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November 21, 1980

On the Pathogenetic Mechanism of Quail Myopathy

JAMA. 1980;244(20):2263-2264. doi:10.1001/jama.1980.03310200015013

To the Editor.—  Many cases of quail poisoning have been recently reported in Algeria,1 but more have been reported in Greece.2,3 Remarkable muscle stiffness, pain, and muscle weakness in conjunction with myoglobinuria are the cardinal findings in this strange myopathy. The clinical syndrome has a short duration (one to three days) and generally a good prognosis. Nevertheless, in a few cases myoglobinuria is severe enough to produce acute renal failure (myoglobinuric nephrosis), which is sometimes fatal. An enzymatic defect in skeletal muscle fibers might explain the vague pathogenetic mechanism of this peculiar syndrome that effects only sensitive persons (211:1186, 1970).2 Quails are probably carriers of an unknown toxic agent that in these particular persons produces rabdomyolysis. A defect in the anaerobic glycolysis of skeletal muscle fibers of sensitive persons was suspected2,3 because of some clinical similarities of the syndrome with McArdle's metabolic myopathy where myophosphorylase is