Atopic dermatitis (AD) is a genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features. It is most commonly associated with IgE antibodies to environmental allergens such as pollens, environmental mites, molds, food allergens, and Malassezia and Staphylococcus organisms. The atopic phenotype is characterized by chronic pruritus, typical lesion distribution, a family history of the disease, and breed predisposition. These signs can be seen in animals with IgE-mediated skin disease, or a condition called "atopic-like dermatitis" (ALD). ALD is defined as a pruritic skin disease in dogs with characteristic features of AD but negative tests for IgE antibodies.
Feline atopic dermatitis has many similarities to canine atopic dermatitis, but cats have a different clinical manifestation of skin hypersensitivity, including at least one of the following reaction patterns: miliary dermatitis, self-induced alopecia, eosinophilic granuloma complex, and head and neck pruritus.
Etiology and Pathogenesis of Atopic Dermatitis in Animals
The etiology and pathogenesis of AD is complex and involves a genetic predisposition, impairment of the normal barrier function of the skin, and immunologic aberrations. Animals with AD are thought to be genetically predisposed to become sensitized to allergens in the environment. Allergens are proteins that, when inhaled or absorbed through the skin, respiratory tract, or GI tract, evoke allergen-specific IgE production. These allergen-specific IgE molecules affix themselves to tissue mast cells or basophils. When these primed cells come in contact with the specific allergen again, mast cell degranulation results in the release of proteolytic enzymes, histamine, bradykinins, and other vasoactive amines, leading to inflammation (erythema, edema, and pruritus).
The skin is the primary target organ in dogs and cats, but rhinitis and asthma can also occur in ~15% of affected animals. Neuronal itch stimulation plays an important role in the initiation and perpetuation of pruritus. IL-31 has been shown recently to be an important pruritogenic cytokine. IL-31 stimulates neurons via its receptors and activation of enzymes of the JAK family. This knowledge has led to the development of new therapies.
