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Fig 6: Whole-body crusts and alopecia due to pemphigus foliaceus in a 10-year-old American Miniature Horse gelding.
Fig 5: Ulceration and crusts on the tail caused by intramammary Malassezia infection in an 8-year-old Danish Warmblood mare.
Immune-mediated diseases
Pemphigus foliaceus This disease is the most common cause in the author’s practice for noninfectious crusts in the horse. It is also the second most commonly seen autoimmune skin disease in the horse, after purpura hemorrhagica. While earlier literature suggested the age of onset of pemphigus foliaceus (PF) may be bimodal, either at an early age (<one year) or in the mature horse (>8 years), studies at UC Davis and elsewhere do not support this; i.e. PF can occur at any age (Vandenabeele et al. 2004; Zabel et al. 2005). Likewise, the UC Davis caseload does not support the previous assertion that Appaloosas are predisposed to PF. Interestingly, a seasonal onset of the disease was present in our horses, with >80% of cases occurring in a period from September to February (Vandenabeele et al. 2004). A recent report describes a donkey whose PF occurred, then regressed, during 2 of its 5 pregnancies (Bourdeau and Baudry 2005). Crusts are the most common lesions, and frequently start
on the face and legs then become generalised (Fig 6). Alternatively, crusts may occur only on the coronary band. Pruritus is variable. Peripheral oedema (‘stocking up’) is common, and a low grade anaemia combined with a leucocytosis may be seen. Diagnosis is by biopsy, showing subcorneal pustules with acantholytic cells. It is very important not to surgically prepare the area to be biopsied, as the answer is usually in the crusts; one can always surgically prepare the leg after taking the biopsy to limit the chances of infection. Because certain strains of Trichophyton sp. of dermatophytes may also cause acantholysis in horses, any histology suggestive of PF should have special stains for fungi performed (Scott 1994). Treatment is corticosteroids at immunosuppressive doses (prednisolone 1 mg/kg bwt q. 12 h, dexamethasone
approximately 0.05–0.1 mg/kg bwt q. 24 h; then taper). There are anecdotal reports of aurothiomalate, a gold salt (Myochrysine)17 being helpful at 1 mg/kg bwt i.m. q. 7 days. Adverse reactions of gold salts, while rare in the horse, would include thrombocytopenia and glomerulonephropathy. There are also reports of azathioprine at 1–3 mg/kg bwt q.
24–48 h being used for various autoimmune skin diseases in horses (Humber et al. 1991; Messer and Arnold 1991; McGurrin et al. 2004). A potential side effect is thrombocytopenia, as horses have low levels of the enzyme thiopurine methyltransferase (White et al. 2000), which is responsible for the metabolisation of azathioprine in other species, including man. However, the author has used azathioprine (1–3 mg/kg bwt for one month, then q. 48 h) in 8 horses with no deleterious effects (White et al. 2005); this is used as a steroid-sparing drug, with corticosteroids in an attempt to eventually decrease the steroid needed. Approximate cost in a 500 kg horse for daily generic azathioprine is $300/month.
Cutaneous vasculitis (aka pastern leucocytoclastic vasculitis, photoaggravated vasculitis) This seems to be more common in California and the western United States (and doubtless, other regions with an excess of sunlight) as a clinical entity. It generally affects mature horses, and produces lesions confined to the lower extremities that (often but not always) lack pigment. Lesions are multiple and well demarcated with the medial and lateral aspects of the pastern the most common sites. Initially, erythema, oozing, crusting, erosions and ulcerations develop, followed by oedema of the affected limb(s) (Fig 7). Chronic cases may develop a rough or ‘warty’ surface. Pruritus is variable but may be intense. The pathogenesis is uncertain: an immune- complex aetiology has been suggested, and the limitation of lesions to nonpigmented areas suggests a role for UV radiation. Drug reactions may be a potential cause; a recent report implicated Staphylococcus intermedius (Risberg et al. 2005). In a review of 72 cases, the most frequent clinical findings
were crusts/scales and oedema of the legs with the most common underlying disease being photo-aggravated dermatitis. Common laboratory findings were anaemia, neutrophilia, hyperglycaemia and hyperglobulinaemia. Histopathological patterns were most commonly cell-poor
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