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Introduction:
10
Equine Atopic Dermatitis
ACVSC Proceedings Dermatology Chapter Science Week 2005
Janet Littlewood
Atopic dermatitis is defined as a genetically programmed disease mediated by
reaginic-antibodies (type I hypersensitivity) in which the patient becomes sensitised
to environmental allergens that are innocuous for non-atopic animals. Classically the
diseases is associated with IgE allergen-specific antibodies, but in some species
evidence supports a role for allergen-specific IgG. The importance of other
components of the immune system are now known to be important in the aetiology
of the disease process.
In humans and dogs there is good evidence that the disease is genetically
programmed and there are reports of familial incidence and breed predispositions in
the horse that suggest genetic involvement. It is well recognised that insect bite
hypersensitivity (IBH, Culicoides hypersensitivity) has a strong familial tendency, and
there are reports of familial occurrence of equine atopy suggesting a genetic
predisposition (Rees 2001). Factors such as susceptibility to sensitisation during early
life and the influence of the presence of parasitic infestation, viral infections,
vaccination and environmental pollutants are of unknown significance in the horse.
Genetically-predisposed individuals mount allergen-specific IgE (and possibly IgG)
antibody responses to environmental (and possibly ingested) antigens. Equine IgE
was isolated and characterised by Suter and colleagues in the early 1980's, with even
earlier documentation of skin-sensitising antibodies. IgE binds to mast cells in the
skin (and elsewhere) via the high-affinity IgE receptor. Cross-linking of mast cellbound
IgE by specific allergens, causes degranulation and release of preformed
mediators, giving rise to the classical erythematous wheal reaction, and synthesis of
new mediators resulting in the recruitment of inflammatory cells to the area.
However, the lesions that develop in atopic humans and dogs at the site of patch
tests more closely mimic those found in the naturally occurring clinical disease.
Atopic individuals show increased numbers of both dermal and epidermal
Langerhans cells, as well as increased numbers of other inflammatory cells.
Epidermal Langerhans cells have been shown to bear allergen-specific IgE molecules
in atopic humans and dogs, further supporting that percutaneous absorption of
allergens is important in the aetiology of the natural disease, probably aided by
epidermal barrier function defects.