Abstract
Food allergy is a recognized clinical entity in dogs and cats and is an important differential to consider in the workup of a pruritic animal. Food can be a trigger factor for canine atopic dermatitis, and food allergy may coexist with feline atopic skin syndrome. Other clinical signs such as urticaria, recurrent pyoderma, and dorsolumbar pruritus can be seen in dogs, and urticaria, conjunctivitis, and respiratory signs can be seen in cats. In both species, gastrointestinal signs may be present. The pathogenesis in dogs and cats is complex and incompletely understood, which limits the development of reliable diagnostic laboratory tests. The diagnosis currently relies on an appropriately performed diet trial with subsequent provocation. This paper briefly reviews food allergies in people and explores our current knowledge of the disorder in dogs and cats.
Definition and Pathogenesis
Adverse food reactions can either have a true immunological basis (food allergy) or can occur as a result of toxic, pharmacological, or idiosyncratic reactions to food (food intolerance). Examples of food intolerance in pets are lactose intolerance, chocolate poisoning (dogs), and bacterial toxins contaminating diets leading to enteritis. There are no confirmed reports of adverse food reactions in dogs and cats causing recurrent or ongoing pruritus with or without gastrointestinal signs. There is evidence of an immunological basis for cutaneous adverse food reactions in dogs; there is a paucity of research into the condition in cats. Consequently, this review will focus on food allergy.
Food allergy is the result of the breakdown of immunological tolerance to food that results in immunoglobulin E (IgE) or non-IgE-mediated immune disorders resulting in clinical disease. In the normal individual, food allergens are presented by local dendritic cells in the gastrointestinal tract and stimulate a regulatory T cell (T-reg) response in the local lymph node. In patients with food allergy, this process is compromised and a specific Th2 response is triggered, which is responsible for B-cell immunoglobulin class switching, and an allergen-specific IgE response is initiated. A non-IgE, cell-mediated reaction may also develop or a combination of both reactions.
Humans
Most cases of food allergy in people are IgE mediated, and there is consistent evidence for food as a trigger in some atopic children. Cell-mediated food allergy in humans is a heterogeneous group of diseases such as eosinophilic oesophagitis and food protein-induced allergic proctocolitis, which primarily affect the gastrointestinal tract.1
The prevalence of (IgE-mediated) food allergy in humans is estimated at around 2.8% in infants rising to 10% at 2 years of age and falling to 7% in adolescents.2 In this age group milk, tree nuts, peanut, and shellfish are the most common allergens. The same authors estimated a prevalence of 10.8% in adults. Certain allergies such as those to peanuts, tree nuts, and shellfish are more likely to persist whereas milk and egg allergies usually resolve. It is estimated that around 33% of children with moderate to severe AD have food allergy.3
The development of food allergy is a complex interaction between genetics, epigenetics, and environmental factors leading to a breakdown in normal tolerance to dietary components. The higher incidence in infants may reflect an immature immune system. It would also appear that specific timing can be critical in infants and the composition of the gut microbiota early in life could be important for the development of allergy in the future.4
In addition to the gastrointestinal route, epicutaneous exposure to allergens is thought to be important in this age group, especially in those affected with AD where inflamed skin facilitates allergen absorption.5
There is insufficient evidence to support the maternal avoidance of foods during pregnancy and lactation or the feeding of a hydrolyzed milk formula and breastfeeding postnatally.6
Class II sensitization to food allergens is more common in later life and occurs after a primary sensitization to pollen allergens with subsequent cross-reactivity with homologous epitopes in vegetables and fruits, the pollen-food allergy syndrome (PFAS).7 The particular foods triggering PFAS varies geographically with birch pollen being the primary sensitizer in Europe.
Adult sensitization to food allergens can also be percutaneous with dairy, wheat, and soy allergies developing as a consequence of the use of skin care products containing these ingredients.2
Dogs
There is less known about the pathogenesis of food allergy in dogs when compared to humans. To develop a hypersensitivity reaction, there is a loss of tolerance to food antigens, which likely arises from a genetic predisposition, alterations in gastrointestinal permeability, local immune surveillance, and dysbiosis of the gut microbiome. The prevalence of food-induced disease is greater in dogs less than 12 months of age with another peak in older dogs. A recent review8 of the onset of food-induced clinical signs in dogs was reported to be less than 6 months (22%) to less than 12 months (38%) with the range extending to 13 years of age. Estimates of the prevelance in dogs vary between 25% and 49% of allergic dogs9–12 and between 8% and 62% of dogs with pruritus.13 In many cases, the clinical presentation is of an AD phenotype (9% to 50%) and food allergens can be demonstrated to cause a flare of the disease.13
Although there is evidence that IgE is involved in the pathogenesis of canine food allergy, lymphocyte blastogenic responses to food allergens also showed a strong correlation with offending allergens in dogs with a confirmed food allergy. Furthermore, the reactivity was attenuated when the dogs were fed an elimination diet.14 This supports a mixed immunological reaction in canine food allergy; while Th cells can stimulate a B-cell response, a delayed-type hypersensitivity can also be initiated.
There is a paucity of studies investigating the development of canine food allergy and most researchers have focused on AD. A prospective study15 followed 90 West Highland White Terrier puppies, a breed known for developing AD, for the first 3 years of life. Of this group, 52% developed clinical signs consistent with AD, and of this 17% were confirmed to have food-related AD.15
In a small study16 looking at the expression of Foxp3 in the canine gut, this was shown to increase with age, suggesting a progressive establishment of oral tolerance. The effect of diet on the gut microbiota has also been studied. The gut microflora was compared between 2 groups of dogs, 1 on a raw diet and the other on commercial feed. The raw-fed dogs were found to have a greater diversity of bacteria in their gut but also a higher incidence of opportunistic pathogens such as Clostridia perfringens,17 and in a small study18 feeding a raw meat diet to Staffordshire Bull Terriers with AD, changes in the skin transcriptome were seen. A number of investigators have looked at whether a dietary modification in pregnancy or early puppyhood could influence the development of AD in later life. In a case-controlled Swedish study,19 the feeding of noncommercial foods to the pregnant bitch had a protective effect on the development of AD in West Highland White Terriers, Boxers, and Bull Terriers. In an owner-reported survey,20 in Finland an association between the consumption of 80% or more of the diet as kibble with added mixed oils and sugary fruit and the development of adult-onset AD was reported. It should be noted that a causal relationship was not established in this study and other management variables of the puppies were not addressed. Whether dietary modifications in these cited studies had an influence on the development of food-induced AD in the dogs was not reported. Further research into whether dysbiosis of the gastrointestinal microbiome is a factor in the development of canine allergic diseases is required.
Allergens
The most common food protein allergens range in size between 15 and 40 kDa although some smaller or larger proteins can be allergenic. They are generally resistant to digestion.
A review21 of allergens reported by owners to provoke a clinical response in cats and dogs with a presumed food allergy between 1985 and 2015 suggested beef, dairy, chicken, and wheat were most common in dogs and beef, fish, and chicken in cats. Our knowledge of clinically relevant component-derived diagnostic (CRD) allergens (specific epitopes) in animals is minimal and was reviewed 2017.22 To date, bovine serum albumin (Bos d6), phosphoglutaminase, and bovine IgG (Bos d7) have been identified in dogs with a clinical allergy to beef.23 Five dogs with clinical hypersensitivity to hens egg had allergen-specific IgE to ovomucoid (Gal d1), ovalbumin (Gal d2), and ovotransferrin (Gal d3),24 and dogs with confirmed fish (cod) allergy had serum IgE specific for tropomyosin and enolase (Gad m2).25 Knowledge of CRD will help with diagnostics and discrimination between cross and cosensitization in the future. A recent investigation26 compared 3 groups of dogs; first, those consuming a diet with no chicken but no clinical hypersensitivity or positive serum IgE to chicken; second, a group with AD and positive IgE titers to chicken (whether the dogs had clinical reactivity to chicken was unknown); and finally, a group of dogs with clinical chicken hypersensitivity confirmed by food challenge. Using immunoblotting and mass spectrometry, 7 major chicken allergens were identified in the chicken-sensitized dogs, 3 of which were recognized allergens in humans and all of which were common to other food sources such as fish, meats, or plants.26 Serum IgE cross-reactivity was demonstrated by the same researchers27 between chicken and fish when serum from dogs with suspected food allergy was examined using ELISA, inhibition ELISA, and inhibition immunoblots. Further serological cross-reaction in the serum of suspected food-allergic dogs has been demonstrated between ruminants (ie, beef and lamb and cow milk),28 poultry, and grains, as well as unrelated sources such as pork and ruminant.29
It is currently unknown whether class II sensitization occurs in dogs. Between 10 and 35% of dogs are naturally sensitized to birch; however, it is unknown whether this is specifically Bet v1, the major cross-reacting allergen in humans, and whether this has clinical relevance to the ingestion of vegetables and fruit by dogs has not been investigated. In Japan, sensitization to Japanese cedar is a common airborne allergen with subsequent PFAS developing to tomato in people. This has been reported in an individual dog.30
While in some cases the specific allergens responsible for clinical reactions in sensitized dogs have been identified the clinical relevance of positive results in dogs with no signs of allergy and the significance of cross-reactivity with homologous allergens remains to be investigated.31
In theory, exposure to “hidden” proteins such as traces of bovine serum albumin and casein in vaccinations32 or infestation with Toxocara canis31 may act as sensitizing allergens.
The research reviewed herein has focused on an IgE-mediated pathogenesis, and further work needs to be directed at the possibility of dysregulation in other immune pathways.
Clinical Presentation
Dogs
In a Swiss study11 in which the allergic population was compared with all registered dogs, West Highland White Terriers, Rhodesian Ridgebacks, and Pugs were predisposed to food allergy, supporting a genetic predisposition to the disease. It should be noted however that these breeds are also commonly affected by canine AD. In the same study,11 gastrointestinal signs were more common in the affected population with food allergy and clinical signs tended to develop earlier, 48% in the food-allergic dogs (< 1 year) as compared with 16% of dogs with AD.
Food-allergic dogs with the atopic phenotype present with pruritus affecting the paws, ventral abdomen, axillae, groin and perineum, face, and ears. Not all these body sites will be affected, and some may present with only pedal pruritus or recurrent otitis for example. Although in young dogs clinical signs may initially be controlled with diet, some of these dogs will subsequently develop environmental hypersensitivities later in life.
Other dogs can present with urticaria,33 recurrent pyoderma, or dorsolumbar pruritus and may also exhibit gastrointestinal signs manifested by soft feces, flatulence, intermittent diarrhea, and clinical signs consistent with colitis.34 Conjunctivitis and sneezing have also been reported in a small number of dogs.34
As food allergy can develop at any age, the onset of pruritus, recurrent otitis, and or recurrent pyoderma should be considered as a differential diagnosis for any dog in which parasite infestation and other causes of pruritus have been comprehensively ruled out.
Cats
The figures for cats are similar with the onset of clinical signs before 12 months in 27% of cases where reported.35 Cats usually present with pruritus, which may be associated with self-induced symmetrical alopecia, miliary dermatitis, head and neck pruritus, the eosinophilic granuloma complex, or a combination of patterns.35 Extracutaneous signs such as conjunctivitis (12%), gastrointestinal (18%), and respiratory signs may also be present.35
Diagnosis
The diagnosis of food allergy in dogs and cats currently relies on performing a diet trial and subsequent provocation. This is currently the only reliable diagnostic test. This should not contain any previously consumed foods and be based on a “novel” or hydrolyzed protein diet. Selection of an appropriate diet therefore relies on a comprehensive diet history obtained from the owner and any other individuals who take care of the animal. Identification and sourcing novel proteins can be challenging and are potentially complicated by the possibility of cross-reaction with apparently unrelated food sources as discussed previously. For this reason, hydrolyzed diets are commonly used (Figure 1). Pivotal to the performance of a successful diet trial are owner education and compliance.36 Time needs to be set aside within a busy clinical setting to explain the premise of the trial and address any potential obstacles, which might arise. Using trained technicians to make regular phone contact with owners during the trial will improve compliance.
A 7-month-old domestic short-haired cat with head and neck pruritus before (left) and after a 7-week-diet trial with a hydrolyzed diet (right).
Citation: Journal of the American Veterinary Medical Association 261, S1; 10.2460/javma.22.12.0548
Composition of the diet
It is increasingly difficult to source a “novel” protein source, ie, one the pet has not previously eaten. In this context, it has been suggested that employing insect-based diets to which the dogs have not had previous exposure and that contain highly valuable digestible proteins might be a reasonable option. However, these contain a source of allergen that is phylogenetically related to house dust and storage mites. Serum containing house dust and storage mite-specific IgE was collected from clinically normal and dogs with confirmed AD. In both groups, the IgE bound to insect (mealworm) proteins on a Western blot with no significant difference seen between the groups.37 It is not currently clear whether these findings represent clinically relevant allergy, sensitization, or carbohydrate moieties causing false positive results. However, a novel protein diet trial based on insects in dogs previously sensitized to house dust and storage mites may not be the optimal choice.
An additional problem is the potential for residues of unlisted food sources to be present in the diet. Various studies have examined pet foods proposed as novel protein diets using PCR, ELISA, or direct microscopy and demonstrated foreign elements in 33 to 83% of these diets, reviewed by Olivry and Mueller.38 The hydrolyzed diets examined did not have food contaminants present.
The use of hydrolyzed diets eliminates the requirement to find a novel protein source. The proteins are generally hydrolyzed to a molecular weight < 5 kDa, which theoretically prevents cross-linking of IgE. The antigenicity of a hydrolyzed diet depends on the degree of hydrolysis; for IgE-mediated food allergy, an extensively hydrolyzed diet is optimal; and regular monitoring of the product batches is desirable. Extensively hydrolyzed elemental diets that contain oligopeptides are also available in certain countries. Hydrolyzed diets usually contain a carbohydrate moiety, in this regard cornstarch appears less likely to induce an IgE reaction in dogs and cats than corn flour.39
A small study40 demonstrated that 10 dogs with proven chicken allergy did not react clinically to an extensively hydrolyzed poultry feather diet < 1 kDa; however, when the diet was only partially hydrolyzed, 40% of the dogs had clinical reactions.
It has been shown however that hydrolyzed proteins can stimulate T-lymphocytes in dogs with suspected food allergy suggesting that these diets may not be uniformly reliable for diet trials, and this supports a cell-mediated pathway of food allergy in dogs.41
Home-cooked diets often are advocated to avoid pet food additives that may cause adverse reactions, although there are no well-documented reports to support this in pets. However, home cooking with a single source of protein should avoid the problem of contamination with foreign proteins in manufactured pet foods discussed above. The diets are usually based on a single protein to which the animal has not been previously exposed; this is usually mixed with a carbohydrate source. Home-cooked diets are usually nutritionally inadequate for maintenance or growth, and clinicians are advised to use recipes available in veterinary textbooks or the services of a diplomate in veterinary nutrition to create balanced diets. In 1 study,42 36% of clients preparing home-cooked food for their dogs discontinued the diet trial prematurely. Another study9 documented a failure rate of 52% of clients, although the failure rate dropped to 27% after better client education was instituted. This emphasizes the importance of client communication if home-cooked diets are used. Clients should also be made aware that preparing home-cooked diets is time consuming and generally more expensive than feeding commercially available foods.
The diet trial and challenge
The diet trial should be continued for a number of weeks, and based on an analysis of previously published studies, 85% of dogs will have improved by 5 weeks and extending the trial to 8 weeks will be adequate for over 95% of dogs. Similar figures for cats are 80% at 6 weeks and over 90% at 8 weeks.43 If gastrointestinal signs are concurrently present, then these can resolve more quickly than the cutaneous signs.
Using anti-inflammatory treatment during the initial phase of the diet trial in dogs has the potential to shorten the duration of the diet trial to 4 to 6 weeks and consequently improve client compliance.44 Prednisolone tapered to 0.5mg/kg daily was administered for a minimum of 2 weeks until affected dogs exhibited an acceptable level of pruritus as assessed by a validated pruritus analog scale. After discontinuing the prednisolone, the diet was continued for a further 2 weeks without an increase in pruritus before a dietary challenge was performed.
If clinical improvement is sustained, then a dietary challenge must be performed to confirm food allergy and relapse of clinical signs demonstrated. In most allergic skin diseases in dogs and cats, the pruritus waxes and wanes over a period of weeks. Great care must be taken with the interpretation of any apparent improvement in response to a restricted diet as an improvement may be due to concurrent topical antimicrobial treatment, better management, or a seasonal effect. Any pet that improves with a restricted diet should be challenged with its original diet, which should include all treats, scraps, biscuits, chews, and dietary supplements. In the majority of cases, clinicians rely on owners to report a relapse. It is worth pointing out that if an animal has concurrent environmental hypersensitivities, then complete resolution of clinical signs is unlikely to occur. These cases can often be more difficult to interpret as pruritus associated with environmental allergen exposure can wax and wane. The author recommends performing the dietary challenge on a weekend when the owners are with their animals, and if there is seasonality to AD, then performing the diet trial during the winter months may be optimal.
In 1 recent prospective study24 including 46 dogs, the median time to relapse after a challenge was 12 hours (range, 1.5 hours to 10 days) with 23.9% within 3 to 6 hours and 60.9% within 12 hours. Pruritus primarily affected the limbs and face. In a previously mentioned study26 with confirmed chicken-allergic dogs, 44% (4/9) became pruritic within 12 hours of challenge. However, in a retrospective review45 of publications between 1990 and 2019, only 9% of dogs and 27% of cats reportedly flared within 24 hours. The time to flare of 50% and 90% of dogs, respectively, was 5 and 14 days and for cats was 4 and 7 days.45 Variability in these reports is likely due to owner observation, specific protein and amount fed, individual variability, and the immune reaction elicited. While an IgE-mediated reaction would be expected to evoke clinical signs within hours of provocation, a mixed or cell-mediated reaction could take considerably longer.
Other Diagnostic Tests
Serum allergy testing for food allergy in dogs has received considerable scrutiny over the years but has been proven to be unreliable in predicting clinical allergy. There are potentially a number of reasons for this. First, serum allergy testing assumes that food allergy in dogs is IgE mediated and serum IgE has a short half-life, and testing is most valid when performed in association with recent exposure.
Specific epitopes can vary with processing; the allergens employed for testing may not resemble those present in pet foods; and additionally, positive reactions on serum allergy testing may not predict clinical hypersensitivity. If serum allergy testing is to be used at all, then foods to which serum antibodies are not detected should be selected for the diet trial.46
Serum was submitted to 2 laboratories for food-specific IgE and IgG from dogs with confirmed food allergy, AD, other skin diseases, and healthy dogs, and the results lacked concordance and were unable to distinguish reliably between the 4 groups.47
These results have been corroborated by other investigators.
Similarly, food allergen-specific IgE is not reliable as a diagnostic tool in cats.48
Western blotting (WB) has been examined as a possible diagnostic tool for dogs with suspected food allergy. Serum from dogs with confirmed food allergy was tested against extracts from diets commonly used in diet trials. While dogs with food allergy had more IgE binding to the extracts than nonfood allergic dogs, the WB could not be recommended as a diagnostic tool.49 Another study49,50 performed WB under nonreducing conditions to preserve conformational epitopes; while the food-allergic dogs demonstrated strong IgE binding to beef and milk compared to the nonfood allergic group, the test was not diagnostically useful.
Measurement of serum food-specific IgG or saliva testing for food-specific antibodies is of limited value in the diagnosis of canine food allergy.51
Intradermal testing has also been shown to be unreliable for the diagnosis of food allergy in dogs.52 Patch testing has also been evaluated as a diagnostic tool. It was shown to have a good negative predictive value, which could be useful in selecting proteins for an elimination diet trial,46 and a recent study53 combining the prick and patch test suggested that this improved the negative predictive value. Patch testing however is not a practical clinical tool as allergens require to be in contact with the skin for 48 hours.
Long-Term Management
The majority of dogs and cats with a diagnosis of food allergy are maintained on an avoidance regime after diagnosis. Dietary indiscretions are treated with short-term antipruritic and anti-inflammatory therapy. It is a clinical observation that many pets will tolerate offending foods later in life; however, good long-term studies on this subject have not been performed.
The goal of food allergy immunotherapy is to induce tolerance to the offending allergens or increase the threshold dose required to elicit an adverse reaction. In at-risk infants, early controlled introduction of peanut/egg is recommended as there is evidence that this is protective against future severe food allergy.54 Additionally, sublingual and epicutaneous immunotherapy is successfully employed in children to induce desensitization.55 In dogs, sublingual immunotherapy has been shown to be well tolerated and effective at reducing the severity of reactions to food after 6 months of therapy in 5 dogs.56
Conclusion
Food allergy is a recognized clinical entity in dogs and cats; however, the details of the aetiopathogenesis remain incompletely understood. At the time of writing, a strict diet trial with a provocative challenge is the standard diagnostic tool. As this relies on owner education and compliance, it presents additional challenges for the busy practitioner. Although commercially available serum allergy tests are available, the results are an unreliable predictor of clinical allergy. Further understanding of the aetiopathogenesis of food allergy in dogs and cats and the clinical relevance of allergen-specific IgE is required to advance our knowledge in this field.
Acknowledgment
The author declares no conflicts of interest.
References
- 1.↑
Cianferoni A. Non-IgE mediated food allergy. Curr Pediatr Rev. 2020;16(2):95–105. doi:10.2174/1573396315666191031103714
- 2.↑
Sicherer SH, Warren CM, Dant C, et al. Food allergy from infancy through adulthood. J Clin Immunol Pract. 2020;8(6):1854–1864. doi:10.1016/j.jaip.2020.02.010
- 3.↑
Bergmann MM, Caubet J-C, Boguniewicz M, Eigenmann PA. Evaluation of food allergy in patients with atopic dermatitis. J Allergy Clin Immunol Pract. 2013;1(1):22–28. doi:10.1016/j.jaip.2012.11.005
- 4.↑
Bunyavanich S, Berin C. Food allergy and the microbiome: current understandings and future directions. J Allergy Clin immunol. 2019;144(6):1468–1477. doi:10.1016/j.jaci.2019.10.019
- 5.↑
Brough HA, Liu AH, Sicherer S, et al. Atopic dermatitis increases the effect of exposure to peanut antigen in dust on peanut sensitization and likely peanut allergy. J Allergy Clin Immunol. 2015;135(1):164–170. doi:10.1016/j.jaci.2014.10.007
- 6.↑
Halken S, Muraro A, de Silva D, et al. EAACI guideline: preventing the development of food allergy in infants and young children (2020 update). Pediatr Allergy Immunol. 2021;32(5):843–858. doi:10.1111/pai.13496
- 7.↑
Mastrorilli C, Cardinale F, Giannetti A, Caffarelli C. Pollen-food allergy syndrome: a not so rare disease in childhood. Medicina. 2019;55(10):641. doi:10.3390/medicina55100641
- 8.↑
Olivry T, Mueller RS. Critically appraised topic on adverse food reactions of companion animals (7): signalment and cutaneous manifestations of dogs and cats with adverse food reactions. BMC Vet Res. 2019;15(1):140. doi:10.1186/s12917-019-1880-2
- 9.↑
Chesney C. Food sensitivity in the dog, a quantitive study. J Small Anim Pract. 2002;43(5):203–208. doi:10.1111/j.1748-5827.2002.tb00058.x
- 10.
Jackson H, Murphy KM, Tater K, et al. The pattern of allergen hypersensitivity (dietary or environmental) of dogs with non-seasonal atopic dermatitis cannot be differentiated on the basis of historical or clinical information: a prospective evaluation 2003–2004. In: North American Veterinary Dermatology Forum, Sarasota, Florida, April 7. NAVDF; 2005.
- 11.↑
Picco F, Zini E, Nett C. A prospective study on canine atopic dermatitis and food induced allergic dermatitis in Switzerland. Vet Dermatol. 2008;19(3):150–155. doi:10.1111/j.1365-3164.2008.00669.x
- 12.↑
Loeffler A, Soares-Magalhaes R, Bond R, Lloyd DH. A retrospective analysis of case series using home-prepared and chicken hydrolysate diets in the diagnosis of adverse food reactions in 181 pruritic dogs. Vet Dermatol. 2006;17(4):273–279. doi:10.1111/j.1365-3164.2006.00522.x
- 13.↑
Olivry T, Mueller RS. Critically appraised topic on adverse food reactions of companion animals (3): prevalence of cutaneous adverse food reactions in dogs and cats. BMC Vet Res. 2017;13(1):51. doi:10.1186/s12917-017-0973-z
- 14.↑
Ishida R, Masuda K, Kurata K, Ohno K, Tsujimoto H. Lymphocyte blastogenic responses to inciting food allergens in dogs with food hypersensitivity. J Vet Int Med. 2004;18(1):25–30. doi:10.1111/j.1939-1676.2004.tb00131.x
- 15.↑
Favrot C, Fischer N, Olivry T, Zwickl L, Audergon S, Rostaher A. Atopic dermatitis in West Highland White terriers–part 1: natural history of atopic dermatitis in the first three years of life. Vet Dermatol. 2020;31(2):106-e16. doi:10.1111/vde.12801
- 16.↑
Junginger J, Schwittlick U, Lemensieck F, Nolte I, Hewicker-Trautwein M. Immunohistochemical investigation of Foxp3 expression in the intestine in healthy and diseased dogs. Vet Res. 2012;43(23):2–14. doi:10.1186/1297-9716-43-23
- 17.↑
Schmidt M, Unterer S, Suchodolski J, et al. The fecal microbiome and metabolome differs between dogs fed Bones and Raw Food (BARF) diets and dogs fed commercial diets. PLoS One. 2018;12(8):e0201279. doi:10.1371/journal.pone.0201279
- 18.↑
Anturaniemi J, Zaldívar-LópezHuub S, Savelkoul FJ, Elo K, Hielm-Björkman A. The effect of atopic dermatitis and diet on the skin transcriptome in Staffordshire bull terriers. Front Vet Sci. 2020;7:552251. doi:10.3389/fvets.2020.552251
- 19.↑
Nødtvedt A, Bergvall K, Sallander M, et al. A case-control study of risk factors for canine atopic dermatitis among boxer, bullterrier and West Highland white terrier dogs in Sweden. Vet Dermatol. 2007;18(5):309–315. doi:10.1111/j.1365-3164.2007.00617.x
- 20.↑
Hemida MBM, Salin S, Vuori KA, et al. Puppyhood diet as a factor in the development of owner-reported allergy/atopy skin signs in adult dogs in Finland. J Vet Intern Med. 2021;35(5):2374–2383. doi:10.1111/jvim.16211
- 21.↑
Olivry T, Mueller RS. Critically appraised topic on adverse food reactions of companion animals (8): storage mites in commercial pet foods. BMC Vet Res. 2019;15(1):385. doi:10.1186/s12917-019-2102-7
- 22.↑
Pali-Schöll I, De Lucia M, Jackson H, Janda J, Mueller RS, Jensen-Jarolim E. Comparing immediate-type food allergy in humans and companion animals-revealing unmet needs. Allergy. 2017;72(11):1643–1656. doi:10.1111/all.13179
- 23.↑
Martín Á, Sierra M-P, González JL, Arévalo MA. Identification of allergens responsible for canine cutaneous adverse food reactions to lamb, beef and cow’s milk. Vet Dermatol. 2004;15(6):349–356. doi:10.1111/j.1365-3164.2004.00404.x
- 24.↑
Shimakura H, Uchiyama J, Saito T, et al. IgE reactivity to hen egg white allergens in dogs with cutaneous adverse food reactions. Vet Immunol Immunopathol. 2016;177:52–57. doi:10.1016/j.vetimm.2016.06.003
- 25.↑
Imanishi I, Uchiyama J, Mizukami K, et al. IgE reactivity to fish allergens from Pacific cod (Gadus macrocephalus) in atopic dogs. BMC Vet Res. 2020;16(1):341. doi:10.1186/s12917-020-02559-1
- 26.↑
Olivry T, Pucheu-Haston CM, Mayer U, Bergvall K, Bexley J. Identification of major and minor chicken allergens in dogs. Vet Dermatol. 2022;33(1):46-e16. doi:10.1111/vde.13029
- 27.↑
Bexley J, KIngswell N, Olivry T. Serum IgE cross-reactivity between fish and chicken meats in dogs. Vet Dermatol. 2018;30(1):25-e8. doi:10.1111/vde.12691
- 28.↑
Bexley J, Nuttall TJ, Hammerberg B, Halliwell RE. Serological cross reactivity between beef, lamb and cows’ milk allergen extracts in dogs. Vet Dermatol. 2017;28(1).31-e7. doi:10.1111/vde.12335
- 29.↑
Baumann SA, Fritz C, Mueller RS. Food antigen-specific IgE in dogs with suspected food hypersensitivity. Tierarztl Prax Ausg K Kleintiere Heimtiere. 2020;48(6):395–402. doi:10.1055/a-1274-9210
- 30.↑
Fujimura M, Ohmori K, Masuda K, Tsujimoto H, Sakaguchi M. Oral allergy syndrome induced by tomato in a dog with Japanese cedar (Cryptomeria japonica) pollinosis. J Vet Med Sci. 2002;64(11):1069–1170. doi:10.1292/jvms.64.1069
- 31.↑
Olivry T, O’Malley A, Chruszcz M. Evaluation of the theoretical risk of cross-reactivity among recently identified food allergens for dogs. Vet Dermatol. 2022;33(6):523–526. doi:10.1111/vde.13110
- 32.↑
Shimakura H, Nasukawa T, Uchiyama J, et al. IgE reactivity to milk components in dogs with cutaneous adverse food reactions. J Vet Med Sci. 2021;83(10):1509–1512. doi:10.1292/jvms.21-0162
- 33.↑
Rostaher A, Hofer-Inteeworn N, Kümmerle-Fraune C, Fischer NM, Favrot C. Triggers, risk factors and clinico-pathological features of urticaria in dogs–a prospective observational study of 24 cases. Vet Dermatol. 2017;28(1):38-e9. doi:10.1111/vde.12342
- 34.↑
Mueller RS, Olivry T. Critically appraised topic on adverse food reactions of companion animals (6): prevalence of noncutaneous manifestations of adverse food reactions in dogs and cats. BMC Vet Res. 2018;14(1):341. doi:10.1186/s12917-018-1656-0
- 35.↑
Santoro D, Pucheu-Haston CM, Prost C, Mueller RS, Jackson H. Clinical signs and diagnosis of feline atopic syndrome: detailed guidelines for a correct diagnosis. Vet Dermatol. 2021;32(1):26-e6. doi:10.1111/vde.12935
- 36.↑
Painter MR, Tapp T, Painter JE. Use of the Health Belief Model to identify factors associated with owner adherence to elimination diet trial recommendations in dogs. J Amer Vet Med Assoc. 2019;255(4):446–453. doi:10.2460/javma.255.4.446
- 37.↑
Premrov Bajuk B, Zrimšek P, Kotnik T, Leonardi A, Križaj I, Jakovac Strajn B. Insect protein-based diet as potential risk of allergy in dogs. Animals (Basel). 2021;11(7):1942. doi:10.3390/ani11071942
- 38.↑
Olivry T, Mueller R. Critically appraised topic on adverse food reactions of companion animals (5); discrepancies between ingredients and labelling in commercial pet foods. BMC Vet Res. 2018;14(1):24. doi:10.1186/s12917-018-1346-y
- 39.↑
Olivry T, Bexley J. Cornstarch is less allergenic than corn flour in dogs and cats previously sensitized to corn. BMC Vet Res. 2018;14(1):207. doi:10.1186/s12917-018-1538-5
- 40.↑
Bizikova P, Olivry T. A randomized, double-blinded crossover trial testing the benefit of two hydrolysed poultry-based commercial diets for dogs with spontaneous pruritic chicken allergy. Vet Dermatol. 2016;27(4):289-e70. doi:10.1111/vde.12302
- 41.↑
Masuda k, Sato A, Tanaka A, Kumagai A. Hydrolyzed diets may stimulate food-reactive lymphocytes in dogs. J Vet Med Sci. 2020;82(2):177–183. doi:10.1292/jvms.19-0222
- 42.↑
Tapp T, Griffin C, Rosenkrantz W, Muse R, Boord M. Comparison of a commercial limited-antigen diet versus home-prepared diets in the diagnosis of canine adverse food reaction. Vet Ther. 2002;3(3):244–251.
- 43.↑
Olivry T, Mueller R, Prelaud P. Critically appraised topic on adverse food reactions of companion animals (1): duration of elimination diets. BMC Vet Res. 2015;11:225. doi:10.1186/s12917-015-0541-3
- 44.↑
Favrot C, Bizikova P, Fischer N, Rostaher A, Olivry T. The usefulness of short-course prednisolone during the initial phase of an elimination diet trial in dogs with food-induced atopic dermatitis. Vet Dermatol. 2019;30(6):498-e149. doi:10.1111/vde.12793
- 45.↑
Olivry T, Mueller R. Critically appraised topics on adverse food reactions of companion animals (9): time to flare of cutaneous signs after a dietary trial in dogs and cats with food allergy. BMC Vet Res. 2020;16:158. doi:10.1186/s12917-020-02379-3
- 46.↑
Bethlehem S, Bexley J, Mueller RS. Patch testing and allergen-specific serum IgE and IgG antibodies in the diagnosis of canine adverse food reactions. Vet Immunol Immunopathol. 2012;145(3–4):582–589. doi:10.1016/j.vetimm.2012.01.003
- 47.↑
Hardy JI, Hendricks A, Loeffler A, et al. Food-specific serum IgE and IgG reactivity in dogs with and without skin disease: lack of correlation between laboratories. Vet Dermatol. 2014;25(5):447-e70. doi:10.1111/vde.12137
- 48.↑
Belova S, Wilhelm S, Linek M, et al. Factors affecting allergen-specific IgE serum levels in cats. Can J Vet Res. 2012;76(1):45–51.
- 49.↑
Favrot C, Linek M, Fontaine J, et al. Western blot analysis of sera from dogs with suspected food allergy. Vet Dermatol. 2017;28(2):189-e42. doi:10.1111/vde.12412
- 50.↑
Pucheu-Haston C, Mougoet I. Serum IgE and IgG responses to dietary antigens in dogs with and without cutaneous adverse food reactions. Vet Dermatol. 2020;31(2):116-e20. doi:10.1111/vde.12810
- 51.↑
Udraite Vovk L, Watson A, Dodds WJ, Klinger CJ, Classen J, Mueller RS. Testing for food-specific antibodies in saliva and blood of food allergic and healthy dogs. Vet J. 2019;245:1–6. doi:10.1016/j.tvjl.2018.12.014
- 52.↑
Kunkle G, Horner S. Validity of skin testing for diagnosis of food allergy in dogs. J Am Vet Med Assoc. 1992;200(5):677–680.
- 53.↑
Possebom J, Cruz A, Gmyterco VC, de Farias MR. Combined prick and patch tests for diagnosis of food hypersensitivity in dogs with chronic pruritus. Vet Dermatol. 2022;33(2):124-e36. doi:10.1111/vde.13055
- 54.↑
Greer F, Sicherer S, Burkes AW, et al. The effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, hydrolyzed formulas, and timing of introduction of allergenic complementary foods. Pediatrics. 2019;143(4):e20190281.
- 55.↑
Sindher SB, Long A, Chin AR, et al. Food allergy, mechanisms, diagnosis and treatment: Innovation through a multi-targeted approach. Allergy.2022;77(10):2937–2948. doi:10.1111/all.15418
- 56.↑
Maina E, Cox E. A double blind, randomized, placebo controlled trial of the efficacy, quality of life and safety of food allergen-specific sublingual immunotherapy in client owned dogs with adverse food reactions: a small pilot study. Vet Dermatol. 2016;27(5):361-e91. doi:10.1111/vde.12358
