• Coat brushings

•   Hair pluck/ skin scrape

•   Swabs

•   Fungal culture

•   Aspirates

•   Impression smears

•   Biopsy/ punch biopsy

•   Allergy testing – intra-dermal, serum

•   Photographs 

• Lice infestation with biting louse (Damalinia equi) and sucking louse (Haematopinus asini).

•   Very common and causes pruritis, scaling and alopecia.

•   Often occurs on winter in poorly managed / congregated horses.

•   Common in cushingoid horses.

•   Diagnosis: demonstration of lice or nits (eggs).

•   Treatment: insecticidal shampoos, sprays or powders usually containing pyrethrins or pyrethroids (eg. Deosan Deosect - cypermethrin). Two applications at 14 day intervals are usually sufficient. 

• Caused by Chorioptes equi

•   Primarily affects distal limbs of heavily feathered horses.

•   Carrier horses with no clinical signs can perpetuate the infection.

•   Infection spread by bedding, brushes, contact.

•   Affected horses stamp and bite limbs. Scaling and exudation are present with secondary

  bacterial infections.

•   Diagnosis: presence of mites in superficial scrapings (denture brush useful).

•   Treatment includes removal of hair and scabs combined with application of insecticides

  including permethrins and fipronil (unlicensed) to affected horses and in contacts. Systemic ivermectin/ avermectin may be useful. Seleen shampoo can reduce pruritis (unlicensed). 

• T. autumnalis (small orange/ yellow coloured mites).

•   Sucking mite – disease associated with nymphal form.

•   Pruritis of head/ legs of grazing horses in late summer / autumn.

•   Diagnose with groomings.

•   Treatment: topical insecticides. 

Adult worms migrate from the small colon/ rectum to lay eggs on the perianal skin

causing pruritis/ tail rubbing. Most modern athelmintics are effective. 

Onchocercal Dermatitis (onchocerciasis / microfilariasis) 

• Seasonal (summer) dermatitis caused by Onchocerca cervicalis microfilaria.

•   Parasite transmitted by Culicoides spp. and other biting insects.

•   Larvae can be found in capillaries of unaffected horses but clinical cases result from type

  1 and 3 hypersensitivity reactions.

•   Causes alopecia and scaling of the head, neck, withers, chest and ventral midline. Can

  be very pruritic.

•   Severe focal dermatitis with pruritis and exudation may develop following the death of

  microfilaria in the skin after administration of avermectins.

•   Diagnosis on clinical signs, poor worming history, season, response to ivermectin. Biopsy

may identify microfilaria. 

• Hypersensitivity to bites of Culicoides spp. midges.

•   Generally common but not in foals. Usually gets progressively worse with age.

•   Commonly affects the mane and tail but can affect the ventral abdomen too.

•   Clinical signs are seasonal. Pruritis is always present and worst at dawn and dusk when

  midges are most active. Aggressive rubbing causes self-inflicted trauma.

•   Diagnosis: clinical signs are often diagnostic. Biopsies, intradermal skin tests and ELISAs

  also available

•   Treatment includes:

  •   Management of skin lesions

  •   Corticosteroids (prednisolone / methyl-prednisolone acetate).

  •   Immunotherapy/ desensitisation treatment offered by a number of labs eg. Greendale

    veterinary diagnostics

  •   Fly repellents eg. “Switch” (permethrin)

  •   Preventing midges biting

    • -  Oil based liquids eg. Benzyl benzoate

    • -  Stabling at dawn and dusk

    • -  Rugs/ hoods eg. Boett rug

    • -  Insect proof stables with meshes

    • -  Fans/ wind prevent midges landing

    • -  Avoid rivers/ water/ woodland as these attract midges 

• Type 1 hypersensitivity reaction to a number of allergens.

•   Causes extreme pruritis and secondary, self-inflicted skin lesions.

•   Diagnosis: exclusion of other differentials. Skin biopsies generally non-specific.

  Intradermal skin testing is useful but has limitations as requires availability of specific allergens and experienced personnel. Serum ELISA or RAST tests to specific allergens may be of use in diagnosis.

•   Identification of an allergen may allow prevention of contact or hyposensitization by immunotherapy.

•   Systemic corticosteroids are useful in the treatment of the condition. 

• Common syndrome with a complex immune-mediated/ allergic aetiopathogenesis.

•   Arises from injected (drugs), ingested (chemical, feeds) or inhaled (pollens, moulds, dust,

  chemicals) antigens/ allergens.

•   Alternatively, can arise from direct skin (changes in bedding, chemicals to wash rugs etc)

  or mucous membrane contact.

•   Physical urticaria occurs without an immunological component eg “Dermatographism” is

  the development of a ‘wheal’ from a blunt scratch.

•   Clinical signs: ‘wheals’ occur within variable time following the instigating factor. These

  typically ‘pit on pressure’ but can be difficult to assess in small lesions. Pruritis varies

  from mild to severe. Some lesions are exudative.

•   Angio-oedema is a subcutaneous form of urticaria which tends to be more diffuse owing

  to lack of restraint of the spread of fluid present in the subcutis.

•   Diagnosis: based on clinical signs but identification of the instigating factor can be

  challenging and unrewarding in isolated occurrences. Skin tests and serum ELISA or

  RAST tests may be useful in some cases. Food elimination trials may be useful.

•   Treatment: initial attacks usually respond well to short courses of corticosteroids. Often a

  single dose of intravenous/ intramuscular dexamethasone or oral prednisolone will

  resolve the clinical signs.

•   Further investigations are warranted in recurrent cases. Identification of an allergen may

  allow prevention of contact or hyposensitization by immunotherapy.

•   Anti-histamines generally have little effect. 

• An autoimmune disease characterised by an exfoliative dermatitis.

•   Results from a type 2 hypersensitivity due to autoantibodies directed against the cell

  membrane of epidermal cells.

•   Clinical signs: include vesicles, pustules, erythematous scaling and crusting, commonly

  begins around the face and limbs. Inflammation around the coronary band, ergot and chestnut is common. Lesions may be painful or pruritic. Systemic signs may include lethargy, inappetance, ventral oedema, pyrexia and weight loss.

•   Biopsy required for diagnosis. Direct immunofluorescence shows intracellular deposits of immunoglobulin in epidermis.

•   Treatment: high (immunosuppressive) doses of corticosteroids (prednisolone at 2-4 mg/kg). Attempts to reduce the dose are often unrewarding and result in deterioration of cases. It is likely that treatment will be life-long. Gold injections may be of use. 

0. Multisystemic eosinophilic epitheliotrophic enteritis / generalised granulomatous enteritis 

• Multisystemic diseases often affecting the gastrointestinal tract as well as the skin.

•   Skin lesions include ulcerative coronitis, alopecia, hyperkeratosis and exudation. Lesions

  can be intensely pruritic.

•   Signs of generalised disease include weight loss, inappetance, diarrhoea, ventral

  oedema, dullness and lethargy. Pyrexia and lymphadenopathy may be present.

•   Diagnosis usually requires biopsy of the skin +/- rectum/ intestine. Hypoalbuminaemia,

  hypoproteinaemia and hyperfibrinogenaemia may be present and glucose absorption

  tests may be indicated.

•   Treatment is usually with corticosteroids but often unrewarding. 

• Strongyloides westeri

•   Foals <2 months old.

•   One method of infestation is by skin penetration, causing pruritis. 

0. Linear keratosis / linear alopecia

   0. Selenium toxicity 

    

• Common skin infection caused by Dermatophilus congolensis.

•   Causes exudation, matted hairs and scabs in areas wetted by rain – primarily the back/

  quarters.

•   Classic ‘paint-brush’ lesions.

•   Treatment includes antibiotics and clipping / soaking of the skin with chlorhexidine to

  remove exudates and scabs.

•   Topical treatments including antibiotic ointments applied as necessary. 

0. Ringworm (Dermatophytosis) 

0. Trichophytosis

•   Commonly caused by Trichophyton equinum var. equinum and Trichophyton equinum var.

  autotrophicum, less commonly by Trichophyton verrucosum and Trichophyton

  mentagrophytes.

•   Spores are highly resistant and survive in stables/ tack for years.

•   Infection relies on the presence of spores and skin abrasion therefore common around the

  girth/ saddle.

•   Lesions appear initially as circular areas of erect hairs followed by alopecia and scaling.

•   Diagnosis: clinical signs, microscopy of a hair pluck / scrape (hyphae and endothrix spores)

  and culture. Infected hairs do not fluoresce with woods lamp.

•   Lesions resolve spontaneously over a number of weeks but treatment limits spread.

•   Topical fungicidal treatments include enilconazole (Imaverol) and natamycin (Mycophyte).

  Sporocidal treatment of the environment also important (natamycin or Virkon). Griseofulvin is

  of limited use and contra-indicated in pregnant mares. 

• Microsporum gypseum, Microsporum equinum and Microsporum canis.

•   Less common than trichophytosis.

•   Clinical picture as above, can be spread by flies.

•   Diagnosis on clinical signs, microscopy of a hair pluck / scrape (hyphae and ectothrix spores)

  and culture. M. equinum and some M. canis may fluoresce with woods lamp.

•   Treatment as above. Additionally, miconazole (Malaseb) licensed for treatment of M. canis in

  dogs and cats is not licensed for use in horse but may be of use. 

•   Rare, cell-mediated autoimmune skin disease

•   Clinical signs: thinning of mane and tail and reasonably circumscribed areas of alopecia.

•   No effective treatment. 

0. Linear keratosis / linear alopecia 

• Rare, idiopathic possibly inherited dermatosis.

•   Unilateral, linear, vertical bands of hyperkeratosis and hairloss on neck, thorax and upper

  hind limb.

•   Predominantly quarterhorses. 

0. Selenium toxicity 

• Caused by ingestion of seleniferous plants (eg. Senecio spp.) or by unnecessary or excessive administration of selenium supplements.

•   Acute poisoning usually results from over supplementation. Cases present with lethargy, weakness, colic, diarrhoea, arrhythmias and dyspnoea. (No dermatological signs).

•   Chronic poisoning causes dramatic loss of mane and tail and thin fragile body hair. Lameness results from laminitis, hoof ‘slippering’ and sloughing.

•   Diagnosis: based on history and assays of selenium in mane/ tail.

•   Treatment: remove the source of selenium and feed diets high in protein. 

0. Congenital Papillomatosis (“Neonatal Wart”)

•   Papilloma virus has the ability to pass the mare’s placenta resulting in viral papillomata

  on the skin of newborn foals.

•   Treatments include ligation or surgical removal. Rarely, spontaneous resolution occurs.

  
  

  Viral Papillomatosis (“Grass warts”)

  •   Generally in horses under 3 years old (often less than 1 year old), caused by equine

    papilloma virus.

  •   Moderately contagious by contact between co-grazing horses.

  •   Lesions appear as small white-grey papules and can be present in huge numbers.

    Usually affects muzzle and lips but can be present on the eyelid, external genitalia and

    limbs.

  •   Usually spontaneously resolve in 3-4 months. Treatment often unnecessary but can

    include autogenous vaccines and surgery. 

• Clinically distinct syndrome caused by a papilloma virus.

•   Common in horses of all ages (but rarely in animals less than 1 year).

•   Lesions begin as small papules that coalesce into white hyperkeratotic plaques.

•   Occur on the inner surface of the pinna.

•   Spontaneous regression does not seem to occur but treatment is not indicated. 

• Most common skin tumour of horses

•   6 types – occult, verrucose, nodular, mixed, fibroblastic, malevolent.

•   Cause not fully understood but bovine papillomavirus widely accepted as having a role.

•   Diagnosis usually based on clinical appearance and submission of photos via Liverpools

  website. Rarely biopsied.

•   Treatment:

o Benign neglect
o AW4-LUDES cream
o Surgery
o Ligation
o BCG injection
o Several other topical medications 

• Melanin pigment depots (melanotic hamartomas) are common in the linings of the guttural pouches and on mucosae.

•   Melanomas are benign tumours of melanocytes and generally cause disruption by space- occupying bulk. Melanomas are largely limited to grey horses and are common around the perineum, sheath, parotid region and less commonly, in guttural pouch, eyelids, lips and iris.

•   Melanosarcomas are rapidly invasive and metastasise but are rare.

•   Diagnosis can often be made on clinical appearance. FNAC or biopsy if necessary.

•   Treatment options include:

  •   Surgical – Excision, cryosurgery

  •   Cytotoxic drugs – intralesional cisplatin

  •   Other: cimetidine orally – 1 paper reported success. Histamine (H2) may be involved in

    tumour growth by activation of T suppresser cells. Cimetidine (H2 blocker) may be effective in rapidly growing tumours. 

• Can affect the skin only but can be part of a multicentric syndrome.

•   Diagnosis is by biopsy.

•   Treatment is limited and prognosis guarded. 

0. Eosinophilic collagen necrosis/ granuloma 

• Common

•   Firm, painless skin nodules associated with degenerative collagen.

•   Usually along back and sides of chest.

•   Diagnosis: Clinical signs and biopsy.

•   Treatment: rarely necessary but includes intra-lesional steroids or surgical excision. 

0. Axillary nodular necrosis 

• Firm painless, sub-cutaneous nodules near the girth and axilla.

•   Biopsies show focal dermal necrosis.

•   Treatment: surgical removal is possible if necessary, or intra-lesional steroids. 

0. Dentigerous cyst 

Swellings in the temporal region arising from tooth germ tissue. Drainage occurs near the ear or through adjacent skin. 

Dermoid cyst 

• Cutaneous cysts most commonly found on dorsal midline.

•   Congenital or hereditary lesions affecting young horses.

•   Contain soft cheese-like material and sometimes coiled hairs. 

0. Epidermoid cyst (atheroma) 

• Developmental cystic structure of epidermis.

•   Most common in false nostril where it is called an ‘atheroma’.

•   Usually a cosmetic problem only. 

•   Invasive tumour of squamous cells. Aetiological factors include UV light (skin and eye forms) and smegma (penile and vulval forms).

•   Diagnosis is by biopsy (or impression smears in ocular forms).

•   Treatment options include:

  •   Surgical – Excision (penile amputation), cryosurgery

  •   Cytotoxic/ antimitotic drugs – intralesional cisplatin

  •   Radiation – Probably the most effective of all treatments eg. Iridium 192 or strontium-90

    probes (beta radiation). Usually limited to specialist centres. 

0. Habronemiasis

•   Ulcerating cutaneous granulating nodules or wounds caused by the larvae of Habronema muscae, Habronema majus and Drachia megastoma.

•   Disease has several forms.
  i) Ophthalmic habronemiasis – presence of yellow granules in conjunctivae and nasolacrimal duct.
  ii) Cutaneous habronemiasis – larvae penetrate wet areas of the face (eg. secondary to epiphora), granulating wounds and the urethral process.

•   Diagnosis is usually made on impression smears and washes.

•   Treatment: oral / topical ivermectin, surgical removal and control of muscid flies. 

Staphylococcal dermatitis 

• Painful skin lesions associated with folliculitis and furunculosis.

•   Caused by S. aureus, S. intermedius and S. hyicus.

•   Treatment with antibiotics based on culture and topical chlorhexidine. 

• Caused by UV radiation, facilitated by lack of protection from pigment and hair.

•   Falls into 2 categories:

  1. a)  sunburn – excessive exposure to UV light.

  2. b)  Photosensitisation – disproportionate response to normal UV exposure. 

     Comes in 2

     forms:

  Primary photosensitisation – results from plant or chemical poisoning eg. St. John’s Wort. The ingested photodynamic agent is delivered to the skin.
  Secondary photosensitisation – digestion of chlorophyll produces a potent photodynamic agent, phylloerythrin, which is normally detoxified and excreted by the liver. Liver failure allows the substance to pass into the bloodstream unchanged and it accumulates in skin. Severe damage to the skin is common. 

0. Leucoderma (vitiligo) 

• Loss of pigment in skin causing depigmented spots.

•   Rarely associated with hairloss except around the eye or perineum and can be idiopathic

  or secondary to surgery, cryosurgery, radiation etc.

•   No treatment is necessary or possible. 

0. Leucotrichia

 White hair (with or without leucoderma).

 (Dermatophilus congolensis)

•   Exudation, scabs and matting of hair of distal (often white) limbs.

•   Diagnosis can be made on examination of a smear. However, mixed infections with

  Staphylococcus spp. and Streptococcus spp. are common.

•   Treatment: antibiotics, anti-inflammatories and soaking of the skin with chlorhexidine to

  remove exudates and scabs. May require clipping of hair. Skin should be dried and topical treatments including antibiotic ointments applied. (Fuciderm and flamazine are useful). Bandaging not always helpful as it may promote moistness of skin. 

0. Pastern / cannon leucocytoclastic vasculitis 

• Skin condition of the unpigmented distal limb.

•   Aetiopathogenesis uncertain but IgG and C3 portion of complement have been detected

  by direct immunofluorescence in vessel walls.

•   Unpigmented skin involvement suggests role of UV light, although this condition is not

  thought to be a true photosensitisation.

•   Clinical signs: erythema, oozing and crusting of the white areas of distal limbs. Can

  appear very similar to ‘mud fever’. Clinical signs are often diagnostic but biopsies reveal

  leucocytoclastic vasculitis, vessel wall necrosis and thrombosis.

•   Evaluation of liver function prudent.

•   Treatment: clipping hair and removal of exudates and scabs with chlorhexidine. Topical

  antiseptics, antibiotics, corticosteroids and sun block may be useful. Consider leg wraps if horse turned out in sun and systemic corticosteroids may be necessary in some cases. 

Coronary band dystrophy/ Coronitis 

• Idiopathic/ immune-mediated defect in cornification of coronary bands. All four hooves show hyperkeratotic changes. The ergots and chestnuts may be involved. Lesions may crack and fissure, bleed and ooze serum.

•   Treatment often unrewarding but includes symptomatic management of lesions, keeping limbs dry and the use of corticosteroids. 

• Inflammation of cutaneous lymphatics usually but not always secondary to a bacterial infection obtained via a small cut / abrasion.

•   Affects hindlimbs more commonly than forelimbs.

•   Usually causes marked swelling of the limb (2-3 times normal size), lameness (which

  can be severe) and serum exudation.

•   Treatment – antibiotics based on culture results, NSAIDs / corticosteroids, potassium

  iodide and diuretics. Hydrotherapy, cleaning with antimicrobials, leg wraps and gentle

  exercise may be beneficial.

•   Ulcerative lymphangitis is commonly associated with Corynebacterium

  paratuberculosis, Staphylococcal spp. and Streptococcal spp. infections. Can result in nodules which may ulcerate, abscessate and drain pus. If fibrosis occurs, disfigurement may be permanent. Chronic lymphatic nodules can potentially be removed. 

• Wound infection that rapidly spreads along tissue planes.

•   Caused by a number of bacteria.

•   Commonly affects the limbs.

•   Causes acute painful swelling, inappetance and pyrexia.

  Treatment – antibiotics based on culture results and NSAIDs. Hydrotherapy, cleaning with antimicrobials and gentle exercise may be beneficial. 

• Inflammatory reaction involving blood vessel walls.

•   Commonly immune-mediated involving type 1 and type 3 reactions.

•   Can result from various infections or the administration of drugs.

•   Causes oedema, necrosis, and ulceration of lower limbs and mucosae.

•   Treatment includes corticosteroids (+/- antibiotics and symptomatic treatments). 

• An immune-mediated vasculitis associated with recovery of an upper respiratory tract infection (most commonly caused by M protein antigen of Streptococcus equi subsp. equi).

•   Immune complexes deposited in the walls of peripheral blood vessels increase vascular permeability and cause oedema, primarily of the limbs. Serum exudation and skin erosions can be marked. Petechial or ecchymotic haemorrhages can occur in the skin and mucosae. Pulmonary and cerebral oedema can develop in the most severe cases and is life-threatening.

•   Signs usually occur 2-4 weeks after respiratory infection.

•   Horses are depressed, inappetant and reluctant to move.

•   Diagnosis can be confirmed with biopsies.

•   Treatment is with systemic corticosteroids and antibiotics, hosing limbs, gentle exercise and leg wraps.