Canine atopic dermatitis (AD) is a common, genetically predisposed inflammatory dermatosis. It is likely to involve complex interactions between skin structure, the immune system and the environment. Most cases are characterized by generation of IgE antibodies that target environmental allergens, although 10-20% of cases appear to be non-allergic (atopic-like dermatitis). Recent findings have greatly improved our understanding of the mechanisms involved in this condition and have prompted the development of hypotheses for pathogenesis.
    There is some evidence suggesting that epidermal barrier defects in atopic dogs can enhance exposure to allergens, irritants and micro-organisms. Such exposure might stimulate keratinocytes to release pro-inflammatory cytokines and chemokines, and express MHCII and adhesion molecules. IgE⁺ binding to FcεRI in the skin is stable and long-lasting. IgE-allergen interactions greatly enhance allergen capture and presentation by Langerhans′ cells to T-cells, and induce mast cells to release cytokines, chemokines, proteases and other pro-inflammatory mediators. This results in an influx of neutrophils, eosinophils, TH2 cells and dendritic cells. TH2 cytokines promote further IgE production, and eosinophil recruitment and activation.
    Self-trauma results in an ongoing cycle of skin damage, keratinocyte activation and pro-inflammatory mediator release. Atopic skin is particularly vulnerable to colonization and infection with staphylococci and Malassezia, which induce further inflammation, keratinocyte activation, and recruitment and activation of dendritic cells and T-cells. Cytokines, chemokines and other mediators recruit and activate allergen-specific and non-specific T-cells that secrete a mix of TH1 and TH2 cytokines. TH1 cytokines contribute to ongoing skin damage and chronic cellmediated inflammation. Resolution fails to occur, possibly because of the failure of T-regulatory cells and other mechanisms that limit activation and inflammation.

    The clinical symptoms and signs of canine atopic dermatitis (AD) have been well described with some variation. These variations likely reflect several problems in recognizing the signs and symptoms of canine AD. The signs, symptoms, and ruling out other mimicking diseases are the basis for making the diagnosis of canine AD. Many aspects such as age of onset, presence of lesions in pruritic areas and the distribution pattern rely on owner observation. Assessment and accurate information are often only obtained after owners have been trained on what they need to observe for. The major differential diagnoses for AD are adverse food reactions, sarcoptic mange, and flea allergy dermatitis. This article will present a review of what is known about clinical AD as well as the observations of the authors and clues used to help differentiate AD from the major differential diagnoses.

    The diagnosis of canine atopic dermatitis (AD) is based on patient history, clinical signs and exclusion of other causes of pruritic disease. When a clinical diagnosis of AD is made, allergy testing can be performed to select allergens for management of environmental allergies through immunotherapy. Allergy testing for canine AD is performed using an intradermal allergy test or a serologic allergy test. Information about each of these tests will be presented in this article. The basic techniques for each test will be described and the pros and cons of each test will be discussed. Patch testing for canine AD will also be briefly discussed.

    Proper diagnosis and treatment of secondary infections is essential for successful management of patients with atopic dermatitis (AD).
• Diagnosis first involves a thorough and concise physical examination and gathering of the history from the client in order to identify behaviors and lesions that are associated with these infections.
• Cytology is the first diagnostic test used to gather preliminary data regarding infections. Based on these results, clinical history, and patient behavioral patterns, further diagnostic testing such as bacterial culture and sensitivity might be appropriate.
• A therapeutic regimen of topical and/or systemic therapy for an appropriate time period is recommended based on test results.
• Patient follow-up via communication with the client and, more importantly, follow-up examination prior to stopping antimicrobial therapy is essential for eliminating infections and preventing the development of resistant organisms.
• There are many challenges resulting from both patient and client idiosyncrasies that need to be taken into consideration when selecting the appropriate therapy. Ultimately, the development and maintenance of open lines of communication between the client and veterinary team, with special attention paid to the client′s understanding of atopic disease and its relationship to secondary infections, are essential to successful therapy.

    This article reviews allergen-specific immunotherapy (ASIT) in veterinary medicine, which is the only specific therapy for atopic dermatitis. Current hypotheses of possible mechanisms of action are outlined. Evidence suggest altered T cell reactivity. Reported success rates for ASIT are between 50 and 65%. However, protocols vary widely and make comparison difficult. The most common adverse effect is increased pruritus. Anaphylactic shock is the most severe but an extremely rare adverse effect. Age of disease onset, duration of disease prior to therapy, and type of allergen or signalment were consistently not shown to affect the success rate.

    Canine atopic dermatitis is a condition that requires long term management, usually for the remainder of the pet′s life, and a multimodal approach to therapy is typically the most beneficial. Antihistamines, fatty acid supplements, glucocorticoids, and cyclosporine are commonly used systemic modulators and typically help control allergy symptoms in most atopic patients.

    Treating dogs with atopic dermatitis involves a multi-modal approach. In addition to allergen avoidance, allergen-specific immunotherapy, and systemic anti-inflammatory medications, topical therapy can be of use. There is no single type of topical therapy (i.e. shampoo, leave-on conditioner, spray, ointment) that is best for every patient, and no single active ingredient (i.e. anti-inflammatory, glucocorticoid, antihistamine, anesthetic) that works in every case. To date, the topical treatment of canine atopic dermatitis remains an art rather than a science.