosis of the lateral cartilage
Sidebone
This is a process of calcification of the cartilage of the pedal or coffin bone. Once hard, the cartilage
may even protrude above the coronet.
Macro: Presence of a large, unevenly shaped, hard, solid, boney area of the collateral cartilage easily
noticed upon palpitations that protrudes out around the coronet; calcification of the cartilage of the
coffin bone.
Micro: Inflammation in the Os pedis bone affects bone forming cells; cartilage is invaded and begins to
calcify.


Diseases of the Bones:
Fractures
Fractures of bone structures in the equine hoof are hard to diagnose and should be
carefully looked for on radiographs. Most often they are caused by trauma.
Macro: Hairline fractures on structures like the Pedal or Navicular Bones
Micro: Inconsistent (fractured) bone tissue

Diseases of the Bones:
Pedal Ostitis
This is another way to say Inflammation of the Pedal Bone. We will consider
the following 3 types:

Rarefactive --can be seen on X-rays as an irregular or rough-looking border of
the edge of the pedal bone; the bone is red and the Haversian canals are
increased in size giving the bone a pumice-stone appearance.
Osteoplastic formation of new bone tissue surrounding the Haversian
canals, the affected bone is denserobliterating the Haversian canals. Often,
the bones are described as feeling more ivory-like.
Necrosis/Caries
Histologically, it appears as a variant of laminitis of the sole affecting its epidermal and corial laminae in the
toe and wing regions.
Diseases of the Bones:
Pyramidal Disease (Buttress Foot)
There is thinning of the cartilage that makes up the
articulation at the pyramidal process. The bone is an
abnormally white color. The cartilage can thin so
much that it is destroyed completely. It begins at the
pyramidal process and can go all the way back to
the articulation and may lead to a fracture further
deforming the hoof. There is also a presence of
inflammation at the coronary band.

Osteochondritis Dissecans
We are dealing with bone flaps or fragments due to a
defect in ossification.
Macro: The bone cartilage intersection found at the
joint is abnormally formed. The bone fails to form
and what is left is a thick cartilage.
The joint should be shiny, white, smooth to the
touch and free of any debris floating in the sinovial
fluid. In OCD, however, the presence of deformities
and rough articulations cause lameness in the horse.
Osteochondritis Dissecans
Both hocks in this picture have severe effusion, as
shown by the red arrows.
Notice how the joint bulges outward.
Most horses with OCD will have a milder degree
of swelling.
Osteochondritis Dissecans
This is an example of how an OCD fragment typically
looks on a radiograph.
The OCD fragment is circled in red.
Notice that the fragment seems to float within a defect
in the main bone.
: Pathological specimen of a Danish sow. A typical osteocondrotic lesion is shown in the form of osteochondritis
dissecans (arrow) of the articular cartilage of the lateral humeral condyle. Haematoxylin and eosin staining.
Bar = 200 microm.

the arrow points to a fracture in the
lateral epicondyle of the humerus.

Figure 1a). Normal development results in a bone (shown in blue) with a subchondral bone plate to which a smooth cartilage cap is
attached (shown in yellow).

Figure 1b). Abnormal development due to a defect in endochondral ossification results in an area of thickened and/or weakened
abnormal bone and cartilage (shown in green).

Figure 1c). Trauma or exercise can further damage the abnormal area as the horse flexes and extends the joint.

Figure 1d). Separation of the abnormal bone and cartilage from the underlying and surrounding tissue results in an OCD fragment,
which can form a flap or can detach and float as a free body within the joint.
Diseases of the Joints:
Navicular Disease of Podotrochleitis
A long term condition that is degenerative. Affecting the Navicular bursa, the Navicular bone and flexor
tendon, leading to an outgrowth of the bone, it is often bilateral.
Cause: Unknown but thought to be affected by traumas, blood supply, and ligaments/joints/bursa/and
other nearby anatomical features of the hoof.
Macro: The affected foot will be narrow and upright. Due to the compression of the Navicular bone, we
will be able to see some changes anatomically to the structures like CARTILAGE DEGENERATION
and even EROSION, FIBROUS BANDS or ADHESIONS form from friction, and it is possible to see an
increase in BONE DENSITY beneath the surfaces of cartilage
Diseases of the Joints:
Navicular Disease

Diseases of the Joints:
Navicular Disease of Podotrochleitis
Micro: Inflammation, obstructed blood vessels and/or decreased blood flow; an increase of fibrous tissue
around the ligament, compressed veins but arteries will see increased blood flow to compensate both
increase the pressure within the bone.
To compensate for this increase in pressure, the body tries to absorb some of the minerals present this
can be seen on a radiograph through the formation of cavities or lollipops. New bone formation may
also be visible by reshaping the Navicular bone to a boat or canoe shape
Arthrogryposis (Congenital Joint Rigidity)

Fotografas de Exmenes por microscopia electrnica donde se aprecia el tejido muscular
normal de un Potrillo (foto izq.) comparado con un caballo con PSSM
(Acumulacin anormal de polisacridos, manchas obscuras prpuras), foto derecha.
Glycogen Storage Disease (Glycogenosis or Glycogen
Branching Enzyme Deficiency)
The tendons of the lower limbs are contracted and
result in high muscle enzymes and liver enzymes in
blood work.
Glycogen Storage Disease (Glycogenosis)
:
Biopsies from normal (left) and GBED-affected (right) horses stained with PAS. Note
globules of abnormal polysaccharide (Arrows) with no normal background pink
staining in the GBED biopsy; Cardiac and skeletal muscle may show PAS+ eosinophilic
cytoplasmic inclusions.
The liver biopsy specimen (Figure 1) shows enlarged hepatocytes with pink material within the
cytoplasm, preserved architecture, and no evidence of fibrosis or inflammation. (16)
Periodic acid-Schiff stain (Figure 2) reveals strong staining within hepatocytes, which dissolves with diastase,
consistent with glycogen (16)
Disorders Associated with Nutritional Imbalances or
Toxins:
Osteomalacia (Adults Rickets)
Due to a lack of vitamin D in diet, calcium and phosphorus concentrations in the
bones is affected and the body begins its search for these two minerals; It is found
stored in bone tissue . This absorption from the bones, however, has debilitating
effects on the animal.

Many horses also suffer from this ailment when they are fed high energy diets to
quicken growth. The bones are unable to keep up with growth of the rest of the body.

Macro: Bones are soft and deformed; Stance is compromised; when cut, internal
structure deformation is obvious.

Disorders Associated with Nutritional Imbalances or
Toxins:
Enzootic Calcinosis
Large deposits of calcium in soft body tissues after consumption of poisonous plants.
These plants increase the absorption of calcium from the intestines of 1,25-
DHcholecalciferol or the active metabolite of vitamin D. This active metabolite causes
the calcification of blood vessels and excess deposits of new bone tissue; both of these
changes lead to major complications in the lower extremities of the horse.
Disorders Associated with Nutritional Imbalances or
Toxins:
Disorders Associated with Nutritional Imbalances or
Toxins:
Selenium Toxicosis
Separation of Keratin layers of the hoof, Keratin dystrophy of the coronary band.
In chronic selenium toxicity, the selenium replaces sulfur in sulfur containing amino
acids (MET and CYS) that are present in the hoof. These two amino acids are
responsible for cell division and growth.
Macro: Separation of the coronary band if severe or fissures if mild that reach down to
the sensitive laminae; oozing of a necrotic exudate, swelling of the coronet; erosion of
the joints (hock and fetlock);
Micro: Soft tissue calcification
Disorders Associated with Antigens:
Epizootic Lymphangitis
Macro: Irregular papulae-like lesions of
different sizes that ooze a green exudate.
Micro: Inflammatory reaction, necrosis,
presence of polymorphonuclear leukocytes but
most of the nodules were infiltrated with
mononuclear cells.
H. farciminosum were oval in shape and
presented structures like an envelope, cell wall,
plasma membrane, capsule and nucleus that
could be seen with an electron microscope.
Micrograph of H. farciminosum showing
the cell envelope (CE),
plasma membrane (PM),
cells wall (CW)
the nucleus (N).
Pythiosis
Macro: the cutaneous lesions are areas of discontinued tissue (ulcers), with various size and shape; they
present a nodular aspectfound around the coronary band of the hoof, the limb has a localized larger volume
and a profound bloody serous exudate.
When this lesion is cut, it has a white appearance and firm consistency with the presence of fistules found in
galleries. These galleries contain white-yellow aggregates of firm consistency with the aspect of coral called
kunkers which are always covered in a purulent exudate.
Micro: (21)
With an HE stain, revealed is a cutaneous inflammatory reaction with focal necrosis; infiltrate of eosinophils (some are
degranulated), neutrophils, and mononuclear cells -- like macrophages, lymphocytes, plasmocytes and sometimes giant
Langerhans cells.
This reaction is found more concentrated in the periphery where the vascularization is greater.
Photo:
Stars = Necrosis with an eosinophilic infiltration
The same photo at 690X
Arrows: Degranulated eosinophils in the periphery
Thin Arrows: Neutrophil infiltration
Curved Arrows: Macrophages
Phaeohyphomycosis
There are two forms of this fungal infection that affect the keratinized cells.
1.)Dermatomycosis
2.) Onychomycosis
Both are very distructive.

Cause: Dreschlera spicifera
Macro: Possible to see multiple plaques and/or nodules that may or may not ulcerate. They are small, of dark color
and contain papulae and pustules that are located on the lower limb.
Micro: Presence of a mixed inflammatory infiltrate found in the dermis. Throughout the slide, multinucleated giant
cells can be seen.
Macro: Possible to see multiple plaques and/or nodules that may or may not ulcerate. They are small, of dark color and
contain papulae and pustules that are located on the lower limb.

Micro: Presence of a mixed inflammatory infiltrate found in the dermis. Throughout the slide, multinucleated giant
cells can be seen.
Osteochondroma
Osteochondroma
Chondrosarcoma
Cartilage-Forming Tumor: This is a malignant tumor that forms cartilage cells from the tumor cells.
These tumors are rare in horses.
Micro: Pleomorphic tumor tissue, large cells with visable mitosis. These cells are surrounded by a
cartilaginous substance. Some of the tissue may be undifferenciated as well as mineralization of the
intercellular tissue.
Tumoral Calcinosis
Localized deposits of calcium in nodules in
subcutaneous tissue or muscles.
Macro: large, hard lump on the lower limb
Micro: calcium deposits in connective tissue, Histologic section of the surgically resected tissue mass (hematoxylin and eosin stain X
180). The lesion consists of lakes of mineral deposits (large arrow) surrounded by zones of granulomatous inflammation, often
containing multinucleate giant cells (arrow head) and other zones of thick fibrous tissue (small arrow).
Fibroma
This is a benign tumor that produces collagen.
Macro: some are soft while most are firm in texture;
they are found in the subcutaneous layer to
intradermal layer of the skinit is possible that it
extends down from the surface to the deeper tissues;
they are well defined and range from 1 to 5cm in
diameter; when cut, the tumor is white-gray in color
and grows into the surrounding tissues
Micro:
The cells are of long, uniform, spindle shape;
collagen and nuclei are in bundles; little or no
nuclear hyercromasia visible; sometimes the
collagen inside the tumor may give off a thick,
classy, eosinophilic appearance
BIBLIOGRAFIA
1. Daradka M, Pollitt CC. Epidermal cell proliferation in the equine hoof wall. Equine Vet J. 2004 Apr;36(3):236-41.
2. Pollitt CC. An autoradiographic study of equine hoof growth. Equine Vet J. 1990 Sep;22(5):366-8.
3. Pollitt CC, Daradka M. Equine Laminitis Basement Membrane Pathology: Loss of Type /V Collagen, Type VII Collagen and
Laminin Immunostaining. Equine Vet J Suppl. 1998(26):139-44.
4. Pollitt CC, Daradka M. Hoof wall wound repair. Equine Vet J. 2004 Apr;36(3):210-5.
5. Oke RA. Unilateral white line disease and laminitis in a quarter horse mare. Can Vet J. 2003 Feb;44(2):145-6.
6. McDiarmid A. Keratoma from the frog corium of a horse. Equine Vet Educ. 2007;19(6):285-7.
7. Nagamine CM, Castro F, Buchanan B, Schumacher J, Craig LE. Proliferative pododermatitis (canker) with intralesional
spirochetes in three horses. J Vet Diagn Invest. 2005 May;17(3):269-71.
8. Stashak TS, Adams OR. Adams' Lameness in Horses. 5th ed: Lippencott Williams & Wilkins; 2002.
9. Rashmir-Raven AM, Black SS, Rickard LG, Akin M. Papillomatous pastern dermatitis with spirochetes and Pelodera
strongyloides in a Tennessee Walking Horse. J Vet Diagn Invest. 2000 May;12(3):287-91.
10. Andalusians-for-you. White Line Disease: What is it? 2005; Available from: http://www.andalusians-for-you.com/treatment-of-
white-line-disease.html.
11. Kuwano A, Yoshihara T, Takatori K, Kosuge J. Onychomycosis in white line disease in horses: pathology, mycology and clinical
features. Equine Vet J Suppl. 1998 Sep(26):27-35.
12. O'Grady SE, editor. Management of White Line Disease. American ASsociation of Equine Practitioners Convention; 2006.
13. Blunden A, Dyson S, Murray R, Schramme M. Histopathology in horses with chronic palmar foot pain and age-matched
controls. Part 1: Navicular bone and related structures. Equine Vet J. 2006 Jan;38(1):15-22.
14. Valberg SP. Glycogen Branching Enzyme Deficiency in Horses. 2009.
15. Anderson WED. Glycogen Storage Disease, Type IV. 2007; Available from: http://www.medscape.com/article/119690-
overview.
16. Leung DHM, Chung CTM, Loomes KMM. A 2-Year-Old Boy With Diarrhea, Failure to Thrive, and Hepatomegaly: The Pertinent
Results. 2009.
17. Li YC, Pirro AE, Amling M, Delling G, Baron R, Bronson R, et al. Targeted ablation of the vitamin D receptor: an animal model
of vitamin D-dependent rickets type II with alopecia. Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9831-5.
18. Aguirre JI. Bone changes caused by experimental Solanum malacoxylon poisoning in rabbits. Pesquisa Veterinaria Brasileira.
2005;25(1).
19. Falah K. Al-Ani AHA, and Hawa B. Banna. Histoplasma farciminosum infection of horses in Iraq. Veterinarski Arhiv Irbid,
Jordan1998. p. 101-7.
20. Banner TAD. Pythiosis: Is Your Horse at Risk? Equus Caballus Magazine. 2008.
21. Reis JLJ, R.H.G. N. Estudo anatomopatolgico e imunoistoqumico da pitiose em eqinos naturalmente infectados. Belo
Horizonte. 2002;54(4).
22. Held JP, Patton CS, Shires M. Solitary osteochondroma of the radius in three horses. J Am Vet Med Assoc. 1988 Sep
1;193(5):563-4.
23. Misdorp W, Van der Heul RO. Tumours of bones and joints. Bull World Health Organ. 1976;53(2-3):265-82.
24. Hig D. Dr. Hig's Veterinary Blog: : . 2006.
25. Bertone AL, Powers BE, Turner AS. Chondrosarcoma in the radius of a horse. J Am Vet Med Assoc. 1984 Sep 1;185(5):534-7.
26. Goulden BE, O'Callaghan MW. Tumoral calcinosis in the horse. N Z Vet J. 1980 Oct;28(10):217-9.
27. Wellsphere. De Fibromas - a comprehensive view - Wellsphere. 2009.