Selenium Toxicity in Breeding Ring-Necked Pheasants (Phasianus colchicus)

Abstract

A flock of breeding ring-necked pheasants received feed with a high selenium content. Within 4 days of eating the toxic feed, the rate of egg production began to decrease, and bird aggression increased. Approximately 12% of the hens died within a week. Necropsy of the hens revealed colorless fluid around the heart and a friable, but otherwise normal, liver. The rapid onset of the problem and signs noted at necropsy suggested toxicosis. Based on analysis, the feed contained 9.3 ppm of selenium. Selenium toxicity was consistent with the histologic diagnosis of degenerative cardiomyopathy, vacuolar degeneration of hepatocytes, and centrilobular hepatic necrosis. After 8 days, the toxic feed was removed and replaced with fresh feed. Egg production, which had dropped to 50%, returned to normal within 10 days of feed replacement. Hatchability of eggs laid from days 8 to 14 after delivery of the toxic feed was 35%. Approximately 10% of the chicks that hatched had deformed beaks and abnormal eyes. Many of the chicks that died in the shell had deformities, bringing the total to more than 50% of all embryos that developed. The selenium content of eggs that had no embryonic development was 2.05 ppm. Hatchability of eggs laid from days 21 to 28 after the toxic feed was delivered was almost 80%, which was slightly lower than normal. The selenium content of these eggs was 0.30 ppm. These results show the rapid onset and correction of selenium toxicity and suggest that specific embryologic defects are diagnostic for selenium toxicity.