Submitted to: Journal of Veterinary Diagnostic Investigation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/1/2011
Publication Date: 3/1/2012
Citation: Davis, T.Z., Stegelmeier, B.L., Panter, K.E., Cook, D., Gardner, D.R., Hall, J.O. 2012. Toxicokinetics and pathology of plant-associated acute selenium toxicosis in steers. Journal of Veterinary Diagnostic Investigation. 24(2): 319-27. Interpretive Summary: Selenium (Se) is an essential element which is necessary for the activity of many enzymes and proteins. Excessive Se in forages, feeds or supplements can result in either chronic or acute Se toxicosis. Chronic Se toxicosis is caused by consuming feeds or forages with high concentrations of Se over a period of weeks to months. Acute Se toxicosis is caused by calculation errors in Se supplements, misformulated feed rations, and ingestion of Se accumulator plants. Over 15,000 sheep died during the summers of 1907 and 1908 in a region north of Medicine Bow, Wyoming and the losses were attributed to the grazing of the Se accumulator plants, woody aster and Gray’s vetch. This report is a description of acute Se toxicosis in steers caused by ingestion of Se-accumulator plants (Aster ascendens) while grazing on a reclaimed mine site. Several dead animals that were necropsied had acute severe myocardial necrosis characterized by edema, myocyte swelling, with hypereosinophilia, clumping and coagulation of myocardial proteins. One animal, died 18 days after exposure, was necropsied and had severe multifocal myocardial fibrosis with extensive hepatic congestion, degeneration, and hemosiderosis. The Se elimination half-lives from serum, whole blood, liver, muscle and hair of the recovering steers were determined. In conclusion these findings indicate that cattle are extremely sensitive to Se toxicity from accumulating plants. We also found that the primary change of acute Se toxicity in cattle is myocardial necrosis with subsequent heart failure seen as passive congestion and centrilobular hepatic congestion with hepatocellular degeneration and necrosis. A small percentage of animals may not die immediately however, if myocardial damage is significant these animals develop myocardial fibrosis and subsequent heart failure. We also found that Se is slowly excreted from some tissues thus, requiring long withdrawal times.
Technical Abstract: Sixteen of about 500 yearling steers died of acute selenium (Se) toxicosis after grazing Se contaminated range for only a few days. Field studies and chemical analyses identified the predominant toxic plant as western aster (Aster ascendens), which contained over 4,000 ppm Se. Several dead animals that were necropsied had acute severe myocardial necrosis characterized by edema, myocyte swelling, with hypereosinophilia, clumping and coagulation of myocardial proteins. Whole blood from 36 surviving steers was collected and analyzed and ten steers with elevated Se concentrations were selected for close monitoring and clinical evaluations. Each steer was weighed and serum, blood, liver, skeletal muscle, and hair were regularly collected after removal from the Se-contaminated range. One animal, died 18 days after exposure, was necropsied and had severe multifocal myocardial fibrosis with extensive hepatic congestion, degeneration, and hemosiderosis. At 180 days post-exposure two of the ten steers were slaughtered, tissues were collected and both had rare, small fibrotic foci in their hearts. The Se elimination half-lives from serum, whole blood, liver, and muscle of the recovering steers were 40.5±8.2, 115.6±25.1, 38.2±5.0, and 98.5±19.1 days, respectively. The Se concentration in hair reached a peak of 11.5±5.3 ppm at 22 days post-exposure. These findings indicate that cattle are sensitive to acute Se toxicosis caused by ingestion of Se-accumulator plants; the primary lesion in cattle is myocardial necrosis; some poisoned animals may develop congestive heart failure weeks after the toxic exposure; and in this study Se was slowly excreted requiring a relatively long withdrawal time.