Merck Manual

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Toxic Myopathies in Ruminants and Pigs


Stephanie J. Valberg

, DVM, PhD, DACVIM, ACVSMR, McPhail Equine Performance Center, Michigan State University

Last full review/revision Apr 2014 | Content last modified May 2014

Plant Toxins

Plant toxins affect both cardiac and skeletal muscle. Clinical signs are not specific for the toxin and include anorexia, cardiac failure with tachycardia, dyspnea, diarrhea, stiffness, muscular weakness, recumbency, and myoglobinuria. Myonecrosis may occur when gossypol is fed. Monogastrics, including young calves, should not ingest feed containing >200 ppm gossypol, whereas mature ruminants may tolerate 20 g of gossypol/head/day. Senna obtusifolia (sicklepod) is prevalent in the southeastern USA, and ingestion of its seeds by swine or ruminants may cause a degenerative skeletal and/or cardiomyopathy. Trematone is a toxic component of white snakeroot (Eupatorium rugosum), which grows in shaded areas of the eastern and central USA, as well as rayless goldenrod (Isocoma wrightii), which is common in the Southwest on open pastures. Ingestion of these plants in quantities of ~2% of body weight can cause a fatal cardiomyopathy and severe skeletal muscle degeneration. Trematone remains active in hay and in the stalks of the dead plants on pasture.


Ionophores added to feeds in excess of recommended levels can cause cardiac and skeletal muscle necrosis. Experimental studies have indicated that LD50 values for monensin are 12, 17, 26, and 21–36, for sheep, pigs, goats, and cattle, respectively. Feed concentrations of 100 g/ton and 400 g/ton have been fatal to sheep and cattle, respectively. Newborn calves dosed with 100 mg lasalocid tid for cryptosporidiosis experience muscle necrosis. Other ionophores include naracin, salinomycin, and laidlomycin. At necropsy, pale areas of myocardial necrosis and pulmonary congestion are usually prominent in cattle. Pigs and sheep tend to have mainly skeletal muscle lesions that appear quite similar grossly and histologically to those of nutritional myodegeneration. Diagnosis requires history of exposure with development of characteristic clinical and pathologic alterations.

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