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Selenium is an essential micronutrient, although ingestion in excess in pigs can cause disease conditions including neurological dysfunction and chronic skin and hoof lesions. Controlled feeding trials in growing swine, using the same Se content in feed sources, resulted in higher concentrations (p < or = 0.05) of Se in blood and organs of pigs fed seleno-DL-methionine compared with those receiving Astragalus bisulcatus or sodium selenate. Clinical signs of Se toxicity including neurological signs of paralysis were more severe and occurred sooner in the A. bisulcatus group than in the sodium selenate or seleno-DL-methionine groups. All five pigs fed A. bisulcatus developed neurological signs of paralysis, and in four the signs occurred within 5 days of the start of treatment. Four of five pigs fed sodium selenate also developed paralysis, but this occurred 4 to 21 days after treatment began. The fifth pig in the group developed signs of chronic selenosis. Two of five pigs fed seleno-DL-methionine developed paralysis on 9 and 24 days, respectively, and the remaining three developed chronic selenosis. Selenium fed to pigs in three forms [plant (A. bisulcatus), sodium selenate, or seleno-DL-methionine] resulted in neurological dysfunction and lesions of symmetrical poliomyelomalacia. These were most severe in the A. bisulcatus group, which also had polioencephalomalacia. Although seleno-DL-methionine caused the greater increase in tissue and blood Se concentrations, this did not correlate with severity of pathological changes, since animals fed A. bisulcatus developed more severe and disseminated lesions.

Certain plants accumulate selenium at levels that render them toxic. One of the principle groups of selenium-accumulating plants is the selenium-accumulating Astragalus. Reports in early literature suggest that selenium is the only toxin in these plants. Sheep fed Astragalus bisulcatus, a selenium-accumulating plant, had signs similar to those observed in locoweed poisoning, and the microscopic lesions from tissues collected from these sheep were similar to those of locoweed poisoning rather than selenium poisoning. This suggests this group of plants contains toxin compounds in addition to selenium.

Three groups of 5 pigs each were fed a high selenium (Se) diet by mixing either Astragalus praelongus (31.6 ppm Se in feed), A bisulcatus (31.7 ppm Se in feed), or sodium selenate (26.6 ppm Se in feed) with commercial hog feed. Ten control pigs were fed only commercial hog chow containing trace selenium (0.44 ppm Se). Pigs were fed for 9 weeks and necropsied when they had ataxia or paralysis. Blood was collected for hematologic and serum biochemical determinations, and samples of various tissues were collected and fixed in neutral-buffered 10% formalin for histologic evaluation or frozen for determination of selenium concentration. All forms of selenium induced clinical signs of weight and hair loss, with cracked hooves and inflamed coronary bands developing in all Na2SeO4-fed pigs and 1 A praelongus-fed pig, but not in A bisulcatus-fed pigs. Serum calcium, phosphorus, and albumin concentrations were unchanged or significantly decreased from prefeeding values in groups fed selenium. Serum aspartate transaminase (AST) activities in Astragalus species-fed groups, and amylase activities and PCV in all groups of pigs fed selenium, were increased. Serum alkaline phosphatase and creatine kinase activities were significantly increased in the A praelongus-fed pigs and significantly decreased in Na2SeO4-fed pigs. Terminal tissue and body fluid selenium concentrations were determined in all groups of pigs fed selenium and compared with values in control pigs. Urine and bile concentrations were increased by the greatest factor (40 to 100x), with tissue concentrations of selenium increased by a lesser factor (6 to 17x).(ABSTRACT TRUNCATED AT 250 WORDS)