Causes and pathogenesis.
The development of atopic dermatitis is complex. In dogs, it is a genetically programmed and heritable disease. In cats, evidence
suggests that the disease is heritable.6 Canine atopy can develop in any dog, but certain breeds are predisposed, such as terriers and retrievers (Table 2).1,7 Geographic gene pools may affect breed predispositions throughout the world.
Table 2. Dog Breeds with a Predilection for Atopic Dermatitis
The immunologic mechanisms involved in the development of atopic dermatitis are the focus of a great deal of study. Part of
the immune response involves an IgE-mediated type 1 hypersensitivity reaction, and it is hypothesized that the pathogenesis
also involves a T cell-mediated reaction.7-9 For many years, it was presumed that allergen exposure and sensitization occurred primarily through inhalation, hence the
name allergic inhalant dermatitis. Percutaneous allergen exposure is now thought to be an important additional part of the pathogenesis; it leads to a cytokine
imbalance and altered T cell-mediated response. Allergens from epidermal exposure become bound to epidermal Langerhans' cells
and are presented to T cells. Th2 cells are then preferentially activated and secrete cytokines, triggering allergen-specific
IgE antibody production.7-9 When allergens cross-link surface-bound IgE antibodies, mast cells degranulate, and preformed and synthesized inflammatory
mediators (e.g., histamine, leukotrienes, and substance P) are released. It is this cascade of reactions that is involved in the production
of pruritus and subsequent development of inflammation.
Key features of the historical presentation.
The owner will report that the dog is pruritic, or you will deduce this from the history; owners may not consider foot licking
and face rubbing to be signs of pruritus.
Uncomplicated atopic dermatitis is a glucocorticoid-responsive disease. However, if marked bacterial and yeast infections
are present, glucocorticoid therapy alone may not alleviate all of the clinical signs. Therefore, a history of unsuccessful
previous treatment with glucocorticoids does not rule out a diagnosis of atopic dermatitis.
The classic age of onset of clinical signs is somewhere between 7 months and 7 years of age, but most dogs develop clinical
signs between 1 and 3 years of age. This historical information may not be available from owners who adopted their dog from
a shelter. Also, if a dog has traveled with the owner through many geographic regions, signs of atopic dermatitis may not
develop until later in life. I have seen dogs develop clinical signs as early as 3 months and as late as 15 years of age.
Clinical signs may be seasonal or nonseasonal; dogs that initially present with seasonal clinical signs may develop nonseasonal
atopy with time. Owners may not be aware of this, but careful review of medical records may reveal the pattern. Breed predisposition
is another important historical clue (Table 2).
Key features of the clinical presentation.
The hallmark clinical sign the clinician is looking for is pruritus or evidence of pruritus, such as excoriations on the body
and face, saliva staining, broken stubbly hairs, and hair lodged between the teeth and gums. However, clinical signs can just
include recurrent ear disease, recurrent acral lick granulomas, or perineal pruritus.The primary distribution pattern is ventral
(Table 3); however, some dogs have only one or two affected areas (e.g., ears or feet). Lesion distribution also tends to be symmetrical, but it is not uncommon for signs to be worse on one side
of the body. The clinical signs of atopic dermatitis can overlap with those of other diseases, including the allergic diseases
Table 3. Common Clinical Features of Atopic Dogs