Experimental models for nutritional myopathy

Nutritional myopathy is a disease affecting young ruminants. The aetiological factors and their relative importance in disease development have been explored. A theoretical model has been developed and tested experimentally. The disease can be produced consistently using a recently developed vitamin E- and selenium-deficient diet. Disease can occur spontaneously in animals maintained on this diet alone over an extended period. Alternatively, myopathy can be induced in deficient animals by feeding polyunsaturated fatty acids such as linoleic and linolenic acid from corn and linseed oils respectively. For ruminants the oils are protected to prevent hydrogenation in the rumen. Because a similar protective mechanism appears to occur with normal ruminant forages such as grass, and the development of disease is so similar to that occurring naturally, polyunsaturated fatty acids are thought to play a major role in the development of the disease. The experimental disease reproduces extensive and consistent lesions of skeletal and cardiac myopathy. Hyaline necrosis occurs in the skeletal muscle fibres of many major muscle groups. In the heart the accumulation of droplets of lipofuscin-like pigment in Purkinje fibres is the initial lesion, followed by necrosis of Purkinje fibres and peri-Purkinje fibrosis. The accumulating pigment has been characterized by fluorescence spectroscopy and histochemical techniques. The cardiac pathology results in detectable electrocardiographic abnormalities and sudden death.