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Incidence of White Muscle Disease
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While white muscle disease used to be commonplace; but reports of this disease in newborn bovine calves are now rare. This may be due to the increased use of vaccinations worldwide. Development of better feeds has also decreased the incidence of Enzootic Muscular Dystrophy. Typically within the first ten days, the newborn receives injections of vitamin E and selenium to prevent the sickness. In cases where white muscle disease is suspected, nutritional deficiencies are usually found.
The Biochemistry of White Muscle Disease Development
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Dietary polyunsaturated fatty acids, unaccustomed exercise, and rapid growth are precipitating factors in developing white muscle disease. Vitamin E and selenium both protect cellular membranes from free radicals, which cause peroxidation of the membrane lipids. Vitamin E decreases hydroperoxide formation, which destroys free radicals both inside and outside of the cell. Selenium is an essential element of the enzyme glutathione peroxidase, an enzyme that works from inside the cell to protect its membranes and organelles from peroxidative damage. With low levels of vitamin E or selenium, cell membranes are damaged, letting too much calcium in and injuring the mitochondria. The mitochondrion, the powerhouse of the cell, is necessary to maintain homeostasis. Injury results in cell death or segmental necrosis.
History of Enzootic Muscular Dystrophy
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In 1953, Doctors Blaxtar and Sharman of the North of Scotland College of Agriculture reported that muscular dystrophy of suckling beef calves was quite commonplace. The disease occurred in 15 to 25 percent of all farms rearing beef cattle, and the incidence on these farms occasionally approached 90 per cent. The disease appeared to be similar to experimental vitamin E deficiency and cod-liver oil toxicity syndrome of calves. It usually occurred in calves born indoors in spring to mothers that had been housed since the previous autumn, and the winter feed tended to be low in alpha-tocopherol (vitamin E). Cod liver oil was the usual treatment.
A Case Study of Congenital Muscular Dystrophy
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Sameeh Abutarbush and Otto Radostits, veterinary doctors at Western College of Veterinary Medicine in Saskatchewan, Canada, studied a thirteen-hour-old Aberdeen Angus female calf who was admitted to their Large Animal Clinic for recumbency and inability to move. Based on the clinical findings, increased serum creatine kinase, and decreased serum vitamin E and selenium levels, the doctors suspected Congenital Muscular Dystrophy. A muscle biopsy, which could have confirmed the diagnosis, was not done. The doctors suspected that the calf's inability to suck had been caused by weakness of the tongue muscles. Further complications were due to lack of protein and immunoglobulins from colostrums. The calf was treated with supportive fluid therapy, vitamin E, and selenium, with a positive outcome. In their 2003 report, they stated that cases of Congenital Muscular Dystrophy are now very rare.
Treatment and Prevention
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Treat early cases of white muscle disease with parenteral injection of vitamin E and selenium. A veterinarian must be consulted for accurate diagnosis and treatment since high levels of selenium are toxic. Measure selenium whole blood levels and alpha-tocopherol plasma levels. Selenium and vitamin E deficiencies may also cause reproductive failure and red blood cell fragility from increased oxidative damage.
Prevent white muscle disease by vitamin E and selenium dietary supplements to pregnant dams, or by strategic oral and/or parenteral vitamin E and selenium to pregnant dams or young animals on pasture.
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Baby Calf Muscle Diseases
White muscle disease, otherwise known as Nutritional Muscular Dystrophy, is caused by a deficiency of vitamin E, selenium, or both. If present at birth, it is known as Congenital Muscular Dystrophy; if onset is later it may be referred to as Enzootic Muscular Dystrophy. It occurs in all farm animal species, especially calves, lambs, kids, and foals. Clinical indices include stiffness, weakness, and recumbency. Clinical diagnosis can be confirmed by elevated levels of muscle enzymes (CK and AST); low levels of vitamin E and selenium in the diet, tissue, and serum; and muscle degeneration. Affected muscles are usually pale at necropsy.