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Veterinary Medicine Notes Endocrinology and Integument 2 Notes

Dermatological Specific Diseases Large Animal Notes

Updated Dermatological Specific Diseases Large Animal Notes

Endocrinology and Integument 2 Notes

Endocrinology and Integument 2

Approximately 192 pages

4th year notes for ENI 2....

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Dermatological specific diseases – large animals

DERMATOPHILOSIS

Dermatophilosis is characterised by an exudative dermatitis with scab formation. It is caused by Actinomycetes, and is often caused by Dermatophilus congolensis.

In horses it is commonly referred to as mud fever and rain scald.

Clinical signs

  • Exudative dermatitis

  • Scale

  • Crust formation

  • Common sites include feet, lower limbs and the dorsum.

Pathogenesis

  • The initial infection requires superficial skin damage.

  • The motile zoospore stage is activated to form a mycelium.

  • The infection is confined to the epidermis, and the zoospore can remain dormant in skin debris and scabs for months in dry conditions.

  • Penetration of the hyphae into the epidermis cause an acute inflammatory reaction.

  • D. congolensis is gram positive, non-acid fast and a facultative anaerobe.

Diagnosis

  • Impression smears of lesions stained in Giemsa or Diff Quick for cytology

  • Histology.

  • Culture and identification.

Treatment

  • Often heals rapidly and spontaneously.

  • The primary problem should be managed, e.g. rain or flies.

  • A short course of antibiotics may be used

  • Erythromycin

  • Penicillin G

  • Ampicillin

  • Amoxicillin

  • Tetracyclines

  • Topical antibacterials may be used

  • Chlorhexidine

  • Benzoyl peroxide

Prognosis

  • Good.

CASEOUS LYMPHADENITIS (SHEEP AND GOATS)

Caseous lymphadenitis is caused by Corynebacterium pseudotuberuclosis, which is a commensal of sheep skin.

Clinical signs

  • Raised lymph nodes

  • Ill thrift

  • Depression

  • Abscesses that are green in colour

  • Pneuomia

Pathogenesis

  • Infection is chronic and follows tissue trauma such as shearing wounds.

  • The bacteria proliferate within macrophages.

  • Transmission is due to eruption of bacteria from lymph nodes of infected animals, which then causes contamination of dipping fluids and equipment.

Diagnosis

  • Clinical signs

  • Sandwich ELISA tests to detect circulating antibodies to phospholipase toxin.

Treatment

  • Antibiotic treatment

  • Topical iodophore shampoo

  • Screening and culling of infected animals.

  • Strict hygiene.

  • Inactivated vaccine available.

Prognosis

  • Good.

EXUDATIVE EPIDERMITIS (GREASY PIG DISEASE)

Greasy pig disease is caused by Staphylococcus hyicus and is characterised by an exudative dermatitis.

Clinical signs

  • Affects pigs <3 months of age.

  • Dark, localised areas of grease and scale

  • Excess sebum

  • If severe, the skin turns black due to necrosis.

  • Systemic illness due to toxin release possible.

Pathogenesis

  • Greasy pig disease is often a secondary condition. Primary causes include

  • Abrasions

  • Faulty procedures for iron injections, removing tails or teeth in piglets.

  • Fighting and skin trauma at weaning.

  • Mange

  • Abnormal behaviour such as tail or ear biting.

  • Highly contagious and persists in the environment for long periods of time.

  • S. hyicus produces an exfoliative toxin that causes separation of cells in stratum spinosum.

Diagnosis

  • Clinical signs.

  • Bacterial culture and susceptibility testing.

Treatment

  • Individuals can be treated with antibiotic injection

  • Sensitive to most antibiotics including penicillins.

  • Topical antibacterial washes may be used.

Prognosis

  • If severe, disease can be fatal.

DERMATOPHYTOSIS (RINGWORM)

Dermatophytes are closely-related fungi that use keratin for growth. Dermatophytosis tends to be confined to superficial layers of the skin, nails, claws and hair.

Clinical signs

  • Circular or irregular lesions

  • Scaling

  • Crusting

  • Alopecia

  • Erythema

  • Follicular papules and pustules

  • Varying pruritus.

Pathogenesis

  • Ringworm in horses and cattle is usually caused Trichopyton verrucosum, and occasionally Trichopyton mentogrophytes.

  • Young animals are particularly affected.

  • Dermatophytes only invade the keratin of growing (anagen) hairs.

  • Transmission is by direct contact with the infected animal, or indirect via contaminated environment.

Diagnosis

  • Woods Lamp examination

  • Uses UV light

  • Green fluorescence will be seen in 50% of cases

  • Trichogram examination

  • Hairs from lesion suspending in 10% KOH

  • Look for hypae or arthrospores

  • Technically difficult.

  • Fungal culture

  • Using plucked hairs from edge of lesion or skin scrape.

  • Sabouraud’s medium that contains cyclohexaimide to inhibit growth of other fungi and gentamicin and chloreotetracycline to inhibit bacterial growth.

  • Red colour change is suggestive of dermatophytosis.

  • Skin biopsies for histopathology and/or culture.

Treatment

  • Griseofulvin treatment.

  • Topical enilconazole treatment (Imaverol)

  • Treatment of in-contact animals and the environment

Prognosis

  • Good.

EQUINE ATOPY

Equine atopy is a hypersensitivity disorder in which the horse becomes sensitised to inhaled or percutaneously absorbed allergens.

Clinical signs

  • Pruritus

  • Urticaria and angio-oedema

  • Excoriations

  • Alopecia

  • Lichenification

  • Secondary infection

  • Nodules

  • Eosinophilic granulomata

  • Tufted papules that may coalesce or crust

  • Eosinophilic mural folliculitis

Pathogenesis

  • Common allergens implicated in equine atopy include dust mites and forage mites.

Diagnosis

  • Serology

  • Intradermal skin testing.

Treatment

  • Allergen avoidance

  • Immunotherapy

  • Corticosteroids

  • Antihistamines

  • Fatty acids

Prognosis

  • Good.

EQUINE CULICOIDES HYPERSENSITIVITY (SWEET ITCH)

Sweet itch is caused by a hypersensitivity reaction to the saliva of biting insects.

Clinical signs

  • Peak onset between 2-4 years.

  • Intense pruritus

  • Commonly affected areas include head, mane, tail, withers and ventral abdomen.

  • Papules

  • Self-excoriation may lead to

  • Alopecia

  • Broken hairs

  • Erosions

  • Ulcers

Pathogenesis

  • Due to both type I and type IV hypersensitivity reactions.

  • Allergen-specific IgE to Culicoides saliva is produced, resulting in mast cell degranulation and histamine release.

  • Often seasonal – seen from spring to late autumn.

Diagnosis

  • History and clinical signs.

  • Allergy testing may be used.

  • Sensitivity and specificity is low.

Treatment

  • Control of pruritus

  • Corticosteroids may be necessary

  • Treatment of secondary bacterial infections.

  • Reduction of Culicoides contact

  • Anti-midge rugs

  • Insect repellants...

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