Food allergy in canines: A review

Full text

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Journal of Entomology and Zoology Studies 2017; 5(6): 1522-1525
E-ISSN: 2320-7078
P-ISSN: 2349-6800
JEZS 2017; 5(6): 1522-1525
© 2017 JEZS
Received: 22-09-2017
Accepted: 24-10-2017
Rakshanda Bhagat
Division of Veterinary Medicine,
Sher-e-Kashmir University of
Agricultural Sciences and
Technology - Jammu (SKUAST-
J), R. S. Pura, Jammu and
Kashmir, India
Amir Amin Sheikh
Department of Veterinary
Physiology and Biochemistry,
College of Veterinary Sciences
and Animal Husbandry,
Jabalpur, Madhya Pradesh,
India
VS Wazir
Division of Veterinary Medicine,
Sher-e-Kashmir University of
Agricultural Sciences and
Technology - Jammu (SKUAST-
J), R. S. Pura, Jammu and
Kashmir, India
Aditya Mishra
Department of Veterinary
Physiology and Biochemistry,
College of Veterinary Sciences
and Animal Husbandry,
Jabalpur (M.P), India
Uttarani Maibam
Department of Veterinary
Physiology and Biochemistry,
International Institute of
Veterinary Education and
Research (IIVER), Rohtak,
Haryana, India
Correspondence
Amir Amin Sheikh
Department of Veterinary
Physiology and Biochemistry,
College of Veterinary Sciences
and Animal Husbandry,
Jabalpur, Madhya Pradesh,
India
Food allergy in canines: A review
Rakshanda Bhagat, Amir Amin Sheikh, VS Wazir, Aditya Mishra and
Uttarani Maibam
Abstract
Food allergy is an immunological response to the ingested allergen present in food like artificial food
additives, beef, canned foods, corn, cow milk, dairy products, dog foods, dog biscuits, eggs, fish, and
food preservatives, meat of different species including pork, mutton and horse meat, oat meal, potatoes,
rice and commonly occurs in dogs and cats. Among all canine species, Labrador and German shepherd
were found to be more prone to food allergy and symptoms are similar to other pruritic skin diseases.
These food allergies are broadly classified into two categories (1) IgE-mediated food allergy (2) non-IgE-
mediated food allergy. Diagnosis can be done by accurate clinical history, parental observations, and
laboratory tests: Skin scrapping, bacterial/fungal culture examination, thyroid test, fecal examination and
skin biopsy, allergic tests: Patch test, Skin Prick Test, Intra-dermal test and Radioallergosorbent test.
Management of these allergies can be done by antihistaminics like Hydroxyzine and Chlorpheniramine,
antibiotics like Cephalexin, Enrofloxacin, antifungals like Ketoconazole, Griseofulvin, Amphotericin-B
and glucocorticoids like Prednisolone, Methyl prednisolone.
Keywords: Food allergy, IgE mediated, non-IgE mediated, Patch test
1. Introduction
Adverse reactions in dogs and cats to allergens present in food is the commonest form of
hypersensitivity and frequently reported to occur next to flea allergic dermatitis and atopic
dermatitis. It is defined as the clinically abnormal exaggerated immunological
reaction/response to the ingested allergen present in food as described by National Institute of
Allergy and Infectious Diseases, 2011. Alternatively the food allergy and food/dietary
hypersensitivity are used interchangeably. All food reactions are not considered as food
allergies [1]. Adverse reactions to food account for 10-20% of all the skin problems been
reported till date [2]. It is associated mostly with the protein component present in the food that
elicits an immunological response that is capable of bridging the two molecules of IgE thereby
triggering degranulation in the mast cells thus causing the release of mediators of
inflammation [3].
2. Classification
Broadly untoward reactions to food are classified on the basis of response elicited into two
types: immunological and non-immunological. Food allergy/food anaphylaxis is categorized
under immunological response which may be IgE mediated or non IgE-mediated. Mostly, it is
of type I (immediate) hypersensitivity reactions, mediated by immunoglobulin E (IgE) but in
some cases both types III and IV hypersensitivity may also be involved. Glycoproteins with a
molecular weight ranging between 10 and 60 kilo Daltons are considered as the antigens which
can cause reaction within minutes to hours, days and can even take longer periods to get
sensitized to present clinical manifestations. Whereas food poisoning, food intolerance and
dietary indiscretion are classified under non-immunological response. Food intolerance is
further subdivided namely reaction due to pharmacological active ingredient, reaction due to
metabolism of certain ingredients, food idiosyncrasy and pseudo allergy [4]. Pharmacological
reaction to food is initiated by stimulation of response to certain pharmacological active agent
present in food having drug like action. Mostly response is seen in intestine causing motility
disorders manifested as diarrhea. An example is monosodium glutamate used as a flavour
enhancer in dogs. In addition, physiological compounds like casomorphins also reported to
alter the gut motility and manipulation of the omega-3 and omega-6 ratio in food causes
alteration of prostaglandin production [5].

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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)

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Journal of Entomology and Zoology Studies
or, in the case of food allergens, food allergy [4]. The food
allergens that trigger such an abnormal response are usually
soluble protein or glycoproteins resistant to degeneration [4].
In dogs, common allergens are derived from beef, chicken,
milk, eggs, corn, wheat, and soy [18]; in contrast, reactions in
cats are more commonly to dairy and fish proteins. As such,
no particular protein is especially ‘allergenic’. Animals are
more likely to respond adversely to dietary components to
which they are commonly exposed. Factors that contribute to
food allergy either interfere with the normal mucosal barrier
(viruses, bacteria, parasites, toxins, etc), lead to an abnormal
presentation of the antigen to the galt, or cause deregulation
of the galt [4].
4.2 Non-IgE-mediated food allergy:
Non-IgE-mediated anaphylaxis or gluten-sensitivity most
likely involves a type iii or iv immunological reaction
although some believe it to be more an intolerance than
immunologic of nature. In gluten-sensitivity, gliadens, one of
the four gluten proteins, induce a non-IgE-mediated mast cell
response as in IgE-mediated food allergy. Gluten sensitivity
was demonstrated in a single cohort of young Irish setters [19].
Hence, the opinion that gluten should be avoided in all cases
of gastrointestinal diseases (or in all dog foods) is flawed.
5. Clinical Signs
Reactions to ingested food components can affect many body
systems and can produce signs involving the skin,
gastrointestinal tract, respiratory tract and central nervous
system. Dermatological signs include pruritus, erythma,
papular eruptions are common and often seen with a
secondary staphylococcal folliculitis infection, otitis externa
(unilateral or bilateral), Urticaria. Occasionally, dogs will be
non-pruritic and exhibit only seborrhoe [20]. Self inflicted
trauma in pruritic cases resulting in excoriation, alopecia and
secondary superficial pyoderma are also noticed.
5.1 Food anaphylaxis is an acute response to ingestion of
food or food additives resulting in various systemic
consequences
 Angioedema or facioconjunctival edema [10].
 Angioedema is typically manifested by large edematous
swellings of the lips, face, eyelids, ears, conjunctiva
and/or tongue, with or without pruritus [10].
 These reactions usually occur within minutes of allergen
exposure and generally subside after one to two hours
 1/4th of dogs with AFR had lesions only in the region [21].
 Adverse food reactions should always be with pruritic,
unilateral or bilateral otitis externa, it may accompanied
by secondary bacterial or Malassezia infections [10].
Other presentations of food allergy include recurrent
superficial pyoderma, pruritic papular eruptions over the trunk
and head [2].Adverse food reactions concurrent to flea-allergic
or atopic dermatitis accounting for 20% to 30% or more of
dogs has been documented [22]. Concurrent GIT signs
(vomiting, diarrhea, frequent defecation, colitis etc) were seen
to occur in 10-15% dogs with skin infections caused by an
adverse reaction to food [23]. Neurological signs, such as
seizures, malaise have been reported [24].Although asthma and
other respiratory signs have also been reported, these clinical
signs are rare [3].
Diagnosis and management
6.1 Diagnosis can be done by
a. Accurate clinical history
b. Parental observations: Clinical symptoms, physical
examination
c. Laboratory tests: Skin scrapping, bacterial/fungal culture
examination, thyroid test, fecal examination and skin
biopsy
d. Allergic tests: Patch test, Scratch tests (Skin Prick Test),
Intra-dermal test and RAST (Radioallergosorbent test).
e. Dietary investigation in the form of elimination diets and
test meals
f. Diet selection: Limited antigen diet, in common use, is of
3 types: Home-cooked diets, commercially available
novel protein diets, Hydrolyzed protein diet.
g. Challenge diet: Dog should be challenged with old diet.
If symptoms do not recur with challenge: improvement
would have been coincidental & if symptoms do recur,
the diet should be switched back to the elimination diet.
h. Gastroscopic food sensitivity testing (GFST)
i. Endoscopic observation of gastric mucosal reaction
following exposure to pure food extracts [25].
h. Colonoscopic food sensitivity test (CFST)
 Allergens injected directly into the mucosa of the colon
 Results observed as wheal and flare reactions.
5.2 Management
5.2.1 Antihistaminic drugs: They counteract the release of
histamine from the mast cells, which is the source of the
itching. Some of the common antihistaminics used are:
Diphenhydramine hydrochloride @ 2mg/kg B.W,
Hydroxazine @ 2.2 mg/kg B.W, Chlorpheneramine @4-8
mg/kg B.W
5.2.2 Antibacterial drugs: Some dogs scratch so severely that
they cause a secondary bacterial infection of the skin called
pyoderma (Staphylococcus intermedius), which intensifies the
itching. Antibiotics that work best for pyoderma include:
Cephalexin @ 22 mg/kg B.W, Enrofloxacin @ 2.5 -5 mg/kg
B.W, Erythromycin @ 10 mg/kg B.W, Clavulanic acid +
Amoxycillin combination @ 13.5 mg/kg BW. The dog should
be bathed with shampoo that will help in controlling the skin
infection, eg. Benzoyl peroxide or chlorhexidine containing
shampoo.
5.2.3 Antifungal drugs: Secondary fungal infections can
occur, especially when the feet are licked constantly. The
commonly used antifungal agents include: Ketoconazole @ 5-
10 mg/kg B.W, Griseofulvin @ 25 mg/kg B.W,
Amphotericin-B @ 0.5 mg/kg B.W. Bathing the dog with a
shampoo containing ketoconazole and chlorhexidine.
5.2.4 T-cell inhibitor: Cyclosporine @ 5mg/kg B.W,
Tacrolimus @ 2 mg/kg B.W
5.2.4 Glucocorticoids: Prednisolone @ 2-4 mg/kg B.W,
Methyl prednisolone @ 1-2 mg/kg B.W
5.2.5 Food supplements: Feed diets balanced with vitamin,
mineral and fatty acid supplements e.g. omega-3 and omega-
6.
6. Conclusion
Food hypersensitivity is a relatively common cause of allergic
skin disease of dogs Symptoms are similar to other pruritic
skin diseases, a methodical approach is required to establish a
definitive diagnosis. Secondary infections of the skin and ears
are common with food allergy, particularly in the dog. These

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Journal of Entomology and Zoology Studies
infections must be resolved prior to completion of an
elimination diet. An 8–12 week elimination diet is the only
reliable way to diagnose food allergy in the dog and cat. If
improvement or resolution of symptoms is seen, the diagnosis
can be confirmed by provocative challenge with the former
diet. Long term management of food allergy in the dog
requires avoidance of the offending allergen(s). The
investigation and diagnosis of food hypersensitivity are
laborious and frustrating.
7. Acknowledgements
The authors would like to acknowledge Dr. V.S Wazir,
Associate Professor, Division of Veterinary Medicine, F.V.Sc
& A.H, R.S. Pura, Jammu for providing me all the invaluable
insights and regular encouragement throughout the whole
study.
8. References
1. Gaschen FP, Merchant SR. Adverse food reactions in
dogs and cats. Veterinary Clinical North American Small
Animal Practice. 2011; 41:361-379.
2. Chesney CJ. Food sensitivity in the dog: a quantitative
study. Journal of Small Animal Practice. 2002; 43:203-
207.
3. Ricci R, Hammerberg B, Paps J, Contiero B, Jackson H.
A comparison of the clinical manifestations of feeding
whole and hydrolysed chicken to dogs with
hypersensitivity to the native protein. Veterinary
Dermatology. 2010; 21:358-66.
4. Day MJ. The canine model of dietary hypersensitivity.
Proceedings of Nutrition Society. 2005; 64(4):458 464.
5. Fritsch DA, Allen TA, Dodd CE, Jewell DE, Sixby KA,
Leventhal PS. A multicenter study of the effect of dietary
supplementation with fish oil omega-3 fatty acids on
carprofen dosage in dogs with osteoarthritis. Journal of
American Veterinary Medical Association. 2010;
236(5):535-539.
6. Mandigers PJ, Van DI, Spee B, Penning LC, Bode P,
Rothuizen J. Chronic hepatitis in Doberman pinschers. A
review. Veterinary Questions. 2004; 26(3):98-106.
7. Hall EJ. Dietary sensitivity. In: Bonagura JD, editor.
Kirk’s Current Veterinary Therapy xiii. ed. Philadelphia:
WB Saunders; 2000, 632-637.
8. Guilford WG, Markwell PJ, Jones BR, Harte JG, Wills
JM. Prevalence and causes of food sensitivity in cats with
chronic pruritis, vomiting or diarrhea. Journal of
Nutrition, 1998; 128:2790-2791.
9. Carlotti DN, Remy I, Prost C. Food allergy in dogs and
cats: a report and review of 43 cases. Veterinary
Dermatology. 1990; 1:55-62.
10. Scott DW, Miller WH, Griffin CE. Immune system and
allergic skin diseases: In Muller & kirk's small animal
dermatology. Philadelphia saunders. 2001; 6:543-666.
11. Rosser EJ, Diagnosis of food allergy in dogs. Journal of
American Veterinary Medical Association. 1993;
203:259-262.
12. Roudebush P, Guilford WG, Jackson HA. In Hand MS,
Thatcher CD, Remillard RL. Adverse reactions to food.
Small Animal Clinical Nutrition. 2010; 5:609.
13. Jeffers JG, Meyer EK, Sosis EJ. Responses of dogs with
food allergies to single-ingredient dietary provocation.
Journal of American Veterinary Medical Association.
1996; 209:608-611.
14. Ohmori K, Masuda K, Kawarai S. Identification of
bovine serum albumin as an IgE-reactive beef component
in a dog with food hypersensitivity against beef. Journal
of Veterinary Medical Sciences. 2007; 69:865-867.
15. Simpson KW. Small Intestinal Disease. In: Thomas,
D.A., Simpson, J.W., Hall, E.J., editors. Manual of
Canine & Feline Gastroenterology. Gloucestershire:
British Small Animal Veterinary Association. 1996;
1:114-150.
16. Harvey RG. Food allergy and dietary intolerance in dogs:
a report of 25 cases. Journal of Small Animal Practice.
1993; 34:175-179.
17. Befus AD, Pearce FL, Goodacre R, Bienenstock J.
Unique functional characteristics of mucosal mast cells.
Advances in Experimental Medicine and Biology. 1982;
149:521-527.
18. White SD. Food hypersensitivity. Veterinary of Clinical
North American Small Animal Practice. 1988;
18(5):1043-1048.
19. Hall EJ, Batt RM. Development of wheat-sensitive
enteropathy in Irish Setters: morphologic changes.
American Journal of Veterinary Research. 1990;
51(7):978-982.
20. Wills J, Harvey R. Diagnosis and management of food
allergy and intolerance in dogs and cats. Australian
Veterinary Journal. 1994; 71(10):322-326.
21. Rosser EJ. Diagnosis of food allergy in dogs. Journal of
American Veterinary Medical Association. 1993;
203:259-262.
22. Jackson HA, Jackson MW, Coblentz L, Hammerberg B.
Evaluation of the clinical and allergen specific serum
immunoglobulin E responses to oral challenge with
cornstarch, corn, soy and a soy hydrolysate diet in dogs
with spontaneous food allergy. Veterinary Dermatology.
2005; 14:181-187.
23. Favrot C, Steffan J, Seewald W. A prospective study on
the clinical features of chronic canine atopic dermatitis
and its diagnosis. Veterinary Dermatology. 2010; 21:23-
31.
24. White SD. Food hypersensitivity. Veterinary of Clinical
North American Small Animal Practice. 1988; 18(5):
1043-1048.
25. Guilford WG, Jones BR, Markwell PJ, Arthur DG,
Collett MG, Harte JG. Food sensitivity in cats with
chronic idiopathic gastrointestinal problems. Journal of
Veterinary Internal Medicine. 2001; 1:7-13.