Page 621 - Small Animal Clinical Nutrition 5th Edition

Skin and Hair Disorders 643

marized in Table 32-1 and discussed in more detail below. least a threefold increase in epidermal cell renewal, may
VetBooks.ir PROTEIN AND FAT change the nutrient requirements of these dogs. However, no
studies to date have evaluated the specific nutrient require-
As mentioned previously, the integument is a metabolically
ments of dogs with severe primary seborrhea vs. age- and
active organ that is affected by the nutritional status of the ani- breed-matched controls. Some authors suggest that primary
mal. Protein and energy are required for the development of seborrhea worsens greatly in dogs with nutritional inadequa-
new hair and skin; fat is the most concentrated source of dietary cies (Scott et al, 1995). Dogs with severe deep pyoderma sec-
energy. Developing hair requires sulfur-containing and other ondary to generalized demodicosis or other underlying dis-
amino acids.Therefore, for normal skin and hair, it is important eases may have increased nutrient requirements above those
for the pet’s food to provide optimal protein quantity, quality found in the normal adult animal.
(appropriate levels of essential amino acids) and digestibility.
Dogs and cats have increased protein and energy requirements Metabolic Epidermal Necrosis
during growth, gestation, lactation and some illnesses. Ab- Metabolic epidermal necrosis is a rare cutaneous disease that
normal skin and hair will often be noted if nutritionally inade- in most cases is a marker for a serious underlying metabolic dis-
quate foods are fed during these stages (Ralston Purina order. In dogs, this syndrome has findings similar to those of
Company, 1987; Huber et al, 1991). Key nutritional factor pro- necrolytic migratory erythema of people and has also been
files for various lifestages of dogs and cats are listed in Chapters termed hepatocutaneous syndrome or superficial necrolytic
13 through 24. Optimal levels of protein and fat, and minimum dermatitis. Clinical features include crusting acral dermatopa-
dry matter (DM) digestibility of foods for dogs and cats with thy with erosions around the mouth, eyes, legs, feet and geni-
skin and hair disorders are listed in Table 32-1. talia (Scott et al, 2001; Angarano, 1993). Hyperkeratosis, ulcer-
Foods inadequate in protein and energy can cause keratiniza- ation of footpads or both conditions is also prominent. The
tion abnormalities, depigmentation of hair and changes in epi- cutaneous syndrome is typically diagnosed in older dogs and is
dermal and sebaceous lipids (Box 32-2). The skin loses its pro- often associated with hepatic cirrhosis, other hepatopathies,
tective barrier function in patients with protein-energy malnu- diabetes mellitus, hyperadrenocorticism, and rarely, glucagon-
trition and becomes more susceptible to secondary bacterial or secreting pancreatic tumors. Metabolic changes often include
yeast infection. Impaired wound healing and decubital ulcers carbohydrate intolerance and marked hypoaminoacidemia
are also sequelae to protein-energy malnutrition. Protein-defi- (Outerbridge et al, 2002).
cient dogs and cats have patchy alopecia and coats that are dry, Specific treatment is aimed at correcting the underlying
dull and brittle. metabolic disease. Unfortunately, most cases are associated with
Telogen defluxion is usually recognized as hair loss associat- irreversible chronic liver disease and hepatic cirrhosis (Chapter
ed with a stressful event (e.g., pregnancy, severe illness, surgery) 68). Symptomatic treatment includes antimicrobials for sec-
that causes the abrupt, premature cessation of growth of many ondary infections, insulin therapy as needed for diabetes melli-
anagen hair follicles and the synchronization of these hair fol- tus, hydrotherapy to help remove crusts and lessen pruritus and
licles in catagen, then in telogen (Scott et al, 2001; Harvey, glucocorticoids. Treatment of hypoaminoacidemia may reverse
1994). Short-term increased requirements of energy, protein the skin lesions. Anecdotal reports suggest that foods for reple-
and other nutrients during growth, gestation, lactation and ill- tion/recovery containing moderate protein levels (Prescription
a
ness may cause telogen defluxion if appropriate nutritional Diet a/d Canine/Feline ), zinc, egg yolks or intravenous
changes are not instituted. Bitches and queens in late gestation administration of crystalline amino acid solutions will reverse
and lactation, and growing puppies and kittens are at risk unless the skin lesions in some patients. b,c A review of 36 canine cases
they are fed nutritionally balanced, highly digestible foods that showed that dogs responded better to therapy with intravenous
meet their increased nutritional requirements. amino acid infusions rather than oral protein hyperalimenta-
Anagen defluxion is a sudden loss of hair due to an unusual tion (Outerbridge et al, 2002).
event (e.g., antimitotic drugs, infectious disease, metabolic dis-
ease) that interferes with anagen, resulting in abnormalities of ESSENTIAL FATTY ACIDS
hair follicles and shafts. Patients suffering from the stress of ill- Functions in the Skin
ness, injury and surgery often require increased amounts of EFA are polyunsaturated fatty acids (PUFA) derived from and
energy, protein, specific amino acids and other nutrients. including the parent EFA, cis-linoleic acid (LA) and α-linolenic
Patients with severe illness that do not receive adequate nutri- acid (ALA). Figure 32-1 summarizes the metabolic pathway of
tional support are at risk for telogen defluxion, anagen deflux- EFA. The skin of adult mice, guinea pigs and presumably other
ion or other coat abnormalities. animals lacks ∆-6-desaturase and ∆-5-desaturase activity
Dogs with severe primary seborrhea may have increased (Chapkin et al, 1987). Thus, the epidermis depends on food to
protein and other nutrient requirements. The calculated epi- supply EFA or the continuous formation of γ-linolenic acid
dermal cell renewal time is approximately seven to eight days (GLA), arachidonic acid (AA) and eicosapentaenoic acid (EPA)
for dogs with primary seborrhea (Kwochka and Rademakers, by the liver, with subsequent transportation to the skin by the
1990; Baker and Maibach, 1987). The hyperproliferative blood (Chapkin et al, 1987; Horrobin, 1989; Campbell, 1990).
nature of the skin of dogs with primary seborrhea, with at In the skin, EFA are principally found in phospholipids, and