Food Allergy

By | 2011-07-24

Food Allergy (Hypersensitivity)

The prevalence of true food allergy is unknown because no reliable diagnostic tests are available. Furthermore, food allergy with gastrointestinal signs may be more difficult to prove than cases in which dermatologic signs prevail. This is partly because other gastrointestinal diseases may also respond (for nonallergenic reasons) to dietary manipulation (Box Conditions that May Improve Clinically in Response to Dietary Modification). The management of food allergy is simple: feed any food that does not contain the allergen, and the animal will be healthy. The difficulty for the clinician lies in the recognition of food allergy and the identification of foods that must be excluded.

Conditions that May Improve Clinically in Response to Dietary Modification

Food allergy

Food intolerance

Small intestinal bacterial overgrowth

Inflammatory bowel disease


Exocrine pancreatic insufficiency


Chronic gastritis

Castroesophageal reflux

Gastric emptying disorders

Portosystemic shunt


Currrent hypotheses of food allergy propose one or a combination of mechanisms that lead to breakdown of oral tolerance: an inadequate mucosal barrier, abnormal presentation of dietary antigens to the mucosal immune system, or immune system dysregulation (see earlier discussion). Such hypotheses could explain both genetic susceptibility to the development of allergy and the development of allergies after a primary gastrointestinal insult that damages the mucosal barrier. For example, viral or parasitic enteritis can both damage the mucosal barrier and provide danger signals in the intestinal mucosa. Active immune responses, rather than tolerance, can then occur to bystander antigens (i. e., sensitization to dietary antigen). Dietary hypersensitivity may involve a variety of mechanisms, including type I (IgE mediated, immediate), type II (immune complex mediated), and type IV (delayed hypersensitivity) reactions.

Clinical Signs

A contemporaneous association between ingestion of a particular food and the onset of signs is suggestive of an immediate (type I) IgE-mediated hypersensitivity, but mixed or delayed reactions are also possible. In such cases the inevitable delay between food ingestion and onset of signs obscures any causative link, particularly if repeated ingestion causes chronic disease.

Clinical signs of food allergy generally involve the skin and gastrointestinal tract (Box Clinical Signs Recognized as Manifestations of Food Allergy). Most case studies have focused on dermatologic signs, with few reports of food-allergic gastrointestinal disease. Systemic signs (anorexia, lethargy) are rarely recorded, and urticaria-angioedema and even anaphylaxis seem rare. Concurrent skin and gastrointestinal signs can occur but have been reported only rarely. However, only 5% of human patients with gluten-sensitive skin lesions (dermatitis herpetiformis) have gastrointestinal signs, yet intestinal histologic examination shows a subclinical enteropathy in 95% of these individuals.

Clinical Signs Recognized as Manifestations of Food Allergy

Systemic Signs



Peripheral lymphadenopathy (cats)



Cutaneous Signs

Primary papules


Pruritus and self-trauma

Secondary pyoderma


Otitis externa

Miliary dermatitis (cats)

Eosinophilic granuloma complex (cats)

Gastrointestinal Signs




Small intestinal — like signs

Colitis-like signs

Abdominal pain, “colic”

Weight loss and / or stunting

Altered appetite

Food-allergic skin disease The major sign of food-allergic skin disease is pruritus, which is nonseasonal and has no characteristic distribution, although pedal pruritus, facial pruritus, and otitis externa may be noted. Excoriation, crusting, scaling, and lichenification arise through self-trauma and may predispose to secondary pyoderma. In cats, food allergy may also result in miliary dermatitis, eosinophilic granuloma complex, or symmetric alopecia.

Food-allergic gastrointestinal disease Signs of food-allergic gastrointestinal disease are not pathognomonic and include vomiting, diarrhea, abdominal pain, flatulence, borborygmi, and weight loss or failure to thrive.


The cornerstone of the diagnosis of a food allergy is the response to dietary manipulation. Clinical signs should resolve on exclusion of the offending dietary component and return with rechallenge. Unfortunately, objective criteria by which to judge such a response are lacking, and other diseases also may respond to dietary manipulation (see Box Clinical Signs Recognized as Manifestations of Food Allergy). Furthermore, diagnosis requires confirmation with rechallenge studies, but many clients refuse to pursue this.

Indirect tests Given the difficulties of diet trials, indirect tests for food allergy have been devised; unfortunately, none are reliable in veterinary medicine.

Antigen-specific serum antibodies to food components can be measured in vitro (by radioallergosorbent testing (RAST] or enzyme-linked immunosorbent assay), and a number of laboratories now offer this commercially. In most situations IgG and / or IgE responses to different food components are assessed. Subjectively, clinicians who use such tests believe them to be of value, but critical appraisal suggests that they are unhelpful. The use of such tests is flawed for many reasons. First, antibodies to food components can be found in normal individuals, therefore the presence of antibody in an affected individual may be incidental. Second, because vaccines may contain bovine serum albumin, individuals may develop antibodies to beef antigens. Third, some tests assess only IgG responses, therefore they may miss humoral responses of other antibody classes and cell-mediated responses. Fourth, because the affinity of antibodies formed to a particular antigen in different individuals may vary, not all may be detected in the immunoassay, and some may not react at all (if the in vitro antigen is not relevant). Fifth, the presence of antibodies does not necessarily prove primary food hypersensitivity, because the antibodies they may have arisen secondary to another underlying disease process (e. g., IBD).

It has been shown that dogs with chronic gastrointestinal disease arising from a number of causes had greater levels of food-specific IgG than healthy or atopic dogs. However, these findings did not correlate with the animals’ response to exclusion diet trials. Thus any perceived benefit of dietary modification after food antigen testing may be coincidental. Given that most clinicians do not go on to prove a causal association by food provocation, such an coincidence is misinterpreted.

Skin testing has also proved unreliable in the diagnosis of food-allergic skin disease.

Gastroscopic food sensitivity testing (GFST), in which dietary antigens are instilled directly onto the gastric mucosa in an anesthetized patient, theoretically should give more specific results for cases presenting with gastrointestinal signs. However, correlation between the results of GFST and the results of clinical challenge trials is poor. The method is tedious, technically demanding, and prone to artifacts and detects only immediate hypersensitivities. Using the colonic mucosa as the testing surface [colonoscopic allergen provocation (COLAP) testing] may be simpler but has not been widely adopted.

Dietary trial Dietary trial is the only reliable way to confirm the presence of dietary sensitivity, although such trials do not distinguish food intolerance from allergy.