Atopy is a well-recognized clinical entity in dogs and is defined as an inherited tendency to develop IgE antibodies and clinical allergy to environmental allergens.3 The most common presenting sign is pruritus, which may be accompanied by dermatologic lesions. There are three management options available: allergen avoidance, symptomatic therapy and immunotherapy.5 The currently preferred therapy is specific allergen immunotherapy, based on the results of intradermal skin testing and the identification of clinically relevant allergens.4 Successful treatment of inhalant allergic dermatitis using an injectable hyposensitization schedule has been reported in the polar bear (Thalarctos maritimus).1
A 13-year-old female sub-Antarctic fur seal (Arctocephalus tropicalis) has been housed at Melbourne Zoo since 1991. In August 1993, the seal presented with evidence of a dermatopathy. Clinical signs included matting of the hair coat with loss of the protective guard hairs over the dorsum. Initially it was felt that poor grooming behavior may have been the cause of the coat abnormalities, as keepers believed that the animal did not use the grooming claws on the hind flippers effectively. Between 1993 and 1996, it became clear that the clinical signs were markedly seasonal (typically, signs first appeared during late autumn and resolved during mid-summer) and that pruritus (seen as rolling while swimming, scratching, and rubbing) was the predominant clinical sign.
Intradermal skin testing was carried out in September 1996, using a panel of 61 aeroallergens. A diagnosis of allergic dermatitis was made based on positive reactions to allergens prepared from weed, grass, tree pollens and some insects. Through 1996–1998, the seal (body weight approximately 32 kg) was given nonsteroidal symptomatic treatment, consisting of oral antihistamines including terfenadine (Teldane®, Hoechst Marion Roussel Australia) at 15–60 mg SID–BID, cetirizine hydrochloride (Zyrtec®, Faulding Pharmaceuticals) at 5–10 mg SID, and essential fatty-acid supplements (562.5 mg eicosapentaenoic acid, 375 mg docosahexaenoic acid, 350 mg cis-linoleic acid, and 5 mg dl-α-tocopheryl acetate orally every other day as Omega 3® Biochemical Veterinary Research Pty Ltd).
The symptomatic treatment was only temporarily successful. Therefore, over a 6-month period during 1998, keepers habituated the seal to receiving small volumes of sterile saline by SC injection, using a tuberculin syringe with a 30-ga needle. Specific allergen immunotherapy was begun in July 1998, using a vaccine containing 10 allergens. These were chosen with reference to the results of the intradermal skin testing and the likelihood of exposure to particular allergens in the surrounding environment. The treatment protocol used was similar to those used in canine immunotherapeutic regimens: immunotherapy was administered in increasing doses once weekly (beginning at 2 protein nitrogen units [PNU]/allergen) for 15 weeks, until the maintenance dose (2000 PNU/allergen) was reached. This was then given every 3 weeks as a maintenance therapy.2
Following the two initial doses of vaccine, the seal presented with transient, non-painful, fluctuant subcutaneous swellings. On examination, these appeared to be areas of localized subcutaneous edema. They developed 3–5 days after each vaccination and were therefore assumed to be vaccine associated. Subcutaneous edema has not been reported as an adverse effect of immunotherapy in other species (Mueller, personal communication). On several subsequent occasions during the loading phase, the seal showed evidence of a mild adverse reaction to the vaccine, being extremely pruritic for 2–3 days following the injection. Vaccine dosage adjustments and treatment with oral prednisolone (0.5 mg/kg SID) for 24 hours prior to and following the vaccination appear to have prevented any further reaction.
At present, the seal is receiving the maintenance dose of vaccine subcutaneously every 3 weeks. Keepers give the injection during a routine feeding session. To date, clinical response indicates that the treatment has been successful, with a marked decrease in the level of pruritus and an improvement in the quality of the hair coat.
The authors would like to thank Drs Sonya Bettenay and Linda Vogelnest (Animal Skin and Allergy Clinic, Mount Waverley, VIC) for providing advice on all aspects of the treatment program, and seal keepers Kim Beasley and Karen Svalesen for habituating “Lucy” to SC injections.
1. Harper, J., S. White, L. Stewart, and J. Pelto. 1988. Inhalant allergic dermatitis in a polar bear. Proceedings American Association Zoo Veterinarians, Pp 97.
2. Mueller, R.S. and S.V. Bettenay. 1996. Long-term immunotherapy of 146 dogs with atopic dermatitis—a retrospective study. Aust. Vet. Pract. 26: 128–132.
3. Nesbitt, G.H., Kedan, G.S. and Caciolo, P. 1984. Canine atopy. Part I. Etiology and diagnosis. Compend. Contin. Educ. 6: 73–84.
4. Nuttall, T.J., K.L. Thoday, A.H.M. van den Broek, H.A. Jackson, G.H. Sture, and R.E.W. Halliwell. 1998. Retrospective survey of allergen immunotherapy in canine atopy. Vet. Rec. 143: 139–142.
5. Reedy, L.M., H.M. Miller. 1989. Immunotherapy. In: Allergic Skin Diseases of Dogs and Cats. W.B. Saunders Co., Philadelphia, PA. Pp: 111–132.