Selenium functions as both a toxin and an essential element. Trace amounts of selenium (0.1-0.3 ppm) 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.
All animal species are susceptible to selenium toxicosis. Poisoning is, however, more common in forage-eating animals such as cattle, sheep, and horses that may graze selenium-containing plants. Poisoning may also occur in swine and poultry consuming grain raised on seleniferous soils or due to error in feed formulation. 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 quite toxic, especially to young animals. Deaths have been reported in baby pigs at a dose of 1.0 mg/kg.
Selenium poisoning in animals is characterized as acute or chronic; in either case, selenium tends to distribute throughout the body. Blood selenium concentration in acute poisoning is much higher than in chronic poisoning. In acute cases, blood selenium may reach 25 ppm; in chronic cases, it stays between 1-4 ppm. Hair may have >5 ppm selenium in chronic poisoning. A “garlicky” odor of an animal's breath is a good clue of selenium toxicosis.
Etiology: Selenium poisoning can result when the dietary selenium exceeds 5 ppm. Severity of the disease depends on the quantity ingested and duration of exposure. Misformulation of swine and cattle feeds is not uncommon. Selenium is absorbed to some degree by all plants, and the earth's surface has been estimated to contain an average of 0.1 ppm selenium. Chronic selenium poisoning (alkali disease) usually develops when animals consume naturally seleniferous forages and grains that contain 5-40 ppm of selenium. Soils capable of supporting seleniferous plants are alkaline in nature and receive <50 cm annual rainfall. Certain plants known as “accumulators” require selenium for their growth and can often accumulate several thousand ppm of selenium. When consumed by animals, these selenium accumulator plants can produce a poisoning called “blind staggers.” Seleniferous plants that are not removed from the soil may decay and thus become a source of selenium for nonseleniferous plants, which in turn may accumulate enough selenium to be a problem for animals.
Selenium occurs in soils in many forms. Selenate is the most soluble form of inorganic selenium, selenite is less available, and selenides and elemental selenium are virtually unavailable to plants. Vegetation with high selenium content has been found consistently in western plains of Canada and Mexico. Most cases of selenium poisoning in the USA have been reported from Colorado, Nebraska, South Dakota, and Wyoming. Selenium toxicosis in dogs, although rare, can occur after ingestion of selenium-containing shampoos or when excess selenium tablets have been given as medication. Selenium toxicosis has also been reported in man.
Diagnosis: 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 between 1-4 ppm. Kidney or liver may contain 4-25 ppm in both acute and chronic poisoning.
