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Por meio de revisão da literatura pertinente foram coligidos e são apresentados os principais dados relativos à intoxicação por selênio em animais domésticos. Foram abordados e discutidos os aspectos epidemiológicos, clínicos, anátomo e histopatológicos e patogenéticos atribuídos a Alkali Disease, Blind Staggers, intoxicação aguda e poliomielomalácia simétrica focal dos suínos. O trabalho tem como objetivo esclarecer pontos obscuros relativos à intoxicação por selênio, bem como alertar para os riscos que a suplementação com esse elemento pode representar.

Selenium in certain soils may be taken up by plants in amounts to render them toxic. Seleniferous forage can be found in most of the western states. Intoxication of livestock by seleniferous plants has been classified as acute and chronic. Acute poisoning results from consumption of plants having high levels of Se; chronic Se poisoning has been described in two forms— alkali disease and blind staggers. Alkali disease is said to result from the consumption of seleniferous grains and grasses, and is manifest by loss of hair, lameness, and loss of weight. Blind staggers is slid to result from the consumption of Se indicator plants and is manifest by wandering, circling, loss of ability to swallow, and blindness. Some research casts doubt on the above classification of Se poisoning. Research using pigs (Sus scrofa domesticus) indicates that the source of Se does not alter the type of lesion or signs of poisoning observed. There are data available that suggest that blind staggers is not related to Se poisoning.

Selenium was first discovered in 1818 by Jons Jacob Berzelius in deposits from the lead chambers of a sulfuric acid plant at Gripsholm, Sweden. Berzelius realized that the new element was related to tellurium which had been discovered in the late 1700’s. For the first 140 years after its discovery Se was thought to be deleterious to humans and animals. In the 1930’s it was shown that certain plants could accumulate Se to levels which are toxic to livestock. The metabolic disorders “alkali disease” and “blind staggers” were shown to be caused by excess dietary intake of Se. In was only in the late 50’s that Se was shown to be an essential nutrient to animals. The discovery of the “Factor-3 effect” (the anti-oxidant capacity of Se, vitamin D and coenzyme Q) by Schwarz and Foltz (1957) brought about this abrupt change. Further studies then indicated that Se interacted with vitamin D on a variety of deficiency disorders in livestock and poultry. In 1984 it was shown that Se was able to prevent cancer in human (Salonen, 1984).

An experiment involving 33 pigs initially weighing 18 kg, was conducted to investigate the effects of a single intramuscular injection of the effects of a single intramuscular injection of selenium (sodium selenite) at different levels on resulting blood and tissue selenium concentrations at various time intervals post-injection and to determine the effect of a single lethal injectable dosage of selenium. Serum samples were collected and analyzed for SGOT and selenium. Hepatic, kidneys and longissimus muscle tissues were collected and analyzed for selenium. The same tissues were collected from those pigs dying of selenosis. Pigs receiving selenium injections of 1.65 to 3.30 mg/kg BW died of selenosis within 4 hr to 6 days with death occurring earlier at the higher dosage levels. Symptoms in order of occurrence were: vomiting, blind staggers, foaming at the mouth, dyspnea, prostration and death. Elevated SGOT activity was observed in the remaining injected pigs at 12 hr post-injection with the enzyme activity increasing as the dosage quantity increased, suggesting mild selenium toxicosis of body tissues.

The nutritional importance of selenium has only recently been discovered. Selenium was originally considered only to be a toxic element after it was found to cause the disabling Alkali Disease and the Blind Staggers in livestock grazing in parts of the western United States during the early 1900’s. These areas were and still are sites of selenium-accumulat ing plants. About 50 years later the beneficial aspects of selenium began to be recognized when Schwarz and Foltz (1) found that selenium prevented liver necrosis in rats.

I. ABSTRACT A selenium-accumulating indicator plant, Astragalus bisulcatus, previously recognized as toxic and thought to be a cause of chronic selenium toxicity described as Blind Staggers, was fed experimentally to sheep. Clinical signs of emaciation, depression, neurological disturbances, and pathologic changes of neurovisceral cytoplasmic vacuolation were observed microscopically in the experimental sheep. These changes are similar to those observed in locoweed poisoning. It is suggested that the principle toxic agent (s) in Astragalus bisulcatus is similar to that of the true locoweeds rather than being selenium related. Further studies feeding other seleniferous indicator plants are being conducted.

I. ABSTRACT Soils in some areas of the world contain such high concentrations of selenium that they produce plants toxic to livestock. Some plants grow only in these seleniferous soils, are referred to as primary selenium indicators, and concentrate high levels of the element in their tissues. Others, referred to as secondary selenium absorbers, can accumulate rather high concentrations of the element when growing on seleniferous soils. A third class of plants, grasses, and grains as well as many others, absorb less selenium, but still often contain enough to be toxic. Three major types of selenium toxicosis have been described. “Blind staggers” is suggested as a chronic type toxicosis resulting from long-term ingestion by sheep and cattle of the primary indicators or secondary absorbers in less than acutely toxic amounts. There is some reason to question the role of selenium in causing this syndrome. “Alkali disease ” occurs in poultry, swine, cattle, and horses that consume grains, forages, or pasture plants containing usually less than 50 but more than 5 parts per million of the element over a period of many weeks or months. Acute selenium toxicosis results when grazing animals consume the primary selenium indicators in amounts sufficient to cause a very rapid toxicosis. Control in all types of selenium toxicoses requires avoidance of seleniferous feeds.

Humboldt, Tenn., April 8, 1905. To the Editor: —I have just read Dr. Albert's letter inThe Journal, April 8, p. 1132, on the identity of meningitis in animals and man. This is an interesting and important subject, especially as the question of contagion is beginning to receive the attention it should have had long ago. I am not familar with the disease in the cow, but I have seen a few cases in man and in horses and have long been impressed with the idea that the disease is the same in both. The disease in the horse is known in this locality as "blind staggers" and there is a popular impression that the horse contracts the disease from eating the "chaff" of old corn, and as it is undoubtedly more common about the time the farmers are cleaning out the corn-cribs preparatory to housing the new crop, it