Author: Dawn Logas
Veterinary Dermatology Center, Maitland, Florida

Definition

Food allergy is an uncommon and poorly understood disease in the horse. Symptoms can be gastrointestinal, dermatologic, or both. The terminology itself is confusing. The term food allergy implies an immunologic reaction to an ingested substance. Not all food allergies are truly allergic in nature. A better term for the condition would be “adverse reactions to food.”This designation includes immunologic and nonimmunologic reactions to food substances. Nonimmunologic food sensitivities include metabolic, pharmacologic, and idiosyncratic reactions. An example of this would be pruritus resulting from the histamine content of a food (e.g., mackerel or tuna), instead of from an allergic reaction to the food itself. Fortunately, clinical symptoms and treatment of immunologic and nonimmunologic food reactions are identical. Therefore, for the sake of simplicity, most clinicians use the term food allergy to indicate adverse reactions to food.

Pathogenesis

Very little is known about the pathogenesis of food allergy in the horse. Most of the research into
food allergy has concentrated on human food hypersensitivities, particularly in children. True food allergies in humans have been classified as type I hypersensitivity reactions for the most part, but type III and IV hypersensitivity reactions are also suspected. Type I reactions (immediate type hypersensitivity) encompass all IgE mediated reactions such as pruritus, erythema, and urticaria. Type III (arthus) hypersensitivities typically cause vasculitic lesions. Type IV reactions (delayed type hypersensitivity) usually cause a papular eruption. All three types of clinical reactions have been observed in the food-allergic horse, but detailed information about the pathogenesis of each type of reaction is lacking. Unfortunately, at this time much of the information known about food allergy in the horse is case-based and anecdotal.

The first stage of any hypersensitivity reaction is the sensitization phase. During sensitization, the antigen is repeatedly presented to T lymphocytes and an abnormal hypersensitivity response occurs instead of tolerance. For a food allergy to occur, an allergen must breach the intestinal mucosal barrier in order to be exposed to the immune system. Normally, the intestinal tract has various mechanisms to prevent the absorption of potentially allergenic substances. Intestinal enzymes break down large molecules into smaller, less antigenic ones. The mucous coating and tight junctions of the intestinal
epithelium do not allow larger, more antigenic macromolecules to pass the intestinal barrier and reach the immune system. Secretory IgA binds to smaller antigenic molecules, thereby preventing their penetration of the mucosa. Intestinal peristalsis also helps by moving large molecules through the intestinal tract at a relatively rapid rate.
Hypersensitivity can result when there is a break in intestinal barrier function and an abnormal immune response to a presented antigen. This can occur in young animals whose intestinal mucosal barrier is not fully developed, in old animals whose intestinal mucosal barrier has begun to degenerate, and in animals with gastrointestinal illnesses that have damaged the intestinal barrier. In these cases, macromolecules (>12 kilodaltons) are able to pass through the mucosal barrier and reach the immune system. Under normal circumstances, especially in the young animal, a CD8 positive T cell response occurs and results in tolerance/anergy. However, if Th2 lymphocytes are activated, a type I hypersensitivity reaction can develop. The reason this abnormal immunologic response occurs in some individuals is still unknown. It may be genetically determined, or may occur secondary to another event such as a heavy parasite load. Parasite antigens cause activation of many T helper cells, some of which may inadvertently react to food antigens instead of parasite antigens. Another possibility is the formation of a hapten-antigen complex. This can occur when a small, theoretically nonantigenic molecule is easily absorbed through the mucosal barrier, then combines with a hapten to form a complex that is now large enough to elicit an immunologic response.
In the diet, water-soluble glycoproteins are thought to act as the base of many of these antigens. These glycoproteins can be found in fresh or prepared foods, supplements, or other additives. Unfortunately, what is not known is which glycoprotein(s) in a particular food item is important, or what part of each particular glycoprotein is antigenic.

Incidence

The true incidence of adverse food reactions in the horse is not known. It is assumed to be uncommon; however, it can be difficult to rule out, so many food-allergic horses may not be properly diagnosed. It is also possible that the condition is recognized and corrected by an owner prior to seeking veterinary attention, so we have no knowledge of these cases. Diet items reported to cause adverse food reactions in horses include alfalfa, barley, beet pulp, bran, buckwheat, chicory, clover, malt, oats, potatoes, St. John’s wort, wheat, feed additives, and feed supplements.