Nutritional influences in dermatological disorders

Scaling skin, alopecia, and skin infections may be the first indication of critical dietary deficiencies

A) Moderate erythema, hypotrichosis, edema, scale, and pruritus of the axilla of a dog with food allergy 72 hours after eating chicken. B) Moderate erythema, hypotrichosis, pruritus, and edema of the ventral neck in the same dog. Photos courtesy Amelia White
Figure 1: A) Moderate erythema, hypotrichosis, edema, scale, and pruritus of the axilla of a dog with food allergy 72 hours after eating chicken. B) Moderate erythema, hypotrichosis, pruritus, and edema of the ventral neck in the same dog.
Photos courtesy Amelia White

The old adage, “You are what you eat” cannot be more true when it comes to the skin. The skin is an important immune organ with functions including a barrier against foreign antigens, immunoregulation, vitamin D production, thermoregulation, nutrient storage, sensory perception, reproduction, and antimicrobial action.

Unbalanced diets cause rapid dysregulation in normal skin health and function. Some systemic diseases prevent absorption of essential nutrients from reputable diets or trigger aberrant immune reactions to normal dietary ingredients. Below are some of the important ways nutrition plays a role in dermatological diseases.

Nutrition and skin function

There are many nutritional requirements to maintain healthy skin and coat. This includes the appropriate balance of dietary-acquired proteins, fatty acids, minerals, and vitamins. Probiotics play a role in regulating skin inflammation. Structures in the skin relying on nutrition include keratin, hair, skin, desmosomes, lipid bilayer, sebum, sweat, nervous tissue, collagen, elastin, proteoglycans, and glycosoaminoglycans.

Protein

Hair is about 95 percent protein and has many sulfur-containing amino acids.1 Skin and hair growth requires 25-30 percent of the daily protein requirement and even more in young, growing dogs.1 The skin is frequently repairing wounds from trauma incurred during normal daily activity. Imbalances in nutrition or relative nutritional deficiencies can lead to delayed wound healing.

Collagen is one of the major components of the dermis, and gives structure and support to the skin. Collagen synthesis is dependent on arginine, glutamine, and cysteine.1 Hair color also is an indicator of a nutritional deficiency, particularly when darker hair coats lighten or lose color intensity. The composition of aromatic amino acids such as phenylalanine, tryptophan, and tyrosine all affect normal hair color.1

Food allergies

Figure 2: A) Ulcerated eosinophilic plaque in periauricular area bilaterally in a cat with food allergy. B) Resolution of dermatitis was achieved after completing a diet trial with a hydrolyzed protein diet.
Figure 2: A) Ulcerated eosinophilic plaque in periauricular area bilaterally in a cat with food allergy. B) Resolution of dermatitis was achieved after completing a diet trial with a hydrolyzed protein diet.

Occasionally, hypersensitivity to dietary ingredients, especially proteins, causes a food allergy. The pathogenesis of food allergy is complex and not completely understood. Food allergy may occur at any age, but immature animals are predisposed.2 Clinical signs include severe pruritus, erythema, papules, urticaria-angioedema, alopecia, and infections (Figure 1).3 Additionally, cats demonstrate lesions of the eosinophilic granuloma complex (e.g. miliary dermatitis, eosinophilic plaque, eosinophilic granuloma, and rodent ulcer) (Figure 2).4,5

Other clinical signs of food allergies include vomiting, diarrhea, loose stools, and flatulence. Clinical signs may occur minutes to days after exposure.6 Lesion localization for dogs is the face, ears, rear, feet, and ventrum, while cats may localized to the face.3 Food ingredients acting as allergens include beef, soy, chicken, fish, milk, egg, pork; however, carbohydrates and preservatives are less commonly implemented.7

The definitive diagnosis for food allergy is achieved by performing a strict eight- to 12-week novel or hydrolyzed protein dietary elimination trial.8 Serology and intradermal testing are not reliable in veterinary medicine.9 If offending dietary ingredients are avoided, then the prognosis is good to excellent.

Superficial necrolytic dermatitis

Superficial necrolytic dermatitis (SND) (also called hepatocutaneous syndrome) is a less-common disease caused by a relative hypoaminoacidemia. Deficient amino acids include arginine, leucine, lysine, methionine, proline, threonine, and valine.10

Other reported changes will depend on the underlying disease process, but may include elevated glucagon, deficiencies in zinc, essential fatty acids, tryptophan, and niacin. This leads to epidermal protein depletion and death of keratinocytes with epidermal necrosis.

Examples of underlying diseases associated with SND are chronic hepatopathy (vacuolar, fibrosis, cirrhosis), diabetes mellitus, pancreatic glucagonoma, and hyperadrenocorticism.10 The highest incidence occurs in older animals with predisposition to the Shetland sheep dog, West Highland white terrier, cocker spaniel, shih tzu, and Scottish terrier.10 Cutaneous signs include severe crusting, erythema and depigmentation of the paw pads, lips, eyelids, nasal planum, axillae, inguinal area, and genitalia (Figure 3).

This disease carries a guarded to poor prognosis, and nutritional supplementation of dietary protein, vitamin E, zinc, and omega fatty acids may temporarily improve the clinical signs. Intravenous (IV) amino acid replacement therapy (10 percent Aminosyn, 25 mL/kg IV over six to eight hours via a central catheter) administered every seven to 10 days may significantly improve dermatological lesions, but it will not reverse the primary disease process.10

Essential polyunsaturated fatty acids (EFA)

Essential fatty acids maintain normal hydration of the skin and regulate inflammation. The EFA required from the diet include linoleic acid and alpha-linolenic acid for dogs, and linoleic acid, alpha-linolenic acid, and arachidonic acid for cats.1 In general, EFA deficiencies are rare and caused by feeding an unbalanced diet, gastrointestinal malabsorption, or storage of food past the expiration date, which can lead to oxidation of EFA.1

Figure 3: Severe palisading crusting and erythema of the paw pads in a dog with superficial necrolytic dermatitis secondary to hepatic cirrhosis.
Figure 3: Severe palisading crusting and erythema of the paw pads in a dog with superficial necrolytic dermatitis secondary to hepatic cirrhosis.

An imbalance in EFA can lead to arachidonic acid deficiency and increased DNA synthesis, which causes epidermal hyperplasia and scaling. These alterations in the skin structure cause decreased production of the cutaneous lipid bilayer leading to increased transepidermal water loss.1

The beneficial effects of EFA supplementation in dermatological diseases is controversial, but they are used to treat adjunctively many conditions including allergic dermatoses, autoimmune dermatoses, hepatocutaneous syndrome, endocrine-related dermatoses, and seborrheic disorders.1,11

Atopic dermatitis is characterized by dysregulation of EFA production, overproduction of pro-inflammatory mediators of arachidonic acid pathway, increased systemic inflammation, and abnormal barrier function. Supplementation with EFA may reduce the clinical signs associated with atopic dermatitis in dogs.1

Vitamins and minerals

The most important vitamins for maintaining skin health are A, D, E, and K. Cocker spaniels, Labrador retrievers, and miniature schnauzers are predisposed to a dermatological condition called vitamin A responsive dermatosis.1,12 The cause is unknown, but a relative deficiency due to inadequate utilization from the diet leads to adult-onset refractory seborrheic dermatitis.

Clinical signs include follicular plugging, epidermal hyperplasia, hyperkeratotic plaques, scaling, crusts, alopecia, and secondary infections. Treatment is vitamin A 10,000 IU orally once daily with fatty meal.1 Side effects of vitamin A are uncommon but include dry eye (xerophthalmia), hepatotoxicity, and teratogenicity.

The most important minerals affecting skin are zinc, copper, and calcium. Unbalanced diets or improper absorption of these minerals can lead to changes in hair coat quality and color, as well as scaling and crusting dermatosis.

Figure 4: Bilaterally symmetrical crusting, alopecia, and erythema of the periocular and perioral areas in a Cavalier King Charles spaniel with zinc responsive dermatosis Syndrome I.
Figure 4: Bilaterally symmetrical crusting, alopecia, and erythema of the periocular and perioral areas in a Cavalier King Charles spaniel with zinc responsive dermatosis Syndrome I.

Zinc is an essential component in numerous enzymatic pathways, including those for protein and carbohydrate metabolism, normal maturation of skin and hair, and various immune functions.1 Zinc deficiency represents one of the most commonly observed nutritional deficiencies in animals. Clinical signs include bilaterally symmetrical erythema, alopecia, crusts, and scale most classically at mucocutaneous junctions, distal extremities, footpads, genitalia, and pressure points. Secondary infections are common1,13-15 (Figure 4).

There are two types of zinc-responsive dermatoses: Syndrome I (relative deficiency) and Syndrome II (absolute dietary deficiency). In Syndrome I, animals fail to absorb zinc from a well-balanced diet. This may be due to abnormalities in gut function or other unknown causes. Arctic breeds such as the Alaskan malamute and Siberian huskies are predisposed, but it can affect any breed.1,13-15 Diagnosis is presumptive based on history, signalment and clinical signs; however, histopathology is confirmatory.

The treatment is oral supplementation with elemental zinc (2-3 mg/kg/day).1,13,15 Occasionally, low-dose corticosteroids provide improvement in clinical lesions because steroids increase intestinal zinc absorption. The prognosis is very good if lifelong supplementation with zinc is continued. Syndrome II is caused by an absolute dietary zinc deficiency or diets high in phytates or calcium, which interfere with zinc absorption.1,15 Another less common cause is prolonged enteritis or diarrhea.

Due to the availability of complete and balanced diets, this type of zinc deficiency is not common. When present, this usually affects young, rapidly growing dogs. Treatment is feeding a complete and balanced diet, and temporary zinc supplementation until clinical signs resolve.

Copper plays an important role in erythropoiesis, coenzyme function, hair pigmentation, reproduction, collagen and elastin synthesis, and iron utilization.1 While copper deficiency is uncommon, animals with it may show signs of pica, stunted growth, diarrhea, depigmentation of hair, anemia, and impaired bone growth.

Calcium is important for many body systems and functions in bone and tooth formation, blood clotting, enzyme activation, muscle contraction, and nerve impulse transmission.1 Calcium’s most important role in cutaneous health is enzyme activation of crucial skin and hair growth pathways. Calcium deficiency is uncommon, but may lead to changes in overall skin and coat health and appearance.

Probiotics

Probiotics promote beneficial intestinal microbiota colonization, improve gut barrier function, and modulate systemic immune system.1,16 Research suggests probiotics decrease allergic clinical signs in atopic dogs, but do not prevent allergic disease formation in predisposed animals.17-19

Probiotics are selected from members of normal, healthy intestinal microbiota and include the species Lactobacillus, Bifidobacterium, and Enterococcus.1,16 These strains have different targets, which induce variable responses in the patient. Studies in mice suggest probiotics can stimulate anti-inflammatory responses and suppress IgE responses related to allergies.20,21 The true benefits of probiotics in allergic veterinary species is still undetermined on a larger level, but they seem to have potential for beneficial therapeutic effects.

Conclusion

Nutrition plays a vital role in the normal appearance and function of the skin and hair coat. Scaling skin, alopecia, and skin infections may be the first indication of critical dietary deficiencies. Utilizing dietary supplements or diets formulated for skin health may be sufficient for the return of a shiny, healthy hair coat over the course of several months. Other times, investigation into systemic diseases may be warranted.

Amelia White, DVM, MS, DACVD is the associate clinical professor of dermatology at Auburn University College of Veterinary Medicine.

References

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4 Halliwell R, Pucheu-Haston CM, Olivry T, et al. Feline allergic diseases: introduction and proposed nomenclature. Vet Dermatol 2021;32:8-e2.

5 Diesel A. Cutaneous Hypersensitivity Dermatoses in the Feline Patient: A Review of Allergic Skin Disease in Cats. Vet Sci 2017;4.

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10 DeMarle KB, Webster CRL, Penninck D, et al. Approach to the Diagnosis of Hepatocutaneous Syndrome in Dogs: A Retrospective Study and Literature Review. J Am Anim Hosp Assoc 2021;57:15-25.

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12 Ihrke PJ, Goldschmidt MH. Vitamin A-responsive dermatosis in the dog. J Am Vet Med Assoc 1983;182:687-690.

13 Hall J. Diagnostic dermatology. Zinc responsive dermatosis. Can Vet J 2005;46:555-557.

14 Colombini S, Dunstan RW. Zinc-responsive dermatosis in northern-breed dogs: 17 cases (1990-1996). J Am Vet Med Assoc 1997;211:451-453.

15 Colombini S. Canine zinc-responsive dermatosis. Vet Clin North Am Small Anim Pract 1999;29:1373-1383.

16 Wernimont SM, Radosevich J, Jackson MI, et al. The Effects of Nutrition on the Gastrointestinal Microbiome of Cats and Dogs: Impact on Health and Disease. Front Microbiol 2020;11:1266.

17 Marsella R. Evaluation of Lactobacillus rhamnosus strain GG for the prevention of atopic dermatitis in dogs. Am J Vet Res 2009;70:735-740.

18 Marsella R, Santoro D, Ahrens K. Early exposure to probiotics in a canine model of atopic dermatitis has long-term clinical and immunological effects. Vet Immunol Immunopathol 2012;146:185-189.

19 Marsella R, Santoro D, Ahrens K, et al. Investigation of the effect of probiotic exposure on filaggrin expression in an experimental model of canine atopic dermatitis. Vet Dermatol 2013;24:260-e257.

20 Shida K, Takahashi R, Iwadate E, et al. Lactobacillus casei strain Shirota suppresses serum immunoglobulin E and immunoglobulin G1 responses and systemic anaphylaxis in a food allergy model. Clin Exp Allergy 2002;32:563-570.

21 von der Weid T, Bulliard C, Schiffrin EJ. Induction by a lactic acid bacterium of a population of CD4(+) T cells with low proliferative capacity that produce transforming growth factor beta and interleukin-10. Clin Diagn Lab Immunol 2001;8:695-701.

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