Diet plays a major role in the maintenance of a healthy coat and skin in dogs and cats. Deficiencies in certain components of the diet such as zinc, vitamin A and polyunsaturated fatty acids (PUFAs) can cause skin disease.
Zinc deficiency
Acquired nutritional deficiencies due to poorly prepared or unbalanced diets are rare in modern times due to the high quality and regulation of commercial foods in developed countries (Miller, 1989; Watson, 1998). Zinc deficiency is a rare condition but it can be seen in young, rapidly growing, large breed dogs fed diets either deficient in zinc or with high levels of plant phytates or calcium and/or fed cereal or soya based diets. The phytates or calcium in the diet competes with zinc for absorption from the bowel, leading to a relative deficiency. Dogs typically present with crusting lesions at the mucocutaneous junctions, pressure points and trunk (Figure 1). Lesions resolve once a more balanced diet is fed (Sousa et al, 1988; Roudebush and Wedekind, 2002).

Another syndrome of zinc deficiency is also seen in young Nordic breeds of dog especially the Siberian husky, Alaskan malamute and Samoyed. These dogs present with zinc deficiency despite the fact they are fed a balanced diet, because they seem to have a congenital inability to absorb zinc from their diets. They present in a similar way to other dogs with acquired zinc deficiency. These dogs respond well to supplementation with zinc but need supplementation for life (Colombini and Dunstan, 1997; White et al, 2001; Roudebush and Wedekind, 2002).
Vitamin A deficiency
Vitamin A is important to maintain healthy skin and epithelial cells. Deficiency is rare because it is readily available in most commercial diets in the form of animal proteins such as liver and fish. Deficiency leads to a poor hair coat with scaling and alopecia (Lewis, 1981; Miller et al, 2013). Vitamin A can also be used to treat some of the keratinization disorders such as idiopathic seborrhea, ichthyosis and sebaceous adenitis (Figure 2).

PUFA deficiency
PUFAs are essential for the production of normal skin. There are two distinct PUFA families, n-6 and n-3 (also known as omega-6 and omega-3) (Table 1). Linoleic acid (LA), gamma-linolenic acid (GLA) and arachidonic acid (AA) are n-6 PUFAs. LA is found in soya and sunflower oil; GLA is found in evening primrose oil and borage oil; AA is found in dairy products and fish. Alpha-linolenic acid (LNA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are n-3 PUFAs. The most important of the n-3 PUFAs EPA and DHA, are found in cold marine fish oils.
PUFA family | Most important n-6 or n-3 | Major nutritional source |
---|---|---|
Omega 6 (n-6) | Linoleic acid | Soya, sunflower oil |
Gamma linolenic acid | Evening primrose oil, borage oil | |
Arachidonic acid | Dairy products, fish | |
Omega 3 (n-3) | Alpha linolenic acid | Cold marine fish oils |
Eicosapentaenoic acid | ||
Docosahexaenoic |
Fatty acid deficiency must be present for several months before changes in the skin and coat are seen (Hansen and Weise, 1943, Lewis, 1981, Miller et al, 2013). Dogs develop fine scaling, loss of hair lustre often with alopecia and skin infection. Commercial food that has been poorly stored or stored for long periods; homemade rations or poorly formulated low calorie diet can be deficient in PUFAs (Lewis, 1981).
Fatty acid deficiency can also occur in dogs with intestinal malabsorption, pancreatic disease or chronic hepatic disease where the disease process leads to a reduced utilisation of fatty acids (Miller et al, 2013). Supplementation with oils especially those rich in LA, GLA and EPA have been shown to improve the quality of dog's skins and can be used in the management of scaling disorders in dogs (Campbell and Dorn, 1992; Campbell et al, 1995). PUFAs have also been shown to be beneficial in dogs with allergy (Gueck et al, 2004; Abba et al, 2005; Noli et al, 2007).
Cutaneous adverse food reaction
Food ‘allergy’ now more commonly referred to as cutaneous adverse food reaction (CAFR) has been described in both the dog and cat (White, 1986; White, 1988; Rosser, 1993; Wills and Harvey, 1994; Paterson, 1995; Kennis, 2006; Verlinden et al, 2006, Gaschen and Merchant, 2011). Most cases of CAFR occur in young animals. Non-seasonal pruritus is a consistent finding (Rosser, 1993, Verlinden et al, 2006; Gaschen and Merchant, 2011) and is often poorly responsive to steroids (Verlinden et al., 2006). The cutaneous signs of CAFR overlap with other allergic skin problems. Dog and cats will commonly traumatise their faces, pinnae and ventral skin (Rosser, 1993) (Figure 3). CAFR is diagnosed by a resolution of clinical signs when an appropriate restricted/novel diet is fed and relapse of signs once the animal is challenged with the original diet. Identifying a truly novel protein diet can be difficult for each animal. Many different commercial and veterinary novel protein diets are available. They contain proteins such as duck, venison, pork, fish and soya. However there is always a risk that a novel protein may cross react with a protein in the dog or cat's current diet or that the protein is not novel to that animal. The advent of the hydrolysed diet over the last 10 years has led to the institution of more effective diet trials as investigation of CAFR (Loeffler et al, 2004; Cave, 2006; Loeffler et al, 2006; Olivry and Bizikova, 2010). The proteins in these diets are treated with water and enzymes to reduce them to sub allergenic sizes so that theoretically they cannot trigger an allergic reaction. There are numerous excellent hydrolysed diets available to help in the diagnosis of CAFR (Bizikova and Olivry, 2016).

Other diagnostic tests such as intradermal skin testing (Jeffers et al, 1991; Kunkle and Horner, 1992), skin patch testing (Bethlehem et al, 2012), and measuring circulating food allergen–specific serum IgE (Jeffers et al, 1991; Hardy et al, 2014) are of no diagnostic value because of their low sensitivity and specificity.
Immunological reactions to food can mimic almost any other skin disease and there are reports in the literature of food triggering a wide range of diseases including vasculitis (Morris and Beale, 1999, Nichols et al, 2001) and erythema multiforme (Itoh et al, 2006).
Contaminated food
Food that is stored poorly can become contaminated with fungi or bacteria. The most important of these are the aflatoxins that are produced by certain molds (Aspergillus flavus and Aspergillus parasiticus). These grow in soil, decaying vegetation, hay and grains. When food contaminated with aflatoxin is ingested it causes primary liver disease but can also produce skin lesions. One report describes clinical signs in 60 out of 65 dogs caused by eating contaminated maize. All 60 dogs died but initially presented with anorexia, jaundice, haematemesis, and melena, and bleeding of the skin, eye, ear, and mouth (Wouters et al, 2013).
Conclusion
Nutrition plays an integral part in the formation and maintenance of normal skin. The principal deficiencies that are recognised in dogs and cats are to zinc, vitamin A and PUFAs. These deficiencies with the exception of zinc-related disease in Nordic breeds are rare. Adverse reactions to food may be immunological or toxic in nature. CAFR are the most common immunological disease described in dogs and cats; most animals present with non-seasonal pruritus. The best way to investigate CAFRs is by feeding a hypoallergenic diet. This can be achieved by using a novel protein diet or ideally by using a hydrolysed diet. A toxic often life-threatening reaction can be seen to food contaminated with bacteria or fungi.