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Professional Version

Acute Selenium Toxicosis


Jeffery O. Hall

, DVM, PhD, DABVT, Utah State University

Last full review/revision May 2014 | Content last modified Jun 2016

Acute oral selenium poisoning due to consumption of plants or mis-mixed diets with concentrations >50 ppm (dosages 1–10 mg/kg or greater, depending on the species, age, and chemical form of selenium) is not common but has caused large losses in cattle, sheep, and pigs. Animals usually avoid plants with high selenium content because of their offensive odor; however, when pasture is limited, accumulator plants may be the only food available. In some cases, plants may not have the profound offensive odor. Young animals are most susceptible to acute parenteral selenium toxicosis with dosages of 0.2–0.5 mg/kg. Clinical signs are different from those of chronic selenosis and are characterized by abnormal behavior, respiratory difficulty, GI upset, and sudden death. Abnormal posture and depression, anorexia, unsteady gait, diarrhea, colic, increased pulse and respiration rates, frothy nasal discharge, moist rales, and cyanosis may be noted. Sheep usually show these signs to a much lesser degree or just become depressed and die suddenly.

Most deaths usually follow within a few hours to 2 days after an acutely toxic consumption or injection of selenium. The major lesions are pulmonary edema, pulmonary congestion, pulmonary hemorrhage, hepatic necrosis, myocardial necrosis, myocardial hemorrhage, and potentially renal necrosis.

Blood or serum selenium concentration in acute poisoning is often higher than in chronic poisoning. Treatment consists of symptomatic and supportive care. Acetylcysteine to boost systemic glutathione concentrations may be beneficial.

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