A sudden increase in mortality, preceded by a short history of respiratory signs and diarrhea, occurred in a backyard flock of 48 game chickens in the Central Valley of California. Necropsy findings included severe generalized linear hemorrhages and/or ulcers in the digestive tract, larynx, and trachea. Histology revealed severe multifocal hemorrhages and necrosis in the mucosa of the respiratory and digestive tracts, vasculitis, and necrosis of lymphoid tissue. The birds were serologically negative to Newcastle disease virus; this was consistent with an acute infection. The avian paramyxovirus type 1 isolated was characterized as velogenic viscerotropic Newcastle disease virus. A thorough epidemiologic investigation was carried out, and no other premises were found to have birds with clinical signs or evidence of exposure. The entire outbreak was limited to the original backyard flock and resolved within 14 days of the onset of clinical signs.

Abstract. In May 1996, 150 grower pigs in 5 California counties were exposed to selenium-contaminated feed distributed by a single feed company. Feed samples from 20 herds had a mean selenium concentration of 121.7 ppm dry weight (range, 22.1-531 ppm). In San Luis Obispo County, 52 pigs in 24 herds were exposed to the feed, and 8 pigs died with signs of paralysis. Bilateral symmetrical poliomyelomalacia involving the ventral horns of the cervical and lumbar intumescence was evident on histologic examination of spinal cord from affected pigs. Of 44 surviving exposed pigs, 33 (75%) exhibited signs of selenosis, including anorexia, alopecia, and hoof lesions. Thirty-nine of 44 pigs (88.6%) had elevated (Ͼ1 ppm) blood selenium concentrations. Surviving exposed pigs were changed to a standard commercial ration containing approximately 0.5 ppm (dry weight) selenium. Blood selenium concentrations were determined weekly for 46 days following removal of the contaminated feed and were compared with values of 20 control pigs fed a standard commercial ration. Mean (ϮSD) blood selenium concentrations of exposed pigs were 3.2 Ϯ 2.6 ppm at the initial sampling and 0.4 Ϯ 0.1 ppm after 46 days. Mean blood selenium concentrations of Յ 0.3 ppm for control pigs at all samplings were significantly lower (P Ͻ 0.001) than concentrations for exposed pigs. Muscle and liver samples of 22 of the 44 exposed pigs were collected at slaughter approximately 72 days after withdrawal of the selenium-contaminated feed. Muscle samples had a mean selenium concentration of 0.36 ppm (wet weight). Liver samples had a mean selenium concentration of 1.26 ppm (wet weight). One liver sample had a selenium value in the toxic range for pigs (3.3 ppm wet weight; reference range, 0.4-1.2 ppm). A 1-compartment pharmacokinetic model of selenium elimination in exposed pigs was generated, and the geometric mean blood selenium elimination half-life was estimated to be 12 days. The 60-day withdrawal time recommended by the Food Animal Residue Avoidance Database was considered sufficient to allow safe human consumption of tissues from exposed pigs.Selenium is an essential trace element for swine, necessary for cells to detoxify peroxides. 29 It is one of the most toxic trace elements 26,33 and has a narrow margin of safety. Toxicosis has been reported in swine after repeated ingestion of feed containing Ͼ5 ppm selenium (dry weight). 4,12,[24][25][26] Signs of selenium toxicosis in swine include anorexia, alopecia, separation of hoof and skin at the coronary band, degenerative changes in the liver and kidney, and poliomyelomalacia. 16,26,27,33 In 1974, the US Food and Drug Administration (FDA) authorized the addition of a sodium salt of selenium to swine feed at a concentration of 0.1 ppm (dry weight) in the complete ration. 32 Current FDA regulations allow a maximum of 0.3 ppm (dry weight) in the complete ration as either inorganic sodium selenite or selenate. 7 Sodium selenite is the most commonly used selenium compound in domestic feed because of its lower cost, a...