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The skin serves as an anatomic and physiologic barrier between the animal body and its environment. It provides protection from physical, chemical and microbiological injury. Its sensory components enable the animal to perceive heat, cold, pain, touch and pressure. Although the skin and hair coat of dogs and cats act in heat regulation, they do not function in the same manner as in animals that do not pant. The skin may help in the synthesis of vitamin D and its deeper layers have important fat storage and insulating qualities.
Perhaps the most important function of skin is to make possible an internal environment for all other organs by maintaining an effective barrier to the loss of water, electrolytes and macromolecules.
A corollary function is the exclusion of external injurious agents (chemical, physical and microbiological) from entrance into the internal environment.
Skin plays a role in the regulation of body temperature through its support of the hair coat and through regulation of the cutaneous blood supply.
Skin is a prime sense organ for touch, temperature, pain and itch.
The flexibility, elasticity and toughness of the skin allow motion and provide shape and form.
The skin surface has antibacterial and antifungal properties.
Changes in the peripheral vascular bed affect blood pressure.
Skin is a secretory organ by virtue of its apocrine and sebaceous glands.
Skin produces keratinized structures such as hair, nails and the horny layer of the epidermis.
The skin is a reservoir of electrolytes, water, vitamins, fat, carbohydrates, protein and other materials.
Processes in the skin (melanin formation, vascularity and keratinization) help determine the coat and skin color. Pigmentation of the skin prevents damage from solar radiation.
The skin functions in some species in a limited way as an excretory organ.
Vitamin D is produced in or on the skin through stimulation by solar radiation.
The skin may be an important indicator of internal disease.
The skin, hair and subcutaneous tissue of a newborn puppy represent 24 per cent of its body weight. By the time of maturity these structures only compose 12 per cent of body weight. Skin is made up of the epidermis and dermis, which are closely associated with the hypodermis (subcutis). It is difficult to dissect these layers from underlying structures since subcutaneous tissue and superficial muscles are attached closely. Some areas of skin are specially modified in thickness and structure to adapt to specific function. The structure of skin is determined embryologically and thick areas transplanted to other skin areas retain their characteristic anatomy in the new site.
Skin is continuous at each body opening with the mucous membrane located there (digestive, respiratory, ocular and urogenital portals). The thickness of various layers of the skin varies greatly from one area to another. In general the skin is thickest over the dorsum and neck and thinnest on the abdomen and sternum and in the auxiliary and inguinal regions. The hair covering also varies in density in each individual. Usually the coat is heavy and thick over the back and sides of the body, but the inside of the ears and flanks and the underside of the tail often are practically hairless.
A. Epidermis
1. Horny layer (stratum corneum)
2. Clear layer (stratum lucidum)
3. Granular layer (stratum granulosum)
4. Prickle layer (stratum spinosum)
5. Basal layer (stratum basale)
B. Epidermal appendages (adnexa)
1. Glands of the skin
a. Sebaceous glands
b. Apocrine sweat glands
c. Exocrine sweat glands
2. Claw (ungues)
3. Hair (pili)
C. Dermis (corium)
10.3.1.1 Hyperkeratosis
Hyperkeratosis refers to an increase in the thickness of the stratum corneum. The type of hyperkeratosis can be further specified by the adjectives orthokeratotic (anuclear) or parakeratotic (nucleated). Hyperkeratosis may be caused by excessive production of keratin or by excessive retention of keratin (ichthyosis). Orthokeratotic and parakeratotic hyperkeratosis are common, non-diagnostic findings in virtually any chronic dermatosis. They simply imply altered epidermopoiesis, whether inflammatory, hormonal, neoplastic, or developmental in nature. Diffuse parakeratotic hyperkeratosis alone is suggestive of seborrhea, zinc-responsive dermatosis, vitamin A-responsive dermatosis, and thallium poisoning.
10.3.1.2 Hypokeratosis
Hypokeratosis is a decreased thickness of the stratum corneum. It is much less common than hyperkeratosis and reflects an exceptionally rapid epidermal turn-over time or decreased cohesion or both between cells of the stratum corneum. Hypokeratosis may be found in seborrheic and other exfoliative skin disorders. It may also be produced by excessive surgical preparation of the biopsy site or by friction.
10.3.1.3 Dyskeratosis
Dyskeratosis is a premature and faulty keratinization of individual cells. Dyskeratosis is also used, though less commonly, to indicate a general fault in the keratinization process and, thus, in the state of the epidermis as a whole. Dyskeratotic cells are characterized by eosinophilic, swollen cytoplasm and condensed, dark-staining nuclei. Dyskeratosis may be seen in a number of inflammatory dermatoses (especially the lichenoid dermatoses and the pemphigus and seborrheic complexes) and neoplastic dermatoses (especially papilloma, squamous cell carcinoma, and keratoacanthoma).
10.3.1.4 Hyperplasia
Hyperplasia is an increased thickness of the noncornified epidermis due to an increased number of epidermal cells. The term acanthosis is often used interchangeably with hyperplasia. However, acanthosis specifically indicates an increased thickness of the stratum spinosum and may be due to hyperplasia (true acanthosis - most common) or hypertrophy (pseudoacanthosis - uncommon). Epidermal hyperplasia is often accompanied by rete ridge formation (irregular hyperplasia resulting in "pegs" of epidermis that appear to project downward into the underlying dermis). Rete ridges are not found in normal haired skin of dogs and cats.
10.3.1.5 Atrophy of the Epidermis
Atrophy is a decreased thickness of the noncornified epidermis due to a decreased size and/or number of cells. An early sign of epidermal or atrophy is the loss of the rete ridges in areas of skin where they are normally present (the nonhaired skin in dogs and cats).
Epidermal atrophy is uncommon in canine and feline skin diseases but is occasionally seen with hormonal (hyperadrenocorticism, hypothyroidism, hyposomatotropism), developmental (cutaneous asthenia), inflammatory (discoid lupus erythematosus) dermatoses.
10.3.1.6 Intercellular Edema
Intercellular edema (spongiosis) of the epidermis is characterized by a widening of the intercellular spaces with accentuation of the intercellular bridges, giving the involved epidermis a "spongy" appearance. Severe intercellular edema may lead to rupture of the intercellular bridges and the formation of spongiotic vesicles within the epidermis. Severe spongiotic vesicle formation may, in turn, "blow out" the basement membrane zone in some areas, giving the appearance of subepidermal vesicles. Intercellular edema is a common, non-diagnostic feature of any acute or subacute inflammatory dermatosis.
10.3.1.7 Intracellular Edema
Intracellular edema (hydropic degeneration, vacuolar degeneration) of the epidermis is characterized by increased size, cytoplasmic pallor, and displacement of the nucleus to the periphery of affected cells. Severe intracellular edema may result in reticular degeneration and intraepidermal vesicles.
Intracellular edema is a common, non-diagnostic feature of any acute or subacute inflammatory dermatosis. Caution must be exercised not to confuse intracellular edema with freezing artifact, delayed fixation artifact, or the intracellular accumulation of glycogen seen in the outer root sheath or normal hair follicles and secondary to epidermal injury.
10.3.1.8 Ballooning Degeneration
Ballooning degeneration is a specific type of degenerative change seen in epidermal cells and characterized by swollen eosinophilic cytoplasm without vacuolization, by enlarged or condensed and occasionally multiple nuclei, and by a loss of cohesion resulting in acantholysis. Ballooning degeneration is a specific feature of viral infections and hence is extremely rare in the skin of dogs and cats. (viral infections in the skin are more common in large animals).
10.3.1.9 Reticular Degeneration
Reticular degeneration is caused by severe intracellular edema of epidermal cells, in which the cells burst, resulting in multilocular intraepidermal vesicles whose septae are formed by resistant cells walls. It may be seen with any acute or subacute inflammatory dermatosis.
10.3.1.10 Acantholysis
Acantholysis (dyshesion, desmolysis, desmorrhexis) is a loss of cohesion between epidermal cells, resulting in intraepidermal clefts, vesicles, and bullae. Free epidermal cells in the vesicles are called acantholytic cells. This process may also involve the outer root sheath of hair follicles and glandular ductal epithelium. Acantholysis is further specified by reference to the level at which it occurs, i.e., subcorneal, intragranular, intraepidermal, or suprabasilar.
Acantholysis may be caused by severe spongiosis (any acute or subacute inflammatory dermatosis), ballooning degeneration (viral infection), proteolytic enzymes released by neutrophils (bacterial and fungal dermatoses, subcorneal pustular dermatosis), and neoplastic transformation (squamous cell carcinoma). A primary, often diagnostic cause of acantholysis is the production of autoantibodies against the intercellular cement substance seen in the pemphigue complex.
10.3.1.11 Microvesicles, Vesicles, and Bullae
Microvesicles, vesicles, and bullae are microscopic and macroscopic fluid-filled, relatively acellular spaces within or below the epidermis. Such lesions are often loosely referred to as blisters. These lesions may be caused by severe intercellular or intracellular edema, ballooning degeneration, acantholysis, hydropic degeneration of basal cells, subepidermal edema, or other factors resulting in dermoepidermal separation (e.g., the autoantibodies in bullous pemphigoid). Microvesicles, vesicles, and bullae may thus be further described as subcorneal, intragranular, intraepidermal, suprabasilar, or subepidermal in location. When these lesions contain larger numbers of inflammatory cells, they may be referred to as vesicopustules.
10.3.1.12 Hyperpigmentation
Hyperpigmentation (hypermelanosis) refers to excessive amounts of melanin deposited within the epidermis and often, concurrently in dermal melanophages. Hyperpigmentation may be focal or diffuse, and confined to the stratum basale or present throughout all epidermal layers. It is a common, non-diagnostic finding in chronic inflammatory and hormonal dermatoses as well as in some developmental and neoplastic disorders. Hyperpigmentation must always be cautiously assessed with regard to the patient's normal pigmentation.
10.3.1.13 Hypopigmentation
Hypopigmentation (hypomelanosis) refers to decreased amounts of melanin in the epidermis. It may be associated with congenital or acquired idiopathic defects in melanization (e.g., leukoderma, vitiligo), toxic effects of certain chemicals on melanocytes (e.g., monobenzyl ether of dihydroquinone in rubbers and plastics), inflammatory disorders that affect melaninization or destroy melanocytes, hormonal disorders, and dermatoses featuring hydropic degeneration of basal cells (e.g., lupus erythematosus). In those hypopigmented dermatoses associated with hydropic degeneration of basal cells, the underlying superficial dermis usually reveals pigmentary incontinence.
10.3.1.14 Crust
A crust is a consolidated, desiccated surface mass composed of varying combinations of keratin, serum, cellular debris, and often microorganisms. Crusts are further described on the basis of their composition:
- (1) serous - mostly serum
- (2) hemorrhagic - mostly blood,
- (3) cellular - mostly inflammatory cells and
- (4) exudative (serocellular) - a mixture of serum and inflammatory cells.
Crusts merely indicate a prior exudative process and are rarely of diagnostic significance. However, crusts should always be closely scrutinized, since they may contain important diagnostic clues:
- (1) dermatophyte spores and hyphae,
- (2) the filaments and coccoid elements of Dermatophilus congolensis, and
- (3) large numbers of acantholytic keratinocytes (pemphigus complex or subcorneal pustular dermatosis). Bacteria and bacterial colonies are common inhabitants of surface debris and are of no diagnostic significance.
10.3.2.1 Collagen Changes
Dermal collagen is subject to a number of pathologic changes. Collagen may undergo
- (1) hyalinization - a confluence and increased eosinophilic, glassy, refractile appearance; seen in chronic inflammation and connective tissue diseases
- (2) fibrinoid degeneration - deposition on or replacement with a brightly eosinophilic fibrillar or granular substance resembling fibrin; seen in connective tissue diseases,
- (3) lysis - a homogeneous, eosinophilic, complete loss of structural detail seen in microbial infections and ischemia,
- (4) degeneration - a structural and tinctorial change characterized by slight basophilia, granular appearance, and frayed edges of collagen fibrils; seen in feline linear granuloma and canine eosinophilic granuloma,
- (5) dystrophic mineralization - deposition of calcium salts as basophilic, amorphous, granular material along collagen fibrils; seen in hyperglucocorticoidism and, rarely, idiopathically,
- (6) atrophy - thin collagen fibrils and decreased fibroblasts, with resultant decreased dermal thickness; seen in hormonal dermatoses.
10.3.2.2 Pigmentary Incontinence
Pigmentary incontinence refers to the presence of melanin granules free within the subepidermal dermis and within dermal macrophages (melanophages). Pigmentary incontinence may be seen with any process that damages the stratum basale and the basement membrane zone, especially hydropic degeneration of basal cells (lichenoid dermatoses, lupus erythematosus, epidermolysis bullosa simplex).
10.3.2.3 Edema
Dermal edema is recognized by dilated lymphatics (not visible in normal skin), widened spaces between blood vessels and perivascular collagen (perivascular edema), or widened spaces between large areas of dermal collagen (interstitial edema). The dilated lymphatics and widened perivascular and interstitial spaces may or may not contain a lightly eosinophilic homogeneous, frothy-appearing substance (serum).
Dermal edema is a common, nonspecific feature of any inflammatory dermatosis. Severe edema of the superficial dermis may result in subepidermal vesicles and bullae, necrosis of the overlying epidermis, and predisposition to artifactual dermoepidermal separation during handling and processing of biopsy specimens.
10.3.2.4 Mucinous Degeneration
Mucinous degeneration (myxedema, mucoid degeneration, myxoid degeneration, mucinosis) is characterized by increased amounts of an amorphous, stringy, granular, basophilic material that separates, thins, or replaces dermal collagen fibrils and surrounds blood vessels and appendages in H and E stained sections. Only small amounts of mucin are ever visible in normal skin, mostly around appendages and blood vessels Mucin is more easily demonstrated with stains for acid mucopolysaccharides, such as Hale's and Alcian blue. Mucinous degeneration may occasionally be seen in numerous inflammatory, neoplastic, and developmental dermatoses and is not an uncommon feature of canine hypothyroidism and lupus erythematosus.
Follicular epithelium is affected by most of the histopathologic changes described for the epidermis. Follicular (poral) keratosis, plugging, and dilatation are common features of such diverse conditions as inflammatory, hormonal and developmental dermatoses. Perifolliculitis, folliculitis, and furunculosis (penetrating or perforating folliculitis) refer to varying degrees of follicular inflammation. Follicular atrophy refers to the gradual involution and disappearance characteristics of hormonal dermatoses. Hair follicles should be closely examined to determine what phase of the growth cycle they are in. A predominance of telogen hair follicles is characteristics of hormonal dermatoses and states of telogen defluxion (stress, disease, drugs).
Sebaceous and apocrine sweat glands may be involved in various dermatoses. Sebaceous glands may be involved in many suppurative and granulomatous inflammations (sebaceous adenitis). They may become atrophic (reduce in number and size, with pyknotic nuclei predominating) and cystic in hormonal dermatoses, in occasional chronic inflammatory processes, and as a senile change. Sebaceous glands may also become hyperplastic in chronic inflammatory dermatoses and in senile nodular sebaceous hyperplasia. Sebaceous gland atrophy and hyperplasia must always be cautiously assessed with regard to the area of the body from which the skin specimen was taken.
Apocrine sweat glands are commonly involved in suppurative and granulomatous dermatoses (hidradenitis). They may become dilated or cystic in many inflammatory and hormonal dermatoses, in apocrine cystomatosis, and as a senile change. The light microscopic recognition of apocrine gland atrophy is a moot point, since dilated apocrine secretory coils containing flattened epithelial cells are a feature of the normal postsecretory state.
The skin tends to react to most forms of injury (traumatic, bacterial, viral, etc.) by inflammation (dermatitis). Grossly, dermatitis is generally characterized by the classical inflammatory manifestation, ie., redness, heat, pain, swelling, and loss of function. Dermatitis in and of itself is not diagnostic unless analyzed closely as to pattern and cell type. Dermatitis may perivascular, diffuse, nodular, vascular, pustular, eosinophilic, neutrophilic (suppurative), or granulomatous, depending on the inciting etiologic agent.
Vesicular and pustular dermatitis show considerable microscopic and macroscopic overlap. This is because vesicles in domestic animals tend to accumulate leukocytes very early rapidly. Thus vesicular dermatitis in these species frequently appear pustular or vesculopustular both macroscopically and microscopically. Intraepidermal vesicles and pustules may be produced by intercellular and/or intracellular edema (any acute to subacute dermatitis reaction), ballooning degeneration (viral infections), acantholysis (the autoantibodies of pemphigus the proteolytic enzymes from neutrophils in microbial infections and subcorneal pustular dermatosis) and hydropic degeneration of basal cells (lupus erythematosus, epidermolysis bullosa simplex, drug eruptions). It is useful to classify intraepidermal vesicular and pustular dermatitis as to their location within the epidermis.
Subepidermal vesicles and pustules may be formed through hydropic degeneration of basal cells (lupus erythematosus) dermoepidermal separation (bullous pemphigoid), severe subepidermal edema and/or cellular infiltration (cellulitis, ectoparasitism), and severe intercellular edema with disruption of the basement membrane zone (spongiotic perivascular dermatitis). Caution is warranted when examining older lesions as reepithelialization may result in subepidermal vesicles and pustules assuming an intraepidermal location. Such reepithelialization is usually recognized as a single layer of flattened, elongated basal epidermal cells at the base of the vesicle or pustule.
The healthy, intact integument is remarkably resistant to bacterial invasion. Colonization of the skin by pathogenic bacteria is usually limited by a lack of moisture, constant desquamation of surface corneocytes, and ecological pressures exerted by the normal flora. Disturbance of any of these factors may allow the establishment of bacterial infection. Once infection is established, it outcome depends on the nature of the organism and on host defenses. Bacterial infection of the skin is called pyoderma. Pyodermas may be classified as primary or secondary and superficial or deep. Primary pyodermas are usually caused by a single organism and have a specific disease pattern. The cause of the initial breakdown of host defenses is usually not identified. Secondary pyodermas are bacterial infections which occurs subsequent to skin injury or disease. Any one or more of a number of organisms may be responsible, though Staphylococcus and Streptococcus spp. are the more common isolates. Superficial pyodermas involve the epidermis, usually heal without scarring, are of short duration, do not involve the regional lymph nodes, and are not associated with systemic illness. Superficial pyodermas are characterized by the formation of papules, transient pustules, and crusts, sometimes localize in the ostial of hair follicles. Histologically, they take the form either of an intraepidermal pustular dermatitis (impetigo) and /or a superficial folliculitis. The predominant inflammatory cell present is the neutrophil. Despite the bacterial cause, the bacterial colonies are not readily apparent in histologic sections. Dermatophilus congolensis is an exception.
Deep pyodermas involve the dermis, with or without the subcutis, often heal with scarring, have a chronic, sometimes recurrent course, usually involve regional lymph nodes and may produce signs of systemic illness. Grossly deep pyodermas take a variety of forms, including papules or pustules with erect hairs emerging from their center, subcutaneous nodules, abscesses, ulcers, or fistulous tracts. Histologically, deep pyoderma may take the pattern of a deep folliculitis, furunculosis, nodular to diffuse, suppurative or pyogranulomatous dermatitis, or panniculitis. In the dog, goat, and horse, furunculosis is often accompanied by tissue eosinophilia. Such reactions are often misinterpreted as "hypersensitivity reactions" or "probable parasite migrations".
Impetigo is a subcorneal pustular dermatitis caused by Staphylococcus aureus and rarely by Streptococcus spp. It occurs commonly in puppies, occasionally in piglets and kittens, and affects the udders of lactating dairy cows and goats. Puppies between 2 weeks and 1 year of age are affected. The disease often occurs as a secondary infection due to unhygienic conditions, poor nutrition, or debilitating diseases (Canine Distemper). The lesions occur on glabrous skin of the axilla, groin, and ventral abdomen. Erythematous macules or papules, 5-10 mm in diameter, develop into superficial pustules containing honey-colored exudate. These rupture to form shallow erosions with an erythematous border and a light yellow crust. The final stage is a hyperpigmented macule. Impetigo in kittens commences on the back of the neck and may spread to the withers, head, ventral chest, and abdomen. Pasteurella multocida and B-hemolytic streptococci are cultured from the superficial pustules. The lesions may developed from excessive wetting of the kitten's neck as they are transported by the queen. The lesions are similar morphologically to those of puppies.
Histologically, impetigo in all species is characterized by intraepidermal pustular dermatitis. Hair follicles are spared. The pustules are usually subcorneal and contain predominantly neutrophils, which may or may not contain intracellular bacteria. Acantholysis is minimal to absent. Focal epidermal necrosis surrounding the pustules is not uncommon.
Botryomycosis, which literally means a fungal infection with lesions resembling a cluster of grapes, is actually a chronic granulomatous disease caused by bacteria, usually Staphylococcus aureus. Botryomycosis occurs in horses, cattle, sheep, pigs, humans, dogs and cats. Lesions usually follow some form of skin trauma and involve the deep dermis and subcutis, occasionally extending to the muscle and adjacent bone. The macroscopic lesions are single or multiple subcutaneous nodules, which often ulcerate and exude a purulent exudate containing tiny, white granules, the so-called grains. The microscopic lesions is pyogranulomatous dermatitis and panniculitis. The predominant inflammatory cells are epithelioid macrophages and neutrophils, but multinucleated giant cells, lymphocytes, and plasma cells will be present according to the stage of the lesion. The macroscopic grains correspond microscopically to round or oval bodies in which a central core of bacterial colony is embedded in a homogeneous matrix. The bacterial colonies are usually Gram-positive cocci. A homogeneous eosinophilic substance, known as Splendore-Hoeppli material, may coat the grains and take the form of a radiating corona of club-shaped bodies.
Dermatophilosis (cutaneous streptothricosis, rain scald, lumpy wool, mycotic dermatitis) is an acute or chronic, superficial pyoderma caused by the actinomycete, Dermatophilus congolensis. (Streptothrix bovis). The disease affected a wide range of species in all age groups. It occurs most often in cattle, horses, and sheep, occasionally in goats, pigs and mules, and rarely in dogs, cats, and humans.
Dermatophilus congolensis is a pleomorphic, Gram-positive bacterium that grows as filamentous, branching septate mycelium. Septation occurs both transversely and longitudinally, giving rise to small coccoid spores known as zoospores. Dermatophilus congolensis cannot penetrate healthy skin. The two most important predisposing factors in the pathogenesis of dermatophilosis are prolonged wetting and mechanical damage to the skin.
The gross lesions of dermatophilosis in cattle usually commence along the dorsal midline between the withers and rump, extending laterally onto the flanks, thoracic wall, shoulders, and neck. The characteristic lesions are raised, roughly circular, thick, laminated, gray-brown scale crusts that are penetrated by tufts of hair. In very severe lesions, the hairs may be buried in thick plaques of scale crust. When individual crusts are forcibly detached, the hair is also epilated. The underlying epidermis is moist and erythematous, and in older lesions raised areas of granulation tissue may be present.
Dermatophilosis affecting the hairy skin of the distal extremities of lambs and weaners in the United Kingdom and Australia has been named "strawberry footrot," although the disease has no relationship to footrot. Small, raised, dome-shaped scale crusts form on the leg, particularly on the anterior aspect of pastern, but may expand and coalesce to cover the leg to the level of the neck or knee. Removal of the dense scale crust reveals shallow ulcers with hemorrhagic pits, supposedly resembling a strawberry.
The microscopic features are unique and best understood by explaining the pathogenesis of the infection. The organism invades and multiplies within the epidermis as branching filaments, which divide in a characteristic multidimensional fashion, giving rise to multiple rows of coccoid organisms. They do not invade the dermis, but induce an extensive purulent exudate beneath the epidermis, separating it from the dermis. The invaded epidermis cornifies and a new epidermis forms under the exudate, which in turn is invaded by hyphae at the periphery of the lesion. A second inflammatory exudate separates the new epidermis from the dermis, and a third epithelium is generated. The process is repeated, resulting in a thick scab composed of alternate strata of cornified epidermis and exudate. The organisms can usually be seen in hematoxylin and eosin stained tissue sections, and are clearly observed as Gram-positive filaments or chains of cocci in sections stained with the Gram's technique.
Swine erysipelas is caused by Erysipelothrix insidiosa, a Gram-positive bacillus which has a wide geographic distribution and a wide host range. The disease occurs in several forms:
These forms may occur together, in sequence, or separately. Acute septicemic erysipelas is characterized by petechial hemorrhages over serous membranes and other tissues. The spleen and lymph nodes may be enlarged and reddened. Bluish discoloration of the skin may occur. Chronic skin lesions are characterized by square, rhomboidal, or diamond shaped, raised, hyperemic, or purple-colored lesions over the body. Also, the ends of the tail and ears may become necrotic. The skin lesions are associated with arthritis and thrombosis of smaller arterioles. Arthritis and endocarditis are chronic lesions caused by the localization of the organism in these sites. Endocarditis is characterized by vegetative thrombi on heart valves (mitral most often). These thrombi may lead to embolism and infarction of various organs. Arthritis may involve one or more legs; the joints enlargement is firm due to thickening of the joint capsule and the capsular ligaments; there may be erosion of the articular cartilage with periostitis and osteitis; ankylosis may occur. Erysipelothrix insidiosa is quite sensitive to penicillin.
Cutaneous lesions occur in the course of a number of viral diseases in domestic animals. Viruses may induce skin lesions on local infection, but the intact integument is resistant to viral penetration, and injection via an arthropod bite or introduction through a cutaneous wound is a prerequisite for infection. An example of local viral infection are papillomas induced by the Papovaviruses. Much more often, viruses localized in the skin during the viremia phase of a systemic infection. Examples include some poxvirus infections, malignant catarrhal fever, and the vesicular stomatidies such as foot and mouth disease. Pantropic viruses, such as those of Canine Distemper and hog cholera, may cause cutaneous lesions, but most viruses causing cutaneous lesions are epitheliotropic. Some epitheliotropic viruses, in particular the Poxviridae, have a predilection for the epithelium of the skin. Other diseases cause primary lesions in the alimentary tract, with lesser involvement of the skin.
Cutaneous viral diseases are more common in food-producing animals than in domestic pets. Some of these diseases, notably sheeppox, cause significant mortality. Others have an economic impact because of their deleterious effect on production. Viral diseases with cutaneous manifestations are rare in dogs and cats. Canine distemper is associated with nasodigital hyperkeratosis so-called hard-pad disease, and pustular dermatitis (impetigo).
The Poxviridae are a large family of complex DNA viruses. Highly epitheliotropic, they cause cutaneous and systemic disease in birds, wild and domestic mammals, and humans. Of the domestic species, only the dogs does not appear to suffer pox infections. Some members of the Poxviridae, including sheeppox, ectromelia, (mousepox) monkeypox, fowlpox, and the now eradicated human smallpox, cause severe systemic disease. Other cause mild, localized disease, for example, pseudocowpox, which chiefly affects the teats of milking cows. A few poxviruses are associated with hyperplastic and neoplastic conditions, such as the Shope fibroma virus of rabbits.
Most of the poxviruses are host specific, but some such as pseudocowpox are zoonotic. Infection is usually achieved by cutaneous or respiratory routes.
Poxviruses induce lesions by a variety of mechanisms. Degenerative changes in the epithelium are caused by virus replication and induce vesicular lesions typical of many poxvirus infections. Degenerative lesions in the dermal or submucosal tissues sometimes result from ischemia secondary to vascular damage, due to virus multiplication in endothelial cells. Poxvirus infections also induce proliferative lesions. Poxviruses replicating in the epidermis, such as contagious ecthyma, typically induce hyperplasia along with degenerative changes.
Pox lesions have a typical developmental sequence. They commence as erythematous macules, become papular, and then vesicular. The vesicular stage is well developed in some pox infections, such as sheeppox, and is transient or nonexistent in others, such as contagious ecthyma. Vesicles develop into umbilicated pustules with a depressed center and a raised, often erythematous border. This lesion is the so-called pock. The pustules rupture, and a crust forms on the surface. This crust may become very thick, as in lesions of contagious ecthyma. Lesions heal and often leave a residual scar. The mucosal lesions are briefly vesicular and develop into ulcers rather than pustules.
Histologically, pox lesions develop as epidermal cytoplasmic swelling and vacuolation, usually first affecting the cells of the outer stratum spinosum. Rupture of the cells produces multiloculated vesicles. The dermal lesions include edema, vascular dilation, a perivascular mononuclear-cell infiltrate, and variable neutrophilic infiltrate. Neutrophils migrate into the epidermis and aggregate in vesicles to form microabscesses. Large intraepidermal pustules may form and sometimes extend into the superficial dermis. There is usually marked epithelial hyperplasia, sometimes pseudocarcinomatous hyperplasia of the adjacent epithelium. This contributes to the raised border of the umbilicated pustule. Rupture of the pustule leads to inflammatory crust formation, which is often mixed with ortho- or parakeratotic hyperkeratosis and colonized by surface bacteria.
Poxvirus lesions contain characteristic intracytoplasmic inclusion bodies. These are single or multiple, or varying size and duration. The more prominent inclusions are designated type A. They are eosinophilic, reflecting their high protein content.
Contagious ecthyma is a poxvirus disease of sheep and goats, with incidental infections occurring in humans, cows, and very rarely, dogs. The disease is caused by a parapoxvirus closely related to pseudocowpox and bovine papular stomatitis. Synonyms for contagious ecthyma include "contagious pustular dermatitis," "infectious labial dermatitis," "soremouth," "scabby mouth," and "orf." Orf is used to describe human infections.
Contagious ecthyma affects sheep of all breeds. It is predominantly a disease of lambs and kids since infection. The gross lesion usually commence at the commissures of the lips and spread around the lip margins to the muzzle.
The lesions develop through the typical pox phases but are much more proliferative. The vesicular stage is transient, and pustules are flat rather than umbilicated. The most significant feature of the gross lesions of contagious ecthyma is the layer of thick-brown grey crust, which may be elevated 2-4 mm above the skin surface.
Pseudocowpox is caused by a parapoxvirus. The virus is closely related to bovine papular stomatitis virus. The infection is common and often unapparent. The disease affects milking cows but spares dry cows, non-milking heifers, and bulls. Morbidity in a herd approaches 100%, but only 10-15% of cows are affected at any one time. The economic significance lies in the effect on milk production, either as a result of sore teats or because of secondary bacterial mastitis. Lesions, which affect the teats, udder, and perineum, commence as erythematous macules and develop into vesicles but do not form the umbilicated pustules seen in cowpox and vaccinia infections.
Sheeppox, caused by a member of the virus genus Capripox, is the most serious of the pox disease of domestic animals. It exists currently in Africa, Asia, and the Middle East. The disease is exotic to the Americas, Australia, and New Zealand. Sheeppox causes extensive economic loss through high mortality, reduced meat, milk, or wool yields, commercial inhibitions from quarantine requirement, and the cost of disease prevention programs.
The sheep is the natural host for the sheeppox virus. Transmission of infection is by direct contact with diseased sheep or indirect contact via a contaminated environment. Sheeppox occurs in all ages of sheep, but the disease is most severe in lambs, with the mortality reaching 80-100%.
Sheeppox is a systemic disease. Infection is usually by the respiratory route but may occur through skin abrasions. The incubation period is 4-7 days and is followed by leukocyte associated viremia. The virus localizes in many organs, including the skin, where the virus concentration is highest 10-14 days postinfection. The initial clinical signs are fever, lacrimation, salivation, serous nasal discharge, and hyperesthesia. The skin lesions develop 1 or 2 days later. They have a predilection for the sparsely wooled areas and typically involve eyelids, cheeks, nostrils, vulva, udder, scrotum, prepuce, ventral surface of the tail, and the medial thigh. The macroscopic lesions follow the typical pattern for pox infections. Sheeppox lesions have a prominent vesicular stage.
Although the virus is introduced percutaneously, the infection is systemic. A leukocyte associated viremia disseminates the virus to the various tissues, including the skin, where greatest virus concentration occurs 9-12 days postinfection. The virus infects a wide range of cells, including keratinocytes, mucous and serous glandular epithelium, fibrocytes, skeletal muscle, macrophages, pericytes, and endothelial cells. Damage to the endothelial cells causes vasculitis. The epidermis shows the typical hydropic changes associated with poxvirus infection. Intracytoplasmic, eosinophilic, homogeneous, occasionally granular inclusion bodies occur in endothelial cells, pericytes, keratinocytes, macrophages, and fibroblasts. Virions in various stages of development are present in these inclusion-containing cells and in peripheral nerves. Neutrophils, macrophages, and occasionally, eosinophils migrate into the dermis in the acute lesions, to be replaced as the lesion ages by a predominantly mononuclear cell population.
Swinepox is caused chiefly by a member of the genus Suispoxivirus. The disease has received relatively little attention as it is usually mild and mortality is negligible. It affects chiefly young, growing piglets but occurs in neonates, indicating that transplacental infection is possible. Normally, swinepox is transmitted by contact. Grossly, swinepox must be differentiated from the vesicular diseases, hog cholera pityriasis rosea, dermatosis vegetan and sunburn. The histologic lesions also follow the pattern for pox infections. The eosinophilic, intracytoplasmic inclusion bodies are quite transient and are not found in older lesions.
Fungal diseases are divided into three categories: the superficial mycosis, the subcutaneous or intermediate mycoses, and the deep or systemic mycoses. The superficial mycoses are caused by fungi that invade the skin and its appendages to a very limited extent. The most important of the superficial mycoses, dermatophytosis, is caused by fungi that grow only in the nonviable keratinized tissue. The intermediate mycoses are caused by a wide range of fungi, which being mostly saprophytic, induce disease only when introduced into the subcutaneous tissues by penetrating cutaneous wounds.
The deep or systemic mycoses are also caused largely by saprophytic fungi. Severe disease results from the infection of immunosuppressed or otherwise debilitated animals, usually by inhalation, although occasionally following skin penetration.
Dermatophytosis (dermatomycosis) (ringworm) is a superficial infection of the keratinized layers of the skin and its appendages caused by a group of taxonomically related mycelial fungi known as dermatophytes. The disease, which occurs worldwide, is common in humans and animals.
The dermatophytes belong to three genera: Microsporum, Trichophyton, and Epidermophyton. Most animal pathogens belong to the first two genera.
Dermatophytes do not invade living tissue but remain confined to the keratinized layer, which they attack with proteolytic enzymes having keratinolytic activity. Inflammatory and immunologic reaction is induced by fungal products permeating the underlying dermis. These produces are chiefly extracellular proteinases such as "keratinase," collagenase, and elastase.
Natural infection is by contact, which may be direct or indirect by exposure to contaminated objects such as grooming equipment or tack. Young animals are most susceptible to dermatophyte infection than adults.
If infection is established, branching septate hyphae colonize the surface stratum corneum, the follicular infundibula, and the hair shafts. The hyphae break up into round or oval arthrospores, either within the hair (endothrix) or on its external surface (ectothrix). In general, Microsporum infections are ectothrix, and Trichophyton both endo- and exothrix.
The initial reaction to dermatophyte invasion has been likened to a contact irritant dermatitis, but one caused by substances released from a microbiologic agent. This results in increased epidermopoiesis, which is reflected histologically by moderate to marked hyperplasia, often with rete-ridge formation, and by ortho- and parakeratotic hyperkeratosis.
The surface epidermis and proximal external root sheath are both affected. The dermal reaction is often mild, consisting of a lymphocytic perivascular infiltrate in the superficial dermis and around adnexa. Folliculitis and a pyogranulomatous furunculosis may develop in severe dermatophyte infections. The hyperkeratosis of the pilar canal and follicular plugging common to all dermatophyte infections predispose to secondary bacterial infection, which may be manifested as a suppurative folliculitis, pyogranulomatous furunculosis, or both.
The gross appearance of the individual lesions of ringworm are variable, but their character is similar, consisting of different degrees of erythema, follicular papules, scaling, crusting, and alopecia. The alopecia results from breakage of the brittle, parasitized hair shafts and is not permanent unless a secondary bacterial folliculitis destroys, the root of the hair follicle. The classical lesion is circular, with peripheral expansion and central healing producing the "ring" appearance; it is the exception rather than the rule in many infections.
Dermatophytosis is a self-limiting infection. Lesions take from a few week so several months regress, depending on the species of fungus and degree of host adaptation.
Dermatophytosis is one of the less common skin infections in dogs. The condition chiefly affects young dog; in older animals it is often associated with debilitating disease or lack of immune competence. The most frequently isolated species is Microsporum canis, followed by M. gypseum and Trichophyton mentagrophytes.
Dermatophytosis is a common disease of cats caused almost exclusively by Microsporum canis. The cat is the natural host for this fungus and acts as a source of infection for other animals and humans.
Sporotrichosis is a chronic disease, primarily of skin and subcutaneous tissues, caused by the dimorphic fungus Sporothrix schenckii. Sporotrichosis occurs in horses, mules, cats, dogs, cattle, and buffalo.
The lesions in horses tend to occur on the distal extremities. In dogs and cats, primary lesions often occur on the head or the distal extremities and spread to other body sites. There are three clinical syndromes associated with sporotrichosis. The mildest form is cutaneous. It is probably the most common form in the dog and cat and is characterized by the formation of single or multiple subcutaneous nodules 1-5 cm in diameter, which tend to ulcerate and discharge a small amount of thick, red-brown purulent exudate. The lesions have a chronic course. The cutaneous-lymphatic form, the most common in equine infections, is characterized by the formation of multiple nodules, arranged in lines along the course of lymphatics which become thick and corded. Ulceration of the nodules leaves deep cratiform lesions that heal slowly.
The microscopic lesion of sporotrichosis is a diffuse and/or nodular pyogranulomatous dermatitis and panniculitis. The fungi grow in tissues in yeast form. They may be extremely sparse and sometimes are demonstrated only by fluorescent antibody techniques or by culture.
The yeasts are round, oval, or cigar-shaped single or budding cells, 2-6 um in diameter. The cigar-shaped forms, considered classical for sporotrichosis, may not be found regularly in tissues.
The term phycomycosis applies to certain mycoses in which culture has not been obtained but the fungus in tissue sections conforms to certain morphologic criteria. The phycomycoses in this context currently include: mucormycosis, oomycosis, rhinosporidiosis, and trichomycetosis. Most of this organisms are characterized by raised, ulcerated, hard (due to extensive fibrosis) gross lesions. Microscopically there is extensive necrosis, fibrosis, and infiltration by epithelioid macrophages (granulomatous inflammation). The extensive necrosis is the result of local infarction due to thrombi produced by the fungi's characteristic proliferation in blood vessels.
Fleas are ubiquitous and obligate parasites. They are not permanent parasites and often leave one host for another. They are not host specific, but there is probably some host preference. Fleas are the most common ectoparasite of cats and dogs. The most important species are Ctenocephalides felis, the cat flea, and C. canis, the dog flea. The clinical manifestations of flea infestation are highly variable. Some animals, despite heavy infestations, remain asymptomatic carries. Others develop flea-bite dermatitis, which is a reaction to the many irritant substances in the fleas's saliva. The lesions are usually distributed over the dorsal lumbar and neck areas and comprise a mild papulocrustaous dermatitis, with or without mild to moderate pruritus. In certain animals, components of the flea saliva are allergenic, resulting in flea allergy dermatitis. Finally, the blood sucking activities of fleas may induce blood-loss anemia in heavily infested animals, particularly in kittens, puppies, or debilitated adults.
10.8.2.1 Sarcoptic Mange
Sarcoptes scabei is responsible for scabies in humans and sarcoptic mange in domestic animals. It is probably the most important ectoparasitism in swine. Sarcoptic mange is common in the dog and may be under-diagnosed. It occurs rarely in the cat. So-called feline scabies is caused by Notoedres.
The pathogenesis of lesions in sarcoptes scabei infestation is due to direct damage inflicted by the parasite mechanically and by the irritant effects of its secretion and excreta, and by an allergic reaction developed against one or more of the extracellular products of the parasites.
The primary parasite-related lesions of sarcoptic mange are erythematous, macules or papules that develop a local scale crust in reaction to the burrowing mites. The lesions of allergic sarcoptic mange largely result from self-trauma induced by pruritus. In the early stages these include erythematous papules, excoriations, hemorrhagic crusts, and patchy alopecia. Chronic lesions include marked alopecia, scaling and lichenification. The distribution of the lesions is characteristic in the various species. In pigs the mites have a predilection for the inner surface of the pinna, where they cause primary lesions. In dogs, the preferred sites are the lateral elbows, hocks, ventral thorax, and margin of the pinna.
Histologically, the lesions vary with the balance between allergic reactions and parasitic infestations. There is a thick scale crust composed or ortho- and parakeratotic hyperkeratosis, serum lakes, neutrophilic debris, and numerous refractile Sarcoptes ova. The epidermis is markedly hyperplastic, with prominent rete-ridge formation and/or pseudocarcinomatous hyperplasia. Dermal lesions include variable vasodilation, endothelial swelling, edema, fibrosis, perivascular mononuclear-cell infiltration, and neutrophilic exocytosis, depending on the development of secondary bacterial infection or epidermal excoriation.
10.8.2.2 Demodectic Mange
Demodex mites are normal inhabitants of the hair follicles or sebaceous glands in all species of domestic animals and in humans. The mites found in the different hosts are regarded as separate species, although they are similar morphologically. The mites are generally named for the host species, as in D. canis of dogs, and D. bovis of cattle.
Demodex mites are part of the normal fauna of the skin in most, if not all, animal species. This implies that small numbers of mites exist in harmony with the host, and it is only when the equilibrium between the host and parasite is altered in favor of the mite that excessive proliferation occurs and lesions of demodectic mange are produced. The most severe expression of demodectic mange is seen in the dog as a generalized dermatitis, which is on occasion fatal.
Demodectic infection in dogs begins when puppies are infected from the bitch via direct skin contact during nursing in the neonatal period. Mites are first observed on the muzzles of newly infected pups. Occasionally this normally benign parasitic infestation is converted into a pathogenic one because of two interrelated factors, genetic predisposition and selective or partial states of immunodeficiency.
The disease in dogs takes two clinical forms. Localized or squamous demodicosis occurs in young dogs 3-10 months of age and is usually self-limiting. The lesions are single or multiple, well-circumscribed, erythematous, scaly, and alopecia patches usually affecting the head around the lips and eyes or on the extremities.
The generalized or pustular form is characterized by patchy to diffuse alopecia, erythema, scaling, and crusting. Secondary bacterial pyoderma is extremely common. The lesions are generalized, are particularly severe on the face or limbs, and feet, and are often pruritic. Peripheral lymphocytic patchy infiltration occurs in approx. 50% of affected dogs. Often the dogs are depressed, febrile, and debilitated, and may die.
Histologically, the localized form of the disease is characterized by a predominantly lymphocytic-plasmacytic perifolliculitis. There is marked follicular hyperkeratosis associated with the presence of demodectic mites in the upper third of the follicle. Large numbers of mites occupy the hair follicles at all levels and also occlude the opening of the sebaceous gland into the pilar canal. Large populations of mites stimulate a proliferative response in the follicular epithelium with marked follicular hyperkeratosis causing follicular plugging. Bacterial proliferation within plugged follicle often induces a neutrophilic folliculitis. The combined effects of follicular keratosis, mite proliferation, and folliculitis lead to follicular rupture and release of mites, bacteria, keratin, sebum, and other irritant products into the dermis. The bacteria, chiefly Staphylococcus spp., induce a suppurative dermatitis, often with abscessation. The keratin and other irritant substances stimulate a granulomatous reaction, chiefly of epithelioid macrophages, but a few multinucleate giant cells may be present. This pyogranulomatous furunculosis of demodectic mange differs from most other types of furunculosis in that eosinophils are rare or absent in the reaction.
Ticks belong to the suborder Ixodidea in the class Arachnida. They are divided into two suborders, the Argasidae and the Ixodidae. The Argasidae are the so-called soft ticks, lacking the scutulum that characterizes the Ixodidae. Otobius megnini, known as the "spinose ear tick," is parasitic to all domestic animals, causing severe parasitic otitis externa, predisposing to bacterial infection or myiasis. Most of the pathogenic species of tick are found in the Ixodidae.
Ticks are most important as vectors for a large number of serious viral, rickettsial. bacterial, and protozoal disease of domestic animals. Ticks also harm their hosts more directly by causing local injury at the site of attachment. If infestation is heavy, fatalities may result. The local injury may predispose to secondary bacterial infection and to screw worm myiasis. Heavy infestations are also capable of causing anemia as a result of the bloodsucking activities of the ticks, but the Ixodidae, which engorge only once at each instar, are much less important in this respect than are the argasid ticks, which as adults engorge repeatedly. Several species of Ixodid ticks are capable of causing paralysis of the host by the injection of toxins in their saliva (tick paralysis).
Stephanofilariasis is a nematode dermatitis that occurs in cattle, and caused by Stephanofilaria stilesi. The parasite causes circumscribed lesions which are located on the ventral abdomen near the midline. The adult forms of the parasite are found either in small cyst with epithelial linings in the base of hair follicles or in the dermis near the epidermis. A zone of inflammatory cell surrounds parasites. The microfilaria are found a short distance from the adults in spaces in the dermal papillae. Lesions along the ventral abdomen are characterized by hyperkeratosis and parakeratosis with an accumulation of exudate.
Lice infestation is referred to as pediculosis. Various species of biting and sucking lice infest domestic animals. Cattle are more commonly infested with Damalina bovis (biting louse) and by Hematospinus eurysternus and Linognathus vituli (sucking lice). In sheep, Damalina ovis and Linognathus are most common. Hematospinus suis occurs with frequency in swine. In general, lice infestation is manifested by pruritis and skin irritation; animals become unthrifty in appearance and develop a rough hair coat.
Immune-mediated skin diseases are those diseases in which the animals own immune system plays a critical role in the pathogenesis and formation of lesions. The two basic types are autoimmune and hypersensitivity (allergic). In autoimmune skin diseases, the animal generates antibodies towards components of its own skin. In hypersensitivity, exaggerated responses by the immune system result in tissue damage. Hypersensitivity diseases can be the result of Type I (anaphylactic), Type II (cytotoxic), Type III (immune-complex), or Type IV (cell-mediated) hypersensitivity.
10.11.1.1 Pemphigus
Pemphigus refers to a group of immune-mediated skin diseases characterized clinically by vesicles, bullae, and erosions, histologically by acantholysis, and immunologically by the development of antibodies directed against surface antigens of squamous epithelial cells. The antigen or antigens against which the antibodies are directed are glycoproteins located on the surface or epidermal cells. The stimulus triggering the immune response is unknown. The binding of pemphigus antibodies to the epidermal-cell surface stimulates the synthesis and secretion of plasminogen activator. It is postulated that the resultant localized increase in plasmin causes loss of epidermal cohesion through proteolysis and leads to the formation of intraepithelial vesicles or bullae.
Different types of pemphigus are recognized. These are divided according to the level within the epidermis at which acantholysis occurs. The reason for the development of acantholysis at different epidermal levels is unknown but may relate to the antigenic specificities of the keratinocytes at different stages of their differentiation.
10.11.1.2 Pemphigus vulgaris
Pemphigus vulgaris has been reported in the dog and cats. The condition is primarily a vesiculo-bullous erosive to ulcerative disorder that may affect the oral cavity, mucocutaneous junctions (lips, nostrils, eyelids prepuce, vulva, anus), skin, or any combination thereof. About 90 per cent of the dogs have oral cavity lesions at the time of diagnosis. Cutaneous lesions occur most commonly in the groin and axillae. Histologically, there is suprabasilar acantholysis with resultant cleft and vesicle formation. Basal epidermal cells remain attached to the basement membrane zone like "a row of tombstones". Neutrophils often invade the vesicles forming an intraepidermal pustule.
10.11.1.3 Pemphigus foliaceus
In pemphigus foliaceus, the acantholytic process occurs at a superficial level in the epidermis (subcorneal), the lesions being typically exfoliative rather than erosive-ulcerative. The fragile vesicopustules rupture to form very shallow ulcers which become covered by thick crust and scale. Lesions tend to appear first on the nose and spread to periorbital areas, the ears, neck, and ventral abdomen. Mucocutaneous and oral lesions are rare. Histologically, there is subcorneal acantholysis, with vesicle and/or pustule formation. When the condition is pustular, differentiation from impetigo is necessary. Differentiation is on the basis of acantholytic cells in the pustule (many in pemphigus, few or absent in impetigo), and involvement of the hair follicle epithelium (present only in pemphigus foliaceus).
10.11.1.4 Pemphigus vegetans
Pemphigus vegetans is characterized by marked (pseudoepitheliomatous) acanthosis, and intraepidermal microabscesses that may occur at varying level in the epidermis. The microabscesses contain predominantly eosinophils and few acantholytic cells.
10.11.1.5 Pemphigus erythematosus
Pemphigus erythematosus may represent a combined form of pemphigus foliaceous and lupus erythematosus. The gross lesions closely resemble those described for pemphigus foliaceous except that they are restricted to the head. Bullous pemphigoid is a chronic, immune-mediated skin disease characterized clinically by large, tense bullae, histologically by the subepidermal location of these bullae, and immunologically by the presence of an antibody to the lamina lucida of the basement membrane zone.
Bullous pemphigoid occurs in dogs and horses. The gross lesions are vesiculo bullous, ulcerative, and crusted in nature. The lesions affect mucous membranes, particularly of the oral cavity, mucocutaneous junctions, skin of the face, ears, axilla, groin, and paws.
Grossly, bullous pemphigoid is usually indistinguishable from pemphigus vulgaris.
Histologically, there is a subepidermal bulla filled with a fibrin net and variable numbers of neutrophils and mononuclear cells. Acantholytic keratinocytes are not present. The basal cells that line the roof of the bulla are not initially degenerate. The floor of the bulla is lined by the basement membrane.
10.11.1.6 Lupus Erythematosus
Lupus erythematosus occurs in two forms: systemic lupus erythematous affects multiple tissues including the skin, and discoid lupus erythematosus is localized to the skin.
Gross skin lesions include erythematous macules and shallow plaques, vesicobullous eruptions, ulcerations, alopecia, and hypopigmentation. Lesions are often widespread, with a predilection for face, ears, and nailbeds.
The microscopic lesions of systemic lupus are variable. The critical diagnostic pattern is an interface dermatitis with hydropic degeneration of basal cells and a lymphohistiocytic infiltrate at the dermoepidermal junction (lichenoid). Pigmentary incontinence, a consequence of the basal-cell degeneration, is a helpful histologic change, as is marked subepidermal vacuolar change. Occasionally this change is sufficiently severe to cause cleft or bulla formation between the dermis and epidermis.
10.11.1.7 Hypersensitivity Diseases:
10.11.1.7.1 Atopy
Atopy (atopic dermatitis, allergic inhalant dermatitis) in humans in defined as a heritable predisposition to develop IgE-mediated hypersensitivity reactions. Overproduction of IgE to ordinarily innocuous stimuli is thought to reflect a dysfunction of suppressor T cells, which normally regulate IgE-synthesizing B cells. The fixation of IgE to mast cells renders certain tissues susceptible to injury on reexposure to the eliciting allergen. The integument is the chief target organ in the atopic dog.
Canine atopy is a common condition accounting for 10% of all dermatologic disease. The usual route of allergen exposure is considered to be respiratory, although ingestion and percutaneous absorption may occur. The primary problem in canine atopy is pruritus. It is doubtful whether a primary lesion of atopy exists. The pruritus initiates an itch-scratch cycle that is central to the pathogenesis of the lesions. The terrier breeds, particularly the West Highland White, are highly predisposed. The Irish setter, Dalmatian, Miniature Schnauzer, Lhasa Apso, and English bulldog are also prone, but all dogs may be affected.
Gross lesions primarily affect the face, the feet, and the axillae. In chronically affected dogs, lesions may become generalized. They develop as a result of self-trauma and vary from erythema, excoriation, crusting, and traumatic alopecia to scaling, hyperpigmentation, and lichenification. Secondary pyoderma occurs in about a third of the cases.
The histologic pattern is of simple, superficial perivascular dermatitis. The most consistent lesions are vasodilation and edema of the superficial dermis, with a mild to moderate perivascular accumulation of mononuclear cells and variable numbers of neutrophils.
10.11.1.7.2 Allergic Contact Dermatitis
Allergic contact dermatitis is a type IV hypersensitivity reaction. The initiating substances are haptens, which are not immunogenic until conjugated with a carrier protein. The carrier is usually an epidermal protein, possible a surface molecule on the Langerhans' cell. The Langerhans' cell, an epithelial macrophage, is responsible for antigen presentation, both locally in the skin and in regional lymph nodes. The specifically sensitized T lymphocytes thus produced are assumed to mediate the delayed hypersensitivity reaction through release of various lymphokines.
The predominant sign in allergic contact dermatitis is pruritus. Lesions have a distribution that reflects the area of contact and tend to involve the glabrous skin, unless the allergen is in a liquid or aerosol form. Primary lesions are erythematous macules, papules, and occasionally, wheals. The lesions are complicated by self-trauma with up to 40% of dogs showing secondary pyoderma. Chronic lesions are crusting, scaling, lichenification, partial to complete alopecia, and hyperpigmentation. Leukoderma rather than hyperpigmentation often occurs in the reaction to plastic food containers.
The elasticity of the skin, the orderly maturation of the epidermis and the quality and luster of the horny appendages reflect in a sensitive but general manner the well-being of an animal. This applies equally to nutritional diseases and diseases of other causes.
Vitamin A is involved in cellular growth and differentiation as well as having specialized function in visual processes and reproduction. Vitamin A has a controlling effect on epithelial differentiation. Deficiency of vitamin A causes squamous epithelia to become hyperkeratotic and secretory epithelia to undergo squamous metaplasia.
Hypovitaminosis A has been reported in all species of domestic animal. It may be secondary to dietary deficiency, decreased intestinal absorption, liver disease, or toxicities such as chlorinated naphthalene toxicity of cattle. The cutaneous lesions of hypovitaminosis A in cattle are a marked scaling and crusting dermatitis; in the pig follicular hyperkeratosis; and in cats, scaling and alopecia. The histologic lesions reflect a severe disturbance in keratinization. There is marked epidermal hyperplasia alternating ortho- and parakeratotic hyperkeratosis, follicular keratosis, and dyskeratosis. The sebaceous glands are hyperplastic.
Zinc is an indispensable trace element found in a large number of enzyme systems. The requirement of swine for zinc is remarkably high and a deficiency of the element leads to a diseases commonly referred to as parakeratosis of swine. This disease is characterized by marked acanthosis and parakeratosis along with some hyperkeratosis. The addition of excessive calcium to swine rations marginal in zinc tends to increase the incidence and severity of parakeratosis. There seems to be an apparent antagonistic effect between calcium and zinc (parakeratosis is most prevalent in pigs receiving mainly vegetable protein and excessive calcium supplement). A deficiency of essential fatty acids will produce cutaneous lesions similar to those of zinc deficiency (these lesions are not influenced by supplements of zinc). Parakeratosis occurs chiefly in pigs from 2 to 4 months of age. Initial gross lesions consist of erythema, and excessive sebaceous secretion. Later, there is excessive growth and keratinization of skin epithelium with the formation of horny crust and fissures. The "crusts" are usually dry on the exposed surface, and are usually easily removed. However, occasionally, secondary infections occur with exudation. In addition to the skin, lesions also occur in the esophagus and on the tongue. Microscopically, there is acanthosis, parakeratosis, and keratinization. Natural zinc deficiency also occurs in ruminants.
Endocrine disorders affecting the skin are associated with various hormonal disturbances. Endocrine dermatoses share many similar gross features, including hypotrichosis or alopecia that is frequently bilaterally symmetrical variable degrees of pigmentary disturbance (hypermelanosis or hypomelanosis), a hair coat that is often coarse, dull, dry, brittle, easily epilated, and fails to regrow normally after being clipped, and variable degrees of seborrheic skin disease and/or pyoderma.
Endocrine dermatoses also have many histologic findings in common. These include ortho- and/or parakeratotic hyperkeratosis, follicular keratosis, follicular dilatation, follicular atrophy, predominance of telogen hair follicles, epidermal hypermelanosis, and sebaceous gland atrophy. These lesions suggest endocrine skin disease but are not pathognomonic. Confirmation of an endocrine dermatosis requires demonstration of a hormone deficiency or excess, lasting response to specific therapy, and demonstration of appropriate lesions in endocrine glands. Secondary seborrheic skin disease and/or pyoderma often complicate endocrine dermatoses. They result in varying degrees of inflammation, from superficial perivascular dermatitis (hyperplastic, spongiotic) to perifolliculitis, folliculitis, and furunculosis.
The skin is the most common site for neoplasia is dogs, horses, cattle, and cats. There is considerable variation in the reported prevalence of skin tumors, the ratio of malignant to benign tumors, and the relative prevalence of different histologic types.
Primary skin tumors can be divided into those of ectodermal and those of mesodermal origin. Those of ectodermal origin are subdivided into tumors of the epidermis and adnexa. Those of mesoderm are divided according to the structural elements of dermis (fibrous tissue, muscle, fat, blood vessels) and leukocyte-related cells of the dermis (histiocytes, mast cells, lymphocytes). Melanocytic tumors occupy a special category of their own. In general, ectodermal neoplasms are behaviorally benign, and those of adnexa are almost exclusively so. Many types of mesodermal tumors, in contrast, are histologically malignant and regularly exhibit locally infiltrative growth and occasionally will metastasize.
Tumor location on the animal is important in judging the potential for malignancy: for example, in squamous-cell carcinoma, those originating on the digits show much more aggressive behavior than those arising elsewhere. Genetic predisposition is important in dogs.
Common skin tumors include papillomas, squamous cell carcinomas, basal cell tumors, sebaceous adenomas, dermoid cysts, melanomas, histocytomas, mast cell tumors and sarcoids, to mention only a few.
SLIDE 1: CANINE SKIN: NORMAL - The skin is shown here diagrammatically. The dark (upper) zone represent the epidermis, which in canine skin is thin and without prominent epidermal pegs. The light (lower) zone represent the dermis.
SLIDE 2: CANINE SKIN: HYPERKERATOSIS - Hyperkeratosis is an increase in thickness of the horny layer of the skin. This condition occurs in normal skin and also on specialized areas such as the digital pads and planum nasale.
SLIDE 3: CANINE SKIN: ACANTHOSIS, HYPERKERATOSIS AND PAR- AKERATOSIS - Observe the prominent rete ridges in the epidermis denoting acanthosis (hyperplasia of the stratum spinosum). The increase in the stratum corneum observed is referred to as hyperkeratosis (orthokeratotic). presence of nuclei in the stratum corneum indicates the more specific conditions of parakeratosis (nucleated).
SLIDE 4: CANINE SKIN: HYPERKERATOSIS AND PARAKERATOSIS - This is a close-up of the stratum corneum from the previous slide. What are the primary causes of these conditions?
SLIDE 5: CANINE SKIN: PARAKERATOSIS - Observe the nuclei in the stratum corneum
SLIDE 6: CANINE SKIN: ACANTHOSIS - In this close-up slide on acanthosis, note that the basal layer is intact, differentiating this condition from neoplasia. What neoplasm of the skin may resemble this condition?
SLIDE 7: BOVINE SKIN: HYPERKERATOSIS - Grossly it can be observed that hyperkeratosis is characterized by scaling and crusting.
SLIDE 8: BOVINE SKIN: HYPERKERATOSIS - Close-up of the previous slide. What is "dandruff?"
SLIDE 9: CANINE SKIN: INTERCELLULAR EDEMA (SPONGIOSIS) - Intercellular edema is edema between keratinocytes. This causes increased distance between individual cells.
SLIDE 10: CANINE SKIN: INTRAEPIDERMAL VESICULAR AND PUSTULAR DERMATITIS - Microabscesses and pustules are microscopic or macroscopic intraepidermal and subepidermal cavities filled with inflammatory cells. Microabscesses and pustules are further described on the basis of location and cell type.
SLIDE 11: CANINE SKIN: MICROABSCESSES - Microabscesses are observed in many dermatoses. This illustrates microabscesses containing many eosinophils located within the epidermis.
SLIDE 12: CANINE SKIN: FOLLICULITIS
SLIDE 13: CANINE SKIN: MACULE - A macule is a circumscribed, flat spot up to 1 cm in size characterized by change in color of the skin. The discoloration can result from several processes; an increased in melanin pigmentation, depigmentation, and erythema or local hemorrhage.
SLIDE 14: CANINE SKIN: PAPULE - A papule is a small, solid elevation of the skin up to 1 cm in diameter. A papule can always be palpated as a solid mass. Many are pink or red swellings produced by tissue infiltration of inflammatory cells, by intraepidermal and subepidermal edema, or by epidermal hypertrophy. Papules may or may not involve hair follicles. Examples are the erythematous papules seen in chronic allergic contact dermatitis of dogs after exposure to plants.
SLIDE 15: CANINE SKIN: CYST - A cyst is an epithelium-lined cavity containing fluid or a solid material. They are smooth, well-circumscribed fluctuant-to-solid masses. Skin cysts are usually lined by adnexal epithelium (hair follicle, sebaceous, or apocrine) and filled with cornified cellular debris or sebaceous or apocrine secretions.
SLIDE 16: CANINE SKIN: SCALE - A scale is an accumulation of loose fragments of the horny layer of the skin (cornified cells). The scale is the final product of epidermal keratization.
SLIDE 17: CANINE SKIN: CRUST - A crust is a dried exudate on the surface on a lesion is formed when dried exudate, serum, pus, blood, cells, scales, or medications adhere to the surface and often mingle with hair. Unusually thick crusts are found in hairy areas because the dried material tends to adhere more tightly than in glabrous skin. Hemorrhagic crusts in staphylodemodicosis are brown or dark red; yellowish-green crusts appear in some cases of pyoderma; tan, lightly adhering crusts are found in superficial pustular pyoderma (impetigo).
SLIDE 18: CANINE SKIN: SCAR - A scar is an area of fibrous tissue that has replaced the damaged dermis or subcutaneous tissue. Scars are the remnants of trauma or dermatologic lesions. Most scars in dogs and cats are alopecic, atrophic, and depigmented. Proliferative scars do occur, and in dark-skinned dogs scars can be alopecic and hyperpigmented. Scars are observed following severe burns and in deep pyoderma.
SLIDE 19: CANINE SKIN: ULCER - An ulcer is a break in the continuity of the epidermis, with exposure of the underlying dermis. A severe pathologic process is required to form an ulcer; therefore, a search for the cause is always indicated. It is important to note the structure of the edge, the firmness of the ulcer, and the type of exudate in the crater. A scar is always left after healing of ulcers.
SLIDE 20: CANINE SKIN: EROSION - An erosion is a shallow ulcer that does not penetrate the basal cell layer and consequently heals without scarring.
SLIDE 21: CANINE SKIN: EXCORIATION - Excoriation is a superficial removal of epidermis caused by scratching, biting or rubbing. Most excoriations are self-produced and caused by pruritus; they invite secondary bacterial infection.
SLIDE 22: CANINE SKIN: LICHENIFICATION - Lichenification is a thickening and hardening of the skin characterized by an exaggeration of the superficial skin markings. Lichenified areas frequently result from friction. They may be normally colored but more often are hyperpigmented.
SLIDE 23: CANINE SKIN: PUSTULE - A pustule is a small, circumscribed elevation of the skin filled with pus. It is technically small abscess (occasionally sterile) that may be intraepidermal or follicular in location. The color is usually yellow but may be pink or red. Examples are acne, folliculitis, and the pustules seen on the abdomen or puppies with superficial pustular pyoderma (impetigo).
SLIDE 24: CANINE SKIN: ABSCESS - An abscess is a demarcated fluctuant lesion resulting from a dermal or subcutaneous acculation of pus. This is not visible on the surface of the skin.
SLIDE 25: CANINE SKIN: TRAUMA - This unfortunate dog was to be injected intravenously. By mistake, the injection was made subcutaneously. Being very irritating to subcutaneous tissues, a perivascular slough occurred.
SLIDE 26: CANINE NECK: NECROSIS and GANGRENE - A rather tight fitting choke-chain was placed around the neck of this dog at approximately 3-months of age. The owner forgot to adjust or remove the chain as the dog grew. Subsequently, the animal was submitted to necropsy with lesions as observed in this slide. Actually, the choke chain was embedded in the skin to some extent. (Give a reason(s) for the death of this dog. What advice would you give the owner? Would you expect to find evidence of necrosis and gangrene associated with the lesion observed in this slide?).
SLIDE 27: CANINE THIGH/LEG: ERYTHEMIA (REDDENING OF THE SKIN) - Observe the erythemia (hyperemia) along the ventral aspect of the thigh and leg. This type lesion represent the acute stage of dermatitis or inflammation. The cause of this condition was not determined.
SLIDE 28: BOVINE SKIN: DERMATITIS - This calf has a bacterial infection of the skin resulting in inflammation (dermatitis). The marked reddening is clearly observable. (What is the term for bacterial infection of the skin?).
SLIDE 29: CANINE SKIN: ACUTE PUSTULAR DERMATITIS (IMPETIGO) - This dog was diagnosed with the viral disease Canine Distemper. Note the acute pustular lesions in the groin region. These are due to secondary bacterial infection of the skin following immunosuppression by the virus.
SLIDE 30: CANINE SKIN: STAPHYLOCOCCAL IMPETIGO - Note nonfollicular subcorneal pustule.
SLIDE 31: CANINE SKIN: STAPHYLOCOCCAL FURUNCULOSIS - Note follicular rupture with resultant pyogranulomatous dermal reaction around hair follicle.
SLIDE 32: PORCINE SKIN: SWINE ERYSIPELAS - This is an excellent example of "diamond skin lesions" associated with swine erysipelas. You should be able to make a tentative diagnosis of this condition of the basis of gross observations if lesions similar to these are found. Remember, the skin lesions are not always typical diamond-shaped. Note the reddened, raised areas over the skin. (What lesions would you expect to find in the joints and heart of this pig? How would you treat this disease?).
SLIDE 33: PORCINE SKIN: SWINE ERYSIPELAS - Observe the well-defined diamond-shape lesion over the skin. (Give a likely pathogenesis for the lesions observed).
SLIDE 34: OVINE SKIN: CONTAGIOUS ECTHYMA - Observe the multiple pustules in the skin of this sheep; also, note the severe reddening of the skin.
SLIDE 35: OVINE SKIN: CONTAGIOUS ECTHYMA - This microscopic section denotes the vesicular changes that occur in the epidermis in association with this disease.
SLIDE 36: HUMAN FINGER: CONTAGIOUS ECTHYMA - This young veterinary student was given the opportunity to examine the mouth of a sheep that had several small ulcers on the lips; no gloves were used. Subsequently, multiple well-defined pustules developed on all parts of the hand. This slide was taken approximately 20 day after infection. (Describe the lesions(s) observed).
SLIDE 37: HUMAN FINGER: CONTAGIOUS ECTHYMA - This is the same lesion denoted in the previous slide but the photo was made 30 days after infection. (Describe the lesions(s) observed).
SLIDE 38: PORCINE BODY: SWINE POX - This is an example of true or natural swine pox; observe the red, raised pock lesions over the skin.
SLIDE 39: PORCINE BODY: SWINEPOX - This is a good example of pock lesions in the healing stages; note the well-defined lesions on the ventral aspect of the body; this pig eventually recovered and went to slaughter. (Discuss the microscopic lesions that you would expect in cases of pox).
SLIDE 40: MICE FEET/TAILS: MOUSE POX (Ectromelia) - This is an example of ectromelia note the ulcerations and rash-like lesions located over the legs and tails. These mice had the systemic form of the disease.
SLIDE 41: MOUSE FEET/TAIL: MOUSE POX (Ectromelia) - This is a close-up view of the previous slide. Observe the well-defined lesions on the feet and tail.
SLIDE 42: CANINE DERMATOPHYTOSIS DERMOGRAM
SLIDE 43: BOVINE BODY: DERMATOMYCOSIS - This is a severe case of ringworm infection in a cow; observe the areas of alopecia and the rough hair coat. (How would you confirm your tentative diagnosis of dermatomycosis?).
SLIDE 44: BOVINE FACE: DERMATOMYCOSIS - Observe the typical rounded and elevated plaques around the eyes, etc.
SLIDE 45: BOVINE SKIN: DERMATOMYCOSIS - Observe organisms associated with the hair follicles.
SLIDE 46: DEMODICOSIS DERMOGRAM
SLIDE 47: CANINE FACE: DEMODECTIC MANGE (ACARIASIS) - This is an example of demodectic mange; lesions in this dog were confined primarily to the head and face. The gross lesions observed are most likely due to a combination factors, including direct irritation by the mites as well-as trauma associated with the severe pruritis.
SLIDE 48: CANINE SCABIES DERMOGRAM
SLIDE 49: FOX HEAD/FACE: SARCOPTIC MANGE (ACARIASIS) - This is one of several foxes found on a university campus; the animals acted rather friendly toward students and others. However, the animals were killed and submitted to necropsy for examination. Examination of the skin revealed the lesions observed in this slide; skin scrapings and histopathologic examinations revealed numerous mites that were identified as Sarcoptic spp. In addition, tissues were submitted to the State Public Health Laboratory for rabies examination. (What tissues, etc. would you submit for rabies examination? Why do you feel tissues from this fox were submitted for rabies examination? Describe the gross lesions observed in this slide. How would you confirm your tentative diagnosis of ascariasis?).
SLIDE 50: CANINE SKIN: WHAT IS YOUR DIAGNOSIS? - This dog had a severe chronic dermatitis and skin sections were examined microscopically. On microscopic examination, abnormal structures were found in hair follicles as observed in this slide; these structures resembled parasites and some were more or less "cigar-shaped! (PLEASE GIVE YOUR DIAGNOSIS AS REQUESTED ABOVE).
SLIDE 51: EQUINE EAR CANAL: SPINOUS EAR TICKS - Otobius spp. is the parasite observed in the ear canal of this horse. (What clinical signs would you expect?).
SLIDE 52: BOVINE SKIN: STEPHANOFILARIASIS - Observe the circumscribed areas of parasitic dermatitis due to S. stilesi; For some reasons, these parasites tend to localize along the midline of the ventral abdomen. (Describe the gross lesions.
SLIDE 53: BOVINE SKIN: STEPHANOFILARIASIS - This view gives the impression that the skin is markedly thickened along the ventral abdomen; hyperkeratosis and parakeratosis were prominent on histopathologic examination. (It is possible to make a tentative diagnosis on the basis of location and appearance of the lesions? What are microfilaria? Name the likely etiologic agent for the condition observed in this slide.
SLIDE 54: BOVINE SKIN: PEDICULOSIS - Observe the lice associated with the skin and hair of the dairy cow; these parasites were numerous on the ventral abdomen. This case of pediculosis was caused by Damalina bovis. (Would you expect to observe evidence of anemia in severely infested animals? You should be familiar with the common lice of domestic animals).
SLIDE 55: BOVINE SKIN: PEDICULOSIS - Pediculosis in this calf was caused by Linognathus spp; observe the parasites over the skin.
SLIDE 56: PORCINE SKIN/HAIR: PEDICULOSIS - These are lice removed from a heavily infested pig; the general condition of the animal was poor. In addition to lice, there were lesions consistent with those of enzootic pig pneumonia.
SLIDE 57: CANINE PEMPHIGUS VULGARIS DEMOGRAM
SLIDE 58: CANINE SKIN: PEMPHIGUS FOLIACEUS - Numerous neutrophils and acantholytic keratinocytes within a subcorneal pustule.
SLIDE 59: CANINE SKIN: PEMPHIGUS VEGETANS - Papillated epidermal hyperplasia, hyperkeratosis, papilomatosis, and several intraepidermal microabscesses.
SLIDE 60: CANINE SKIN: BULLOUS PEMPHIGOID - Subepidermal vesicle and lichenoid band of inflammatory cells
SLIDE 61: PORCINE BODY: PARAKERATOSIS OF SWINE - This pig is from a group that received an experimental ration lacking in zinc with excessive calcium. The growth was stunted in comparison with controls; Observe the patchy areas of alopecia, rough hair coat, and the thickened skin (especially in legs).
SLIDE 62: PORCINE SKIN: PARAKERATOSIS OF SWINE - This is an advance case of parakeratosis; note the scaly appearance of the skin, etc. Discuss the role of calcium in the disease known as parakeratosis. Discuss the gross and microscopic changes associated with zinc deficiency in pigs).
SLIDE 63: BOVINE SKIN: PAPILLIOMATOSIS - Cutaneous papillomatosis in the bovine (as well as in other species) it transmissible and caused by a viral agent. Observe the papillary structures which formed subsequent to proliferation of the epidermis over the dermal papillae (thus, dermal connective tissue is drawn out into long cores for the papillae). This disease is self-limiting and resolution occurs spontaneously.
SLIDE 64: CANINE SKIN: MAST CELL TUMOR - Observe the multiple neoplastic masses found over the body of this dog; Mast cell tumors occur with frequency in the dog and they must be differentiated from histocytomas.
