THE MERCK VETERINARY MANUAL
Print Topic

Sections

Chapters

Overview of Food Allergy

-
-

Adverse food reactions comprise allergic reactions termed food allergy as well as nonallergic reactions termed food intolerance. On a practical level, these terms are frequently interchanged, because the precise immunologic processes of most adverse food reactions are usually not known. Immunologic reactions types I, III, and IV are thought to be the most likely causes, but this is conjectural for most reported cases in small animals. Food allergies are very rare in herbivores. In this chapter, the more commonly used term food allergy will be used for all adverse food reactions.

Food allergy is ~10% as common as atopic dermatitis in dogs and perhaps as common as atopic dermatitis in cats. The history is that of a nonseasonal pruritus, with little variation in the intensity of pruritus from one season to another, in most cases. Most reports do not suggest a breed predilection; however, one report indicated an increased relative risk in Labrador Retrievers, West Highland White Terriers, and Cocker Spaniels. Food hypersensitivities have been reported in Soft-Coated Wheaten Terriers in association with protein-losing enteropathy and nephropathy. The age of onset is variable, from 2 mo to 14 yr old. One report indicated that most food allergies begin at <12 mo of age. In adult-onset food allergy, most dogs have been fed the offending allergen for >2 yr.

The distribution of pruritus and lesions varies markedly between animals. Ear canal disease that manifests as pruritus and secondary infection with bacteria (usually Staphylococcus pseudintermedius, Pseudomonas spp) or yeast (Malassezia pachydermatis) are common and may be the only presenting complaint. Other patterns seen include blepharitis, generalized pruritus, generalized seborrhea (scaling), a papular eruption, or a distribution pattern that may mimic that of atopic dermatitis (feet, face, and ventrum) or flea allergy dermatitis (dorsal lumbosacrum and hindlegs). The most common areas of involvement include the ears, feet, inguinal region, axillary area, proximal anterior forelegs, periorbital region, and muzzle. The degree of pruritus is usually moderate to severe. Response to glucocorticoids varies from poor to excellent.

There is no reliable diagnostic test other than a strict food elimination diet. Serologic testing and intradermal testing for food allergens have proved unreliable. The ideal food elimination diet should be balanced and nutritionally complete and not contain any ingredients that have been previously fed. Many diets contain novel protein or carbohydrate sources (eg, venison and rice). However, if a previously fed ingredient is present in the elimination diet, and the animal is allergic to that ingredient, the diet trial will be a failure. Another option is the use of hydrolyzed protein diets, in which the protein source is hydrolyzed to small molecular weights that are not allergenic. It is estimated that hydrolyzation of the protein may still trigger an allergic response in ~10% of animals allergic to the unhydrolyzed form.

The trial diet should be fed for up to 3 mo. The key point in any food elimination diet trial is that only the designated food ingredients can be fed. Thus, no flavored toys, medications, or toothpaste are allowed. If marked or complete resolution in the pruritus and clinical signs occurs during the elimination diet trial, food allergy can be suspected. To confirm that a food allergy exists and that the clinical improvement was not just coincidental, the animal must be challenged with the previously fed food ingredients and a relapse of clinical signs must occur. The return of clinical signs after challenge is usually between 1 hr and 14 days. Once a food allergy is confirmed, the elimination diet should be reinstituted until clinical signs resolve, which usually takes <14 days. At this point, previously fed individual ingredients should be added to the elimination diet for up to 14 days. If pruritus recurs, the individual ingredient is considered positive for having a causative role in the food allergy. If pruritus does not recur, the individual ingredient is not considered important in causing the clinical signs.

The number of offending food allergens varies from one to five ingredients. The most frequently identified causative allergens in canine food allergy include beef, chicken, eggs, corn, wheat, soy, and milk. Once the offending allergens are identified, control of the food allergy is by strict avoidance. Concurrent diseases (such as atopic dermatitis or flea allergy) may complicate the identification of underlying food allergies. Infrequently, a dog will react to new food allergens over time.

Clinical presentations of food allergy in cats include miliary dermatitis, feline symmetric alopecia, eosinophilic granuloma complex (primarily the eosinophilic plaque), and severe head and neck pruritus. No breed, sex, or age predilection is seen. Age of onset varies from 3 mo to 11 yr. In one study, however, 46% of affected cats became symptomatic at ≤2 yr of age, and Siamese cats represented 30% of the cases.

Response to glucocorticoids is variable, but about two-thirds of cats show excellent response initially. Many cats develop a poor response to glucocorticoids with repeated treatments. As with canine food allergy, an elimination diet should be fed for up to 3 mo. The elimination diet should not contain any previously fed ingredients. Food elimination diets can be difficult in cats because many cats are reluctant to change diets. Cats should not be starved or forced into eating a new elimination diet because of the serious nature of hepatic lipidosis that may be induced by prolonged anorexia.

Time until relapse of pruritus after challenge with the offending food varies from 15 min to 10 days. The most frequently identified food allergens in cats include fish, beef, milk, and chicken. Avoidance of the offending allergens will control the clinical signs associated with the food allergy.

Last full review/revision May 2013 by Stephen D. White, DVM, DACVD

Copyright     © 2009-2015 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Whitehouse Station, N.J., U.S.A.    Privacy    Terms of Use    Permissions