The exact etiology in most clinical cases is not well understood. Food allergy is defined as an immunologically based reaction to food. Immunologic mechanisms of types I-IV have been hypothesized.
The exact etiology in most clinical cases is not well understood. Food allergy is defined as an immunologically based reaction to food. Immunologic mechanisms of types I-IV have been hypothesized. A recent report measured cell-mediated immunity (via lymphocyte blastogenesis against food allergens( in both proven food allergic dogs and healthy dogs. The significantly higher responses of the food allergic dogs to the foods they were allergic to lends some credence to the role of cell-mediated immunity in this disease1. On the other hand, another recent report found that in 10 dogs allergic to either beef, cow's milk, or lamb, all the dogs had specific IgE antibodies against bovine IgG, (There may be some evidence that this reaction could be due to fetal calf serum used in the vaccines – although this needs to be investigated further).3 In further contrast, food intolerance is a general term describing any adverse reaction to food that does not have an immunologic basis, including food poisoning (caused by the direct action of a toxin). From a practical basis, the mechanism of action does not impact the clinician faced with a potential case of chronic food-caused cutaneous disease. It is theorized that most food allergens are proteins.
No sex predilection has been reported for food allergy in dogs or cats. In some studies, no breed predilection was noted. In contrast, two studies found that certain dog breeds may have a risk for the development of food allergy: Soft-Coated Wheaton Terrier, Dalmatian, West-Highland White Terrier, Collie, Chinese Shar Pei, Llasa Apsa, Cocker Spaniel, Springer Spaniel, Miniature Schnauzer, Labrador Retriever Dachshund and the Boxer. Breed data from Colorado State University shows that retrievers may be at greater risk to develop food allergy than other breeds of dogs.
While the age at presentation has been reported as variable, several researchers now feel that at least 33% of their cases in dogs are of animals less than 1 year of age4. Clearly, while food allergy may occur at any time in animal's life, it should always be considered as a differential of pruritus in the young dog.
History and Clinical Signs
The most common clinical sign of food allergy is non-seasonal pruritus which is usually generalized. Pruritus may also be primarily directed at the feet or ears. Very rarely, food allergic dogs with skin lesions but without pruritus have been reported. The most common primary dermatologic lesions are papules and erythema; common secondary lesions are epidermal collarettes (usually indicating a pyoderma) pyotraumatic dermatitis (‘hot spots') hyperpigmentation, and seborrhea. Clinical signs of food allergy have been reported in Cocker Spaniels identical to the idiopathic seborrhea associated with that breed. Food allergy as the underlying cause of idiopathic onychodystrophy (misshapen, splitting claws [nails]) has been reported in 2 dogs.
Food allergy in cats may present as pruritus of the head and face, milliary dermatitis, or one of the manifestations of the eosinophilic granuloma complex.
Reported concurrent gastrointestinal (GI) signs among dogs with cutaneous signs of food allergy are rare; it is unknown if this is due to a true dearth of GI signs or if in fact changes in the stool of these dogs were relatively subtle and/or were not noted or volunteered by the owners while obtaining the history. However, a recent report documented 20 dogs with both pruritus and GI signs typical of colitis: fecal mucus, fecal blood, tenesmus and increased fecal frequency. Both cutaneous and GI signs resolved upon feeding the dogs an elimination diet. Lymphocytic-plasmacytic colitis has been linked to food allergy in cats and cheetahs.In one study, having both GI and skin signs increased the likelihood of a diagnosis of food allergy, in a small number of cats.
Neurologic signs such as malaise and seizures rarely have been reported. The author feels that malaise may be under-reported, as an increase in energy level (‘acting like a puppy, feeling better') is often noted upon feeding the dog a diet without the offending allergen; this may occur before cessation of pruritus. Respiratory signs such as asthma have also been reported, but seem to be quite rare.
Concurrent hypersensitivities have been reported in dogs, and include atopic dermatitis, flea allergy dermatitis, intestinal parasite allergy and even an allergy to bovine insulin.6 A dog has been reported with a cross reaction between exposure to pollen of Japanese cedar and ingestion of tomatoes. Concurrent pyoderma and/or Malassezia pachydermatis infection is also common. Dogs may have pyoderma (superficial or deep) as the only clinical sign of food allergy: These dogs are often clinically normal (i.e., non-pruritic) while receiving antibiotics. Therefore it becomes quite important to diagnose and treat secondary infections, as persistence of pruritus due to these infections may confound the ability of the clinician to diagnose the underlying allergy.
The ideal method of diagnosis is the feeding of an elimination (“hypoallergenic”) diet. The experience of the author and of other researchers has been disappointing in the use of serologic or intradermal skin tests to diagnose food allergy in pets in North America.
The elimination diet ideally contains one protein and one starch. These must be based on previous exposure of the dog to various food stuffs. Important to remember is that dogs who live in households with cats tend to have been exposed to fish, through their consumption of either cat food or cat feces. At UC Davis we often start dogs with pork and potatoes, although pinto beans and potatoes may also be used. Based on non-exposure, rabbit, duck, and tuna are also options. We have also used ‘exotic' foods like elk when feasible. Other than fresh water, nothing else should be fed to the dog during the elimination diet trial. This means that vitamins and chewing toys must be eliminated, and that flavored medications (such as certain ecto/endoparasite preventatives) should be replaced by other, equally effective non-flavored preparations. Protein-flavored toothpaste should be replaced by the malt-flavored variety. Because the elimination diet is not a balanced one, owners should be warned that the dog may lose weight, develop a ‘dull' haircoat or scaling, or be hungrier than usual. In cats, we often use pork and tapioca (the latter made with water rather than milk).
Because many owners are unable or unwilling to cook for their pet for the time period needed, the dermatology service at UC Davis uses commercially available limited-antigen diets. For dogs these would include Purina LA (salmonid); Iams FP (fish and potato) and KO (kangaroo and oats); IVD (now owned by Royal Canin) duck, venison, whitefish, or rabbit plus potato; Hills D/D (duck or fish and rice); or Waltham fish and rice (also now owned by Royal Canin). For cats these would include IVD duck, venison, or rabbit plus potato; Hills D/D feline; or Iams lamb and barley. Another option for animals who already have been fed many foods, or whose dietary history is unknown, is the use of hydrolyzed protein diets, in which the protein source is hydrolyzed to small molecular weights, thus avoiding the body's ‘immunologic radar'. Such foods for dogs include Purina HA (hydrolyzed soy) , Hills Z/D, or DVM Exclude; for cats the author has used Hills feline Z/D, or Purina HA for cats. Usage of a commercially prepared diet will give an approximately 90% chance of determining a food allergy; however, none of these diets will work for all animals, and failure of an animal to improve on such a diet may warrant trying another one, or a home-cooked diet in another trial.
The length of the elimination diet is somewhat controversial, however, our observations have justified a dietary trial of 8 to 12 weeks. Persistence of some pruritus at 12 weeks into the diet trial may indicate the need for continuing the diet, but may also indicate the presence of concurrent hypersensitivities. In cases where antibiotics are given to treat secondary infections, or oral corticosteroids for severe pruritus, the diet must be continued for a minimum of 2 weeks past discontinuation of these treatments, in order to properly judge its efficacy.
Upon resolution of clinical signs with the feeding of an elimination diet, the animal should be challenged with its regular diet to confirm the diagnosis of a food allergy. Recurrence of clinical signs is usually noted within two weeks. At that point the animal is given its elimination diet again, and the owner may then elect to challenge with suspected allergens, each allergen being given one to two weeks at a time. The most common proven allergens in the dog are beef, chicken, milk, eggs, corn, wheat, and soy ; in the cat, fish, beef, milk and milk products. Allergies to more than 2 allergens are uncommon. Once the offending allergens are identified, commercially prepared dog foods that do not contain them may be fed to the dog. In cases in which the owners refuse to do provocative testing, one of the limited antigen pet foods may be used as a maintenance diet.
Zinc-responsive dermatosis consists of two syndromes. Syndrome I has been identified in Siberian huskies and occasionally other breeds and is typified by crusting and scaling of the mucocutaneous junctions, elbows and foot pads. These dogs are thought to have a genetic defect in zinc absorption from the intestines. Therefore, this disease will often occur in dogs fed normal, balanced diets. Diagnosis is based on breed, physical examination and histopathology, which shows marked follicular and epidermal parakeratotic hyperkeratosis. Treatment is the addition of zinc supplement to the diet indefinitely. Zinc sulfate, zinc methionine, or zinc gluconate may all be used; a dosage of 2-3 mg of elemental zinc/kg is recommended. Rarely, these dogs seemed to respond better if an essential fatty acid supplement is also given. A parenteral zinc preparation is available in Europe. Clinical signs usually are greatly improved within four to six weeks. Intact females may respond to lower dosages of zinc after being spayed.
Syndrome II occurs in rapidly growing puppies that are often fed poor-quality dog food or over-supplemented (especially with calcium) diets. These dogs are thought to have a relative zinc deficiency, possibly caused by a combination of low zinc intake and calcium or phytate- (plant protein) binding of the zinc. Clinical signs are generalized crusting plaques with extensive crusting and fissuring of the foot pads. Diagnosis is by history, clinical signs and histopathology (which resembles that of Syndrome I). Response to zinc therapy is dramatic, though changing to a balanced diet may be all that is necessary. Supplementation with zinc is usually not needed after maturity.
Interestingly, zinc-responsive dermatosis has also been reported in the dingo (Canis dingo) and the red wolf (Canis rufus) .
Superficial necrolytic dermatitis
Also known as SND, hepatocutaneous syndrome, epidermal metabolic necrosis, or diabetic dermatosis, this disease is being seen with increased frequency in dogs, and has also been reported in the cat20 and a red fox (Vulpes vulpes)21. The cutaneous lesions include crusting, erythema, exudation, and alopecia periorally and periocularly, around the genitals, and the distal extremities, as well as hyperkeratosis and ulceration of the footpads. The skin disease may precede the onset of the signs of the internal disease. Histopathologic findings include superficial perivascular-to-lichenoid dermatitis, with marked diffuse parakeratotic hyperkeratosis and striking inter- and intracellular edema limited to the upper half of the epidermis (‘red, white and blue sign').22 Diagnosis is usually made by clinical signs, confirmatory histopathology, and an ultra-sound finding of both hyper- and hypo-echoic areas in the liver (‘Swiss-cheese' or ‘honey comb' pattern).
Superficial necrolytic dermatitis resembles the glucagonoma syndrome (necrolytic migratory erythema) of humans, which is usually associated with hyperglucagonemia and a glucagon-secreting alpha-cell neoplasm of the pancreas. Hyperglucagonemia has also been documented in dogs with this syndrome; however, dogs tend to have hepatic parenchymal damage much more commonly than gluconomas. Dogs with SND have profoundly low levels of plasma amino acids.
Therapy is best effected with the infusion of amino acids (ex: Amnosyn®) given intravenously in a central vein, at an approximate rate of 60-80 mg/kg/24 hr. Osmalality and/or neurologic signs should be monitored (although problems are relatively uncommon). This is often performed on a daily basis for 2-3 days, and may need to be repeated on a q 3-6 week basis.
An alternative is the use of oral medications: ProCel® Powder (1 scoop/5kg q12h; Global Health Products www.globalhp.com 1-800-638-2879), scrambled eggs (? /day), elemental Zn (2 mg/kg/ day), and sAME (or similar liver protectants).
When the underlying disease can be treated (drug-induced hepatopathy, removal of glucagonoma) and secondary skin infections (bacterial and/or yeast) are treated, these dogs have usually responded well for variable lengths of time, sometimes for more than one year.
Pansteatitis is caused by the consumption of high levels of unsaturated fatty acids and/or the insufficient intake of vitamin E, leading to inflammation of adipose tissue. This disease usually has been related to fish-based diets. However, non-conventional diets such as pig brains have also been implicated.The disease has also been reported in a lion (Felis leo).
Clinical signs include painful, nodular-to-irregular subcutaneous masses and draining tracts, pain on abdominal palpation (due to involvement of the abdominal fat), inappetence, depression and fever, though not all signs will be present in all cats. Less commonly ascites, pleural effusion, subcutaneous edema may be present. Neutrophilia and leukocytosis are common findings. Grossly, adipose tissue may be yellow or discolored, and firm to hard (dependent on the presence of mineralization). Histological examination shows necrosis of fat cells, severe inflammation of the interstitial tissue with neutrophils, giant cells and macrophages containing acid-fast droplets of ceroid pigment. Treatment has been reported as vitamin E (alpha-tocopherol 50 mg/kg q24 h), prednisolone (1 mg/kg q12 h), and changing the diet to a fish-free, balanced cat food.Pain management is very important! Even with these treatments, 25% or more of these cats will die or be euthanized due to poor response.
Ishida R, Masuda K, Kurata K, Ohno K , et al. Lymphocyte blastogenic responses to inciting food allergens in dogs with food hypersensitivity. J Vet Intern Med 2004;18: 25-30.
Martin A, Sierra MP, Gonzalez JL, et al. Identification of allergens responsible for canine cutaneous adverse food reactions to lamb, beef and cow's milk. Vet Dermatol 2004;15:349-356.
Ohmori K, Masuda K, Maeda S,et al. IgE reactivity to vaccine components in dogs that developed immediate-type allergic reactions after vaccination. Vet Immunol Immunopathol. 2005;104:249-256
Rosser EJ: Diagnosis of food allergy in dogs. J Am Vet Med Assoc 203:259-62, 1993.
Denis S, Paradis M.: L'allergie alimentaire chez le chien et le chat. 2. Étude rétrospective. Med Vét Québec 24:15-20, 1994.
White SD: Food hypersensitivity in the dog: 30 cases. J Am Vet Med Assoc 188:695-8, 1986.
Carlotti DN, Remy I, Prost C: Food allergy in dogs and cats: A review and report of 43 cases. Vet Dermatol 1:55-62, 1990.
Mueller RS, Friend S, Shipstone M, et al. "Diagnosis of canine claw disease - A Prospective Study of 24 Dogs". Vet Dermatol 2000; 11: 133-41.
White SD, Sequoia D: Food hypersensitivity in cats: 14 cases (1982-1987). J Am Vet Med Assoc 194:692-5, 1989.
Rosser EJ: Food allergy in the cat: a prospective study of 13 cats. In: Ihrke PJ, Mason I, White SD, eds. Advances in Veterinary Dermatology Vol 2. Oxford: Pergamon Press, 1993; 33-9.
Paterson S: Food hypersensitivity in 20 dogs with skin and gastrointestinal signs. J Sm Anim Pract 36:529-534, 1995.
Guillford WG, Markwell PJ, Jones BR, et al. Prevalence and causes of food sensitivity in cats with chronic pruritus, vomiting or diarrhea. J Nutrition 1998;128(12 Suppl):2790S-2791S.
Fujimura M, Ohmori K, Masuda K, et al. Oral allergy syndrome induced by tomato in a dog with Japanese cedar (Cryptomeria japonica) pollinosis. J Vet Med Sci 2002;64:1069-70.
Jeffers JG, Meyer EK, Sosis EJ. Responses of dogs with food allergies to single-ingredient dietary provocation. J Am Vet Med Assoc 1996; 209: 608-11.
Harvey RC: Food allergy and dietary intolerance in dogs: a report of 25 cases. J Sm Anim Pract 34:175-179, 1993.
White SD, Bourdeau P, Rosychuk RAW et al. Zinc-responsive dermatosis in dogs: 41 cases and literature review. Vet Dermatol 2001, 12: 101-110.
Stringfield, C. Case Report: Amber Girl. Zoo View 1997; 31 (2): 14-5.
Kearns K, Sleeman J, Frank L, Munson L. Zinc-responsive dermatosis in a red wolf (Canis rufus). J Zoo Wildl Med 2000; 31: 255-258.
Outerbridge CA, Marks SL, Rogers QR. Plasma amino acid concentrations in 36 dogs with histologically confirmed superficial necrolytic dermatitis. Vet Dermatol 2002; 13:177-186.
Kimmel SE, Christiansen W, Byrne KP. Clinicopathological, ultrasonographic, and histopathological findings of superficial necrolytic dermatitis with hepatopathy in a cat. J Am Anim Hosp Assoc. 2003; 39:23-27.
Van Poucke S, Rest JR. Superficial necrolytic dermatitis associated with hepatic lipidosis in a redfox (Vulpes vulpes). Vet Rec 2005;156:54-55.
Gross TL, Song MD, Havel PJ, et al. Superficial necrolytic dermatitis (necrolytic migratory erythema) in dogs. Vet Pathol 1993; 30: 75-81.
Tidholm A, Karlsson I, Wallius B. Feline pansteatitis: a report of five cases. Acta Veterinaria Scandinavica 1996; 37: 213–217.
Koutinas AF, Miller WH, Kritsepi M et al. Pansteatitis (steatitis, ‘yellow fat disease') in the cat: a review article and report of four spontaneous cases. Vet Dermatol 1993;3:101–106.
Summers BA, Sykes G. Pansteatitis mimicking infectious peritonitis in a cat. Journal of the American Veterinary Medical Association 1982;180:546–549.
Niza MM, Vilela CL, Ferreira LM. Feline pansteatitis revisited: hazards of unbalanced home-made diets. J Feline Med Surg 2003;5:271-277.
Bone WJ. Pansteatitis in a lion (Felis leo). J Am Vet Med Assoc 1968;153:791-792