Subclinical nutritional myopathy was induced in 5-month-old sheep by feeding them a diet low in vitamin E and selenium. Subsequently clinical myopathy was induced by dosing with protected polyunsaturated fatty acids. Plasma activities of creatine kinase (CK), pyruvate kinase, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase and aldolase, enzymes of muscle origin, all remained above their reference ranges in clinically affected sheep, but fluctuated widely. Similar fluctuations occurred in subclinically affected animals, resulting in some activities being within the reference ranges and some above, at different times. Plasma malondialdehyde, an indicator of lipid peroxidation, proved of no diagnostic value. Terminal plasma CK activities were significantly correlated with microscopic damage in the vastus lateralis (VL), but not the vastus intermedius (VI) or the tensor fascia lata (TFL) muscles. AST was the most highly correlated with damage in VI and VL. In two clinically affected sheep successfully treated with an oral dose of alpha-tocopherol acetate all enzymes decreased steadily to within their reference ranges, at rates probably related to their plasma half-lives. These results suggest that measurement of plasma CK activity would be useful in monitoring recovery of treated sheep.
The diagnostic performance of plasma tests for muscle enzymes was measured in sheep from flocks affected by clinical and sub-clinical nutritional myopathy. Parallel combinations of tests for creatine kinase (CK), alanine amino transferase (ALT), aspartate amino transferase (AST) and lactate dehydrogenase had higher diagnostic sensitivity than CK alone. The enzymes ALT and AST showed the highest correlation with the degree of muscle damage. A parallel combination of tests for plasma CK and ALT as well as tests for plasma alpha-tocopherol and red cell glutathione peroxidase are recommended for the diagnosis of nutritional myopathy and a decision on the appropriate treatment. The number of false negative results based on a diagnosis from the microscopic examination of single muscles was higher than for the parallel combination of tests. The number of false negatives was highest for the vastus intermedius and lowest for the tensor fascia lata. Diagnosis using a panel of blood tests has the advantages of overcoming problems of inadequate muscle sampling, a larger number of sheep in the flock can be tested and a more rapid diagnosis can be obtained.
Nutritional myopathy occurs as both a clinical and subclinical disease in weaner sheep in Western Australia during summer and autumn. The effect of subclinical nutritional myopathy (SCNM), caused by vitamin E deficiency or combined vitamin E and selenium deficiency, on liveweight and wool was investigated. During the period of SCNM there was no significant difference in liveweight gain in sheep with and without the disease in any of the experiments. Initial liveweight in one experiment was significantly (P < 0.05) higher in sheep that were to develop SCNM during the course of the experiment. In vitamin E deficient-selenium adequate SCNM, there was no difference in wool growth over the period of the disease and no differences in any of the wool measurements at shearing. At 2 sites, the greasy and clean fleece weights were significantly (P < 0.05) greater in a group of sheep diagnosed with more severe SCNM compared with sheep without SCNM. It was concluded that unlike the clinical disease, SCNM was unlikely to cause any economic loss.
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