You’ve all had it or know someone who’s horse has it; “mud fever” and “greasy heel” are all too familiar terms for pastern dermatitis. An occupational hazard of being an equid living in the British climate maybe? And I’m sure you know of a secret recipe for the elixir of treatment, but you’ll have to kill me if you tell me. I wish. The truth is Equine Pastern Dermatitis (EPD) is not a single disease, but a “cutaneous reaction pattern” of the horse and the finding of a dermatitis in the fetlock and pastern region does not point towards a definitive diagnosis but is only of a symptom of change.
EPD should be considered then a syndrome, rather than a diagnosis and it is uncovering the underlying etiology prior to treatment that is key to maximizing treatment, as well as minimizing failures and frustration. To achieve a positive therapeutic outcome, treating the predisposing and perpetuating factors is just as important as addressing the primary cause of EPD.
The clinical signs are usually visible on a close examination of the pastern area but this can be more difficult in the heavily feathered breeds. The signs of dermatitis are most commonly redness of the skin, scabs, crusting and pain in the area affected, and in some cases such as with chorioptic mange the skin is very itchy with aggressive rubbing and biting of the area or foot stamping is seen. In more severe cases the irritation can sometimes extend along the entire lower limb, progressing from redness and scaling to oozing of fluid (serum) from the skin, matting of hair, and development of crusts. Chronic cases can become very ugly indeed, as the skin becomes thickened and swollen. It may even develop bumpy, mass-like tissue. This condition is very painful for the horse, and can cause mild to severe lameness in some cases. It can be unilateral (one sided), or bilateral (involving both right and left limbs). It may affect all four legs and even be found on other areas of the horse, especially white haired sites.
Most cases are due to bacterial folliculitis (deep bacterial infection of hair follicles), are rightly classical mud fever and follow a mixed infection involving more than one type of bacteria, most frequently isolated are Dermatophilus congolensis (also causing Rain Scald) which is thought to survive ubiquitously in mud, and Staphylococcus species, a normal finding on healthy skin which further thrives on damaged areas. When the skin is damaged by either environmental (wet paddocks/abrasive surfaces) or managemental (poor stable husbandry) factors, or by systemic disease (Cushings, liver disease), then overgrowth of the bacteria is common.
Other causes which will also promote bacterial overgrowth however, should not be discounted without consideration and include contact irritation from caustic substances, Chorioptic mange mites particularly in feathered breeds, fungal infection or ringworm – usually Trichophyton or Microsporum spp, sarcoidosis and sarcoids, vasculitis (usually more specifically termed pastern leukocytoclastic vasculitis or PLCCV) a severe autoimmune disease of white skin on the limbs trigged by sunlight exposure, and photosensitization or photo-activated vasculitis (white skin again becomes badly burned and reactive despite normal UV light exposure) usually due either to liver disease or the ingestion of certain (St John’s wort and buckwheat amongst others) but also often unrecognised photosensitizing toxic plants which accumulate in the skin and, once activated, cause localized inflammation and vasculitis. In some drafts (Clydesdales and Shires and other Draughts), an immune-mediated problem with a genetic component similar Darier-White disease in humans is also suspected. An additional point to always remember is that strangles infections can occasionally result in a significant vasculitis, known as purpura haemorragica, typically presenting 2-4 weeks after an infection. Whilst not generally limited to the limbs and with other clinical features (urticaria, mild swelling of the extremities, depression, anorexia and occasionally mucosal haemorrhages), its possible involvement highlights the importance of consideration and examination of the whole horse.
Diagnosis invariably starts with careful history taking (noting previous illness, drug administration, association with sunlight etc). In some cases it may be possible for your vet to make a diagnosis based on examination and clinical appearance alone, but in order to investigate and identify the causal agent, other tests are often required such as: skin scrapes, sticky tape samples, swabs for fungal or bacterial culture and antibiotic sensitivity, haematological and biochemical blood tests, serological testing, possible nasophayngeal swabs or guttural pouch sampling for S.equi infections and full thickness punch biopsies. Despite this, the primary cause is often difficult to identify and may never be determined. Long-standing cases which have already received some treatment are likely to be the most difficult to diagnose accurately, so it is advisable to seek professional help early. Sometimes a secondary infection can be present as well as the original disease and overwhelm primary treatment.
Treatment is orientated around identifying and removing the stimulus if possible, reducing the subsequent inflammation and providing supportive and preventative care. The following general principles for treatment apply to most cases but specific treatment options will vary depending on the cause of the dermatitis:
The limbs should be kept dry, so stabling may be necessary. Feathers may need to be clipped to get good access to the skin for topical therapies. If a parasite, bacteria or fungus is suspected, specific medication should be used. Cream or oil may be needed to aid scab removal, which can be very painful. A dilute antiseptic solution can be used to gently clean the skin. A topical antiseptic, antifungal or steroid cream may be useful. If sunlight is aggravating the condition, bandaging can be used to prevent exposure.
Often therapies are multi-modal requiring both systemic (steroids for vasculitis/auto-immune disease or antibiotics for deep bacterial infection) and local (local wound washes) to achieve resolution. Early treatment usually sees resolution within four weeks; however, relapsing or difficult cases may require a more prolonged treatment course.
Preventative care is always difficult to definitively advise; over-washing of limbs is not recommended due to removal of the natural bacterial flora, care of the horses bed &/or paddocks is challenging and it is common that the condition is simply ‘managed’ or reduced to an acceptable level with regular medical maintenance undertaken to prevent flares.