Nutritional Dermatoses

2. Nutritional Dermatoses

Nutritional dermatoses may be specific (identified deficiency of a particular nutrient or group of nutrients) or non-specific: associated with general underfeeding, poor digestibility of the food or a gastrointestinal absorption problem.

Specific Deficiencies

Nowadays, specific nutritional deficiencies are rare. They may, however, be observed in dogs fed with a poor-quality commercial food or an unbalanced homemade food.

Vitamin Deficiencies

Vitamin A

Retinol, a fat soluble vitamin, is essential to the differentiation of epithelial cells. As a consequence, retinol deficiency causes a general keratinization problem, with scaling. In the only case in dogs described in the literature, these problems were associated with visual deficiencies and digestive problems (Scott et al., 2001).

Vitamin E

Vitamin E is a generic term covering two classes of fat soluble molecules: tocopherols (α, β, γ, δ) and tocotrienols (α, β, γ, δ). Each of these eight different forms has a specific biological activity. α-tocopherol is the most widespread form of vitamin E in animal foods and organisms: it is the form with the greatest biological antioxidant activity in the cell membranes (Figure 3).

Figure 3. Tocopherol Isomers.

Deficiencies of vitamin E are rare and usually due to foods whose fats are poorly stabilized (Scott & Sheffey, 1987). Vitamin E is actually a natural antioxidant, being consumed during oxidation. An experimental deficiency in dogs provokes the appearance of dry seborrhea, diffuse alopecia, erythroderma, secondary pyoderma and anomalies of the immune system.

B Vitamins

B vitamins are water soluble and play a role as coenzymes for the cellular enzymes involved in energy metabolism and tissue synthesis. They are provided in food and some are synthesized by gastrointestinal flora. Deficiencies are rare. A correctly formulated commercial food stored in good conditions contains vitamins in sufficient quantities and supplementation is not necessary.

The dermatological manifestations of such deficiencies vary depending on the vitamin:

• Riboflavin deficiency (vitamin B2), sensitivity to light: xerosis localized to the periorbital and abdominal regions.
• Niacin deficiency (nicotinamide or vitamin PP), occurring with food low in animal nutrients: pruriginous dermatitis of the abdomen and hind limbs.
• Biotin deficiency (vitamin B8 or H), mainly described in animals fed with an excess of egg whites, which contain avidin, a molecule that complexes the biotin and prevents its absorption in the intestine: erythema, facial and periorbital alopecia, generalized scaling, leukotrichia, dull and brittle hair.

Trace Element Deficiencies

Trace elements are mineral substances that act at very low concentrations in the organism. The trace elements most directly related to the beauty of the coat are iron, zinc and copper.

Zinc

Deficiencies in zinc intake are typically caused by foods high in phytates, which chelate zinc. These are most often foods of poor quality that are high in whole meal cereal containing a lot of bran. This intake deficiency is also observed with foods oversupplemented with calcium or in breeds with an inability to absorb zinc. Zinc is a cofactor in a very large number of metabolic pathways, and a deficiency provokes immunity problems and keratinization with scaly, crusty periorificial thickening observed in the skin. The differential diagnosis is not always easy. Therefore it is important to confirm the clinical diagnosis in a histopathological biopsy. Zinc deficiency is characterized by major parakeratosis in the epidermis and the follicles.

In contrast to other types of dermatopathies related to metabolic disorders of zinc (Table 5), a simple deficiency can be controlled by rebalancing the diet and controlling secondary infection. In previous classifications, this deficiency is termed generic dog food disease or type-2 zinc responsive dermatitis (common in large-breed dogs) (Figure 4).

Figure 4. Hyperkeratosis of the elbow in a Fox Terrier due to zinc deficiency. (© P. Prélaud).

Copper

Copper is a component of many carrier enzymes or proteins. A deficiency is observed mainly in puppies fed a homemade food without supplementation or with excessive zinc, calcium or iron content. The deficiency leads to changes in the coat with discoloration beginning in the face, and a thin coat with dull and brittle hairs (Figure 5) (Zentek & Meyer 1991).

Figure 5. Leukotrichia (pilary depigmentation) in a Scottish Terrier puppy due to malnutrition. (© P. Prélaud).

Iodine

While an iodine deficiency could theoretically disturb the synthesis of thyroid hormones, these phenomena are unusual in dogs and generally without clinical consequence. The daily iodine requirement of a beagle is in the order of 140 µg. A reduction in total thyroxin is only observed when concentrations are under 20 - 50 µg/day, there is no however, in free thyroxin and no signs of a hypothyroidism (Feldman & Nelson, 2004).

The quantity of trace elements provided in the food does not correspond to the quantity actually available to the organism. The level of absorption depends on the chemical form in which they are provided and their dietary environment. There are interactions between the different elements. So calcium absorption competes with the absorption of zinc, copper and iodine. The percentage of trace element absorption is often under 30%.

When the trace elements are provided in the organic form chelated with amino acids their absorption is clearly improved. Therefore they are better utilized by the organism. For example, in the presence of an excess of calcium in the ration, which inhibits zincabsorption, loss of zinc in the feces increases. Conversely with the chelated form, assimilation is not affected (Figure 6) (Lowe & Wiseman, 1998).

Figure 6. Influence of the form of zinc intake on hair growth. (From Lowe et al., 1998).

A chelated trace element is made up of a metallic ion linked to three amino acids. This element weighs less than 1500 Daltons. Normal trace element absorption efficiency varies from 5% to 30%. When trace elements are chelated, the absorption efficiency can be in excess of 60%.

Essential Fatty Acid Deficiency

Essential fatty acids are so termed because they are not synthesized by the organism. As is the case with most vitamins they must be provided by the food. They are primarily the precursors of two families of PUFA, omega 6 fatty acids and omega 3 fatty acids.

• Linoleic acid, a precursor of fatty acids of the omega 6 family, is abundant in most vegetable oils. It represents more than 70% of the fatty acids in evening primrose oil and more than 50% in sunflower oil, wheat, corn and soy.
• Alpha linolenic acid, a precursor of fatty acids of the omega 3 family, is found in green vegetables, fruits, grasses and plankton, and is found in concentrated form in the oil of plants like soy and flax. The oils of fish from cold waters contain very high levels of two long-chain fatty acids derived from alpha linolenic acid: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These two fatty acids participate in the fluidity of the cell membranes.

PUFA fulfill four main functions:

• Incorporation in the structure of the cell membrane, which gives it its flexibility and permeability
• Production of eicosanoids (leukotrienes, prostaglandins)
• Maintenance of the skin barrier permeability (especially omega 6)
• Cholesterol metabolism and transport

PUFA deficiencies are observed only in animals suffering from malassimilation or animals fed with poor-quality diets or diets that have been overheated for a lengthy period. The cutaneous signs include xerosis, dull hair and a keratoseborrheic disorder. The response to PUFA supplementation is rapid.

Overall Protein Deficiency

Low-quality or overcooked food will undergo modification due to Maillard reactions and the digestibility will be reduced. Hair growth and the regeneration of the skin mobilizes almost 30% of protein intake and such protein deficiency leads to keratinization problems and diffuse alopecia with dull, brittle hair. Protein deficiencies are also observed in dogs presented with a chronic debilitating disease or bitches at the end of gestation or in lactation, if the dietary intake is not adapted.

The low digestibility of proteins may favor the development of dietary hypersensitivity (Cave & Marks, 2004).

Specific Amino Acid Deficiencies

Aromatic Amino Acids: Tyrosine, Tryptophan

These amino acids are essential to the synthesis of the melanins responsible for hair pigmentation: pheomelanin (red, brown) and eumelanin (black). A dietary deficiency leads to a lightening of the coat or the red dening of black hairs (see above).

Sulfated Amino Acids: Methionine, Cystine

Methionine and cystine are essential to the growth of hair, as they participate in the production of keratin (Figure 7). These amino acids are abundant in animal proteins and are rarely deficient in dog food, with the exception of non-supplemented vegetarian diets.

Figure 7. Structure of a keratin molecule. (From Credille, 2002).

Dogs are however less sensitive than cats to such deficiencies.

Metabolic Diseases

Migratory Necrolytic Erythema

Migratory necrolytic erythema (or superficial necrolytic dermatitis, hepatocutaneous syndrome) is a serious dermatosis due to a severe amino acid deficiency. It originates from chronic liver dysfunction (tumor, cirrhosis, functional failure induced by the administration of phenobarbital (March et al., 2004)) or less commonly from a pancreatic tumor (glucagonoma). It is most often a deficiency of amino acids, essential fatty acids and zinc (Campbell & Lichtensteiger, 2000; Scott et al., 2001; Outerbridge et al., 2002; Turek, 2003).

There is no breed or sex predisposition. The patients are usually old. Dermatological lesions are mucocutaneous and pedal in distribution, and are characterized by erythema associated with major, painful hyperkeratosis (Figure 8a - Fig. 8d). The diagnosis is based on skin biopsies and the identification of the cause of the deficiency (prolonged Phenobarbital intake, biochemical imbalance, liver and pancreatic ultrasound, biopsies). If the cause cannot be treated, the prognosis is poor.

Figure 8a. Hyperkeratosic, ulcerated foot lesions. (© P. Prélaud).  

Figure 8b. Ulcerated, crusty periorificial lesions. (© P. Prélaud).

Figure 8c. Close-up of the lesions in Figure 8b: wide ulcers on the face and firmly attached scabs. (© P. Prélaud).

Figure 8d. Perianal erosions. (© P. Prélaud).

However, with appropriate nutrition intervention the condition of these animals can be quickly improved, and in some cases recovery or a very long remission is possible. Treatment involves intravenous infusion of amino acid solutions (Table 6) or administration of egg yolks and supplementation of essential fatty acids and zinc, at the same dosages as for zinc responsive dermatosis (Table 7).

Zinc gluconate is preferable to zinc methionine complex, as it is less hepatotoxic. These nutritional measures are associated with a discontinuation of antiepileptics, antibiotic therapy and administration of analgesics (opioids), especially when the foot lesions affect locomotion.

Lethal Acrodermatitis in the Bull Terrier

Lethal acrodermatitis in the Bull Terrier is a rare autosomal recessive genetic dermatosis. It is probably a disorder of zinc metabolism, rather than a problem with zinc absorption. The animals present in poor general condition from a very early age (two weeks), with erythematous and keratoseborrheic lesions in the extremities of the limbs (Figure 9) and the face. The digits are thicker. There are serious systemic symptoms including bronchopneumonia, bone deformation, cataracts, and gastroenteritis. This disease is accompanied by a severe immune deficiency and is fatal in all cases.

The diagnosis is based on anamnestic data and histopathological confirmation. The supplementation of zinc is ineffective.

Figure 9. Erythema, scaling and ulcers on the extremities of a Bull Terrier puppy suffering from lethal acrodermatitis. (© E. Bensignor).

Zinc Responsive Dermatosis

Type 1 Zinc responsive dermatosis is not a metabolic disease as such, but results from an abnormality in the intestinal absorption of zinc. It is mainly observed in Nordic breeds of dogs, but many other canine breeds can be affected, including Beaucerons, German Shepherd dogs, Boston Terriers, Bull Terriers and Great Danes.

The initial lesions are localized to the periorificial zones and the digits: erythema, scaling, which progress to firmly attached crusts (Figure 10a, Figure 10a & Figure 11). Pruritus is present in the case of secondary infection. A febrile syndrome is sometimes associated with the condition. The diagnosis must be confirmed by histopathological examination of a biopsy. The differential diagnosis is sometimes difficult. It includes leishmaniasis in endemic areas, scabies, pemphigus foliaceous or dermatophysis (White et al., 2001).

Figure 10a. Hyperkeratosis of the pads of a Siberian Husky presenting with zinc responsive dermatosis; note the cracking on one of the pads. (© P. Prélaud).

Figure 10b. Periocular Hyperkeratosis (firmly attached crusty scaling) on a Siberian Husky presented with zinc responsive dermatosis. (© P. Prélaud).

Figure 11a. Crusty scaling in a Fox Terrier presented with generic dog food disease. (© P. Prélaud).

Figure 11b. Crusty perioral scabs in a Basset Hound fed with a generic food (generic dog food disease). (© P. Prélaud).

Figure 11c. Localized scrotal hyperkeratosis of zinc responsive dermatosis. (© P. Prélaud).

Figure 11d. Zinc responsive dermatosis: Skin biopsy of crusty squama lesions (X 400, HE); note the major parakeratotic hyperkeratosis (persistence of knots in the corneocytes). (© P. Prélaud).

Zinc supplementation is generally sufficient and a clinical improvement follows in less than a month. In case of failure, the administration of low-dose glucocorticoid therapy for three weeks will achieve a rapid improvement in the clinical signs (e.g., oral administration of prednisolone at 0.1 - 0.2 mg/kg/day for three weeks). The treatment is usually lifelong (White et al., 2001).

The various types of dermatitis due to zinc deficiency (food high in phytates or calcium and low in essential fatty acids) have several features in common including an identical histological appearance, hyperkeratosis of the mucocutaneous junctions and the pads. Treatment is based on balancing the diet and administering zinc for three to four weeks (Table 7).

Dietary Hypersensitivities

The term dietary hypersensitivity covers all the dermatoses caused by the ingestion of a food that provokes a harmful reaction in a healthy individual. These hypersensitivities, also termed intolerances, can be of non-immunological or immunological origin (Johanson et al., 2001). An immunological hypersensitivity is a dietary allergy. The clinical manifestations are highly diverse and include gastrointestinal, respiratory, cutaneous, renal or generalized involvement (Figure 12).

Figure 12. Classification of hypersensitivity reactions defined by the European Academy of Allergy and Clinical Immunology (EAACI).  

Etiology

Non-immunological Hypersensitivity

The non-allergic reactions are highly diverse. Some foods may cause urticaria or aggravate an atopic dermatitis if they are high in:

• Histamine: tomatoes, spinach, beef, pig liver, fresh crustacea, tuna, dry sausage, cheese
• Histamine liberator compounds: chocolate, strawberries, fish, pork, ovomucoid
• Tryptamine: chocolate, cooked cheese (Prélaud, 1999).

Gastrointestinal Allergies

The development of an allergic reaction depends on the nature of the dietary antigens, their presentation to the digestive immune system and genetic factors.

Break in Immune Tolerance

The immune response to ingested antigens is generally an immune tolerance reaction. The immune reaction is inhibited when the antigens are present in low concentrations.

When the antigen concentration is high, anergy or even deletion phenomena may occur (Chehade & Mayer, 2005). This immune tolerance is an active phenomenon that depends on several factors related to the individual and the antigen (Table 8).

A hypersensitivity reaction may be triggered by the following factors: augmentation of intestinal permeability, chronic digestive problems, high insoluble antigen content, and individual predisposition to hypersensitivity reactions.

Dietary Allergens

The foods most often implicated in the studies on dietary hypersensitivity in dogs are meat (beef, chicken, lamb), eggs, dairy products and soy, but any dietary protein is potentially allergenic. The very nature of the allergens implicated in these allergies is well known in human medicine, where the major allergens and their structural particularities have not been defined in the dog (Breiteneder & Mills, 2005).

When it comes to dogs, our knowledge is very limited. The overwhelming majority of allergens identified in dogs are proteins of large molecular weight - 40 - 70 kD. The main allergens of beef and cow's mild for dogs may be heavy chains of immunoglobulin G (Martin et al., 2004). There were however crossed sensitivities between cow's milk and beef in dogs. The allergy to casein in cow's milk has also been demonstrated in the animal models presenting spontaneous dietary allergies (Jackson & Hammerberg, 2002). Lastly, some muscle enzymes common to many species of mammal could explain the crossed reactions between lamb's meat and beef in dogs. This is the case for phosphoglucomutases (Martin et al., 2004).

In contrast to humans, there are no cross reactions between pollens and food (with the exception of the cross reaction between tomato and the Cryptomeria japonicum pollen) (Fujimura et al., 2002).

Predisposing Factors

All the factors contributing to immune tolerance can favor the development of dietary hypersensitivity.

Maldigestion

The great majority of dietary proteins, which are allergens or potential allergens, are broken down by the gastric and intestinal enzymes, although only amino acids or small peptides are normally assimilated by the mucosa of the small intestine. If digestion is defective, the quantity of antigens in the digestive immune system and their molecular weight is much greater, which is conducive to the break in tolerance. This explains why a chronic intestinal inflammatory disease or exocrine pancreatic failure is conducive to the development of dietary hypersensitivity.

Intestinal Permeability Problems

An increase in intestinal permeability, by greatly increasing the quantity of allergens presented to the immune system, can break the condition of tolerance and induce deleterious immunological reactions. The inflammatory reaction increases the intestinal permeability and a vicious circle of maintenance of the phenomenon is maintained.

Vaccinations

Vaccinations provoke an increase in the synthesis of IgE in dogs (Hogen-Esch et al., 2002). This increase of IgE synthesis to dietary allergens in the experimental models of dietary allergy is however not accompanied by the appearance of symptoms.

Atopy

By definition, an atopic condition predisposes the animal to the development of allergic reactions, be they aeroallergens or dietary allergens (Prélaud & Olivry, 1998).

Symptoms

The skin symptoms of dietary hypersensitivity are highly variable and sometimes rather vague. The clinical presentation may be that of atopic dermatitis, general or local pruritus, or major acute (skin rash, urticaria) or chronic keratinization problems (Figure 13a - Figure 13c).

Figure 13a. Urticaria visible only after clipping in a Yorkshire Terrier. (© P. Prélaud).

Figure 13b. Chronic urticaria on the abdomen of a dog presented for dietary hypersensitivity. (© P. Prélaud).

Figure 13c. Facial angioedema due to a vaccine allergy in a French Bulldog puppy. (© P. Prélaud).

Urticaria and Angioedema

The most common causes of urticaria in dogs are allergies to medication (vaccines, anti-inflammatory drugs, anti-infection drugs including antibiotics, anti-viral, anti-fungal agents, allergens, etc) or reactions to anthropod bites (Table 9). A dietary cause is less commonly identified. In this case, it may be due to an immunological phenomenon (immediate allergic reaction), the ingestion of a food that is high in vasoactive amines or anaphylactiod reactions (mastocyte degranulation without IgE intervention).

The allergic reactions to vaccines have some things in common with dietary allergies, in that, in the majority of cases, the allergy is due to residues of calf fetal serum in cell cultures (IgG bovines) or to protein additives (casein, gelatins) (Ohmori et al., 2005). As a consequence, it is possible that these vaccine reactions are due to dietary sensitivities to these same proteins, as some vaccinal allergic reactions are observed during initial vaccination, so theoretically without prior sensitivity to the vaccine.

Atopic Dermatitis and Atopic-like Dermatitis

Atopic dermatitis is a chronic pruriginous dermatitis of the face and the extremities, characterized by a genetic predisposition to developing hypersensitive reactions to environmental allergens. The allergy to aeroallergens is not however demonstrated in 20 - 25% of referred or university atopic dermatitis cases.

This phenomenon, which is also described in humans, has led the European Academy of Allergy and Clinical Immunology (EAACI) to propose the term atopic dermatitis syndrome, covering all cases of atopic dermatitis of whatever cause, with or without a demonstrated allergy.

In canine medicine, the term atopic-like dermatitis was recently proposed by the International Task Force on Canine Atopic Dermatitis (ITFCAD) to designate cases of atopic dermatitis without a demonstrable allergy. All these variations of definition are the origin of confusion and controversy. If the results of allergological explorations are taken into account, as they are in human medicine, it is impossible to differentiate an atopic dermatitis due to aeroallergens from an atopic dermatitis due to dietary allergens (Hillier & Griffin, 2001; Jackson et al., 2005) (Figure 14a - Figure 16).

Figure 14a. Periocular erythema and alopecia in an atopic dog presented with dietary hypersensitivity. (© P. Prélaud).

Figure 14b. Erythema of the surfaces of the concha auriculae showing the existence of otitis externa in an atopic Labrador. (© P. Prélaud).  

Figure 14c. Perioral erythema in an atopic dog. (© P. Prélaud).  

Figure 14d. Interdigital erythema in an atopic dog. (© P. Prélaud).  

Figure 15a. Abdominal and stifle fold erythema in an atopic Fox Terrier (classic form of atopic dermatitis). (© P. Prélaud).  

Figure 15b. Erythema, papules and excoriations in the groins of a French Bulldog presented with a classic form of atopic dermatitis. (© P. Prélaud).  

Figure 15c. Severe form of atopic dermatitis in a Cairn Terrier: major lichenification, and abdominal and inguinal hyperpigmentation. (© P. Prélaud).  

Figure 15d. Severe form of atopic dermatitis, with widespread alopecia, erythema and lichenification lesions in a Poodle (complication of Malassezia dermatitis). (© P. Prélaud).  

Figure 16a. Chronic recurring otitis externa in an atopic Poodle. (© P. Prélaud).  

Figure 16b. Perinipple lichenification, a minor form of atopic dermatitis in a French Bulldog. (© P. Prélaud).  

As a consequence, its diagnosis may be based on criteria tied to anamnesis and clinical signs comparables to those proposed in human medicine (Prélaud et al., 1998) (Table 10).

In approximately 30% of atopic animals, the condition is significantly improved by an elimination diet. This suggests that dietary hypersensitivities could be considered as major factors in the etiology of canine atopic dermatitis (Chesney, 2001 & 2002). As a consequence, when confronted with all the symptoms of canine atopic dermatitis, it is necessary to envisage the existence of dietary hypersensitivity in patients with the following clinical signs (Prélaud, 2004):

• Bilateral otitis externa
• Bilateral cheilitis
• Bilateral pododermatitis
• Local or widespread Malassezia dermatitis
• Erythematous or lichenified dermatitis of the large folds
• Hyperhidrosis

Regardless of whether the clinical form is benign, classic or severe (Table 11), a hypoallergenic and highly digestible elimination diet is mandatory.

Local or General Pruritus

Dietary hypersensitivity may also manifest itself in the form of local pruritus, which is most often bilateral. The lesions generally consist of erythema associated with a self-induced alopecia (Figure 17a and Figure 17b).

Figure 17a. Local pruritus in the extremity of limbs leading to alopecia and erythema in a Collie presented with dietary hypersensitivity. (© P. Prélaud).  

Figure 17b. Same dog as in Figure 17a after a month-long elimination diet. (© P. Prélaud).  

Pyotraumatic Dermatitis (Hot Spots)

Dietary hypersensitivity is one of the causes of recurring pyotraumatic dermatitis. This diagnostic hypothesis must however be envisaged after the infection has been controlled (Figure 18) and the most common hypotheses such as demodetic mange (especially in Labrador Retrievers and Rottweilers), flea allergy dermatitis (FAD) and lack of hygiene in dogs with a dense undercoat have been eliminated.

Figure 18. Pyotraumatic furonculo-sis in a Retriever; note the papules and furuncles around the hot spot, which are visible only after clipping. (© P. Prélaud).  

Recurring Superficial Pyoderma

Atopy and less often food allergy is the most common underlying cause of recurrent superficial pyoderma. No specific breed or age group is predisposed. Generally, the lesions (papules, pustules, crusts, epidermal collarettes) are first observed in the regions of predilection: abdomen and inguinal region (Figure 19a & Figure 19b). They can spread all over the body. The response to antibiotic therapy is always good, but recurrence will be rapid after the antibiotic therapy has been stopped.

Figure 19a. Papular lesions of recurring superficial pyoderma in a German Shepherd. (© P. Prélaud).  

Figure 19b. Papular lesions of superficial pyoderma in an atopic French Bulldog. (© P. Prélaud).  

The diagnosis is based on identifying the lesions and conducting a cytological test to find neutrophilic leukocytes with some evidence of cocci phagocytosis. The differential diagnosis is that of all recurring superficial pyoderma and comprises at least the exclusion of an ectoparasitic or another allergic dermatitis (FAD, atopic dermatitis). Once all the causes of recurrence have been ruled out (Table 12), an elimination diet must be initiated.

Diagnosis

The diagnosis of dietary hypersensitivity is based on the elimination of other causes of pruritus (especially infections and parasites) and the beginning of an elimination diet.

It is tempting to measure specific dietary allergen IgE dosages to identify a dietary allergy or to eliminate some foods from the diet. At this time, such an approach is totally unjustified. The few studies that have been published show that allergy tests lack reliability in this capacity (Jeffers et al., 1991; Kunkle & Horner, 1992; Hillier, 1994; Ermel et al., 1997; Mueller & Tsohalis, 1998; Jackson & Hammerberg, 2002; Foster et al., 2003; Jackson et al., 2003; Wilhelm & Favrot, 2005).

This approach is justified only in the case of an immediate pure allergy, as in human medicine. In humans, the positive result of measurement of specific IgE for peanuts, eggs or cow's milk is an excellent predictor in a patient presented with anaphylactic reactions. For the evaluation of atopic dermatitis, the value of these tests is as poor as it is in canine medicine (Sampson, 2004).

Practicalities of Elimination Diets

The principle of an elimination diet is based on the administration of a diet containing proteins that the animal has never previously ingested. It is vital that an elimination diet be rigorously followed. The compliance with such a diet is its main limitation.

Monitoring of Dietary Habits

An elimination diet must be prescribed only after a highly detailed investigation and with the clear consent of the owner. The diet preparation phase conditions the subsequent implementation.

It is not easy to keep a log of the food ingested by the dog, because the dietary sources are highly varied. The questionnaire during the consultation should focus on describing the food itself and identifying all the extras and potential hidden sources of food consumption. If necessary, the owner must be asked to keep a log of all the food consumed over a two-week period. The diet supplements and medication that may contain protein palatability factors (e.g., liver) must also be taken into account.

Choice of Food

Protein Sources

The ideal is to use sources of proteins and carbohydrates that the dog has never previously ingested. That is why venison, duck, rabbit and white fish are the most often used ingredients (tuna, which is high in histamine, should be avoided). Protein hydrolysates with a low molecular weight to ensure low immunogenicity and high digestibility can be used whatever the source. (The available hydrolysates are generally extracted from poultry or soy proteins.)

Homemade Preparations

Homemade preparations must be based on a limited number of sources of protein and carbohydrate (Table 13). The significance of homemade preparations is connected with the control of raw ingredients. Dogs that are used to preparations of this type often find them more palatable than dry commercial foods.

The use of homemade diets is limited by the practicability of such a preparation, especially for large dogs. They are increasingly rare for companion dogs because even for a period of one or two months the preparation of the homemade diet can prove very difficult.

The imbalance of these diets can be easily compensated if the diet has to be followed for more than two months or if the dog is a puppy. However, the supplementary constraints imposed on owners may become limiting factors in the good observance of the diet (Tables 14-15).

Commercial Foods

There are a great number of commercial foods labeled "hypoallergenic" or "for allergic dermatitis". Three categories can be distinguished.
- Foods with proteins that mostly come from selected sources: they cannot be considered acceptable for an elimination diet as the protein sources are highly diverse.
- Foods with proteins that exclusively come from selected sources: these are more acceptable. This is the only category that has been subjected to controlled studies and the results are sometimes disappointing (Vroom, 1994; Leistra et al., 2001; Leistra & Willemse, 2002).
- Foods formulated on the basis of protein hydrolysates are in principle less allergenic than non-hydrolyzed preparations. The purpose of the hydrolysate is to fractionate the proteins into small peptides of low molecular weight. So in practice these hydrolysate-based diets are the most suited to a commercial elimination diet (Biourge et al., 2004; Loeffler et al., 2004).

Hydrolysis reduces the molecular weight and intrinsic antigenicity of the food, and also renders it more digestible. These two properties act in synergy to offer less stimulation of the gastrointestinal immune system.

The major advantage of hypoallergenic commercial foods is their ease of use. This however, does not mean that the owner should neglect the constraints of such a diet. The prescription of a commercial diet goes hand in hand with a warning against the possibilities of food consumption over and above the base diet.

The use of protein hydrolysates raises many questions in both human and veterinary medicine. Only the studies of cohorts in human medicine come close to answering any of them.

• Is a highly hydrolyzed food more effective than a traditionally hydrolyzed food? This has not been shown in either veterinary or human medicine (Osborne & Sinn, 2003).
• Is a hydrolysate more effective than a homemade diet for dogs? There are no studies that demonstrate an advantage for any one type of food.
• Is it worthwhile using a hydrolyzed food on a patient at risk after the appearance of symptoms? This has been shown only in infants when they cannot be breastfed (Osborne & Sinn, 2003).

Concomitant Treatments

Antibacterial and systemic steroid therapy may be required when an elimination diet is initiated. The prescription of flavored medication must be avoided. If the medication must be administered by mouth with a food, any potential source of protein must be avoided, such as butter, cheese, ice cream, and meat. Honey is preferred.

The effectiveness of the diet is interpreted six weeks after the end of the course of medication.

Special Cases

Multi-pet Households
If more than one animal lives in the household, access to the other animals' bowls must be avoided or all animals must be given the elimination diet.

Puppies
Balancing a homemade ration for a growing animal requires special consideration (see the examples for homemade rations at the end).

If a puppy has to follow an elimination diet it is important to ensure that the diet is properly formulated for the special needs of growth. (© Hermeline/Doxicat).

Aging Dogs
In older dogs, the fairly short length of the elimination diet should not pose any problems in the case of a commercial food or a balanced homemade ration (see the examples for homemade rations at the end). On the other hand, the use of standard foods may be problematical: for example, meat as lean as venison may lead to weight loss. It is also important not to abruptly change the dog's habits.

Difficult Dogs
For difficult dogs, two or three days may be needed to obtain normal consumption of the food. While feeding should begin with a palatable supplement, after four weeks a supplement of a different nature must be selected and used for the following four weeks (e.g., beef gravy, then fish).

Associated Diseases
In cases with an associated disease, it is preferable to use a hydrolysate-based commercial food and to closely monitor the concurrent disease (e.g., serum fructosamine concentrations after 15 days of the diet in a diabetic dog).

Monitoring the Diet

Compliance with the diet can be difficult, and information and motivational visits are often necessary. Every member of the family must be informed of forbidden foods that could affect the interpretation of the trial (Table 15).

Regular appointments are needed to monitor compliance with the diet. This will allow the potential secondary effects of the elimination diet to be identified, which are refusal to eat or digestive problems. A two-day fast is tolerated. In the case of failure, a new diet must be initiated. To limit the appearance of digestive problems, a period of gradual dietary transition from the previous diet of at least four days is recommended.

Depending on the food, weight gain or weight loss may ensue. Owners must be informed so that they can monitor the dog's weight and body condition score and adjust the quantities given when necessary.

Length of the Diet

There is consensus on the duration of 6 - 8 weeks to 10 - 12 weeks at most. Continuing the diet after this period will be useless if no improvement has been observed.

Interpretation of the Results

The appreciation of clinical improvement is simple when it is spectacular, but more difficult when it is partial. Photographs and lesional scores (simplified CADESI: Table 16) or pruritus scores (Table 17) may prove highly useful.

More is needed if the food is to be identified as the cause of the genesis of pruritic dermatitis than the observation of a significant improvement. A certain number of dogs do not have any recurrence when they ingest the initial food again. As a consequence, a provocative test must be conducted in order to correctly interpret the effects of an elimination diet.

Provocation

There are two options: either the previous diet is given or a new protein source is introduced every one or two weeks. The latter option will identify the foods responsible for the hypersensitivity.