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Vitamin E displays the greatest versatility of all vitamins in the range of deficiency signs. Deficiency signs differ among species and even within the same species. Blaxter (1962) reported that muscular dystrophy seemed to be the one syndrome commonly encountered in all species. White muscle disease (WMD), also known as nutritional muscular dystrophy, a serious muscle degeneration disease in young animals, is the major clinical sign of a vitamin E-selenium deficiency in newborns. White muscle disease occurs in all laboratory and farm animals as well as in camels, buffalos, and kangaroos. Muscular dystrophy is reported in a number of wild animals, the condition in antelope, for example, being indistinguishable from WMD in cattle or sheep (NRC, 1985b). Fundamentally, this is Zenker's degeneration of both skeletal and cardiac muscle fibers. Connective tissue replacement that follows is observed grossly as white striations in the muscle bundles.
Muscular degeneration is reported for dogs with vitamin E deficiency; however, steatitis or yellow fat is the most common indication of the vitamin deficiency in cats. Godwin (1975) reported that electrocardiograms of WMD showed a progressive development of a characteristic abnormality and a fall in blood pressure, therefore suggesting that the fundamental change occurring in the vitamin E-selenium deficiency is circulatory failure.
Confirmation of a low vitamin E and/or selenium status in animals is obtained when specific deficiency diseases associated with a lack of these nutrients are present. Likewise, gross lesions and histopathological examinations provide definite evidence of vitamin E and/or selenium deficiency. Unlike dogs, there are few studies which establish the vitamin E status of cats. Diagnosing of steatitis can be made on biopsy or necropsy findings of yellow to orange-brown fat. Histopathologic examination reveals fat necrosis, septal panniculitis, and ceroid within fat vacuoles, macrophages, and giant cells.
Muscular damage as a result of vitamin E and/or selenium deficiencies causes leakage of intercellular contents into the blood. Thus elevated levels of selected enzymes, above normal concentrations for particular species, serve as diagnostic aids in detecting tissue degeneration. Serum enzyme concentrations used to follow incidence of nutritional muscular dystrophy include serum aspartate aminotransferase, lactic dehydrogenase, creatine phosphokinase, and malic dehydrogenase. Enzyme tests are very sensitive, and an elevation of enzyme activity in serum is usually discovered before any pathological changes or clinical signs appear (Tollersrud, 1973). Dogs with muscular dystrophy have had elevated serum creatine phosphokinase (Worden, 1958; Van Vleet, 1975; Sheffy, 1979).
Dogs deficient in vitamin E have an increased erythrocyte fragility as determined by the dialuric acid hemolysis assay (Sheffy and Schultz, 1978; Pillai et al., 1992). In vitamin E-deficient dogs, Pillai et al. (1992) reported that dialuric acid hemolysis (R = -0.89) and spontaneous hemolysis (R = -0.91) increased with declining plasma alpha-tocopherol concentration.
Immune function is altered in vitamin E-deficient dogs and can be used as an additional indicator of vitamin E status. Vitamin E-deficient dogs had significant reduction in antibody titers to canine distemper and infectious canine hepatitis vaccines compared to normal dogs (Sheffy and Schultz, 1978). Dogs deficient in vitamin E had severe impairment of lymphocyte function as assessed by in vitro blastogenic responses to concanavalin A, phytohemagglutinin, pokeweed mitogen and streptolysin O. (Sheffy and Schultz, 1978; Langweiler et al., 1981). The suppression of lymphocyte function was shown to be associated with the presence of a serum immunosuppressive factor, which could be counteracted in vitro by vitamin E, reducing agents, and synthetic antioxidants such as 2-mercaptoethanol, dithrotritol, butylated hydroxytoluene and ethoxyquinone (Langweiler et al., 1983).
Nutritional status with respect to vitamin E is commonly estimated from plasma (or serum) concentration. There is a relatively high correlation between plasma and liver levels of alpha-tocopherol (and also between amount of dietary alpha-tocopherol administered and plasma levels). This has been observed in rats, chicks, pigs, lambs, and calves within rather wide ranges of intake. Plasma tocopherol concentrations of 0.5 to 1 µg per ml are considered low in most animal species, with less than 0.5 µg per ml generally considered a vitamin E deficiency. Thus, plasma alpha-tocopherol concentrations can be used for assay purposes without the necessity of liver biopsy or animal slaughter.
Plasma vitamin E, as true in other species, is an indicator of vitamin E status. Hayes et al. (1970) related plasma tocopherol concentrations of dogs with pathological evidence of vitamin E deficiency. As vitamin E deficiency developed and progressed in dogs, plasma alpha-tocopherol decreased from baseline values of 20.5 to 31.3 µg per ml to 0.07 to 0.1 µg per ml by 90 weeks (Pillai et al., 1992).
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Definite clinical cases of vitamin E deficiency have been well documented in dogs. Particularly prominent indications of vitamin E deficiency were degeneration of skeletal muscle associated with muscle weakness, degeneration of testicular germinal epithelium and failure of spermatogenesis, failure of gestation, weak and dead pups, and brown pigmentation (lipofuscinosis) of intestinal smooth muscle (NRC, 1985).
Van Kruiningen (1967) reported a brown bowel in malabsorbing boxer dogs with granulomatous colitis, and the condition was eventually reproduced experimentally by Hayes et al. (1969), who fed varying levels of polyunsaturated fat to vitamin E-deficient weanling puppies over a 16-week period. The puppies developed an increased susceptibility to hemolysis of red blood cells as well as brown bowel, mild muscle degeneration, and neuralaxonal dystrophy.
A retinal degeneration was described by Hayes and Rousseau (1970) and reproduced experimentally (Riis et al., 1981) in puppies fed a diet containing stripped corn oil. In as few as three months, ophthalmoscopic lesions were visible, which represented lipid peroxidation and disruption of photoreceptors with accumulation of lipofuscin pigment. Retinal degeneration associated with vitamin E deficiency in hunting dogs was reported by Davidson et al. (1998).
The effect of vitamin E deficiency on reproduction has been reported by Anderson et al. (1939; 1940) and Elvehjem et al. (1944), who described a nutritional deficiency syndrome in puppies from bitches fed evaporated or pasteurized milk diets for extended periods of time. Lactating dams and puppies developed festering skin lesions, and the puppies developed muscle weakness and hemorrhages of body cavities and brain. Other pups were stillborn or died shortly after birth. The syndrome was alleviated by weekly feeding of 40 mg of vitamin E to the bitch during pregnancy.
A combined vitamin E-selenium deficiency described by Van Vleet (1975) included muscle weakness, subcutaneous edema, anorexia, depression, dyspnea, and coma. Pathologic examination revealed extensive skeletal muscle degeneration and regeneration, focal subendocardial necrosis, lipofuscinosis, and renal mineralization.
A deficiency of vitamin E has been implicated in the development of certain dermatological disorders in dogs (Anderson et al., 1939; Worden, 1958; Sheffy, 1979; Scott and Walton, 1985; Scott and Sheffy, 1987; Miller, 1989; Codner and Thatcher, 1993) (Illus. 1). The occurrence of these skin disorders has been associated with decreased blood levels of vitamin E.
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It has been postulated that a subclinical vitamin E deficiency causes suppression of the immune system, which in turn increases a dog's susceptibility to demodex (skin lesions caused by the demodectic mange mite, Demodex canis). When a group of dogs with demodicosis was treated with supplemental vitamin E, significant improvement was reported. However, other researchers have been unable to reproduce these results.
Scott and Sheffy (1987) experimentally produced vitamin E deficiency skin disorders. They were characterized clinically by an early keratinization defect (seborrhea sicca), a later inflammatory stage (erythroderma) and a tendency to develop secondary pyoderma. The vitamin E anti-inflammatory effect may be related to stabilization of cell and lysosomal membranes against damage induced by free radicals and peroxides. By reducing oxidative damage to cells, vitamin E may inhibit immune-mediated or neoplastic skin diseases associated with ultraviolet irradiation.
Vitamin E therapy has been reported to be effective in dogs with discoid lupus erythematosus (Scott et al., 1983) and has been suggested as therapy for dogs with dermatomyositis (Illus. 2) (Muller et al., 1989; Hargis et al., 1985). Vitamin E supplementation has also been evaluated in dogs with acanthosis nigricans. Eight dachshunds with primary acanthosis nigricans showed improvement after 60 days of vitamin E therapy (200 mg twice daily) (Scott and Walton, 1985). All dogs responded with gradual elimination of pruritus, inflammation, lichenification, greasiness, and odor.
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Steatitis or "yellow fat disease" has been noted when sources of highly unsaturated fatty acids (e.g., tuna fish oil, cod liver oil, and unrefined herring oil) have been fed in the absence of adequate supplemental vitamin E. Known as yellow fat after the peroxidized ceroid in adipose tissue, it was characterized by extreme hyperesthesia, fever, and a marked rise in leucocytes, primarily as neutrophils and eosinophils. Anorexia, weight loss, listlessness or overt neurological dysfunction and muscle spasms, harsh haircoat, and palpable lumps in the subcutaneous fat were characteristic (Case et al., 1995). Additional signs were focal interstitial myocarditis and, rarely, muscle fiber degeneration, focal myositis of the skeletal muscle and periportal mononuclear infiltration in the liver (Gershoff and Norkin, 1962). Affected cats are often lethargic, febrile, and exhibit pain on gentle palpation. Subcutaneous and abdominal fat may feel firm or lumpy, and draining tracts may develop. The best way of confirming the condition is histological examination of a fat biopsy (Case et al., 1995). Microscopically, the fat shows focal neutrophilic infiltration with some mononuclear cells. Acid-fast ceroid pigment is present as globules and as peripheral rings in the fat cell vacuoles (NRC, 1986). The white blood cell count is usually elevated (24,000 to 70,000 mg per ml), primarily as a result of neutrophilia, and reflects the degree of fat necrosis.
Vitamin E deficiency in cats became a significant clinical problem when fish products were first used in commercial cat foods that contained inadequate levels of tocopherol (Munson et al., 1958; Cordy, 1954). Later cases of the disease occurred in cats that were fed diets consisting wholly or largely of canned red tuna or fish scraps. Red tuna packed in oil contains high levels of PUFA and low levels of vitamin E. The addition of large amounts of fish products to a cat's diet appears to be the primary cause of this disease in pet cats (Harvey, 1993; Watson, 1998).
Stephan and Hayes (1978) induced severe vitamin E deficiency with hemolytic anemia and steatitis by feeding a diet containing 15% stripped safflower oil without alpha-tocopherol. Clinical signs of deficiency were prevented by supplementing with alpha-tocopheryl acetate at 100 IU per kg (45.5 IU per lb) diet.
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