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Pathogenesis of Canine Atopic Dermatitis
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Canine atopic dermatitis has been defined by the ACVD task force as a genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features, most commonly associated with IgE antibodies to environmental allergens.
The development of atopic dermatitis in a genetically susceptible individual involves the interaction between the animal and various substances in the environment that act as allergens. Subsequent immunological activation leads to allergen presentation and processing, proliferation of lymphocyte subpopulations, and the activation of the IgE/mast cell system.
Genetic Susceptibility
To become atopic, a dog must inherit genes from its parents that cause immunological abnormalities that result in excessive IgE synthesis. this genetic susceptibility makes the condition more common in certain breeds. Genetic involvement also means that atopic dermatitis usually starts at a young age, typically between 6 months and 3 years of age.
The Allergens Involved
Numerous proteins are involved in triggering the immunological pathways that culminate in atopic dermatitis:
• House dust and grain mite antigens (Dermatophagoides farinae, Dermatophagoides pteronyssinus, Acarus siro, Tyrophagus putrescantiae, Euroglyphus maynei).
• Human and animal danders (derived from the continuous desquamation of corneocytes).
• House dust (a mixture of dust mite antigens, human and animal danders, bacteria, fungal spores, and fibres).
• Pollens (from trees, weeds and grasses). • Moulds (from the household or from crops)
• IgE may also be produced to allergens from staphylococci and Malassezia organisms. Studies in the dog have demonstrated that the major allergen in Dermatophagoides farinae is a high molecular weight (98/109 kD) enzyme which is present in the mite’s digestive tract. This chitinase has been designated as Der f 15. Subsequently, another protein with a molecular weight of 60kD designated Der f 18 has been characterised as a major allergen for dogs. [...]
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