1. Dermatosparaxis

Figure 13.1. Foal. Neck and Withers. Dermatosparaxis. A large tear is evident in the skin of the neck and dorsal thorax. Differential diagnosis: epitheliogenesis imperfecta.

Figure 13.2. Horse. Dorsal Back. Cutaneous Asthenia. Note the loose, hyperextensive areas of skin. Minor trauma easily damages skin of affected animals. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Cutaneous asthenia (dermatosparaxis) is considered an inherited autosomal recessive congenital condition resulting in faulty assembly of collagen, the major structural protein in the dermis. The condition is seen in the American Quarter horse and rarely in other breeds. It is characterized by loose, hyperextensible, and unusually fragile skin that is torn by minor trauma. Animals appear normal at birth but develop skin wounds by 6–12 months of age. Tears in the skin may be preceded by hematomas or seromas. The affected skin may be palpably thin, very stretchy, and velvety. The patches of thinned, hyperextensible, fragile skin are often sunken below the surface of surrounding, normal skin. The legs, shoulders, and saddle areas are most often affected. The diagnosis is usually made by clinical lesions and breed association. Microscopically, collagen fibers may be smaller and sparser, and the dermis may be thin compared with normal skin.

2. Epidermolysis bullosa

Figure 13.3. Foal. Epidermolysis Bullosa. Ulcers overlying the point of the hip, stifle, and lateral hock.

Epidermolysis bullosa (EB) refers to a rare group of hereditary and congenital diseases caused by defects in the structural proteins in the basement membrane zone that result in weakening of the dermal epidermal junction. The pathogenesis of the different forms are not completely studied in the horse, but in other species that have been studied document mutations in genes that lead to defective formation of keratin intermediate filaments or anchoring proteins such as collagen types VII and XVII, laminin, plectin, and integrins.

Foals may appear normal at birth but quickly develop subepidermal vesicles and bullae that eventuate into extensive sharply demarcated regions of ulceration. Areas of the body subject to friction or minor trauma such as the tongue, oral mucosa, and pressure points over bony prominences are most often affected. Foals may slough the entire hoof capsule.

EB is most often seen in draft horses but has also been documented in other types of horses. Expression of the condition can be variable due to the different subtypes of EB, but there is no cure for the condition, and extensive ulcerations can lead to euthanasia.

1. Coronary band disease

Figure 13.4. Horse. Coronary Band. Ulcerative Coronitis. Ulcerative lesions on the coronary band. (Courtesy of Dr. E.G. Clark, Calgary, Canada.)

The coronary band region of the foot can be involved in a number of different more widespread cutaneous or systemic disease processes. Lesions of the coronary band can be proliferative, hyperkeratotic, vesicular, ulcerative, or necrotizing. Conditions to consider when faced with coronary band lesions are pemphigus foliaceus, vasculitis, vesicular stomatitis, multisystemic epitheliotropic disease, sarcoidosis, vitamin A deficiency, selenium toxicity, hepatocutaneous syndrome, dermatophilosis, dermatophytosis, or coronary band dysplasia, to name a few.

Differentiating between these conditions depends on evaluation of a complete history and physical examination, concurrent cutaneous lesions, evidence of systemic disease, biopsy interpretation, and tissue culture and sometimes response to therapy. A few examples of conditions primarily affecting the coronary band are discussed here.

Coronary band dysplasia (coronary band dystrophy) is a condition of the horse characterized clinically by extensive crusting, proliferation, and hyperkeratosis and often exudation of coronary bands. Although most affected horses are not lame, chronic lesions can lead to hoof wall deformities that can lead to fissuring and cracking of the hoof wall and eventual lameness. The condition is symmetric.

Figure 13.5. Horse. Hooves. Selenium Toxicosis. Coronary Band Ulcers. Cracking and brittle hooves that slough from the coronary band, exposing the sensitive laminae.

Histologically, the lesions are characterized by marked epidermal papillary hyperplasia and parakeratotic hyperkeratosis. Suppurative to eosinophilic inflammation and pustule formation and epidermal dysplasia have been reported. Most cases are reported in draft breeds, but clear breed dispositions are not well established. The cause of the lesions is not known and has been speculated to be a type of cornification disorder.

Selenium is a metalloid that acts as an antioxidant and also competes with sulfur in the formation of some proteins such as keratin. Chronic exposure to sublethal doses of selenium occurs in horses and other ungulates feeding on plants that accumulate selenium from the selenium rich soil found in Utah, Colorado, Montana, South and North Dakota, Wyoming, Arizona, Kansas, and Nebraska. Soil in parts of many other countries may be high in selenium as well. Chronic selenium ingestion leads to weight loss and alopecia and hoof wall deformities consisting of rings and grooves and possible sloughing of the hoof wall. Lameness is common. Cutaneous lesions are characterized histologically by atrophic, hyperkeratotic hair follicles.

2. Linear alopecia

Linear alopecia is a rare cutaneous condition occurring most often in young Quarter horses. It is characterized clinically by one or more vertically oriented 2- to 10-mm-wide and from 3 cm to 1 m in length linear areas of alopecia with variable crusting and scaling. The lines of alopecia are most often noted on the neck, shoulder, or thorax. The cause is unknown but speculated to be a form of an immune-mediated attack on follicles or a manifestation of keratinocyte-altered cytokine production that incites inflammation. The diagnosis is made by histologic examination of the affected regions that reveals a lymphocytic to lymphohistiocytic to granulomatous mural folliculitis with giant cells. Follicular destruction may occur. The condition is usually asymptomatic and most often permanent.

Figure 13.6. Mare and Foal. Whole Body. Linear Alopecia. Linear alopecia and linear crusting affecting both animals. mare and foal. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Figure 13.7. Horse. Lateral Neck. Linear Alopecia. Vertical bands of alopecia and crusting. Scars should be considered as a differential diagnosis. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

3. Seborrhea

Figure 13.8. Horse. Head. Seborrhea. Note large areas of alopecia and white scales. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Seborrhea is a disorder of cornification leading to scaling and crusting. It occurs in the horse most often secondary to other inflammatory, nutritional, or infectious conditions of the skin or in conjunction with systemic disease. In many cases, a specific cause cannot be identified. In the horse, seborrhea most often occurs in the mane and tail or anterior surface of the rear cannon bone region (cannon keratosis) and leads to excessive production of white scale and variable degrees of alopecia. In some cases, seborrhea can affect large areas of the body. Histologically, there is acanthosis and hyperkeratosis with variable degrees of inflammation.

1. Leukotrichia and leukoderma

Acquired loss of pigment of the hair (leukotrichia) or skin (leukoderma) can occur secondary to trauma such as burns, freezing, inflammation, or immunologic attack on either melanocytes or cells containing melanin. Exposure to compounds (found in some rubber objects) that inhibit melanogenesis can also lead to depigmentation in areas of contact. The skin and hair may be affected independently or in concert, depending on the underlying cause. Leukotrichia can occur in various patterns such as spots (spotted leukotrichia) or lines (reticulated leukotrichia). The condition can wax and wane or be permanent.

2. Vitiligo

Vitiligo refers to an acquired form of depigmentation of the skin that may be due to antimelanocyte antibodies or other mechanisms that disrupt melanin formation.

Figure 13.9. Horse. Head and Neck. Fading Arabian Syndrome. Color fading of hair of head and neck. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Figure 13.10. Horse. Muzzle. Chronic Cheilitis. Fading Arabian Syndrome. Depigmentation of the lips and muzzle. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Figure 13.11. Horse. Perivulvar Region. Fading Arabian Syndrome. Perivulvar depigmentation. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Fading Arabian syndrome is a form of vitiligo in young horses, frequently less than 2 years of age. Affected animals develop the characteristic pale, depigmented macules seen in vitiligo, around the eyes, lips, muzzle, hooves, anus, and genitalia.

1. Actinic dermatitis

Ultraviolet radiation damages skin. Lightly pigmented and sparsely haired skin is most vulnerable to absorption of ultraviolet radiation, but other factors such as altitude, latitude, ozone layer, and smog can also influence the degree of radiation reaching the skin. The nose, eyelids, and genital areas of the horse are most often affected, but any lightly pigmented, nonhaired region of skin is susceptible. Ultraviolet radiation stimulates light-absorbing molecules in the skin leading to energy production from electron transfer and free radical production that damage DNA, enzymes, and other cellular proteins. Damaged nucleoproteins can lead to cell death or mutations that can lead to preneoplastic changes and potential development of squamous cell carcinomas or hemangiosarcomas of the skin. Acute lesions are recognized as burns and are characterized by erythema, edema, and possible bullae formation. Chronic exposure leads to gross lesions of alopecia, scaling, and crusting that correspond to epidermal hyperplasia, hyperkeratosis, and erosions. The epidermis over time will become dysplastic and may eventuate into a squamous cell carcinoma. Dermal lesions include congestion, fibrosis, and buildup of collagen and elastin fibers. Dermal hemangiomas and hemangiosarcomas may also develop.

2. Photosensitization

Photosensitization dermatitis occurs when photodynamic agents are deposited in skin that is subsequently exposed to sunlight. Lesions occur on poorly haired, lightly pigmented, sun-exposed skin. This anatomic distribution is key to establishing the cause of the lesions. There are several types of photosensitization. In primary, or type 1, photosensitization, the horse ingests plants or drugs that contain photoreactive agents that are deposited in the skin.

In type 2 photosensitization, animals are born with an inability to properly metabolize erythrocyte breakdown products, and the photoreactive hematoporphyrins are deposited in the skin. This type has not been reported in the horse.

Type 3 photosensitization occurs in horses with hepatocellular damage or biliary obstruction that impairs the excretion of the photoreactive chlorophyll catabolite, phylloerythrin.

Type 4 photosensitization is reserved for poorly understood cases of photosensitivity in which no pathogenesis can be defined.

Finally, some cases of photosensitization occur after contact with photosensitizing agents, and in these cases, lesions are limited to areas of potential contact such as muzzle, extremities, or ventrum.

Cutaneous lesions of photosensitization are similar regardless of the cause. Initial gross lesions consist of erythema and edema that can progress to vesicle formation and ulcers with exudation and tissue necrosis. Histologically, the changes correspond to the initial gross lesions and include subepidermal vesicle formation, coagulative necrosis of the epidermis and dermis with edema, and fibrinoid degeneration of the vasculature. The tissue sloughs, and pruritus is often a feature. Clinical differentials include chemical or thermal burns and other vesicular and necrotizing conditions of the skin. A careful consideration of the sites affected, exposure to plants or other potential sources of photodynamic agents, and evaluation of liver function is usually needed to determine the cause of the photosensitizing dermatitis.

Figure 13.12. Horse. Head. Focal Erythematous, Exudative, Ulcerative Dermatitis. Photosensitization. Nonpigmented skin is affected. (Reprinted from Illustrated Guide to Equine Diseases, Sameeth M. Abutarbus, Figure 5-61a, Page 302, Wiley-Blackwell, 2009.)

3. Photoactivated vasculitis

Photoactivated vasculitis occurs in horses and affects white-haired extremities. The pathogenesis of this condition is not clearly defined. Horses have normal liver function and no history of ingestion or cutaneous exposure to photoreactive agents. Not all white-haired extremities are affected, and protection from sunlight does not always lead to resolution of the lesions. Lesions are found on lower extremities and are characterized by erythema, edema and serum exudation. Erosions and ulcers may form. Histologically, there is a vasculitis of the superficial dermal vascular plexus and epidermal erosion or ulceration and dermal edema with mild hemorrhage. In chronic cases, the epidermis becomes hyperplastic and hyperkeratotic.

Figure 13.13. Horse. Distal Hind Limbs. Focal Exudative Dermatitis. Equine Photoactivated Vasculitis. There is evidence of alopecia, erythema, and serum exudation on lower portion of legs. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

1. Hypersensitivity dermatoses

a. Atopy

Figure 13.14. Horse. Neck. Atopy. Areas of hyperpigmentation. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Figure 13.15. Horse. Back of Head. Atopy. Areas of excoriation. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Atopy is a genetically based enhanced or exaggerated immunoglobulin E–mediated immune response (allergic response) to inhaled or transepidermal environmental antigens. It most often manifests as pruritus. Clinical lesions are usually the result of self-trauma and include alopecia, hyperpigmentation, and excoriations. The condition manifests as recurrent urticaria in some horses. The face, ears, legs, and ventrum are the areas most often affected. The mane and tail may also be affected. Microscopically, there is a nonspecific perivascular dermatitis with variable numbers of lymphocytes, histiocytes, and eosinophils. In some horses, there may be an eosinophilic folliculitis or the presence of eosinophilic granulomas. The major differentials are insect and food allergy.

b. Culicoides hypersensitivity

Figure 13.16. Horse. Skin over Abdomen. Culicoides Hypersensitivity. Alopecia, crusting, and scaling of the ventral midline.

Culicoides hypersensitivity results in severe pruritus, focal alopecia, and self-mutilation. Gross lesions vary from papules, nodules to erosions, crusts, and alopecia.

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Culicoides hypersensitivity – Fact sheet

Definition

• Most common allergic dermatosis of horses
  
• Intensely pruritic
  
• Hypersensitivity to salivary antigens of Culicoides gnats (also known as biting midges, punkies, no-see-ums)
  
• Combined hypersensitivity reaction; type 1 (immediate and late phase) and type 4 (delayed type)
  
• Gnats usually feed on mane, belly, and tail
  
• Also referred to as sweet itch, Queensland itch, muck itch, summer itch, summer eczema, summer fungus
  
• Culicoides sp. implicated as vectors for Onchocerca cervicalis

Incidence

• Very common
  
• Occurs worldwide
  
• Age of onset approximately 1–4 years
  
• Seasonal: spring and summer
  
• Often more severe each year
  
• May occur year-round, especially in tropical and subtropical climates

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Culicoides hypersensitivity – Pathologic features

Gross findings

• Multifocal papules that may cause hair to stand erect
  
• Secondary lesions include alopecia, broken hairs, crusting, and scaling
  
• Lesions often on the head, neck, withers, tail, and ventral midline but vary depending on species of Culicoides involved
  
• May cause depigmentation

Microscopic findings

• Superficial and/or deep perivascular dermatitis, usually eosinophilic and edematous
  
• Possible lymphocytes and mast cells
  
• Possible spongiosis, hyperkeratosis, and acanthosis
  
• Sterile eosinophilic folliculitis may be seen in conjunction with hypersensitivity reactions
  
• Possible ulcerations

Differential diagnosis

• Ectoparasitism
  
• Other hypersensitivity dermatoses

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c. Urticaria/Angioedema

Thought to be due to a type 1 hypersensitivity reaction with numerous proposed etiologies, including (but not limited to) drugs, arthropod bites/stings, contact allergens, and temperature extremes. These lesions are often pruritic.

Figure 13.17. Horse. Whole Body. Dermal Edema, Multifocal. Urticaria (Hives). Multifocal to coalescing, swelling, and edema of the dermis. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Figure 13.18. Horse. Neck. Dermal Edema. Urticaria, Multifocal (Hives). Multifocal swelling. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

2. Autoimmune dermatoses

a. Bullous pemphigoid

Figure 13.19. Horse. Body. Ulcerative Dermatitis, Multifocal. Bullous Pemphigoid. Severe, multifocal ulceration, secondary to ruptured vesicles and bullae present around the lateral flank and abdomen.

Bullous pemphigoid is an autoimmune disease, with antibodies directed against hemidesmosomal proteins that anchor the cells of the stratum basale to the extracellular matrix. Vesicles and bullae develop that progress to ulceration, in which the entire epidermis lifts off the dermis. Crusting is frequently present. Lesions in horses are often generalized with both cutaneous and mucocutaneous sites affected; however, sloughing of the oral mucosa in particular is often marked.

Figure 13.20. Horse. Nonglandular Stomach. Ulcerative Gastritis. Bullous Pemphigoid. Extensive, coalescing ulceration of the squamous cell lining.

b. Pemphigus foliaceus

Figure 13.21. Horse. Head. Vesicular and Pustular Dermatitis, Multifocal. Pemphigus Foliaceus. Severe annular crusting and alopecia on the face.

Figure 13.22. Horse. Pectoral Region. Vesicular and Pustular Dermatitis, Multifocal. Pemphigus Foliaceus. Numerous pustules with annular areas of crusting and alopecia on chest.

Gross lesions may range from pustules to vesicles, bullae, erosions, and/or ulcers. Appaloosas and Thoroughbreds are predisposed. Pemphigus foliaceus is the most common autoimmune dermatosis in the horse; it begins on the face, ventrum, or legs and may become generalized within a few months. Although the primary lesion of pemphigus foliaceus is pustular and vesiculobullous, these lesions are often very short lived, and there is progression to crusts, erosions, and (often annular) alopecia. Other lesions include matted hair coat, scaling, and hair tufting.

c. Lupus erythematosus

Figure 13.23. Horse. Body. Exfoliative Dermatitis. Systemic Lupus Erythematous (SLE). Note the extensive alopecia, scaling, and depigmentation. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Figure 13.24. Horse. Nose and Muzzle. Exfoliative Dermatitis. SLE. Severe scaling. (Courtesy Dr. E.G. Clark, Calgary, Canada.)

Lupus erythematosus in the horse is a rare and incompletely defined immune-mediated disease that can have lesions limited to the skin or the skin can be involved as part of the systemic condition. The lesions are exacerbated by sunlight. Cutaneous lesions in either condition are most often characterized by patchy alopecia, scaling, and leukoderma of the face, neck, and trunk. Depigmentation of the periocular region, lips, and nostrils is common. Cases of systemic lupus erythematosus may also have lymphedema, weight loss, polyarthritis, anemia, uveitis, thrombocytopenia, or a variety of other conditions indicating systemic disease. The diagnosis of cutaneous lupus is based on biopsy findings of a lymphocytic hydropic interface dermatitis with basal cell apoptosis and pigmentary incontinence and possible areas of basement membrane thickening.

3. Other immune-mediated dermatoses

a. Alopecia areata

Figure 13.25. Horse. Skin. Lymphocytic Mural Folliculitis. Alopecia Areata. Aggregates of lymphocytes surround hair bulbs. The lymphocytic infiltration of anagen hair bulbs is often associated with apoptosis of the developing follicular epithelial cells in outer root sheath and matrix. (H&E)

This disorder is an uncommon cause of alopecia in the horse that is the result of a T lymphocyte mediated attack on the bulb region of anagen (growing follicles). Autoantibodies against follicular antigens have been demonstrated in the horse. Clinically, horses present with demarcated areas of partial to complete hair loss affecting the trunk, head, mane, or tail. Alopecia can be extensive and is sometimes associated with depigmentation. The lesions are usually smooth, often hyperpigmented, and have no clinical evidence of inflammation or pruritus. There are no clear breed, age, or sex predispositions. In chronic cases, inflammation may be absent and histologic changes are limited to small telogen follicles or mild peribulbar fibrosis. The condition can wax and wane or be permanent.

b. Amyloidosis

Figure 13.26. Horse. Chest. Plaques of Alopecia and Leukoderma. Amyloidosis. Large areas of nodular expansion of the skin of the pectoral region of the horse.

Figure 13.27. Horse. Head. Rhinomegaly with Ulcerative Dermatitis. Amyloidosis. The nasal portion of the head has a swollen appearance. Differential diagnosis: nutritional fibrous osteodystrophy (bran disease).

Cutaneous amyloidosis in the horse is characterized clinically by papules, nodules, or plaques most often found on the head, neck, shoulder, or pectoral region. The lesions are not associated with systemic disease and are most often asymptomatic, although some horses with cutaneous amyloidosis may have also have deposits of amyloid in the upper respiratory tract and regional nodes. Lesions vary from 0.5 to 10 cm in diameter and are usually covered by normal skin. The amyloid present has been determined to be AL amyloid derived from immunoglobulin light chains. Clinical differentials include other cases of nodular dermal lesions in the horse such as eosinophilic granulomas, granulomatous inflammation of infectious etiology, or neoplasms.

1. Habronemiasis

Figure 13.28. Horse. Leg. Granular Ulcerative Dermatitis. Cutaneous Habronemiasis (summer sores). An exophytic granular tissue with alopecia is present.

The lesion is considered to be a hypersensitivity reaction to dead and/or dying larvae and develops in areas of moisture such as the genitalia, periocular region, or in preexisting wounds. The nematodes are transmitted by flies that are drawn to areas of moisture or trauma, with eventual aberrant deposition and dermal migration of these larval gastric spiruid nematodes (Habronema majus [microstoma], H. muscae, and H. megastoma). Habronemiasis frequently induces pruritic gross lesions that include single to multiple ulcerative granulomas that rapidly progress and on cut section may contain numerous small caseous to gritty yellow granules (similar in appearance to the “kunkers” seen in pythiosis, but without the typical branching pattern). Differential diagnoses for cutaneous habronemiasis include exuberant granulation tissue, pythiosis, bacterial or fungal granulomas, sarcoids, and squamous cell carcinoma. Habronema is a common secondary infection, especially in ulcerated lesions.

2. Onchocerca

Figure 13.29. Horse. Head. Focal Alopecia and Depigmentation. Microfilarial Dermatitis. Cutaneous Onchocerciasis. Alopecia, scaling, and crusting around the face, head, and mane.

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