Acute oral selenium poisoning due to consumption of plants or mis-mixed diets with levels >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.
The majority of deaths usually follows within a few hours to 2 days after consumption or injection. The major lesions are pulmonary edema, pulmonary congestion, pulmonary hemorrhage, hepatic necrosis, myocardial necrosis, myocardial hemorrhage, and potentially renal necrosis.
Blood and serum selenium concentration in acute poisoning is often higher than in chronic poisoning. Treatment consists of symptomatic and supportive care. Acetylcysteine to boost glutathione levels may be beneficial.
Last full review/revision March 2012 by Jeffery O. Hall, DVM, PhD, DABVT