Merck Manual

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Canine Atopic Dermatitis


Karen A. Moriello

, DVM, DACVD, Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison

Last full review/revision Jul 2013 | Content last modified Jul 2013

Clinical Findings:

There is no sex predilection in canine AD. There are breed predilections, but the prevalence within a breed largely depends on the genetic pool and region. Breeds predisposed to development of AD include Chinese Shar-Pei, Wirehaired Fox Terrier, Golden Retriever, Dalmatian, Boxer, Boston Terrier, Labrador Retriever, Lhasa Apso, Scottish Terrier, Shih Tzu, and West Highland White Terrier. The age of onset is generally between 6 mo and 3 yr. Clinical signs usually occur on a seasonal basis but may be seen year-round with time. Pruritus is the characteristic sign of AD. The feet, face, ears, flexural surfaces of the front legs, axillae, and abdomen are the most frequently affected areas. Primary lesions consist of erythematous macules, patches, and small papules. Lesions that develop secondary to self-trauma include alopecia, erythema, scaling, salivary staining, hemorrhagic crusts, excoriations, lichenification, hyperpigmentation, superficial staphylococcal pyoderma, Malassezia and bacterial overgrowth, and allergic otitis externa. Chronic or recurrent otitis is the only complaint in a small number of animals.


The diagnosis is challenging and is based on signalment, clinical signs, and disease history and not on laboratory tests. Prospective studies have revealed the following clinical features compatible with a diagnosis of AD: onset of clinical signs before 3 yr of age, dogs that live mostly indoors, glucocorticoid-responsive pruritus, pruritus without skin lesions, affected front feet, affected ear pinnae, nonaffected ear margins, and nonaffected dorsolumbosacral areas. These clinical signs can overlap with other diseases, so parasites, pruritic microbial overgrowth, food allergy, and flea allergy need to be excluded. Allergy testing (intradermal or serologic) is a diagnostic aid that measures increased levels of tissue-bound or circulating IgE; alone, it is not diagnostic but rather reflects exposure. The primary reason to pursue intradermal or serologic allergy testing is to identify the offending allergens in an individual animal and to formulate specific immunotherapy. Test results are significant only if the offending allergens identified are compatible with the history or seasonality of pruritus. Animals with classic clinical signs but negative allergy tests are given the diagnosis of ALD. Immunotherapy would be difficult if not impossible in these animals.


AD and ALD cannot be cured. Client education is important, because this is a lifelong disease that requires lifelong management and regular progress checks. Management options depend on the severity of the clinical signs and whether the pruritus is seasonal or year round.

Avoidance of allergens: This may be the best choice, but it is difficult, if not impossible, to do unless a specific allergen can be identified.

Relief from pruritus: By definition, this is a pruritic skin disease; itching may be relieved via antipruritic drugs alone or in combination with allergen-specific immunotherapy (ASIT [see below]).

Bathing and coat hygiene: Bathing dogs with AD may decrease pruritus. In dogs with a history of flares due to microbial overgrowth, routine use of antimicrobial shampoos can be of benefit. Except for the use of lipid-containing shampoos, there is no evidence of benefit from shampoos or conditioners that contain oatmeal, pramoxine, antihistamines, or corticosteroids.

Recognition and control of flare factors: A relapse of clinical signs in a dog that is otherwise well controlled should prompt an investigation into what caused the exacerbation of pruritus. Recognized flare factors include, but are not limited to, fleas, food and environmental allergens, secondary microbial overgrowth, and poor coat hygiene. These need to be investigated before using systemic antipruritic drugs.

Antipruritic drugs for acute flares: In many dogs, the flare may present as allergic otitis, and topical use of otic corticosteroids may be adequate. There is good evidence for a short course of a topical triamcinolone or hydrocortisone aceponate spray for local pruritus. If the pruritus is too severe or extensive to be controlled with topical formulations, then oral steroids may be needed. Options include prednisone, prednisolone, or methylprednisone administered PO at 0.5 mg/kg, once to twice daily, until clinical signs are in remission. Tacrolimus, cyclosporine, or essential fatty acids are unlikely to be beneficial for acute flares.

Antipruritic drugs for chronic AD: Systemic reviews of clinical trials have not shown conclusively that omega-3 and omega-6 essential fatty acids alone are likely to reduce pruritus. Use may help improve coat quality. Cyclosporine can provide relief similar to that seen with glucocorticoids. A reported 50% reduction in pruritus in 70% of dogs with AD given cyclosporine A parallels the response seen with glucocorticoids but with fewer adverse effects. Some animals can be maintained comfortably with this drug alone. Tacrolimus ointment provides a benefit in animals with more localized lesions. However, drugs in this category tend to be more expensive than other symptomatic treatments. Another option is oclacitinib (a Janus kinase inhibitor), which has been shown to be safe and effective in control of pruritus.


Immunotherapy or ASIT is arguably the best treatment option for AD, because it is the only therapy that potentially leads to remission of signs without addition of other medications. It remains the treatment of choice of most dermatologists and allergists. ASIT attempts to increase an animal’s tolerance to environmental allergens (subjectively measured when an individual is exposed to an identified allergen without developing clinical signs). Although the mode of action is not completely understood, the primary theory states that IgG increases during the first few months of hyposensitization and exerts a blocking effect on circulating allergens by binding them and preventing mast cell degranulation. Another theory states that immunotherapy causes a shift away from TH2 toward TH1 by enhancing γ-interferon expression. After an injection, however, allergen-specific IgE levels may also increase when immunotherapy is initiated due to a response to the additional allergen load from the immunotherapy injections. This may result in increased pruritus in some animals. Reducing the amount of allergen given often alleviates this reaction, and with time, allergen-specific IgE levels decrease. However, decreased IgE levels and clinical improvement are not always directly correlated.

ASIT can be administered via injections or allergy drops, which are equally effective. Immunotherapy is best considered for animals with problematic clinical signs that occur for several months during the year. For injections, the animal must also be cooperative enough to receive allergy injections. For allergy drops, the owner must be able to handle the animal's mouth and be able and willing to administer the drops twice a day every day. The criteria for successful hyposensitization include appropriate interpretation of test results, careful selection of allergens, adequate control of secondary infections, control of other allergies (food or flea), systematic administration of immunotherapy injections, and periodic communications between the owner and veterinarian. The longterm commitment needed from both the owner and the veterinarian for successful immunotherapy cannot be overemphasized. The owner must be willing to follow instructions accurately, be patient, and communicate effectively with the veterinarian. The veterinarian must recognize and treat other primary or secondary causes of pruritus and manage flare factors (eg, otitis, pyoderma, Malassezia dermatitis, insect hypersensitivity) as they occur and guide the owner through these challenges until improvement is seen. Symptomatic therapy is required in almost every case during the induction period and at various times of the year (see above).

Allergen selection is determined by correlating the positive allergens on the test results with the prominent allergens during the time of year when the animal is symptomatic. If the test shows positive results for pollens that have no clinical relevance (eg, high pollen count during a period when the animal is not pruritic, positive reaction to an allergen not in the geographic area), then either the allergic reaction is mild (subthreshold) or it is a false-positive reaction. Either way, the allergen is not included in the allergen mixture.

Allergen protocols vary but usually have induction and maintenance periods. During the induction period, the dosage of allergen gradually increases until an arbitrary maintenance dosage is reached. Once the maximal dosage is given, this maintenance level is continued. The interval between maintenance dosages may vary from 3–4 days to 3 wk. Adjustments in the interval are based on the animal’s response. Owners are advised not to expect much response for 6 mo and are asked to commit to at least 1 yr of therapy before deciding the usefulness of immunotherapy. The best assessment of response is to compare the degree of disease or discomfort between similar seasons.

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