Atopic dermatitis is a common dermatosis of dogs defined as a genetically-predisposed inflammatory and pruritic skin disease with characteristic clinical features that is associated with IgE antibodies, most commonly directed against environmental allergens.2 We now recognize a parallel condition termed ‘atopic-like dermatitis’ (ALD) that must be differentiated from AD. Patients with ALD have the same constellation of clinical signs as those with AD, but in ALD, an IgE response to environmental or other allergens cannot be documented by usual methods (Box 1).2
Pathogenesis. The pathogenesis of canine AD is not fully understood. Whereas the traditional dogma stressed the importance of IgE-mediated early and late-phase hypersensitivity reactions to airborne allergens, evidence is now mounting to suggest that epidermal barrier defects might also contribute to disease pathogenesis.3 The current theory on the pathogenesis of canine AD can be summarized as follows.3,4 In the acute phase of the disease, putative epidermal barrier defects are thought to facilitate contact of environmental (and possibly microbial) allergens with epidermal immune cells. Epidermal antigen-presenting cells capture allergens with allergen-specific IgE, and then migrate to the dermis and regional lymph nodes. Microbial products and immune cell-derived inflammatory mediators activate keratinocytes, which, in turn, release more chemokines and cytokines. Immunoglobulin E-coated dermal mast cells release histamine, proteases, chemokines and cytokines following contact with allergens. There is an early influx of granulocytes (neutrophils and eosinophils), allergen-specific T-lymphocytes and dermal dendritic cells. Eosinophils degranulate and release proteins that induce dermal and epidermal damage. Type-2 helper T lymphocytes release cytokines promoting IgE synthesis and eosinophil survival. Microbes, self-trauma and neuromediators might also contribute to persistent inflammation in chronic skin lesions. There is a continuous cycle of chemokine release that leads to the influx and activation of leucocytes and the release of additional pro-inflammatory mediators. The failure to down-regulate pro-inflammatory mechanisms is followed by self-perpetuating cutaneous inflammation. Despite these advances in our knowledge of the pathogenesis of canine AD, the mediators that elicit the sensation of pruritus have not been elucidated. Importantly, histamine does not appear to provoke pruritus in dogs in contrast to humans and mice.5
Table Box 1. . International Task Force on Canine Atopic Dermatitis disease definition
| Canine atopic dermatitis: A genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features associated with IgE antibodies most commonly directed against environmental allergens.|
| Canine atopic-like dermatitis: An inflammatory and pruritic skin disease with clinical features identical to those seen in canine atopic dermatitis in which an IgE response to environmental or other allergens cannot be documented.|
|Halliwell R. Revised nomenclature for veterinary allergy. Veterinary Immunology and Immunopathology 2006; 114: 207–8.|
Clinical Signs and Diagnosis
It is not within the scope of this document to provide a detailed discussion of the many facets (and controversies) in the diagnosis of AD. However, the authors wish to summarize our current understanding, and emphasize several critical elements, which we believe are most frequently misunderstood.
The diagnosis of canine AD relies primarily on the patient’s signalment, clinical signs and disease history, and not on a laboratory test. 6,7 Atopic dermatitis is a diagnosis based on the finding of a constellation of typical history and clinical signs with the subsequent elimination of other conditions that might mimic it. Most atopic dogs usually begin manifesting signs between 6 months and 3 years of age. There is no known gender predisposition. In general, dogs have a history of pruritus with or without recurrent skin or ear infections. A history of lacrimation, ocular congestion or sneezing/rhinorrhea could be indicative of concurrent atopic conjunctivitis and rhinitis respectively. Signs might be seasonal or nonseasonal with or without seasonal exacerbation, depending principally upon the allergens involved as flare factors and the pet’s environment.
Primary skin lesions usually consist of erythematous macules, patches and small papules. Most patients, however, present with lesions that occur secondary to self-trauma, for example excoriations, self-induced alopecia, lichenification and hyperpigmentation. The distribution of canine AD skin lesions is variable and likely depends upon the chronicity of the disease and allergens involved. Body areas that commonly exhibit lesions are the face, concave ear pinnae, ventral neck, axillae, groin, abdomen, perineum, ventral tail, as well as flexural and medial aspects of extremities. The dorsal and ventral paws are often involved and otitis externa is also commonly seen. Periocular and perinasal lesions might reflect co-existing pruritic atopic conjunctivitis and rhinitis respectively.
It is critically important to recognize that other dermatoses can mimic AD, or be superimposed on it. These diseases are usually of parasitic (especially scabies, and, occasionally demodicosis), infectious (e.g. Staphylococcus superficial pyodermas, Malassezia dermatitis) or of other allergic origin. Such diseases must be ruled-out or controlled before the diagnosis of AD is made. The principles of diagnosis and treatment of these clinically similar conditions are beyond the scope of these guidelines; practitioners should refer to recent reviews for best practice recommendations in their respective countries.
A set of criteria – a type of ‘checklist’– has been recently recommended as an aid for diagnosing AD in dogs (Table 2).8 One should remember, however, that these criteria are not absolute; approximately one of five cases (20%) could be misdiagnosed if these parameters were to be applied strictly! However, with the proper rule-out of ectoparasitoses and skin infections, the specificity of these criteria is expected to increase markedly. Finally, it is important to keep in mind that, in early stages of AD, lesions are unlikely to be seen at all characteristic sites, and pruritus might be present without observable lesions.
Table 2. Favrot’s 2010 criteria for canine atopic dermatitis
|1. Onset of signs under 3 years of age|
|2. Dog living mostly indoors|
|3. Glucocorticoid-responsive pruritus|
|4. Pruritus sine materia at onset (i.e. alesional pruritus)|
|5. Affected front feet|
|6. Affected ear pinnae|
|7. Nonaffected ear margins|
|8. Nonaffected dorso-lumbar area|
|A combination of five satisfied criteria has a sensitivity of 85% and a specificity of 79% to differentiate dogs with AD from dogs with chronic or recurrent pruritus without AD. Adding a sixth fulfilled parameter increases the specificity to 89% but decreases the sensitivity to 58%.|
The relationship between canine AD and cutaneous adverse food reactions (CAFR or ‘food allergies’) has long been the subject of controversy. Recently, this Task Force supported the concept that CAFR might manifest as AD in some canine patients, or, in other words, that food components might trigger flares of AD in dogs hypersensitive to such allergens (Box 2).9 It should be noted that, in addition to clinical signs typical of AD, CAFR could also manifest as other syndromes, such as urticaria or pruritus without lesions or with lesions at unusual sites (e.g. flanks, dorsum, perineum, around the lips).
There is consensus that the use of allergen-specific IgE serological or intradermal tests cannot be used for the initial diagnosis of AD in dogs.10,11 Many normal and atopic dogs exhibit positive reactions with either test, thereby markedly decreasing the tests’ specificity for the diagnosis of AD. Using a serologic test or intradermal test as a primary criterion for diagnosing AD will, therefore, lead to misdiagnosis. However, such tests can be used for the following reasons: (i) to document whether or not the disease is associated with allergen-specific IgE (i.e. determining whether the dog suffers from AD or ALD), (ii) to implement allergen-avoidance interventions (e.g. house dust mite elimination measures), and/or (iii) to select allergens to be included in immunotherapy preparations. These interventions will be discussed below in greater detail.
Table Box 2. . Excerpts from the International Task Force on Canine Atopic Dermatitis position on the relationship between food allergy and atopic dermatitis in dogs
| Food allergy (also known as adverse food reaction) is an aetiological diagnosis. In dogs, cutaneous clinical manifestations of food allergies have been reported as focal, multifocal or generalized pruritus, otitis, seborrhoea, superficial pyoderma and also, in some dogs, as atopic dermatitis. These cutaneous manifestations can often be accompanied with digestive signs.|
| Atopic dermatitis, in dogs and humans, is a clinical diagnosis. It can be exacerbated by an exposure to allergens, which can be of environmental (e.g. mites, pollens), microbial and also, in some dogs, dietary origin.|
| Position statement: the International Task Force on Canine Atopic Dermatitis supports the concept that cutaneous adverse food reactions (food allergies) might manifest as atopic dermatitis in some canine patients, or, in other words, that food components might trigger flares of atopic dermatitis in dogs hypersensitive to such allergens.|
| Implications for clinical practice: Food allergies can manifest clinically, in some dogs, as atopic dermatitis, but not every dog with food allergy will manifest it as atopic dermatitis. Atopic dermatitis can be exacerbated by food allergens, but not every dog with atopic dermatitis will have dietary-induced flares. Every dog diagnosed with nonseasonal (i.e. perennial) atopic dermatitis should undergo one or more dietary restriction-provocation challenges (i.e. ‘elimination diets’) to determine, and then eliminate, any dietary allergens that might cause flares of the disease.|
| Olivry T, DeBoer DJ, Bensignor E, Prélaud P for the International Task Force on Canine Atopic Dermatitis. Food for thought: pondering the relationship between canine atopic dermatitis and cutaneous adverse food reactions. Veterinary Dermatology 2007; 18: 390–1.|
The major objective of these practice guidelines is to improve the care of dogs with AD. The recommendations were made by a committee of the International Task Force for Canine AD for the benefit of general practitioners. This article is divided into two distinct sections: (i) the management of acute flares of AD, and (ii) the treatment of chronic skin lesions of AD. Case scenarios are provided as examples of situations that can occur in practice and that would benefit from the interventions recommended in these sections. Treatment options are listed in a particular order, but this does not mean that all recommendations are advised or needed in that specific sequence. First and foremost, practitioners shall examine the validity of these recommendations in the context of their patient, the pet owners and the availability and cost of the products in their respective countries. Again, veterinarians must remember that it is often necessary to combine several interventions in order to achieve a satisfactory outcome.