Deficiency diseases-selenium and vitamin e deficiency, Biology

Selenium and vitamin E deficiency

Selenium is an essential micro-mineral required for various physiological functions and for immunity against a variety of diseases. It is an important component of enzyme glutathione peroxidase, a vital component of antioxidant defence of the body. Vitamin E acts as free radical scavenger and prevents oxidative damage to cell membrane. Dietary deficiency of either selenium or vitamin E or both is associated with deficiency of either or both the nutrients .An important metabolic interrelationship exists between selenium and vitamin E in prevention of oxidative damage and diseases caused by their deficiency. Selenium and vitamin E act synergistically in potentiating immune response, prostaglandin biosynthesis, blood clotting and anticancer activities. The two micronutrients are required for amelioration of various joint problems and skeletal and skin diseases. In most species of animals, deficiency of either selenium or vitamin E or both is associated with muscular dystrophy. A conditioned Vitamin E deficiency has been reported due to presence of polyunsaturated fatty acid in the diet. Incidences of selenium deficiency diseases are reported worldwide, and certain myopathies in farm animals have been found to respond to selenium treatment.

Clinical findings:
Nutritional (enzootic) muscular dystrophy, retained placenta and resistance to mastitis in cattle, nutritional muscular dystrophy in horses, nutritional (enzootic) muscular dystrophy, ill-thrift, bone marrow abnormalities and reproductive inefficiency in sheep, and mulberry heart disease, hepatosis dietetica, exudative diathesis, nutritional muscular dystrophy and anaemia in pigs are considered to be associated with deficiency of either  vitamin E or selenium or both the micronutrients. Sudden death after exercise without any clinical signs may be seen in the animals affected with acute enzootic muscular dystrophy. Affected calves exhibit sudden onset of dullness and severe respiratory distress. Blood stained or frothy nasal discharge may be noticed in some cases. Muscular stiffness, arrhythmias, and tachycardia are also seen. Affected calves, lambs and foals usually assume lateral recumbency and are unable to stand. The heart and respiratory rates are usually increased, but temperature is low or slightly elevated. Death of affected animals may occur within 6-12 hours with 10% case fatality rate.

Subacute muscular dystrophy is relatively a milder and the commonest form in rapidly growing calves (white muscle disease) and in young lambs (stiff lamb disease). Sick animals are usually recumbent and unable to stand. However some may stand for few minutes with stiff and staggering gait, severe weakness of leg muscles and trembling. Gait in calves is marked by movement of hocks. Lambs show stiffness and goose-stepping gait. Involvement of diaphragm and intercostals muscle causes respiratory distress with laboured and abdominal type respiration. Elevated heart rate  and transient fever are also seen. Protrusion of scapula over vertebral column and its separation from thorax (Flying scapula) is reported in heifers grazing over selenium deficient pasture. Sick animals respond favourably to the treatment.Congenital muscular dystrophy has been associated with low selenium and vitamin E levels in serum in newborn calves. In foals, muscular dystrophy occurs most commonly during first few months of age. The common clinical signs are failure to suck, recumbency and unsteadiness and trembling when foals are forced to stand. Aspiration pneumonia and stunting are common complications of muscular dystrophy in foals. Adult horses show signs of stiff gait, myoglobinuria, depression, inability to eat, and oedema of head and neck.

Subclinical nutritional muscular dystrophy has been reported in apparently normal animals and can be identified by increased activities of creatine phosphokinase enzyme, and abnormal electrocardiogram.Mulberry heart disease develops due to selenium and Vitamin E deficiency in growing piglets below four month age. Affected pigs are often found dead without premonitory signs. Live animals show severe dyspnoea, cyanosis and recumbency. The condition is commonly diagnosed on post-mortem by lesions of extensive haemorrhages, necrotic spots on myocardium alongwith transudation in the serous cavity.Hepatosis dietetica is a rarely occurring spontaneous condition in pigs below four months of age, which are reared indoor on high grain -selenium and vitamin E deficient diets. Mostly piglets are found dead without any signs. Occasionally, there will be dyspnoea, severe depression, vomiting, staggering, diarrhoea and state of collapse. Both Mulberry heart disease and hepatosis dietetica are characterized by muscular dystrophy.

Diagnosis: Measurement of plasma creatine kinase (CK) is the most commonly used laboratory test for diagnosis of nutritional muscular dystrophy. The CK activities in affected cattle, sheep and pigs are increased usually above 1000 IU/l or even higher. The test is also useful in monitoring the treatment progress. Aspartate aminotransferase (AST) also indicates muscle damage. In acute cases, AST activity may increase to 300-900 IU/l in calves and 2000-000 IU/l in lambs. Estimation of selenium content in forages and grains, soil and animal tissue, blood and milk; vitamin E status in serum and glutathione peroxidase activity in blood and tissues are also used to support diagnosis of the disease.

Treatment and Prevention: Intramuscular administration of a mixture containing 3 mg selenium and 150 IU/ml of á-tocopherol at dose rate of 2 ml/45 kg body weight is recommended treatment for calves, foals, and lambs. One treatment is usually sufficient. The therapy is also used for prophylactic treatment. Control and prevention measures include providing appropriate levels of selenium and vitamin E in the diet. A slow releasing preparation of barium selenate is available for use in cattle and sheep. The dose is 1 mg selenium per kg body weight subcutaneously. Muscular dystrophy in calves and lambs can be prevented by providing selenium and vitamin E in the diets of the cows or ewes at 0.1 mg/kg DM (1g/day in cows; 75 mg in ewes) during pregnancy.  In some circumstances levels upto 1 mg/kg DM is recommended. Selenium deficient rations of pregnant cows and ewes should be supplemented with mineral mixture containing selenium (14.8 mg/kg) and vitamin E (2700 IU/kg) during the later two third of gestation and for the first month of lactation.

Posted Date: 9/19/2012 2:29:41 AM | Location : United States

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