Atopy is a pruritic (itchy) skin disease of cats that is caused by an allergy to substances in the environment that are contacted through the air, either by absorption through the respiratory tract or contact through the skin. Atopy is thought to be an inherited disease, as litermates can have concurrent atopy[1]. It can be difficult to diagnose in cats and, therefore, is probably under-diagnosed. Symptoms of atopy usually begin relatively early in life, often by one year of age. Symptoms usually are seasonal at first, with most cats showing clinical signs in the summer months when airborne allergens (such as plant pollens) are present in higher concentrations. As atopic cats age, their symptoms tend to become less seasonal as they become allergic to more substances. Eventually, their itchiness can occur year-round. Cats with atopy are usually itchy, particularly the hands and feet. The skin may be red and irritated due to scratching, and the ears may also be inflamed. The symptoms of food allergy are difficult to distinguish from those of atopy and 50% of pruritic cats may be caused by food allergy[2]. Triggers of atopic dermatitis in cats include:

  • airborne pollen and dust
  • diet
  • household (non-pathogenic) fungi, such as Dermatophagoides farinae and D. pteronyssinus[3]


  • 1 Pathology
  • 2 Clinical signs
  • 3 Diagnosis
  • 4 Treatment
  • 5 References



Mast cells predominate in the perivascular infiltrate in skin lesions of allergic cats. Mast cells, however, may predominate in other non-allergic conditions such as pemphigus foliaceous and is not a reliable indicator of atopy. Blood tests which show eosinophilia is of limited value since several conditions including endo- and ecto-parasites may produce similar blood profiles.

The primary theory that supports how atopy is elicited in cats is via Th-2 (helper) cell activation. Allergic dermatitis in cats is not a well understood disease, however the human model for atopy does not contradict what is found experimentally in cats. In humans, Th-2 cells infiltrate the skin and synthesise associated cytokines, including IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-18, tumour necrosis factor-alpha (TNF-ά), transforming growth factor-beta (TGF-ß), and interferon-gamma (INF-γ). This appears to be most likely model in cats[4].

In cats, Immunoglobulin E (IgE) is the primary antibody involved in the initiation of the immediate allergic response. IgE activation can be elicited by a wide range of hypersensitivities by the cat to endo- and ecto-parasites (including fleas and ear mites), fungus, mosquitoes, dietary allergens/additives/preservatives and inhaled allergens (dust mites, chemical aerosols and smoke). In a skin sensitivity test performed by the University of Bristol on 100 cats, 60% of cats showed hypersensitivity to fungi (Dermatophagoides pteronyssinus and D. farinae), 26% were hypersensitive to fleas, 32% to pollen, 32% to dust mites (Tyrophagus spp) and 32% showed no allergic sensitiviity to any allergens when injected intradermally. The dominant allergens appear to be dust mites, fleas and to some extent pollen allergens[5].


Clinical signs

Chewing at the paws, scratching the face or rubbing it on the ground or with the paws, scratching the ears and shaking the head. Clinical presentations include miliary dermatitis, feline symmetrical alopecia, eosinophilic granuloma complex (primarily the eosinophilic plaque), and severe head and neck pruritus. The age of onset is variable but usually begins before 5 yr of age. The pruritus and dermatologic lesions may be seasonal or year round. Siamese, Burmese, and other purebred cats have an increased relative risk as compared with domestic short- or longhaired cats.

Lesions seen in atopy:

  • Periocular
  • Preauricular
  • Scales and crusts at the junction of haired and non-haired skin on the footpad
  • Perifacial

Skin lesions described are erythema, papules, and crusted papules (miliary dermatitis), excoriations and linear crusts, exudative lesions and eosinophilic plaques. Eosinophilic plaques may occur as single lesions or often found together with other lesions. Eosinophilic ulcers are less common signs of atopy in cats.

Sneezing is reported as an accompanying sign in about 50% of cases. Also chronic coughing and asthma may occur, although the association has not be proven reliably. Lymphadenopathy may be seen if skin damage is severe and secondary infection has occurred.



Diagnostic tests are necessary to rule out other skin diseases, as well as to support the diagnosis of atopy. These tests may include a complete medical history and perform a thorough physical examination, especially checking the ears and the skin of the face and paws. Often, abnormalities may not be detected on the physical examination of cats with atopy. Occasionally, redness between the toes or around the muzzle of the face is the only finding. Also, skin scrapings are taken to eliminate other diagnoses such as demodectic or Sarcoptic mange (caused by mites). Fungal cultures may also be taken to rule out ringworm (dermatophytosis). Eosinophilic granuloma complex is a similar disease but often is associated with oral ulcers, raised plaques in the flanks or groin region or large circular lesions[6].

Diseases that are consistent with atopy include miliary dermatitis, symmetric alopecia, eosinophilic granuloma complex, head and neck pruritus. Other diseases have similar clinical signs, including Ringworm, flea allergy dermatitis, various mite infestations (eg, Cheyletiella sppDemodex sppNotoedres sppSarcoptes sppOtodectes spp), mosquito bite hypersensitivity, food allergy dermatitis, autoimmune disease (eg, pemphigus foliaceus), and cutaneous neoplasia.



Response to steroids is excellent in most cases initially; however, efficacy decreases over time. A drug such as methylprednisolone acetate (Depo-Medrol®) given as a depot injection (20mg per cat, subcutaneously) will often induce remission of signs in the majority of atopic cats for a period of 6-8 weeks and appears to be more effective than daily oral prednisolone tablets. Intradermal allergy testing and hyposensitization procedures are similar to those used in dogs, but the testing is more difficult to read because the reactions to intradermal injections of allergens are less dramatic in cats than in dogs. Drugs such as chemotherapeutic agent, Cyclosporin are not recommended unless the severity justifies it use. Complication have been reported[7][8].

Parasite control/treatment should be considered a primary treatment in the initial consultation, with a broad-spectrum anthelmintic for endo- and ecto-parasites such as ivermectin. It is also vital to impress on clients the need for vigilant monthly control of parasites even if the cats are indoor dwelling and have no access to outdoors.

Provision of a high quality diet that is free of preservatives and low in game meat is also a serious consideration. Anecdotal evidence suggests that white meat is preferable to red, and cooking reduces the potential allergen presentation via the gut. Prescription diets such as Hill’s Feline Z/D have resulted in anecdotal improvement of symptoms. Considering the wide range of potential causes of atopy in cats, a multifactorial therapy must be instigated and maintained.

The hyposensitization response is similar to that seen in dogs but immunotherapy has generally been shown to be variable in producing any clinical improvement of signs in the cat. However, Feline allergen specific immunotherapy (ASIT) is considered to be a safe and effective treatment for feline atopy. ASIT is defined as the practice of administering gradually increasing quantities of an allergen extract to an allergic subject. The purpose of which is to reduce or eliminate the symptoms associated with subsequent exposures to the causative allergen. ASIT offers an effective and safe treatment option for cats. Reported success rates range for 60 to 78% in feline atopic patients. Additionally, the reported incidence of side effects in feline atopic patients undergoing ASIT is very low and mainly anecdotal[9].



  1. ↑ Moriello KA. (2001) Feline atopy in three littermates. Vet Dermatol 12(3):177-81
  2. ↑ Waisglass SE, Landsberg GM, Yager JA, Hall JA. (2006) Underlying medical conditions in cats with presumptive psychogenic alopecia. J Am Vet Med Assoc 228(11):1705-9
  3. ↑ Gilbert S, Halliwell RE (1998) Feline immunoglobulin E: induction of antigen-specific antibody in normal cats and levels in spontaneously allergic cats. Vet Immunol Immunopathol 63(3):235-52
  4. ↑ Roosje PJ, Thepen T, Rutten VP, van den Brom WE, Bruijnzeel-Koomen CA, Willemse T. (2004) Immunophenotyping of the cutaneous cellular infiltrate after atopy patch testing in cats with atopic dermatitis. Vet Immunol Immunopathol 101(3-4):143-51
  5. ↑ August, J.R. (2006). Consultations in feline internal medicine. Elsevier Saunders, Missouri
  6. ↑ Roosje PJ, Whitaker-Menezes D, Goldschmidt MH, Moore PF, Willemse T, Murphy GF. (1997) Feline atopic dermatitis. A model for Langerhans cell participation in disease pathogenesis. Am J Pathol 151(4):927-32
  7. ↑ Last RD, Suzuki Y, Manning T, Lindsay D, Galipeau L, Whitbread TJ. 2004) A case of fatal systemic toxoplasmosis in a cat being treated with cyclosporin A for feline atopy. Vet Dermatol 15(3):194-8
  8. ↑ Robson DC, Burton GG (2003) Cyclosporin: applications in small animal dermatology. Vet Dermatol 14(1):1-9
  9. ↑ Trimmer AM, Griffin CE, Rosenkrantz WS. (2006) Feline immunotherapy. Clin Tech Small Anim Pract 21(3):157-61

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