farrier! :
This is the best I could come up with right away.
Yhttp://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/213302.htm
Here is the text from the link
Chronic selenium poisoning
Chronic selenium poisoning usually develops when livestock consume seleniferous forages and grains containing 5-50 ppm of selenium for many weeks or months. Naturally occurring seleno-amino acids in plants are readily absorbed. Until recently, 2 types of chronic selenium poisoning were recognizedalkali 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. Excess sulfate (>2% 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, responsible for locoism, produces the signs.
Clinical Findings:
Alkali disease has been reported in cattle, sheep, and horses. Affected animals are dull, emaciated, and lack vitality. The most distinctive lesions are those involving the keratin of the hair and hooves. The animal has a rough hair coat and the long hairs of the mane and tail break off at the same level giving a bob tail and roached mane appearance. Abnormal growth and structure of horns and hooves results in circular ridges and cracking of the hoof wall at the coronary band. Extremely long, deformed hooves that turn upwards at the ends may be seen. Subsequent lameness is compounded by degeneration of joint cartilage and bone. Reduced fertility and reproductive performance occurs especially in sheep. Reproductive performance may be depressed with a dietary level of selenium lower than that required to produce typical signs of alkali disease. Other lesions may include anemia, liver cirrhosis and ascites, and atrophy of the heart.
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 the embryos 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 leached by agricultural water and concentrated in lakes by runoff.
Blood levels of selenium in chronic cases are usually 1-4 ppm. Other changes in blood include decreased fibrinogen level and prothrombin activity; increased serum alkaline phosphatase, ALT, AST, and succinic dehydrogenase; and reduced glutathione. Hair may have >5 ppm selenium in chronic poisoning. A garlicky odor on the animals breath may be noted.
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Treatment and Control:
There is no specific treatment for selenium toxicosis. Eliminating the source and exposure and 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. Addition of arsenic salt at 0.00375% to enhance biliary excretion of selenium or use of a high-protein diet to bind free selenium may help reduce incidence of selenium poisoning in cattle.
Soil and forages should be tested regularly in high-selenium areas.
This is the best I could come up with right away.
Yhttp://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/213302.htm
Here is the text from the link
Chronic selenium poisoning
Chronic selenium poisoning usually develops when livestock consume seleniferous forages and grains containing 5-50 ppm of selenium for many weeks or months. Naturally occurring seleno-amino acids in plants are readily absorbed. Until recently, 2 types of chronic selenium poisoning were recognizedalkali 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. Excess sulfate (>2% 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, responsible for locoism, produces the signs.
Clinical Findings:
Alkali disease has been reported in cattle, sheep, and horses. Affected animals are dull, emaciated, and lack vitality. The most distinctive lesions are those involving the keratin of the hair and hooves. The animal has a rough hair coat and the long hairs of the mane and tail break off at the same level giving a bob tail and roached mane appearance. Abnormal growth and structure of horns and hooves results in circular ridges and cracking of the hoof wall at the coronary band. Extremely long, deformed hooves that turn upwards at the ends may be seen. Subsequent lameness is compounded by degeneration of joint cartilage and bone. Reduced fertility and reproductive performance occurs especially in sheep. Reproductive performance may be depressed with a dietary level of selenium lower than that required to produce typical signs of alkali disease. Other lesions may include anemia, liver cirrhosis and ascites, and atrophy of the heart.
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 the embryos 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 leached by agricultural water and concentrated in lakes by runoff.
Blood levels of selenium in chronic cases are usually 1-4 ppm. Other changes in blood include decreased fibrinogen level and prothrombin activity; increased serum alkaline phosphatase, ALT, AST, and succinic dehydrogenase; and reduced glutathione. Hair may have >5 ppm selenium in chronic poisoning. A garlicky odor on the animals breath may be noted.
Back to top
Treatment and Control:
There is no specific treatment for selenium toxicosis. Eliminating the source and exposure and 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. Addition of arsenic salt at 0.00375% to enhance biliary excretion of selenium or use of a high-protein diet to bind free selenium may help reduce incidence of selenium poisoning in cattle.
Soil and forages should be tested regularly in high-selenium areas.
