Equine Dermatology – Flashcards

-Lice (Damalinia equi, Haematopinus asini) -Mange (Chorioptes equi, Sarcoptes scabei var equi, Psoroptes equi, Demodex) - Sweet Itch (Equine insect hypersensitivity, Queensland Itch) - Oxyuris equi - Habronemiasis (Habronema muscae, H. majus, Drachia megastoma) - Atopy

Obligate parasites, seen in winter when there is congregation of horses and little sunlight. Damalinia equi - biting louse, 99% of cases. Like dorsum of back and sides of neck. Haematopinus asini - sucking louse, less common. prefer neck, tail, and limbs. Clinical signs - pruritis leading to rubbing, biting, with seccondary patchy alopecia, non-symmetrical moth-eaten pattern, may have loss of condition. Diagnosis - clinical signs, groomings, micro- and macroscopic examination. Treatment - whole body washes or powders, organophosphates, rotenone 2% powder.

Chorioptes equi - most common. "Leg and tail mange". Non-burrowing mite, seen in winter. Clinical signs are restlessness, foot stamping, head shaking, pruritis, self excoriation. Generalized infection result in moth-eaten appearance and weight loss, irritability, exercise intolerance. May have secondary bacterial infections. Sarcoptes scabei var equi - Rare burrowing mite transmitted by direct contact. Extremely pruritic, excoriation, alopecia, crusting, licenification. Begins at the head and spreads down the body. Psoroptes equi - body mange, young stabled horses. Scale and fluid eating. Moderate to severe pruritis, around ears, mane, body, and tail head. Head shaking and tail rubbing Demodex - uncommon, can be found in normal horses, not pruritic. Diagnosis - clinical signs, patterns. ID of parasites. Treatment - Ivermectin, Insecticidal shampoo or powder.

Most common skin allergy in the horse, hypersensitivity to salivary antigens of Culicoides spp. Most horses affected at 4-5 years, gets worse with age. Clinical signs - seasonal, tail swishing, rubbing, restless, excoriation, can lead to serum oozing, crusting, melanotricia. Chronically can see lichenification of affected areas. Diagnosis - clinical signs, season, elimination of ectoparasites, biopsy often unrewarding. Treatment - fly control, stabling, fly sheets, masks, insecticides, fly repellent, steroids.

Inhabit terminal region of small colon and rectum, migrates out the anus, lay eggs on perianal skin. Mid-summer. Rare due to use of avermectins. Clinical signs - perianal irritation, tail rubbing, broken hairs at tail base. Diagnosis - clinical signs, ID of eggs (adhesive tape technique) Treatment - avermectins

Stomach nematodes. Seasonal disease (flies), granulating nodules or wounds ("summer sores"). Opthalmic form - conjunctival get cheese granules overlying conjunctiva. Lacrimal - deep, circular, granulating ulcer below medial canthus of the eye. Cutaneous form - chronic wetting of the skin causing excoriation, parasitic colonization, granulating skin lesions, ulcerating lesions.

Rare, frustrating to diagnose. Inherited Type I hypersensitivity. Potential allergens - pollen, grasses, trees, moulds, feathers, etc. Clinical signs - recurrent intense pruritis with no obvious primary lesion. Diagnosis - difficult, eliminate all other causes of pruritis, intradermal testing, serum testing, skin biopsies, questionable results. Treatment - removal of underlying etiological agent, if you can find it. Steroids, hyposensitization.

Dermatophilosis Dermatophytosis (ring worm) Pemphigus foliaceus. Serum, chemical, fecal, and urinary scalding. Telogen defluxion Stud Crud

Rain scald. One of the most common and important skin infections in the horse. Dermatophilus congolensis. Usually associated with prolonged moist conditions. Clinical signs - see exudation, matted hair, excessive scab formation, allopecia, may have pruritis, classic paint-brush tufting of hair. Head, neck, dorsum and throrax most commonly affected. Winter form - matting or hair and scabs with underlying purulent exudate, overlying pus and ulcerated skin, easier to feel than see. Summer form - smaller lesions, scabs palpable as braile like lumps under the skin. Diagnosis - important to rule out any other cause non-pruritic allopecia. Demonstration of railroad tract cocci on smears, culture. Treatment - Sunlight, local bathing with chlorhexidine or iodine based washes, skin must be kept dry, parenteral penicillin for 3-5 days.

Ring worm. Common, contageous. Trichophyton equinus var equi, Microsporum equinum. Clinical signs - small edematous plaques begining on girth, shoulder, chest, face, then small tufts of erect hairs easily plucked. Only puritic in the early stages. Healing lesions silvery in color. Can become generalized. Diagnosis - history of contact with infected horses, clinical signs, hairs in 10% KOH will reveal hyphae and spores, fungal culture on Sabourauds agar. Treatment - self limiting in 6-12 weeks, sunlight, control.

Type II (autoimmune) hypersensitivity reaction. Clinical signs - early see vesicles and pustules with superficial erosion, form epidermal collerettes, scaling, crusting.Usually starts around face and neck, rapidly spreads, leads to extensive allopecia. Painful/irritating. Chronically see diffuse crusting and scaling with extensive allopecia. Diagnosis - biopsy is gold standard. Direct immunoflorecence - look for intracellular deposits of immunoglobulin in epidermis Treatment - steroids. Poor prognosis, may be better in young horses.

Commonly associated with wounds, application of foreign material, fecal and urinary incontinence. Treatment - removal or irritating factors, cleaning and drying area, emollient creams.

Sudden acute traumatic episode, illness, pyrexia leads to hair cycle arrest in resting phase. See signs 4-6 weeks later. Spectacular progressive alopecia. Resolves spontaneously when next hair cycle starts. Diagnosis - history, microscopy of hair shafts (uniform diameter, clubbed non-pigmented roots, no root sheath). Biopsy (hair follicles in resting phase) No treatment.

Common, non-puritic scaling and crusting on the dorsal aspect of the hind limbs. treatment - washing and drying may alleviate the signs.

PPID Vitiligo Leukoderma Reticulated leukotrichia Arabian Fading Syndrome

See endocrine lectures, see hirsutism and hyperhiderosis.

Inherited and normal in the Appaloosa breed. Can affect other breeds, may be heritable. Idiopathic or may follow primary damage to melanocytes. Benign condition Clinical signs - see depigmented circular areas, increasing in number (not size). No treatment.

"Aquired vitiligo" - common. Get loss of melanocytes due to a variety of causes - pressure injury, cryosurgery, surgery, other skin disorders Clinical signs - ill defined patches of white hair in characteristic locations (point of the withers, girth, distal limbs, immediately behind the ears - from saddle, bandages, cribbing straps). No treatment

Mainly seen in Quarter Horses, Thoroughbred, Standardbred. Unknown etiology. Clinical signs - sudden onset of severe pain along with vesicles and crusts, temporary allopecia, new hair comes in white but underlying skin maintains pigmentation. Clinical course of 3 months. No known treatment.

"Pinky syndrome", Arabians and Welsh Mountain ponies. See dipigmentation of muzzle, lips, periorbital tissues. Clinical diagnosis. No treatment.

Staphylococcal folliculitis "Scratches" Hyperelastosis cutis

S. aureus, S. intermedius Clinical signs - rapid developing, localized, inflammatory purulent skin lesions assoicated with severe pain, often associated with tack areas. Diagnosis - clinical signs, direct smear/culture from lesions. Treatment - clipping, bathing with chlorhexidine soap, systemic antibiotics.

"Greasy heel syndrome"; "mud fever"; "Ideopathic pastern dermaittis". Most common equine exudative disorder. Caused by a loose conglomeration of diseases with similar clinical features. See scaling, erosion, exudation, and pyoderma. Clinical signs - erythema, oozing, crusting, allopecia on the plantar or palmar surface of the pastern, crusts are deep and strongly adherant to underlying tissue, can become significantly lame as horizontal fissures develop. Treatment - eliminate all possible causes, remove hair and necrotic tissue (anesthesia), topical antiseptic washes, NSAIDs, antibiotics.

HERDA autosomal recessive connective tissue disease decreased collagen, fragmentation, disorientation collagen fibers. Young QH Clinical signs - loose, wrinkled, hyperextensibe and fragile skin. Damaged skin repairs very slowly. Treatment - no effective treatment, remove from breeding program and minimize trauma.

Papillomatosis or Warts Aural plaques Eosinophilic collagen necrosis Coital examthema Urticaria

Viral skin disease caused by equine papilloma virus, affects basal cell layers of the epithelium. Incubation 60-70 days, moderately contageous, self-limiting. Usually seen in young animals 6mo you 4 years old. Clinical signs - multiple, single, or coalescent pink or grey vegetative lesions, commonly on muzzle, lips, face, distal limbs, gentialia. DDx - squamous cell carcinoma, sarcoid. Treatment - not usually required, autogenous vaccines. Juvenile warts are not self limiting, and will need to be surgically removed. Can be anywhere on the body.

Possibly caused by fly bite irritation or papilloma virus. Clinical signs - flat, hyperkeratotic, flaking, pink-grey proliferative lesions on the inner surface of the pinnae, non-painful. Treatment - leave it alone! Will not resolve, but the cure is frequently worse than the disease. Look at as a minor blemish.

One of the most common nodular skin diseases. Firm dermal nodules associated with degenerative collagen. Possible the result of insect bits of low grade trauma. Clinical signs - girth or saddle area, firm, painless, well circuscribed subcutaneous nodules. Non-puritic, no overlying allopecia. Diagnosis - clinical signs often diagnostic. Biopsy shows focal necroboiosis of collagen fibers and heavy eosinophilic infiltration. older lesions may mineralize. Treatment - check tack for poor fit or pressure. Intralesional inject of very small doses of triamcinolone or methylprednisone. Systemic sterioids may be helpful in the early stages of the disease.

Caused by EHV3, a venereal disease, can also be transmitted by fomites, inhalation, or droplets. Incubation 5-7 days. Can become latent and may recur during times of stress. Clinical signs - multiple rapidly developing papules-pustules on the penis or vulva, swelling and edema may occur, regress in 3-5 days and become healthy granulation tissue by 10-14 days. Diagnosis - clinical signs, viral isolation, serology (paired sera 4 weeks apart). Treatment - none, do not breed until completely cleared of active lesions.

Very common, a symptom of a disease rather than a specific disease; many possible causes. Immunologic and non-immunologic factors trigger release of mediators from mast cells, basophils, produce wheals. Clinical signs - acute or peracute, see edematous lesions of the skin (wheals). No central focus of inflammation. Treatment - steroids, antihistamines.