Atopic dermatitis


Ralf S. Mueller, DipACVD, FACVSc
Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University
Fort Collins, CO 80523, USA
Conférence présentée en 2003 lors des journées du Groupe de Travail Belge en Dermatologie Vétérinaire

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Atopic dermatitis

  • Atopic dermatitis used to be defined as a type 1 hypersensitivity with production of IgE specific for airborne allergens. This mast cell-bound IgE was supposed to be cross-linked by inhaled airborne allergens. Cross-linking leads to mast cell degranulation with release of inflammatory mediators and subsequent clinical signs. Today, most dermatologists and allergists agree that although inhaled allergens may be responsible for allergic rhinitis and allergic asthma, atopic dermatitis is triggered by percutaneous absorption of allergens which explains most of the predilection sites in the dog, i.e. interdigital, axillary, ventral and facial dermatitis.
  • Allergen-specific IgE has been demonstrated on the surface of Langerhans cells, providing a link between delayed type hypersensitivity and atopic dermatitis. Development of clinical signs may or may not occur with increased allergen-specific IgE concentrations, IgE may not be central to the pathogenesis of atopic dermatitis. T cell reactivity and cytokine release in patients with atopic dermatitis differ from normal individuals and normalize after successful immunotherapy, pointing to the central role of T cells in the disease.
  • In humans, atopic dermatitis may be caused by percutaneously absorbed airborne allergens, but also by ingested food allergens and as food reactions in the dog and cat are clinically indistinguishable from nonseasonal atopic dermatitis, we may consider adverse food reaction a part of atopic dermatitis rather than a completely separate entity.
  • In the dog, breed predilections vary with location and time but have been reported in Cairn Terriers, West Highland White Terriers, Scottish Terriers, Lhasa Apsos, wire-haired Fox Terriers, Dalmatians, Pugs, Irish Setters, Boston Terriers, Golden Retrievers, Boxers, English Setters, Labrador Retrievers and Miniature Schnauzers. In Australia, German Shepherd Dogs, Rottweilers, Bull Terriers, Boxers and West Highland White Terriers seem to be predisposed.
  • The disease classically starts in dogs of young age (as young as 3 months in some dogs).
  • About 80% of atopic dogs initially show the signs seasonally, but as many eventually have nonseasonal clinical signs.

Clinical signs

The skin lesions are usually associated with self trauma, secondary pyoderma and secondary seborrhoea. Atopic otitis externa (seen in 50% of atopic patients) initially involves the pinna and the vertical ear canal alone and can sometimes be the only sign of atopic dogs. Other typically involved sites are feet, face and axillae or at least predominantly facial and ventral. With pedal inflammation, either the interdigital spaces are affected (dorsal or palmar/plantar surface) or dogs lick their carpal and tarsal areas. Some will do both. Pruritus on the tailbase points more towards involvement of flea bite hypersensitivity, pruritus underneath the tail in the perianal area points towards tapeworms, blocked anal glands, atopy or food allergy. Conjunctivitis can be seen in many cases (sometimes due to rubbing the periocular area and sometimes without involvement of periocular skin at all), as well as hyperpigmentation, salivary staining, lichenification, alopecia and (in 10-20%) hyperhydrosis. Non-cutaneous clinical signs reported are rhinitis and asthma. In the cat, the disease can be seasonal or nonseasonal. No breed predilection has been reported. The majority of the atopic cases is reported to first exhibit clinical signs between six months and two years of age, but we have seen quite a number of cats starting at an older age. The cutaneous signs are very variable. Facial pruritus and pruritic ears are common features. A thorough otoscopic exam is essential. Treatment with proper topicals will often lead to resolution and relapse some time after cessation of medication. The nails and mucocutaneous junctions should be examined, lesions in these areas are suggestive of autoimmune disease such as pemphigus foliaceus or lupus erythematosus that may cause crusting and pruritus of the face and the ears. Miliary dermatitis may be associated with atopic dermatitis in the cat. Another common clinical presentation is noninflammatory symmetric alopecia. Pruritus may be obvious to the owner, but many cats are so-called hidden groomers or closet lickers and owners never observe them licking or rubbing. Some of the owners will strenuously deny that possibility. Lesions of the eosinophilic granuloma complex include rodent ulcers (typically ulcerated upper lips), linear granulomas (classically alopecic, inflammed, linear lesions on the back of the thighs) or eosinophilic plaques (red, ulcerated plaques most commonly on the belly which are usually very itchy) and can all be due to atopic disease. Incidence of atopy among allergic cats is reported to be around 15% of all allergies, however these figures may be too low.


Diagnosis is made by history, physical examination and ruling out differential diagnoses. Intradermal testing or serum testing is used when hyposensitization or allergy shots are considered and offending allergens need to be identified to formulate the extract for this therapy.

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