Download Nutrition and skin diseases in veterinary medicine

Clinics in Dermatology (2010) 28, 686–693
Nutrition and skin diseases in veterinary medicine
Patrick Hensel, Dr. med. vet.
Department of Small Animal Medicine and Surgery, College of Veterinary Medicine of the University of Georgia,
501 DW Brooks Drive, Athens, GA 30602, USA
Abstract Veterinarians are confronted with a variety of food and nutrition-related skin diseases, with
cutaneous food adverse reaction the most common in small animal dermatology. In addition to canine
atopic dermatitis, cutaneous food adverse reaction has been an area of interest for extensive research for
the last decade. Nutritional deficiencies and toxicoses are rare these days due to commercially available
high-quality diets; however, poorly stored diets, inadequate husbandry of exotic pets, or problems in a
farm animal environment may result in zinc, vitamin A, vitamin C, and fatty acid, or copper deficiency.
Inherited deficiencies due to abnormal zinc absorption through the gastrointestinal tract must be
considered in Nordic breed dogs and goats.
© 2010 Elsevier Inc. All rights reserved.
Introduction
Cutaneous food adverse reaction
Veterinary dermatologists are confronted with various
food- and nutrition-related skin diseases. The most
common one is cutaneous adverse food reaction (CAFR)
in dogs and cats. Skin diseases caused by nutritional
deficiencies or toxicoses are less common, but are seen
in farm animals and exotic animals due to inappropriate
husbandry. Hereditary nutritional deficiencies have been
reported in Nordic breed dogs and goats. The clinical
presentations among these diseases vary, and lesions such
as alopecia, coat discoloration, seborrhea, hyperkeratosis, and pruritus may be seen. These diseases can affect
many animals in a herd due to husbandry-related
problems, or may affect a single animal, as seen with
CAFR or inherited zinc-responsive dermatosis in Northern
breed dogs.
Adverse food reactions are divided into two categories:
immune-mediated and non-immune-mediated reactions.
Although food hypersensitivity is believed to be immunemediated, the reactions in most dogs are non-immunemediated, which are referred to as food intolerance. Food idiosyncrasy, food toxicity, and food poisoning, anaphylactic food
reaction, pharmacologic, and metabolic food reactions are all
forms of food intolerance (Figure 1). Tolerance and exclusion of
food allergens requires an intact gastrointestinal (GI) barrier,
which is supported by four mechanisms within the GI wall:
E-mail address: [email protected].
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doi:10.1016/j.clindermatol.2010.03.031
1. integrity of the mucosal barrier provided by morphology and functionality of the enterocytes, presence of
immunoglobulin (Ig) A, effective digestion, quality and
composition of the food, and presence of inflammation;
2. immune response regulated by M cells in the Peyer
patches;
3. elimination of formed immune complex through the
mononuclear phagocytic system of the liver and the
mesenteric lymph nodes;
Nutrition, skin diseases in veterinary medicine
Fig. 1 Classification of adverse food reaction. CAFR, Cutaneous
adverse food reaction; Ig, immunoglobulin.
4. tolerance of antigens reaching the mucosa provided by
the suppressor function of the gut associated lymphoid
tissue (GALT).1,2
CAFR in dogs and cats caused by a hypersensitivity has
been associated most commonly with a type I hypersensitivity reaction; however, type III and type IV hypersensitivity
are possible immunologic mechanisms.3
Theoretically, any food has the potential to induce adverse
reactions; but so far only a limited number of food ingredients
have been identified in veterinary medicine. Many different
food ingredients are used and are commonly combined in
commercially available dog and cat foods, which makes the
identification of a specific food allergen very difficult.
Several studies determined that the most common foods
responsible for causing CAFR are beef, dairy products,
wheat, and to some degree lamb, soy, and fish in companion
animals.4-11 Food additives, such as dyes and preservatives,
are also a concern, but scientific evidence could be
established only in two cats, so far.12,13 Adverse reactions
to multiple food ingredients are not unusual and have been
identified in 35% to 50% of food-allergic dogs and cats.14,15
Cross-reactivity among food allergens is another concern.
The results of a recent study showed that bovine IgG was
identified as a major allergen in cow's milk and appeared to
be a source of cross-reactivity with beef and probably lamb.16
CAFR is recognized as a potential cause of nonseasonal
pruritic skin disease and occasional GI signs in dogs and cats.
The exact prevalence of CAFR is not well established, but
a few studies determined that the prevalence of CAFR in
dogs with nonseasonal pruritus may range between 14%
and 24%.5,17,18 Sex, breed, or age predilection could not
be confirmed, but a higher risk for certain breeds, such as
Boxers, West Highland White Terriers (Figure 2, A-D),
retrievers, Cocker/Springer Spaniels, and others has been
reported.5,6,14,18-20 CAFR can occur at any age, and most
authors report an age range of as early as 4 months to 14
years,11 whereas other authors suggest that a contact time of
1 to 2 years is necessary to develop clinical symptoms.5,6,20
The typical clinical presentation of adverse food reactions
in dogs is nonseasonal pruritus of variable intensity affecting
687
face, ears, feet axillae, inguinal, or perineum.5,6,14,20 CAFR
often cannot be distinguished from canine atopic dermatitis,
pyoderma, Malassezia dermatitis, and skin diseases caused
by ectoparasites, such as sarcoptic and demodectic mange
and fleas.3,11 Dogs also commonly present with a combination of food adverse reaction, atopy, and flea bite
hypersensitivity.5,15,19
Depending on severity and duration, the following skin
lesions can be found: erythema, papules, excoriations,
epidermal collarettes, seborrhea, and otitis.5,6,14,19,20 In
severe, chronic cases, the skin becomes lichenified, accompanied with marked hyperpigmentation, seborrhea, alopecia,
secondary superficial pyoderma, and Malassezia dermatitis
(Figure 2 A-D). The most common presentation in cats is
generalized or localized pruritus around the neck and face
(Figure 3), miliary dermatitis, traumatic alopecia, eosinophilic plaques, granulomas, and indolent ulcers.4,5,20-22
Diagnosing a food adverse reaction in veterinary
medicine can be very challenging and depends heavily on
correct food selection, food trial duration, and owner
education and compliance. Several attempts have been
made to find a valuable method to diagnose CAFR, but the
most effective diagnostic method in dogs and cats is still a
strict elimination diet trial.7,17,23-29 Challenging the pet
with its previous diet and a relapse of the clinical signs is
considered necessary to confirm the CAFR. Because many
owners are reluctant to challenge their pet with their previous
diet, CAFR can also be identified by adding a single
ingredient to the elimination diet for 1 to 2 weeks.7,26 If
no relapse is observed, the ingredient is considered safe to
give. It is very important during an elimination diet trial
that no treats, table food, flavored heartworm and flea
preventatives, or medication with gelatin capsules are fed
to the animal.3,26 Although most dogs and cats respond
within 3 to 4 weeks into a diet trial, improvement is
sometimes not seen for 10 to 13 weeks.5,14,15,19,30
The three groups of elimination diets used in veterinary
medicine are home-cooked diets, commercially available
novel protein diets, and hydrolyzed protein diets. Homecooked diets are considered superior due to the lack of
additives and by-products but are difficult to balance
nutritionally, especially for long-term management, and
may be more time consuming to prepare, which may have a
negative effect on owner compliance. Study results indicate
that home-cooked diets may be more effective than
commercially available equivalents.4,6,28,31
Commercially available novel protein diets are composed of a single protein that is not used in over-the-counter
diets, and a carbohydrate source, such as potato and or
oatmeal. Venison, duck, rabbit, and kangaroo are currently
used as novel protein sources in commercial veterinary
prescription diets.
Commercial hydrolyzed diets are considered real hypoallergenic diets and results from studies indicate that, for
example, dogs sensitive to soy did not develop a reaction
to hydrolyzed soy.23,32 In up to 50% of dogs with CARF,
688
P. Hensel
Fig. 2 A-D, Chronic cutaneous food adverse reaction in a West Highlight White Terrier: marked lichenification, hyperpigmentation,
erythema, and alopecia on ventrum and front and hind legs.
a partially hydrolyzed diet may worsen the clinical signs
and so it must be concluded that hydrolyzed prescription
diets may reduce but do not eliminate immunologic and
clinical allergenicity.33
Despite these concerns, the use of hydrolyzed diets for
the diagnosis of CAFR in dogs and cats became more
popular, especially because diets containing hydrolyzed
chicken liver, casein, or soy have become commercially
available. 26 An evaluation of the efficacy of these
veterinary prescription diets reported a success rate of
60% to 75%.11,34 Concurrent complications, such as
superficial pyoderma, Malassezia dermatitis, or bacterial
or yeast otitis externa, often need to be treated at the same
time the elimination diet trial is instituted. Because some of
these patients are severely pruritic, anti-inflammatory
therapy is necessary. Symptomatic therapy must be
discontinued for the last 2 to 3 weeks of the diet trial to
assess effectively the response to the elimination diet.26
The prognosis of CFAR is very good if the offending
allergen is identified and as long as patient and owner
compliance is guaranteed. Occasional recurrences of the
skin problems may occur because some patients may
become sensitive to the new protein after 2 to 3 years.30
Whether animals can become tolerant to a food allergen
after an extended period of avoidance, as reported in people,
has not been proven, but natural hyposensitization seems to
be rare.
Zinc-responsive dermatosis
Zinc is an important mineral for many critical biologic
functions, such as cellular metabolism, which is crucial for
the maintenance of a healthy coat and skin.35,36 Zinc
deficiency is rare but has been reported in various species,
Nutrition, skin diseases in veterinary medicine
689
Fig. 3 Cutaneous food adverse reaction: severe facial pruritus
resulting in extensive excoriations and alopecia in a cat.
including dogs, goats, sheep, alpacas, llamas, and horses.37-44
Goats, South American camelids, and Nordic breed dogs,
such as Siberian Huskies and Alaskan Malamutes, seem to
be affected more commonly.36,37,39-41
Zinc-responsive dermatosis has been divided in two
syndromes: syndrome I is considered to be a hereditary zinc
deficiency resulting in decreased capability of absorbing zinc
from the intestines seen in the Nordic breed dogs and
probably in goats.40,45 Skin lesions develop despite sufficient dietary zinc and most commonly appear in young-adult
dogs.35 Syndrome II occurs in puppies of fast-growing
breeds, such as Great Dane, Doberman Pinscher, German
Shepherd, or Labrador Retriever, or in young-adult animals
fed a zinc-deficient diet.46
Early skin lesions demonstrate erythema, followed by
alopecia and crusting around the muzzle, eyes, and ears
Fig. 4 Zinc-responsive dermatosis: facial alopecia and hyperkeratosis in a Bernese Mountain Dog. (Photo courtesy of C. Sousa.)
Fig. 5 Zinc-responsive dermatosis: marked lichenification,
hyperpigmentation, and hyperkeratosis on the cranioventral chest
of an alpaca.
(Figure 4). Hyperkeratosis may also develop in areas such
as the anus, vulva, prepuce, scrotum, and footpads. In
goats, llamas, and alpacas, the hyperkeratosis tends to
be more severe, hard, and dry, affecting mainly the
dorsum, legs, udder, face, and ears (Figure 5).36,40,43
Pruritus may also develop, especially after the development
of secondary pyoderma.
In either syndrome, serum or hair zinc levels may be
abnormal. Alpacas and llamas, in general, have lower
serum zinc concentrations than do sheep and goats, with no
obvious difference between animals with or without skin
lesions, which makes proper interpretation of serum test
results difficult.36,43
Diagnosis is made by the assessment of a complete
history, physical examination, and skin biopsy specimens.
The characteristic histologic finding in dogs is a marked
diffuse and epidermal/follicular parakeratosis, whereas in
goats and alpacas/llamas, a mixed (parakeratotic and
orthokeratotic) epidermal and follicular hyperkeratosis is
usually present.36,40,43 Superficial perivascular dermatitis
can be found in all species.
Zinc supplementation in animals with syndrome II
usually results in a good response and resolution of the skin
lesions within 2 to 6 weeks. Most common preparations for
the treatment of zinc-responsive dermatosis are elemental
zinc (2 to 3 mg/kg/d), zinc sulfate (10 mg/kg/d), zinc
gluconate (5 mg/kg/d), or zinc methionine (1.7 mg/kg/d).36,39
In patients with lack of response to oral zinc supplementation,
intravenous injection with sterile zinc sulfate (10 to 15 mg/
kg) has been effective.47 Zinc supplementation for patients
with syndrome I is typically lifelong.
690
P. Hensel
Vitamin A-responsive dermatosis and
vitamin A deficiency
Deficiency, as well as excessive supplementation of
vitamin A, has been associated with skin lesions, such as
poor coat quality, alopecia, seborrhea, crusting, increased
susceptibility of secondary pyoderma, Malassezia dermatitis,
and poor wound healing in dogs, horses, caged birds,
and reptiles.36,48,49
Vitamin A-responsive dermatosis in dogs is a rare
condition characterized by an abnormality of cornification
that occurs in adult dogs, predominantly Cocker Spaniels,
but also in Labrador Retrievers and miniature Schnauzers.36,50 Owing to the breed-specific occurrence, a
hereditary etiology is suspected, but the mode of
inheritance is not known. The skin lesions typically present as multifocal areas of alopecia, erythematous plaques,
scaling, crusting, follicular plugging with frond-like
keratinous debris mainly localized on the ventral and
lateral chest (Figure 6), and ceruminous otitis. Analysis of
skin biopsy specimens combined with vitamin A supplementation is routinely used to confirm the diagnosis of a
vitamin A-responsive dermatosis.50 The histopathologic
hallmark of vitamin A-responsive dermatosis is orthokeratotic epidermal and predominantly follicular hyperkeratosis. Therapy consists of oral supplementation of 10,000
IU of vitamin A (retinol), once daily with food. A
response and clinical resolution to therapy should be seen
within 3 to 8 weeks. Treatment must be continued and is
lifelong for most patients.
Vitamin A deficiency in captive reptiles and caged birds,
especially parrots, is common when nutritional requirements are not met. Seeds are commonly deficient in vitamin
A, and so birds fed seeds exclusively often develop a
deficiency resulting in hyperkeratotic skin, white plaques in
Fig. 6 Vitamin A-responsive dermatosis: marked ventral hyperkeratosis and seborrhea on the ventrum of an American Cocker
Spaniel. (Photo courtesy of C. Sousa.)
Fig. 7 Vitamin A deficiency: nostril distortion and rhinolith due
to squamous metaplasia in an African gray parrot. (Photo courtesy
of S. Divers.)
the oral mucosa, rhinitis, and blepharitis (Figure 7).51 In
reptiles, especially in box turtles, vitamin A deficiency is
characterized by periocular edema, conjunctivitis, squamous
metaplasia, hyperkeratosis of the skin and mouth parts, and
aural abscesses (Figure 8).49,52 Therapy consists of a diet
change (adding carrots and cod liver oil), and intramuscular
injections of vitamin A (2000 IU/kg in reptiles and 5000
to 20,000 IU/kg in birds).49
Vitamin C deficiency
Almost all mammals, except humans and guinea pigs,
produce L-ascorbic acid.53 Vitamin C deficiency is a
common problem in guinea pigs that are fed a commercial
Fig. 8 Vitamin A deficiency: conjunctivitis due to squamous
metaplasia in a box turtle. (Photo courtesy of S. Divers.)
Nutrition, skin diseases in veterinary medicine
691
Surgical repair and oral or subcutaneous daily supplementation of 10 to 20 mg/kg has been used successfully to
manage this condition.
Vitamin C deficiency has also been reported in growing
calves, aged 2 to 10 weeks, fed a diet low in vitamin C
content.58 Skin lesions range from nonpruritic seborrhea,
crusting, alopecia, easy hair epilation, erythema, petechiae,
and ecchymoses, starting on the head and limbs (Figure 10).59
Fatty acid deficiency
rabbit chow or outdated commercial guinea pig chow as the
sole diet.54 Guinea pigs are incapable of endogenous
synthesis of vitamin C because they are unable to produce
the enzyme L-gulono-γ-lactone oxidase, which is necessary
to convert glucose to ascorbic acid.55 For this reason guinea
pigs have an absolute dietary daily requirement of 10 mg/kg,
rising to 30 mg/kg in pregnancy.56 Skin lesions associated
with vitamin C deficiency are cutaneous petechiae, ecchymoses, hematomas, ulcerations, generalized seborrhea, and
poor coat quality (Figure 9).54,56 Treatment of vitamin C
deficiency consists of correcting the diet and the administration of subcutaneous injections of vitamin C (50 to 100 mg
daily) until clinical manifestations resolve, followed by
daily oral supplementation.56,57
Although vitamin C deficiency is rare in reptiles, it has
been associated with gingival bleeding and spontaneous
skin ruptures in snakes, especially boas and pythons.49
Dogs and cats are unable to synthesize linoleic acid; thus,
a dietary source is essential in both species. In addition, cats
exhibit low δ-6 desaturase activity and cannot meet their
physiologic requirement for arachidonic acid through
biotransformation from linoleic acid.60 Consequently, linoleic acid and arachidonic acid both are considered essential
nutrients for cats.61 Fatty acid deficiency has become rare
due to the use of commercially available high-quality pet
diets; however, commercial dry food that has been poorly
preserved or a home-cooked diet could potentially result in
fatty acid deficiency. Oxidation of fat during storage,
especially at higher temperatures, is a great concern because
the essential fatty acids are destroyed when fat becomes
rancid. Animals may also develop fatty acid deficiency in
association with intestinal malabsorption, pancreatic disease,
and chronic hepatic disease.
Clinical signs may not be obvious for several months and
usually start with mild scaling and loss of luster of the hair
coat. Over time the degree of seborrhea increases (Figure 11)
and the skin becomes more greasy and thickened, followed
by secondary skin infections and pruritus.36
Specific testing methods to diagnose a fatty acid
deficiency are not available, and so a diagnosis must be
made according to the response to treatment. Therapy in
Fig. 10 Vitamin C deficiency: generalized multifocal areas of
erythema and alopecia in a calf.
Fig. 11 Fatty acid deficiency: dry seborrhea with a dull hair coat
in a dog.
Fig. 9 Vitamin C deficiency: ulcerative foot pad lesions and poor
coat quality in a guinea pig. (Photo courtesy of S. Divers.)
692
such patients consists of switching the diet to a food with a
high fatty acid content or by adding an essential fatty acid
supplement composed of ω-6, ω-3, and vitamin E.
Resolution of mild skin lesions should be observed during
a period of 3 to 8 weeks but may take up to 6 months in
severe cases.
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