Experimental myopathy in vitamin E- and selenium-depleted calves with and without added dietary polyunsaturated fatty acids as a model for nutritional degenerative myopathy in ruminant cattle.

Fourteen calves, 14 weeks old, fed a low vitamin E and selenium diet based on sodium hydroxide-treated, selenium-deficient barley showed a rapid decline in plasma alpha-tocopherol, a gradual decline in erythrocyte glutathione peroxidase (GSHPX) activity, elevated plasma creatine kinase (CK) activity, teeth grinding and (in three cases) electrocardiographic changes, but no clinical abnormalities after 127 to 137 days. Necropsy of six depleted calves at that stage revealed pale muscles in two animals and mild histopathological lesions of skeletal myopathy in all six calves. Ten control calves were fed a similar diet supplemented with alpha-tocopherol and selenium. Plasma alpha-tocopherol and erythrocyte GSHPX activity remained high in these calves and no clinical abnormalities or evidence of myodegeneration were observed. When protected linseed oil was fed as a source of polyunsaturated fatty acids to the remaining eight depleted calves, rapid elevations in plasma CK activity and linolenic acid associated with a variety of cardiopulmonary and locomotory signs, electrocardiographic changes and myoglobinuria occurred within six to 11 days. Necropsy revealed widespread severe skeletal myodegeneration (eight calves) and myocardial lesions (five calves) with preferential involvement of the left ventricular myocardium. Clinical signs and pathological changes were similar to those reported in field outbreaks of nutritional degenerative myopathy in ruminant cattle and establish the experimental regime as the first successful model for reproduction of this disease.