http://www.merckvetmanual.com/mvm/index ... 206924.htmThe 3 main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various dietary and environmental factors.
Encephalomalacia is seen in commercial flocks if diets are low in vitamin E, an antioxidant is either omitted or not present in sufficient quantities, or the diet contains a reasonably high level of an unstable, unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, as the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, assuming the deficiency is not too advanced. Encephalomalacia may or may not respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.
The classical sign of encephalomalacia is ataxia, which results from hemorrhage and edema within the molecular and granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the molecular and granular layers of the cerebellar folia. Due to its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant. The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants will prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E, or in chicks fed vitamin E-depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E are also less susceptible to lipid peroxidation in the brain. The fact that antioxidants can help prevent encephalomalacia but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma.
A vitamin E deficiency accompanied by a sulfur amino acid deficiency results in a severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenker’s degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results in an increase in lysosomal enzymes, the function of which appears to be the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy showed that the addition of selenium at 1-5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E-deficient diet that was low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which by itself had no effect on the disease.
Studies on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have brought some order to the previous confusion about the role of vitamin E in chick nutrition. It is now apparent that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in the prevention of muscular dystrophy in the chicken. Glutathione peroxidase is soluble and is therefore located in the aqueous portions of the cell, while vitamin E is located mainly in the hydrophobic environments of membranes and in lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in the prevention of deficiency signs. "
http://www.avianmedicine.net/articles/vitamin-e.docdoc on vit E
http://ohioline.osu.edu/sc167/sc167_05.html(a few excerpts)
"....Researchers have found that selenium counteracts the toxicity of other elements such as silver, cadmium and mercury, but it is unlikely that these would play any role in practical poultry nutrition. A greater possibility was the presence of higher concentrations of copper and zinc that would interfere with normal metabolism. Both copper and zinc are used as dietary supplements in feed manufacturing. Broiler rations commonly contain copper supplements providing 120 to 240 ppm in addition to the 5 to 8 ppm included in the trace mineral mix. These levels have been used for years, because they improve performance and are believed to protect against fungal and perhaps other diseases.............Copper-selenium interaction studies showed that copper level influenced the requirement of chicks for selenium (Jensen, 1975b). Adding 800 or 1,600 ppm copper to a diet containing .2 ppm selenium caused high mortality and a high incidence of exudative diathesis and muscular dystrophy. Raising the selenium to .5 ppm prevented the mortality and the pathological conditions. Adding 2,000 ppm or more of zinc also caused high mortality, exudative diathesis and muscular dystrophy in chicks fed a similar diet. Raising the selenium level also prevented these effects.............
Involvement of Selenium in Poultry Diseases
In 1973, I joined the Poultry Science Department at The University of Georgia. A parasitologist on the faculty said he frequently observed a high incidence of greenish, gelatinous edema over the breasts in experimental birds exposed to coccidiosis. Coccidiosis is a major disease in chickens. The edema suggested an inadequate level of dietary selenium. We conducted experiments in which we inoculated chicks with a mixture of five coccidial species at two weeks of age. The chicks received a practical diet with or without selenium and/or vitamin E (Jensen et al., 1978). Mortality in chicks fed the unsupplemented diet reached levels as high as 68%, while those given selenium or vitamin E had much lower mortality.
Many studies have shown that selenium and vitamin E play a role in enhancing the immunity of animals. We studied the effect of these nutrients on the development of immunity to Eimeria tenella in young chicks. The chicks, fed diets with and without .25 ppm selenium or 100 IU vitamin E, were immunized at two weeks of age, then challenged with a high dose of E. tenella at about four weeks. Diet did not influence body weight at time of challenge, but the weight gain six days post-challenge was significantly greater in those fed the supplemented diets (Colnago et al., 1984).
During the conduct of the coccidial immunity experiments pens of chicks had to be kept in two different houses. At three weeks of age the chicks in only one house contracted Malabsorption Syndrome. This disease, also called Pale Bird Syndrome, occurs worldwide in broiler flocks. The etiology of this disease is still not determined, but it appears to be caused by a combination of viral and bacterial agents. Because the chicks were fed diets with and/or without selenium and vitamin E, the effect of these nutrients on the severity of the disease could be observed (Colnago et al., 1983). Thirty-four percent of the chicks fed the basal died, while selenium and vitamin E reduced it to a normal level. The combination of the two nutrients also significantly improved body weight gain...........................
....Selenium and Vitamin E Deficiency Diseases in Poultry
Deficiency diseases in chicks involving inadequate vitamin E or selenium include encephalomalacia, exudative diathesis, nutritional muscular dystrophy and nutritional pancreatic atrophy. Only vitamin E or some synthetic antioxidants prevent the first disease. Either selenium or vitamin E prevents exudative diathesis. To produce muscular dystrophy, the diet must be marginal in cystine. Vitamin E will prevent it, but selenium is only partially effective. Thompson and Scott (1969) found that pancreatic atrophy resulted from a specific deficiency of selenium and that vitamin E (100 IU/kg) could not prevent it. Later studies by Whitacre and Combs (1983), however, showed that very high levels of vitamin E or synthetic antioxidants could prevent the disease.
A vitamin-selenium deficiency in turkey poults differs from that in chicks. The major sign is muscular dystrophy, particularly of the gizzard and heart, but also of the breast muscle. In contrast to chicks, adding high levels of sulfur-containing amino acids has no influence on the myopathy (Walter and Jensen, 1963). Muscular dystrophy in turkeys is caused primarily by a selenium deficiency with vitamin E modifying the amount of selenium needed to prevent the disease.................."
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