SELENIUM TOXICITY IN ANIMALS
The toxic effects of selenium were first discovered in the 1930s when livestock ate certain plants of some wild vetches of the genus Astragalus, which accumulated toxic amounts of selenium from the soil (Moxon, 1937). The identification of selenium accumulator plant species (some Astragalus species) in the environment is an indication that grasses and other forages will also have accumulated selenium, and therefore is a risk to livestock grazing them. Soil and herbage levels of Se exceed 5 mg/kg and 3 mg/kg dry matter respectively in 90% of toxic fields (Roger et al., 1990). Addition of too much selenium to feeds, improper uses of selenium containing injectable or feeding livestock forages or feed grown in soils rich in selenium can result in selenium poisoning (Hatch, 1982). Tiwari et al. (2006) compared the acute toxicosis caused by organic selenium (selenomethionine) found in plants with that caused by the supplemental, inorganic form of selenium (sodium selenite) and reported that in an acute oral exposure, selenium from selenomethionine is twice as bioavailable, but can be slightly less toxic than sodium selenite. They also found that sodium selenite, but not selenomethionine administration resulted in decreased liver vitamin E concentration. Lambs receiving 2, 3, and 4 mg/kg body weight as sodium selenite and 4, 6, and 8 mg/kg body weight as selenium methionine had visible evidence of reduced feed intake, depression, reluctance to move, and tachypnea following minimal exercise. Major histopathological findings in animals of the high dose groups included multifocal myocardial necrosis and pulmonary alveolar vasculitis with pulmonary edema and hemorrhage. Some investigators (Casteignau et al., 2006) reported on selenium toxicosis due to errors in dosage of selenium in swine feed that resulted in an initial episode of diarrhea followed by dermatological and neurological signs; the most obvious sign being marked hind limb paresis. Cutaneous lesions consisted of diffuse alopecia, multifocal skin necrosis and coronary band necrosis of the hooves. Central nervous system lesions comprised of a severe bilateral polio-encephalomalacia of the ventral horns. In general therefore, elemental Se is relatively non toxic whereas organic Se found in plants and grains is more toxic to livestock. Several hundred deaths have been reported in sheep from acute/subacute selenium intoxication following grazing of seleniferous plants growing on reclaimed phosphate mines in southeastern Idaho (Fessler et al., 2003). Natural selenium toxicosis was reported from seven states of the USA. Over supplementation with selenium was reported as a cause of toxicosis in 15 states (Edmondson, et al., 1993). Chronic selenosis is often reported in India in winter season with the symptoms of hair loss, cracks on skin, hooves and horns, leading to elongation and sloughing of hooves, lameness, ataxia and recumbency (Gupta et al., 1982). In an experimental study with buffalo calves, adverse effects appeared when the whole blood selenium concentrations increased above 2 µg/ml, with mortality occurring when blood levels exceeded 3.4 µg/ml (Deore et al., 2005). Circumstances in which selenium poisoning occur are quite variable. The Se levels of dairy cows are highest in the winter when indoor feeding of Se-rich concentrates is practiced in Norway (Ropstad et al., 1988). Sugarcane foliage from seleniferous areas can accumulate high levels of selenium ranging from 7.9 to 67.5 mg/kg. These selenium levels were 6-14 times higher than those from non-seleniferous areas (Dhillon and Dillon, 1991). Researchers from India (Ghosh et al., 1993) reported Selenium toxicities in grazing buffaloes of the subHimalayan areas of West Bengal showing gangrenous syndrome of the extremities, skin cracks or sloughing, detachment of hooves, emaciation and eventually recumbency and death. Selenium poisoning should be generally suspected based upon a variety clinical signs including weight loss, poor growth rates, lameness, defective hoof growth, horizontal ridges or cracks in the hoof wall, hair loss, infertility and acute deaths especially when errors are made in mixing of selenium into animal feeds or overdosing injectable selenium products. A garlicky odor on the animals’ breath may be detected. Hematological changes in selenosis cases may include decreased fibrinogen levels and prothrombin activity, increased serum alkaline phosphatase, alanine aminotransferase (ALT), aspartate aminotranferase (AST), and succinic dehydrogenase and reduced glutathione levels. Serum or liver Se levels exceeding 2ppm is indicative of acute toxicity. In chronic cases hair analysis with >5 ppm selenium is confirmatory. Forage analysis in which the Se levels exceed 5ppm should be considered hazardous to livestock health. Selenium accumulator plants may contain as much as 15,000ppm of Se. Livestock grazing plants growing in soils containing in excess of 0.5ppm are at risk of developing selenosis (Rosenfeld, 1964). The Environmental Protection Agency (EPA) has set a chronic ecotoxicity threshold of 5 µg/L in water.
Selenium is an essential element with narrow margin of safety having difference between adequate and potentially toxic concentrations in the diet being approximately 10 to 20 fold. Selenium is an important component of many selenoenzymes and proteins like glutathione peroxidase which acts as an antioxidant in the body. So, in order to prevent deficiency and resulting diseases like white muscle disease in sheep and cattle, exertional myopathy in horses, exudative diathesis in poultry and hepatosis dietetica in pigs, supplements with selenium content of 0.2–0.3 ppm are added to their diets. The maximum tolerable concentrations for selenium in most livestock feed is considered to be 2–5 ppm.
Etiology
Although all animal species are susceptible to the toxic effects of Selenium poisoning but it is more common in forage eating animals such as cattle, sheep, horses and other herbivores that may graze selenium containing plants. Plants accumulate selenium if the element is available at high concentrations in the soil but pH and moisture content of the soil have greater influence on the relative bioavailability of selenium to plants. Generally selenium is mostly bioavailable to plants when they grow on more alkaline soils with low rainfall (<50 cm). The alkalinity and low moisture content of the soil tend to allow more of the selenium to be retained as the oxidized form of selenate for plant uptake. Because low moisture in the soil decreases the anaerobic environments to greater depths, drought conditions could allow for more selenium in the soil to be oxidized into forms which are readily available for plant uptake 1 Based on their relative requirements and ability to accumulate selenium, Selenium accumulating plants have been classified as : 2 Obligate indicator plants require large amount of selenium for growth and contain high selenium concentrations open more than 1000 to 10000 ppm and include species of Astragalus, Stanley, Oonopsis. 3 Facultative indicator plants absorb and tolerate higher concentrations of soil selenium, with accumulations ranging from trace amounts to a few thousand ppm, but they do not require selenium for growth and include species of Aster, Castilleja, Grindelia, Atriplex, Gatierreaia, and Comandra. 4 Non-accumulator plants, such as most grasses, passively absorb much lower amounts of selenium from the soil, resulting in trace amounts to a few hundred ppm. In Punjab, the districts which are most prone to Selenium toxicity are Hoshiarpur>and Nawanshahr. All the affected villages of these districts lie in the foothills of the Shivalik range. As per a study, it has been observed that for the past several years, selenium has been transported through floodwaters from the Shivalik mountain to these areas. Also the paths of seasonal rivulets in the region, which originate in the hills and end in the vicinity of these villages have been traced which may account for the high selenium content of the soil. For soil, the safe limit arrived at by PAU is 0.5 ppm and any amount above this would lead to plants containing more than 5 ppm of the element. It has been evaluated that when selenium levels in a plant go beyond 5 ppm, it becomes toxic for consumption. If the amounts are in excess of 100 ppm, white patches start to appear on the plants (the condition is described as snow-white chlorosis) which are common in crops grown in these villages. Another factors that seem to have aggravated the problem is the cropping pattern of the region. Significantly, though crops such as maize, sorghum and oat are relatively safe, certain others are known to attract high amounts of selenium. Over the past 10-12 years, areas which have switched from the maize-wheat pattern to that of rice and wheat are the worst-hit.
Toxicity
Excess selenium produces three general toxic effects : 1 The direct inhibition of cellular oxidation reduction reactions by depleting glutathione and S-adenosyl methionine reserves. 2 The production of free radicals that cause oxidative tissue damage. 3 The replacement of sulphur containing amino acids in the body with selenium or seleno- amino acids. Loss of these disulfide bonds can alter the three-dimensional configuration of proteins potentially resulting in loss off or diminished enzyme activity. The most commonly altered sulphur containing amino acids are methionine and cysteine, which are replaced with selenomethionine and selenocysteine respectively. Replacement of these amino acids with selenium containing amino acids also effects cell division and growth especially susceptible are the keratinocytes and the sulphur containing keratin molecule itself. Thus Selenium weakens the hooves and hair which tend to fracture when subjected to mechanical stress.
Acute Selenium Poisoning
Acute oral selenium poisoning due to consumption of plants or diets with concentrations >50 ppm is not common but if occurs can result in large losses in cattle, sheep, and pigs. It occurs rarely because animals usually avoid plants with high selenium content because of their offensive odor but during drought conditions or when pasture is limited, accumulator plants may be the only food available. Young animals are most susceptible to acute parenteral selenium toxicosis with dosages of 0.2–0.5 mg/kg. Clinical signs are characterized by abnormal behavior, respiratory difficulty, GI upset, and sudden death. Abnor- mal posture and depression, anorexia, unsteady gait, diarrhea, colic, increased pulse and respiration rates, frothy nasal discharge, moist rales, and cyanosis may be noted. Sheep usually show these signs to a much lesser degree or just become depressed and die suddenly. Most deaths usually follow within a few hours to 2 days after an acutely toxic consumption or injection of selenium. The major lesions are pulmonary edema, pulmonary congestion, pulmonary hemorrhage, hepatic necrosis, myocardial necrosis, myocardial hemorrhage, and potentially renal necrosis. Treatment consists of symptomatic and supportive care. Acetyl cysteine to boost systemic glutathione concentrations may be beneficial.
Subchronic Selenium Toxicosis
In pigs that are fed a diet supplemented with selenium >20–50 ppm for >3 days develop a subchronic selenium toxicosis characterized by neurologic abnormalities. Animals are initially ataxic and uncoordinated, followed by anterior paresis, then quadriplegia. Even though neurologic impairment is occurring, the pigs continue to eat, which would indicate neurologic damage that is not centrally mediated. The hooves develop cracks and impaired growth similar to those seen in cattle. In sows, conception rate decreases and the number of stillborn births increases. Lesions of subchronic toxicosis include focal symmetric poliomyelomalacia, which is most prominent in the cervical and thoracic spinal cord. Death may result from complications of permanent paralysis. Hoof and hair damage is similar to but in most cases less severe than that seen in chronic selenium toxicosis.
Chronic Selenium Toxicosis
(Alkali disease) 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). Hitherto, 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. Alkali disease has been reported in cattle, sheep, and horses and animals become inactive, weak, anorexic, lame, emaciated, anemic, and lack vitality. The most important and 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 leading to subsequent lameness which 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 necrosis. 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. Developmental and teratological effects including underdeveloped feet and legs, malformed eyes, crooked beaks and ropy feathers are also observed. In selenium-poisoned animals, some alterations in blood chemistries occur like 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 even after exposure has been stopped. Forages should be tested regularly in high-selenium areas to evaluate year-to-year risk. Also in high-selenium zones, farmers should be recommended to apply one tonne of gypsum per hectare every alternate year which may slow the selenium absorption by crops by up to 70 per cent.
Compiled & Shared by- Team, LITD (Livestock Institute of Training & Development)
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