Exudative diathesis

In 1956 selenium was identified (123) as an essential micronutrient iu nutrition. In conjunction with vitamin E, selenium is effective iu the prevention of muscular dystrophy iu animals. Sodium selenite is adrninistered to prevent exudative diathesis iu chicks, a condition iu which fluid leaks out of the tissues white muscle disease iu sheep and infertility iu ewes (see Eeed ADDITIVES). Selenium lessens the iacidence of pneumonia iu lambs and of premature, weak, and stillborn calves controls hepatosis dietetica iu pigs and decreases muscular inflammation iu horses. White muscle disease, widespread iu sheep and cattle of the selenium-deficient areas of New Zealand and the United States, is insignificant iu high selenium soil areas. The supplementation of animal feeds with selenium was approved by the U.S. EDA iu 1974 (see Eeed additives). Much of selenium s metaboHc activity results from its involvement iu the selenoproteia enzyme, glutathione peroxidase. 

To some extent the vitamin E requirement may be lessened by the presence in the diet of synthetic antioxidants and by selenium. Much evidence supports a relationship between the nutritional need for selenium and that for vitamin E. Lack of either causes muscular dystrophy in many animals as well as severe edema (exudative diathesis) in chicks. Since vitamin E-deficient rats have a low selenide (Se2 ) content, it has been suggested that vitamin E protects reduced selenium from oxidation.) Vitamin C (ascorbic acid), in turn, protects vitamin E. 

Observations on deficiency symptoms in the cardiovascular system were also made [29, 30]. In chicks, exudative diathesis, a condition in which plasma moves from the capillaries into surrounding, particularly subcutaneous, tissue, was studied and found to be associated with lipid peroxidation [31]. In cardiac muscle, a necrotizing myopathy was found in vitamin-E-deficient mice [32], rats [33], rabbits [34] and ruminants [35], Blood abnormalities, associated with increased susceptibility of erythrocytes to haemolysis, figure among reports of the effects of vitamin E deficiency [36, 37]. 

Gross necropsy lesions of a selenium deficiency are identical to those of a vitamin E deficiency (NRC, 1994) and include exudative diathesis and myopathy of the gizzard. Paleness and dystrophy of the skeletal muscles (white muscle disease) are also common. The incidence and degree of selenium deficiency may be increased by environmental stress. Selenium is generally included in trace mineral premixes. Common sources for supplementation of poultry diets are sodium selenite and sodium selenate. Selenium yeast is also used in conventional diets. 

In growing chicks, a deficiency can result in (i) encephalomalacia or crazy chick disease (ii) exudative diathesis, an oedema caused by excessive capillary permeability or (iii) muscular dystrophy. Encephalomalacia occurs when the diet contains unsaturated fats that are susceptible to rancidity. Some antioxidants, in addition to vitamin E, are also effective against encephalomalacia. Exudative diathesis is prevented by dietary selenium, and muscular dystrophy is a complex disease influenced by vitamin E, selenium, and the... 

Cantor, A.H., Langevin, M.L., Noguchi, T., and Scott, M.L. 1975c. Efficacy of selenium in selenium compounds in feedstuffs and selenium compounds for prevention of exudative diathesis in chicks. J. Nutr. 105, 106-111. 

Vitamin E-deficient animals show exudative diathesis, in which there is leakage of blood plasma from capillaries into subcutaneous tissues, apparently the result of abnormal permeability of capillary blood vessels. There is an accumulation of (usually green-colored) fluid under the skin. This responds to synthetic antioxidants or selenium. 

Studies with animals have revealed an interesting pattern of relahorLships involving Se and vitamin E nutrition. In chicks, experimentally induced deficiencies in both S5e and vitamin E result in exudative diathesis, muscular dystrophy, and pancreatic atrophy. The first two problems can be prevented by vitamin E... 

Characteristic lesions of vitamin E deficiency in animals include necrotizing myopathy (inaccurately referred to as nutritional muscular dystrophy), exudative diathesis, nutritional encephalomalacia, irreversible degeneration of testicular tissue, fetal death and resorption, hepatic necrosis, and anemia. Several of these conditions are directly related to peroxidation of unsaturated lipids in the absence of vitamin E, and others can be prevented by synthetic antioxidants or vitamin E. 

The spatial heterogeneity of selenium content in rocks, various soils, and especially the peculiarities of its translocation from soils to plants, lead to the formation of so-called selenium biogeochemical provinces (see Chapter 7 Biogeochemical mapping ). These provinces are characterized by a deficient or excessive concentration of this trace metal in all links of biogeochemical food webs. Selenium deficiency in fodder crops is related to the less than 30 ppm content of this element (Table 8). This leads to myopatia (white colored animal tissues), necrotic degeneration of kidney, exude diathesis. The addition of sodium selenite is used for prevention of these diseases. 

Schwarz observed that rats maintained on yeast diets developed a fatal necrosis of the liver, which could be prevented either by vitamin E and cysteine, as well as by a third factor ( Factor 3 ), which was recognized to be an organic selenium compound (Schwarz and Foltz 1957). Sodium selenite and other inorganic and organic selenium compounds were generally found to have lower Factor 3 activity. Other selenium-responsive disorders are White Muscle disease in sheep, calves, and horses, hepatosis dietetica and mulberry heart disease in swine, and exudative diathesis and pancreatic fibrosis in chickens. In goats, selenium deficiency adversely affected growth, reproduction and milk performance (Anke et al. 

With regard to the nutritional aspects of selenium metabolism, the essentiality of this element was established in studies which demonstrated that a number of deficiency diseases " such as exudative diathesis in chicks and turkeys, necrotic liver degeneration in rats and swine and white muscle disease which is a nutritional type of muscular dystrophy often affecting young lambs and calves, could be overcome or prevented by administering small doses of selenium. 

Vitamin E (a-, P-, y-tocopherol) Sterility, encephalomalada, exudative diathesis Antioxidant, protection against peroxide ... 

On the basis of present experience, this diet can be simplified and improved by omitting skim milk powder, cod liver oil, yeast, and paper pulp, and introducing gelatin and pure vitamins. Increase of the content of lard to 30% will accelerate the onset of enceplialomalacia. Addition of a trace of selenite will eliminate appearance of exudative diathesis which might result from the simplification of the diet. 

While these studies were in progress, exudative diathesis, another disease in chicks, was described, and shown to be a consequence of vitamin E deficiency (Dam and Glavind, 1939a, b). 

The diets first used for the production of exudative diathesis contained casein and cod liver oil (Table II). 

Though this diet sometimes also produced encephalomalacia, the exudative diathesis was the predominant symptom. On the contrary, diet No. 108 of Pappenheimer and Goettsch almost never produced exudative diathesis. (According to present knowledge, this must have been due, at least in part, to a higher content of selenium in diet 108.)... 

The fat components of these diets were essential for the development of the symptoms. When the fats were eliminated, encephalomalacia never appeared and exudative diathesis was very rare. Furthermore, the symptoms did not appear when the cod liver oil in diet 182 was made thoroughly rancid either before it was added to the diet, or after the mixed diet was left to stand in shallow trays at 50°C for 1 week, whereupon the iodine value dropped to 62 (Dam, 1943). 

The fact that autoxidation was going on in the adipose tissue of chicks suffering from exudative diathesis produced by cod liver oil (5%) was demonstrated by Dam and Oranados (1945a) by direct determination of... 

According to present knowledge, the essential feature of this diet is that its content of selenite (and vitu-niin K) is sufficient to prevent exudative diathesis when cod liver oil is omitted, but not when cod liver oil or other polyunsaturated fat is present. The diet can be simplified by omitting gum arable and yeast and introducing pure vitamins. If cod liver oil is replaced by a small amount of ethyl linolenate, enoephalomalacia is avoided but exudative diathesis will still occur. 

It was found later (cf. Dam, 1953) that certain redox dyes and certain other unphysiological antioxidants fed at a higher level than that required for a-tooopherol could delay and ameliorate the exudative diathesis. Presumably, this is due to conservation of vitamin E in the tissues of the animal. Possibly it spares tocopherol in the dietary cod liver oil, which... 

The next important development came when Torula yeast was used in place of casein in diets for the production of exudative diathesis in chicks (Scott et al., 1955 Bieri et al., 1957). 

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