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2) atopic dermatitis (environmental allergy); or 3) drugs. Less commonly urticaria may be caused by vasculitis (including purpura haemorrhagica), dermatophytes, or pemphigus foliaceus. Note: it is important to remember that urticaria due to any of these diseases is not always pruritic.
Scales and crusts: when focal, pyoderma or dermatophytes. When more generalised, pemphigus foliaceus or equine sarcoidosis (these latter 2 diseases are often not pruritic).
Ulcers/scaling on white pigmented areas: photosensitivity, photo-aggravated (aka pastern leucocytoclastic) vasculitis.
Alopecia. When a horse is pruritic, this can be caused by almost any disease. However, circular areas of alopecia are suggestive of a folliculitis, such as pyoderma or dermatophytes.
Lesion location Ventral midline dermatitis: if linear or widespread, Culicoides or black flies (Simulium sp.). If focal, horn fly (Haematobia sp). Rarely, Chorioptes mites.
Distal limbs: vasculitis (may be seen in pigmented as well as nonpigmented skin), Chorioptes mites. Rarely, contact allergy, atopic dermatitis, dermatophytes.
Face: atopic dermatitis, black flies (especially between rami of mandible), stable flies (Stomoxys calcitrans).
Trunk pyoderma: dermatophyte, vasculitis, atopic dermatitis, lice, chiggers (Trombiculids), food allergy.
Dorsal trunk: Culicoides (may be confined to just mane and tail).
Cranial trunk stable flies (Stomoxys calcitrans).
Caudal trunk (‘tail-rubbers’): Culicoides, pinworms (Oxyuris sp), atopic dermatitis, yeast (Malassezia spp.: these may be between the mammary glands of mares or the preputial fossa of males but the pruritus evident by tail rubbing). Rarely food allergy.
Pruritic diseases
Ectoparasites Culicoides species (‘no-see-ums’, midges, gnats) may feed either on the dorsal or ventral surfaces of the horse, affecting the mane, saddle and rump, or cause a ventral midline dermatitis (the latter in a diffuse pattern; Fig 1). Papules, crusts and alopecia are found at these body locations. The adult gnats are 1–4 mm. The Culicoides’ bites induce a hypersensitivity response via salivary antigens (Wilson et al. 2008); this condition is termed Culicoides hypersensitivity, Queensland itch, sweet itch etc. There is evidence that a hereditary predisposition to develop the hypersensitivity occurs. While there are a number of species of Culicoides, the 2 most commonly suspected of causing the allergic response are C. variipennis and C. nubeculosis. Anumberof studieshaveattempted to define the nature of
the hypersensitivity response. One study (Wilson et al. 2001) found serum antibodies to Culicoides salivary gland antigens in
Fig 1: Crust and alopecia on ventral midline due to ventral-feeding Culicoides in an 8-year-old Quarter Horse gelding.
both healthy horses exposed to Culicoides bites and in horses with insect ‘dermal’ hypersensitivity. In contrast, no antibodies weredetected in serum from native Icelandic horses whichhad not been exposed to Culicoides. Another study confirmed the presence of certain subclasses of IgE and IgG antibodies to various salivary protein extracts of C. nubeculosis in European horses (Hellberg et al. 2006). Further evidence for a hypersensitivity response was demonstrated in a study in which intradermal injection of a Culicoides antigen extract induced T lymphocyte and eosinophil accumulation in the skin of affected horses (McKelvie et al. 2001). While no sex predisposition has been noted, Icelandic
horses may have a higher incidence of allergic reactions to the Culicoides insects than other breeds. The disease is quite uncommon in horses younger than one year, with an onset usually at age 2–4 years. Culicoides hypersensitivity may be seasonal, at least during the first few years in temperate climates. Diagnosis is primarily by clinical signs; commercially available Culicoides antigens are available in the USA1; their efficacy in both diagnosis and treatment is still being evaluated (Kolm-Stark and Wagner 2002). However, a study in Europe showed that intradermal testing and histamine release tests were more accurate than serological testing for antibodies to salivary proteins of C. nubeculosus and C. sonorensis (Langner et al. 2008). Therapy is aimed at insect control, especially:
1. Stabling horses at sunrise and sunset – peak feeding hours. 2. Ultrafine setting or screens placed in windows (60 squares to the square inch).
3. Fly control, especially keeping horses away from standing water and the use of permethrin repellent products on the animal. Usually these are 2% permethrin sprays, but 44–65% permethrin spot-on formulations, marketed for dogs (and thus used off-label) have been used successfully as well. Sprays must frequently be applied more often than the label recommends (i.e. daily, at least at first.) The author has had some success using a nonpesticide product available as either a spray or a stick ‘roll on’ (Shield and Sheen)2.
4. Overhead or stall fans (draughts interfere with the insects’ flight).
5. ‘Dresses’ that physically obstruct the insects from reaching the skin.
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