Chronic selenium poisoning usually develops when livestock consume seleniferous forages and grains containing 5–50 ppm of selenium for many weeks or months, although chronic exposure to high concentrations of inorganic selenium can also produce chronic selenosis. Naturally occurring seleno-amino acids in plants are readily absorbed and inserted into proteins in place of their corresponding sulfur-containing amino acids (ie, selenomethionine in place of methionine or selenocysteine in place of cysteine). Until recently, 2 types of chronic selenium poisoning were discussed in the literature: alkali disease and blind staggers. Blind staggers is no longer believed to be caused by selenium but by sulfate toxicity due to consumption of high-sulfate alkali water and/or high sulfur-containing forages. Excess sulfate (>1% of diet) leads to polioencephalomalacia and the classical signs of blind staggers. Animals consuming milk vetch (Astragalus bisulcatus) have demonstrated clinical signs similar to blind staggers. Although milk vetch contains high levels of selenium, evidence now indicates that the alkaloid swainsonine in milk vetch is responsible for locoism and produces the clinical signs.

Clinical Findings

Alkali disease has been reported in cattle, sheep, and horses. Affected animals are inactive, weak, anorexic, lame, emaciated, anemic, and lack vitality. In addition, the most distinctive lesions are those produced by damage of the keratin of the hair and hooves. For horses, the predominant clinical manifestation is lameness due to founder. The animal has a rough hair coat and the long hairs of the mane and tail break off, giving a “bob” tail and “roached” mane appearance. Abnormal growth and structure of horns and hooves result in circular ridges and cracking of the hoof wall at the coronary band. Extremely long, deformed hooves that turn upward at the ends also may be seen. Subsequent lameness is compounded by degeneration of joint cartilage and bone. Reduced fertility and reproductive performance occurs, especially in sheep and cattle. Reproductive performance may be depressed with a dietary selenium content lower than that required to produce typical signs of alkali disease. Other lesions may include liver cirrhosis, ascites, and myocardial necrosis/scarring.

Birds also may be affected with chronic selenium toxicosis. Eggs with >2.5 ppm selenium from birds in high selenium areas have low hatchability and embryos that are usually deformed. Teratologic effects include underdeveloped feet and legs, malformed eyes, crooked beaks, and ropy feathers. This has been a problem with waterfowl in southern California, where selenium was concentrated in lakes by runoff.

In selenium poisoned animals, some alterations in blood chemistries occur. These changes include decreased prothrombin activity, fibrinogen, and glutathione, as well as increased serum alkaline phosphatase, ALT, AST, and succinic dehydrogenase.

Treatment and Control

There is no specific treatment for selenium toxicosis. Eliminating the source and exposure, as well as symptomatic and supportive care of the animal, should be started as soon as possible. Addition of substances that antagonize or inhibit the toxic effects of selenium in the diet may help reduce the risk of selenium toxicosis. A high-protein diet, linseed oil meal, sulfur, arsenic, silver, copper, cadmium, and mercury have reduced selenium toxicity in laboratory animals, but their use under field conditions is limited. However, some of the poor reproductive performance associated with selenium poisoning can be decreased by copper supplementation. Addition of arsenic salt at 0.00375% to enhance biliary excretion of selenium or a high-protein diet to bind free selenium has historically been used to reduce incidence of selenium poisoning in cattle. However, this has minimal to poor overall efficacy. Chronically selenium-poisoned animals are less likely to thrive than herdmates, even after exposure has been stopped.

Forages should be tested regularly in high-selenium areas to evaluate year-to-year risk.

Last full review/revision March 2012 by Jeffery O. Hall, DVM, PhD, DABVT