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, two 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 those of 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 neurologic clinical signs.
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 impaired with a dietary selenium content
lower than that required to produce the other typical signs of alkali disease.
Other lesions may include liver cirrhosis, ascites, and myocardial
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 May 2014 by Jeffery O. Hall, DVM, PhD, DABVT