White Muscle Disease
White muscle disease is a myodegenerative disorder of cattle that results from selenium deficiency. There are two forms of white muscle disease; a congenital form that affects the cardiac muscle, and a delayed form that is associated with either cardiac or skeletal muscle.
White muscle disease is a myopathy resulting from low levels of dietary selenium and vitamin E. Feeds grown in areas where the soil is deficient in selenium results in decreased uptake by the plant thus making the feed selenium-deficient. Vitamin E deficiency can be caused by large amounts of unsaturated fatty acids and other peroxide-forming substances in the diet. Another mechanism for selenium deficiency in cattle is the result of antagonistic effects of certain metals such as silver, copper, cobalt, mercury and tin.
Calves affected by the congenital form of white muscle disease usually die within 2-3 days of birth due to cardiac muscle degeneration. These calves will show signs of dyspnea due to cardiac failure as pericardial and pleural effusion develop. On necropsy, the heart will show white, chalky subendochondral plaques that are most noticeable in the left ventricle. The result is damage to cardiac muscle cells and Purkinje fibers.
Cattle affected by the delayed form or white muscle disease may exhibit signs ranging from general unthrift and stiffness, to walking with an arched back and spending more time recumbent, depending on the level of selenium in the diet. Often, the delayed form is brought on by vigorous exercise but if chronically affected, cattle can display splayed toes and a relaxation to the shoulder girdle. If a calf is affected severely it may die of starvation due to an inability to nurse properly due to weakness. The skeletal muscle lesions associated with the delayed from of white muscle disease are usually bilaterally symmetrical and can affect one or more muscle groups. The muscle will have white striations and feel dry and chalky due to abnormal calcium deposits.
Calves affected by white muscle disease can usually be diagnosied based on the characteristic signs and lesions. However, in mild cases, laboratory studies such as histologic examination and levels of glutathione peroxidase, AST, and CK may be necessary.
Cattle affected by white muscle disease have been treated with sodium selenite and vitamin E in sterile emulsion. This can be administered SC or IM, at 1 mg selenium and 50 mg (68 IU) of vitamin E per 18 kg (40 lb) body wt. If necessary, the treatment may be repeated two weeks later, but no more than four doses total should be given. In calves affected with simple vitamin E deficiency, treatment with dietary supplementation using α-tocopherol or substances rich in vitamin E can be used. Calves have been cured using 600-mg of α-tocopherol initially; followed by daily doses of 200-mg. Any polyunsaturated fats should be removed from the diet as these may be causing the vitamin E deficiency.
Preventing white muscle disease can be accomplished at many levels. First, soil deficient in selenium can be supplemented with selenium at 4 g/acre (10 g/hectare) in fertilizer. Second, feed known to be grown in selenium-deficient soils needs to be supplemented with additional selenium. In the USA, federal law controls supplementing feed with additional selenium so it is important to contact the appropriate authorities prior to beginning. Selenium can be supplemented in the form of sodium selenite, which contains 45.65% selenium. The recommended level of supplementation is 0.3 ppm selenium, calculated on the basis of total dry-matter intake. This needs to be thoroughly mixed and carefully measured to prevent accidental intoxication. Additional methods of preventing white muscle disease in cattle involve giving additional selenium to the cattle directly in the form of SC or intraruminal selenium pellets, selenium-fortified salt or mineral mixtures, or giving cows 15 mg of selenium, PO or SC, usually as sodium selenite, 4 wk prior to expected parturition. This will help prevent white muscle disease in calves born to these cows.
Smith, B.P. Large Animal Internal Medicine, 3rd Ed. Mosby-Elsevier Publishing. St. Louis, MO. 2009. pp.1279-1282.
Merck Veterinary Manual Online: http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/91002.htm