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Journal of Entomology and Zoology Studies
Metabolic reaction to food is due to genetic error of
metabolism that is inborn in nature. Chronic hepatitis in
Doberman dogs is a classical example. Inability to excrete
copper causes copper toxicosis leading to chronic hepatitis in
these dogs [6]. Indigestible or unabsorbed products (lactulose),
or deficiency of certain enzymes (lactase) can result in a
metabolic food reaction [7].
Food idiosyncrasy is mostly mechanical in nature as occurs
due to less fibre in the diet or the presence of certain
indigestible (bones) products [8]. In contrast production of
histamine (ingestion of Tuna fish and Shell fish) which is
responsible for mast cell degranulation is categorized under
pseudo allergy. [2]. defined Canine food allergy
/hypersensitivity as a non-seasonal pruritus (regional or
generalized) with involvement of ears, feet, inguinal or
axillary areas, face, neck, and perineum. Erythema with a
papular rash including alopecia, excoriations, scales, crusts
and hyperpigmentation of the affected skin areas. It is very
difficult for the clinician to distinguish atopic dermatitis and
food allergy based on clinical signs although seasonality of
occurrence, response to steroid therapy can give useful hints.
In Atopic dermatitis there is a genetic predisposition of
developing hypersensitivity reactions (type 1) to substances
present in environment such as dust, pollens etc.
3. Predisposition, contributing factors and etiology
3.1 Predisposition and contributing factors
Food allergy has no age predisposition [9], no sex predilection
in dogs (Chesney, 2002) with no seasonality of occurrence
[10]. Labrador and German shepherd were found to be more
prone to food allergy [2] although any breed including mixed
breeds may be affected. [11] Reported 33%, 51% and 16%
incidence in < 1 year, 1-5 years and 5-11 years of dogs
respectively. Protein and carbohydrate source in pet food,
certain foods and food ingredients, any disease that increases
intestinal permeability (e.g. viral enteritis), selective IgA
deficiency, poorly digestible protein and other allergic disease
[12].
3.2 Etiology
The offending antigen is usually a basic food ingredient in the
animal’s diet responsible for the food allergy. A wide range of
dietary ingredients responsible for food hypersensitivity
includes artificial food additives, beef, canned foods, corn,
cow milk, dairy products, dog foods, dog biscuits, eggs, fish,
food preservatives, meats of different species including pork,
mutton and horse meat, oat meal, potatoes, rice flour, soy,
wheat, kidney beans. A prospective study was conducted in
25 dogs to characterize specific food ingredients causing
adverse reactions [13]. Single-ingredient stimulation trials were
conducted with beef, chicken, chicken eggs, cow milk, wheat,
soy and corn. Among all the ingredients, beef and soy were
found to cause most cutaneous adverse reactions, although all
ingredients induced clinical signs in at least one dog. 36%
percent of dogs reacted to one protein and the mean number
of suspected allergens per dog was 2.4. Recently in 15
different experimental studies, representing 278 dogs from
different continents were assessed to check ingredients that
are commonly associated with adverse food reactions. These
experimental studies showed beef, dairy products and wheat
accounted for 69% of reported cases where as lamb, chicken
egg, chicken and soy accounted for 25% of the dogs. In 10
experimental studies conducted on 56 cats, beef, dairy
products and fish were associated with food reactions in 80%
of the animals [12]. In one beef allergic dog, bovine serum
albumin was found to be the target of anti-beef IgE [14]. A
study carried on 10 dogs, it was found that major allergen in
cow’s milk that cause allergic reactions is bovine IgG and
because of high homology of bovine IgG with ovine
immunoglobulins it can be a possible source of cross-
reactivity with beef and lamb (similar to meat allergy in
humans). Cow’s milk is a wholesome food containing about
20 protein components [15]. The milk-protein fractions are thus
subdivided into casein proteins (78-86%) and whey protein
(14-24%). β-lactoglobulin is the most allergic component,
followed by casein, lactalbumin, and bovine serum albumin.
Dogs that were allergic to cow’s milk could not eat cheese
and vice versa [16]. Hidden allergens can also be a problem
with food allergies including a number of oils such as corn
and soy. A milk protein (Sodium caseinate), is often added to
improve the packaging qualities in canned tuna is also
responsible for the allergic reaction.
4. Pathogenesis
A food allergy arises when there is a reproducible reaction to
a specific food or food additive with a proven immunological
basis. There are two types: an IgE mediated and a non-IgE-
mediated response.
4.1 IgE-mediated food allergy
It is commonly believed that food allergy is, in most cases, an
IgE-mediated type 1 reaction (Gell & Coombs classification)
[7]. However, it is documented and reported to occur by other
types also including notably type iii and iv [4]. In type 1
hypersensitivity reaction, specific allergen triggers the IgE
sensitized mast cells which causes release its pharmacological
mediators thus setting in the process of inflammation. Clinical
signs mostly depend on system/tissue in which reaction
occurs. It may include dermatological, respiratory,
gastrointestinal signs, or a combination. Several reasons are
responsible for how an allergen can induce abnormal response
in food allergy.
Firstly, the allergen may have the ability to penetrate the
physiological mucosal barrier. The components of this barrier
include digestive enzymes, gastric acidity, peristalsis, the
surface mucus, enterocyte tight junctions, and the
immunological barrier of intraluminal IgA. After penetrating
the mucosal barrier, the allergen will interact with
gastrointestinal associated lymphoid tissue (galt). The galt is
formed by the Peyer’s patches, diffuse lymphoid tissue in the
lamina propria, enterocytes, and intraepithelial lymphocytes
[4]. The immune response in the galt usually leads to a Th2-
mediated response in which the cytokines interleukin IL-4 and
IL-5 stimulate IgA production and immune responses
involving mast cells and eosinophils. In a type i reaction, the
antigen is presented by an antigen-presenting cell to a Th2
cell, which then produces IL-4 and IL-10. These cytokines
stimulate B cell proliferation and induce IgE production. The
resultant IgE binds to mast cells and sensitizes them. If the
allergen reaches the sensitized mast cell, it releases histamine,
proteases, as well as several leukotrienes and prostaglandins.
IL-4 produced by Th2 cells influences, among others, tnf-α
and tnf-β production [17].
Normally, an antigen will induce oral tolerance, which is an
active response and is designed to limit the unnecessary and
wasteful activity of galt in response to ‘harmless’ luminal
antigens, such as those from endogenous microbiota. If, for
whatever reason, this normal tolerance is abolished, the
antigen induces an inappropriate immune response to
endogenous flora (resulting in Inflammatory Bowel Disease)