equine canker (pathologic anatomy)

Anatomic Pathology

of the Lower Limb / Hoof of the Horse

Anatomy of the Limb

Anatomy of the limb - Bones

Anatomy of the Limb – Inner Structures

Anatomy of the Limb:

Anatomy of the Limb - Inner Hoof

Histology of the Limb

Anatomy of the Limb - Inner Hoof

Histology of the Hoof

Hoof structure

Primary and Secondary Epidermal Lamella

Hoof Innervation

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 LaxityFlexor Contracture

CongenitalAcquired

PyusitisBowingDeviationsRotationsFetlock Valgus Carpal Valgus Weak HeelsContracted FootFlat-FootPumiced Foot, Dropped Sole or Convex SoleRinged or Ribbed Hoof

Club FootCrooked Foot or Unequal Foot

Angular Limb Deformities and Faulty Conformation Proper

Angular Limb Deformities :

Angular Limb Deformities

Angular Limb Deformities :

Contracted Flexor Tendons :

• Polydactyly

Complications from Faulty Conformation: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 CornsWhen 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.

Dry Corn• 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.

Chronic Corn• 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)Complete2)Incomplete

Degree:1)Simple2)Complex

Age:•Old•New

Origin:•High•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

Wounds of the Keratogenous MembranePuncture 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.

Disorders of the Foot:

• 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


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.


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.


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

Keratoma

• 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


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


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


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


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 hoof’s 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.


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.

Diseases of the Lateral Cartilages:

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

SideboneThis 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 denser—obliterating 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.

Diseases of the Bones:• Osteochondritis

DissecansWe 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.

Congenital and Inherited Disorders:

• 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.

Congenital and Inherited Disorders:

• Osteochondritis DissecansThis 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.

http://en.wikipedia.org/wiki/Lateral_epicondyle_of_the_humerus




Osteochondritis Dissecans

• 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


• Navicular Disease


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)

• Fotografías de Exámenes por microscopia electrónica donde se aprecia el tejido muscular normal de un Potrillo (foto izq.) comparado con un caballo con PSSM

(Acumulación anormal de polisacáridos, manchas obscuras púrpuras), 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.


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.


Toxins:


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).

Disorders Associated with Antigens: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 690XArrows: Degranulated eosinophils in the periphery

Thin Arrows: Neutrophil infiltrationCurved Arrows: Macrophages


Phaeohyphomycosis

• There are two forms of this fungal infection that affect the keratinized cells.

1.)Dermatomycosis2.) 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.

Tumors of the Hoof:

Osteochondroma

Tumors of the Hoof:

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.

Tumors of the Hoof:

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).

Tumors of the Hoof: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 skin—it 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

Tumors of the Hoof:

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

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