Canine Atopic Dermatitis

Disease State

Prevalence and Etiology

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder in dogs, affecting approximately 10–15% of the canine population globally.^1,2 AD is responsible for nearly 60% of canine dermatological diagnoses in veterinary practice.² AD most commonly manifests in young to middle-aged dogs, with clinical onset typically occurring between 1 and 3 years of age. In certain geographical regions, the prevalence of AD surpasses that of flea allergy dermatitis.³

Multiple risk factors contribute to the development of canine atopic dermatitis (CAD), including^2,4–6:

• Genetic predisposition with a higher incidence of AD diagnosed in Labrador Retrievers, Golden Retrievers, and West Highland White Terriers⁷
• Epidermal barrier dysfunction leading to increased transepidermal water loss and enhanced allergen penetration
• Imbalanced T-lymphocyte cytokine responses, particularly a Th2-skewed immune profile⁸
• Elevated cutaneous mast cell degranulation contributing to local inflammation and pruritus
• Increased susceptibility to secondary bacterial and yeast infections due to trauma from itching

The multifactorial etiology and combination of unique factors in each patient can make CAD difficult to diagnose and treat.

Immunology

The immunopathogenesis of CAD is driven by dysregulated activation of T helper 2 (Th2) lymphocytes, which play a central role in initiating and perpetuating skin inflammation. Th2 cells secrete a range of pro-inflammatory cytokines, including interleukin (IL)-4, IL-5, IL-13, IL-17, IL-22, IL-31, and thymic stromal lymphopoietin (TSLP). These cytokines contribute to epidermal barrier dysfunction and promote cutaneous inflammation.

Among these cytokines, IL-31 is particularly noteworthy for its role in pruritus.¹⁰ IL-31 binds to its receptor on peripheral sensory neurons, triggering pruritogenic signaling and promoting itch perception in both dogs and humans.¹¹ It is highly upregulated following epicutaneous allergen exposure in dogs sensitized to house dust mites.¹⁰

CAD is characterized by distinct acute and chronic immunologic phases:

• Acute Phase⁸: Lesions are predominantly infiltrated by Th2 lymphocytes. Activated Th2 cells secrete cytokines (e.g., IL-4, IL-5, IL-6, IL-9, IL-10, IL-13) that promote B cell class switching to IgE, stimulate eosinophil recruitment, and induce mast cell degranulation. These responses culminate in immediate hypersensitivity reactions and amplify the inflammatory cascade.
• Chronic Phase⁸: Chronic lesions show a mixed Th1/Th2 profile, with increased Th1 cell infiltration. Resulting Th1 cytokines such as interferon-gamma (IFN-γ), tumor necrosis factor-beta (TNF-β), and IL-2 mediate delayed-type hypersensitivity and sustain cellular inflammation by activating macrophages and cytotoxic T cells. IFN-γ also acts to downegulate Th2-mediated IgE synthesis, reflecting a regulatory shift in the chronic disease state.

This biphasic cytokine expression pattern—Th2 dominance in early acute lesions transitioning to Th1 predominance in chronic lesions—defines the dynamic immune response in CAD.

Clinical signs

Clinical signs associated with CAD can demonstrate a seasonal or non-seasonal pattern depending on allergen exposure.  Pruritus is the hallmark clinical sign.⁹ In the acute phase, erythema is commonly observed. With chronicity, the skin often develops lichenification and hyperpigmentation secondary to persistent inflammation and mechanical trauma from the scratching, licking, and/or chewing. Recurrent secondary bacterial and yeast infections are common, further intensifying pruritus and cutaneous inflammation.

Focal or patchy alopecia typically results from self-inflicted trauma. Lesions generally follow a characteristic distribution, predominantly affecting the periorbital and perioral facial regions, pinnae, interdigital spaces of the paws, axillae, inguinal region, ventral abdomen, ventral neck, and perianal area.