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Selenium Toxicosis: Introduction |  |
| Selenium is an essential element that has a narrow margin of safety. Feed supplements containing 0.1-0.3 ppm selenium are added to the diet to prevent deficiency diseases such as white muscle disease in cattle and sheep, hepatosis dietetica in pigs, and exudative diathesis in chickens. The maximum tolerable level for selenium in most livestock feed is considered to be 2 ppm or as high as 5 ppm, although some believe that levels as high as 4-5 ppm can inhibit growth. |
| Selenium is a component of the glutathione peroxidase enzyme that acts as an antioxidant during release of energy. In excess, selenium has 2 general effects: the direct inhibition of cellular oxidation/reduction reactions, and the replacement of sulfur in the body. The inhibition of numerous cellular functions by high levels of selenium results in acute generalized cytotoxicity. The replacement of sulfur by chronic intake of selenium leads to altered structure and function of
cellular components. Altered sulfur-containing amino acids (methionine, cystine) affects cell division and growth. Especially susceptible are the cells that form keratin (keratinocytes) and the sulfur-containing keratin molecule. Selenium therefore weakens the hooves and hair, which tend to fracture when subjected to mechanical stress. |
| Etiology: |
| All animal species are susceptible to selenium toxicosis. However, poisoning is more common in forage-eating animals such as cattle, sheep, and horses that may graze selenium-containing plants. Plants may accumulate selenium when the element is found at high levels—generally in alkaline soil with little rainfall (<50 cm). Selenium accumulating plants have been categorized. Obligate indicator plants require large amounts of selenium for growth and contain high
concentrations (often >1,000 ppm). Facultative indicator plants absorb and tolerate high levels of soil selenium accumulating up to 100 ppm under these conditions, but they do not require selenium. Nonaccumulator plants passively absorb low levels of selenium (1-25 ppm) from the soil. Poisoning may also occur in swine and poultry consuming grain raised on seleniferous soils or, more commonly, due to error in feed formulation. Selenium toxicosis after ingestion of
selenium-containing shampoos or excess selenium tablets is rare in pets. Several factors are known to alter selenium toxicity; however, in general, a single acute oral dose of selenium in the range of 1-5 mg/kg is lethal in most animals. Parenteral selenium products are also quite toxic, especially to young animals, and have caused deaths in baby pigs, calves, and dogs at doses as low as 1.0 mg/kg. |
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| Diagnosis: |
| Severity of selenium toxicosis depends on the quantity ingested and duration of exposure. Poisoning in animals is characterized as acute, subchronic, or chronic. Diagnosis is based on clinical signs; necropsy findings; and laboratory confirmation of presence of high selenium levels in an animal’s diet (feed, forage, grains), blood, or tissues (kidney, liver). Selenium levels in the diet >5 ppm may produce signs after prolonged exposure. Levels of 10-25 ppm could produce
severe signs. In acute toxicosis, the blood selenium concentration may reach 25 ppm, and in chronic toxicosis, it may be 1-4 ppm. Kidney or liver may contain 4-25 ppm in both acute and chronic poisoning. |
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