Atopy is the predisposition to allergic disease in response to environmental allergens. The highest rate of positive allergen reactions is against molds followed by house dust. Tree, grass and weed pollens can also cause this disease. Flea allergic dermatitis and parasitic infections such as sarcoptic mange (scabies) and otodectic mange also cause allergic-type reactions. Many dogs have positive reactions to allergens in the insect group (fleas, mosquitoes, and cockroaches). Currently, there is evidence indicating that abnormal skin barrier function contributes to the disease, which is similar to that seen in humans with atopic dermatitis. This barrier controls absorption of external irritants and allergens. Impairment of the skin barrier can be caused by a primary defect or is a consequence of inflammation. Once the barrier function has been impaired, progressive worsening of this function occurs. Thus, impaired barrier function might play a key role in the development and aggravation of the clinical signs.
Females tend to more affected than males. Though any breed can develop atopy, several breeds have a marked predisposition including the Cairn Terrier, West Highland White Terrier, Shar-Pei, Scottish Terrier, Lhasa Apso, Wirehaired Fox Terrier, Dalmatian, Irish Setter, Boston Terrier, Pug, Golden Retriever, Boxer, English Setter, Labrador Retriever, and Miniature Schnauzer The onset usually occurs 1-3 years of age, with the exception of the Shar Pei which can begin as young as 3 months.
Canine atopic dermatits is a disease of young animals, with the peak age of onset between six months and three years. It is a chronic relapsing condition and most dogs will require ongoing, usually life-long, therapy. It is therefore important to understand the long-term safety of therapeutic interventions to balance efficacy and adverse effects in order to maintain a good quality of life. Dogs with atopic dermatitis usually have physical signs commonly seen in other skin diseases, such as flea bite hypersensitivity, food hypersensitivity, contact dermatitis, scabies, intestinal parasite hypersensitivity, folliculitis, pelodera dermatitis, and hookworm dermatitis. In cats atopic dermatitis often mimics various causes of symmetric alopecia, indolent ulcer, eosinophilic plaque and eosinophilic granuloma.
Diagnosis of allergies is a complicated task. The investigation of a suspected allergic dog should include rigorous treatment for external parasites and secondary bacterial and yeast infections which often complicate and contribute to the itch. A diagnosis of food intolerance is made in 2-10% of 'itchy' dogs. It can be controlled without using drugs and is worth ruling out by introducing an elimination diet followed by dietary challenge to confirm the diagnosis. Elimination diets are time consuming and require considerable owner commitment. It can be up to 3 months before the dog stops scratching. Once other causes of itch have been ruled out, specific tests to detect allergic antibodies to environmental allergens can be undertaken to confirm the diagnosis of atopy.
Skin tests can be used to determine the allergens to which the animal is hypersensitive. It is essential to understand that a positive skin test means only that the patient has skin sensitizing antibodies, not necessarily a clinical allergy. False results can often occur. Reasons for false positives include: irritant test allergens, bacterial or fungal contaminated test allergens, skin sensitizing antibody only, poor technique, substance causes non-immunogenic histamine release "irritable" skin.
Unfortunately, dogs rarely 'grow out' of their allergies and most atopic dogs require lifelong therapy. Various treatments are available and your veterinarian will recommend the best regime. Ciclosporin (Atopica; Novartis Animal Health; cyclosporine, cyclosporin A or CsA) has been licensed for canine atopic dermatitis (AD) since 2002. Adverse effects have been reported in 55 per cent of 759 dogs in 15 clinical trials. Gastrointestinal reactions were most common, but were mild and rarely required intervention. Unacceptable gastrointestinal problems requiring cessation of treatment were rare; in one study this was reported in only two of 266 dogs. Hirsutism and/or hypertrichosis is frequently reported in dogs treated with ciclosporin. Initially, some animals experience a heavy shedding approximately four to six weeks after initiation of ciclosporin therapy. The hair follicles then begin to produce new growth, resulting in the growth of a thicker and glossier haircoat. Hirsutism or hypertrichosis is a benign consequence of ciclosporin therapy. It is rarely clinically significant, but individual dogs may need more frequent grooming to prevent matting of the coat. Ciclosporin decreases staphylococcal and Malassezia infections, and at the recommended dose is not a risk factor for other infections, neoplasia, kidney failure or high blood pressure. Bacterial infections (including gingivitis, pyometra and respiratory tract infections) have been seen in dogs treated with ciclosporin, but these are uncommon and no more frequent than in the general canine population. Diabetes mellitus is rare in dogs treated with ciclosporin. It has been associated with West Highland white terriers in Europe. Ciclosporin therapy is not a risk factor for neoplasia at standard doses used to manage canine atopic dermatitis. However, because of the potential impact on tumor growth and development, ciclosporin is contraindicated in the presence of neoplasia.4
Affected animals should not be used for breeding. The breeders of atopic animals should be informed if a particular sire and dam produced affected offspring and this should influence decisions regarding future breeding. Neem oil can be considered as effective and is beneficial for dogs with atopic dermatitis. Recent findings suggest that daily application of a 0.0584% hydrocortisone aceponate (HCA) spray not only provided short-term alleviation of clinical signs associated with atopic dermatitis, but also improved skin barrier function, which is associated with the disease.