Selenium Elimination in Pigs after an Outbreak of Selenium Toxicosis

Abstract

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...

Intoxicação por selênio em suínos no Sul do Brasil

“…Os achados clínicos e patológicos dos surtos aqui descritos são compatíveis com os casos de intoxicação espontânea e experimental por selênio em suínos (Harrison et al 1983, Wilson et al 1983, 1988, 1989, Castell et al 1985, Saford 1990, Stowe et al 1992, Schultz & Hoffmann 1995, Panter et al 1996, Penrith & Robinson 1996, Banholzer & Heinritzi 1998, Davidson-York et al 1999, Casteignau et al 2006, Nathues et al 2010. Os achados histológicos sugerem um diagnóstico provável de intoxicação por selênio, pois o excesso de ingestão de selênio é a única causa conhecida de poliomielomalácia simétrica focal em suínos (Wilson et al 1983(Wilson et al , 1988.…”

“…Após 42 dias da retirada da ração os suínos que não morreram apresentaram níveis hepáticos de selênio inferiores a 1,73ppm, o que difere dos achados de Davidson-York et al (1999) que, após 72 dias da retirada da ração com excesso de selênio, ainda detectaram um animal com nível de 3,3ppm de Se no fígado. Não foi observada correlação entre altos níveis de selênio no fígado e a severidade das lesões histológicas, dados semelhantes aos encontrados na literatura (Panter et al 1996, Davidson--York et al 1999. A porcentagem de animais com paralisia nos surtos variou de 15 a 16%, dados semelhantes já foram descritos (Davidson-York et al 1999).…”

“…Não foi observada correlação entre altos níveis de selênio no fígado e a severidade das lesões histológicas, dados semelhantes aos encontrados na literatura (Panter et al 1996, Davidson--York et al 1999. A porcentagem de animais com paralisia nos surtos variou de 15 a 16%, dados semelhantes já foram descritos (Davidson-York et al 1999). Todavia outros trabalhos já demostraram mortalidades menores (2,8%) (Harrison et al 1983) e maiores (100%) (Nathues et al 2010).…”

“…Quando presentes, as lesões podais são caracterizadas inicialmente por um avermelhamento na borda coronária, que se torna enegrecida e posteriormente há o desprendimento do casco (Harrison et al 1983, Casteel et al 1985, Banholzer & Heinritzi 1998, Hélie et al 1998, Davidson-York et al 1999, Kim & Mahan 2001, Casteignau et al 2006. As lesões medulares são confinadas às intumescências (Harrison et al 1983, Sanford 1990, porém em animais com evolução mais crônica podem ser observadas em outros segmentos da medula espinhal, como observado no suíno 8.…”

“…Alguns autores descrevem lesões mais severas em intumescência lombar do que na intumescência cervical (Harrison et al 1983, Wilson et al 1983, 1988, Casteel et al 1985, Sanford 1990, Stowe et al 1992, Penrith & Robinson 1996, Davidson-York et al 1999. No presente estudo a intensidade das lesões nas intumescências variou, com cinco casos mais acentuados na intumescência lombar, dois na intumescência cervical e três casos sem diferença na intensidade entre essas duas regiões.…”