Salt and Trace Minerals for Livestock, Poultry and Other Animals
SELENIUM FOR ANIMALS
Selenium has become one of the most widely recognized nutrient deficiencies in the U.S. USDA scientists estimate that beef, dairy and sheep producers lose $545 million yearly due to selenium deficiency (331). Selenium was recognized as a potentially toxic mineral many years before it was identified as an essential nutrient. It was not until 1957 that the role of selenium in preventing liver necrosis in the rat and exudative diathesis in chicks was recognized. Selenium is present in all cells of the body, but the concentration is normally less than 1 ppm. Toxic concentrations in liver and kidney are normally between 5 and 10 ppm (215).
Selenium is an important part of the enzyme glutathione peroxidase. This enzyme destroys peroxides before they can damage body tissues. Vitamin E is also effective as an antioxidant. Therefore, both selenium and vitamin E prevent peroxide damage to body cells. This aids the body’s defense mechanisms against stress. Most feeds contain compounds that can form peroxides. Unsaturated fatty acids are a good example. Rancidity in feeds causes formation of peroxides that destroy nutrients. Vitamin E for example, is easily destroyed by rancidity. Selenium spares vitamin E by its antioxidant effect as a constituent of glutathione peroxidase.
Selenium and vitamin E are interrelated. Both are needed by animals and both have metabolic roles in the body in addition to an antioxidant effect. In some instances, vitamin E will substitute in varying degrees for selenium, or vice versa. However, there are deficiency symptoms that respond only to selenium or vitamin E. Although selenium cannot replace vitamin E in nutrition, it reduces the amount of vitamin E required and delays the onset of E deficiency symptoms.
Selenium plays a critical role in increasing the immune response in animals. For example, Dimitrov et al. (169) reported that pretreatment of polymorphonuclear neutrophils from selenium deficient pigs, with selenium, restored their oxidative metabolism, which is closely related to the ability of the neutrophils to kill microorganisms. Researchers (170) recently showed that adding 0.2 mg selenium and 20 mg vitamin E per kg diet increased antibody titers to parainfluenza3 virus. Titer levels increased more initially due to selenium supplementation, but responses to vitamin E were greater than for selenium to a secondary challenge. These authors concluded their paper by stating, "It may be necessary to reevaluate established recommended intakes for nutrients that may be classified as immuno-stimulatory."
Selenium is important in sulfur amino acid synthesis. Sulfur amino acids protect animals against several diseases associated with low intakes of selenium and vitamin E. This protection is believed to be due to the antioxidant activity of selenium and vitamin E. Therefore, the sulfur amino acids, methionine and cystine, can spare vitamin E and selenium through their antioxidant role.
Selenium can be added to diets of all food animals. Either sodium selenite or sodium selenate can be used. Selenium is added to feed as follows: Up to 0.1 ppm in complete feed for swine, beef cattle, dairy cattle, sheep, poultry, rabbits, dairy goats, etc. Turkeys may be fed 0.2 ppm and small pigs up to 50 pounds, may be fed up to 0.3 ppm. Horses and other non-food animals (game birds, zoo animals, laboratory animals, etc.) can be fed up to 0.1 ppm selenium in the total diet.
In August 25, 1997 Federal Register, FDA published a final rule which adopted, without change, the provisions of an interim rule published in the Federal Register on October 17, 1995 (60 FR 53702) regarding the approved use of selenium as a food additive in animal feeds. The current selenium food additive regulations (Title 21 Part 573.920 in the Code of Federal Regulations) provides for the use of sodium selenate or sodium selenite as sources of selenium for selenium supplementation of complete feeds for chickens, swine, turkeys, sheep, cattle, and ducks at a maximum level of 0.3 ppm; in feed supplements for limit feeding of sheep not to exceed an intake of 0.7 milligrams per head per day and in beef cattle not to exceed an intake of 3 mg per head per day; in salt-mineral mixtures for free-choice feeding for sheep at levels up to 90 ppm at a rate not to exceed an intake of 0.7 mg per head per day and for beef cattle at levels up to 120 ppm at a rate not to exceed an intake of 3 mg per head per day. Updates to this ruling should be available at (311). http://www.fda.gov/cvm/CVM_Updates/selenium.html
Excess selenium in animal diets must be avoided. However, selenium is no more toxic than some of the other trace minerals. Using the pig as an example, the toxic level of selenium is 5 to 10 ppm in the diet, which is 50 to 100 times the current level of 0.1 ppm selenium allowed by the Food and Drug Administration in most swine diets. This margin of safety for selenium is greater than for copper, zinc, iron and possibly manganese for the pig. Therefore, selenium can be used if proper precautions are taken in its addition to animal diets. These same precautions should be taken with the addition of other trace minerals. The National Research Council publications show that the following levels of selenium in the total diet are toxic: swine, 5 to 10 ppm; chickens, 5 to 20 ppm; diary cattle, 3 to 5 ppm; beef cattle, 8.5 ppm; horses, 5 to 40 ppm; and sheep, 3 ppm. All of these animals require selenium at a level of 0.1 ppm in the total diet (except the turkey, which requires 0.2 ppm, and the baby pig, 0.3 ppm). Therefore, there is a significant safety factor between the level needed in the diet and what is toxic. Generally, higher levels of protein, sulfur and arsenic will partially protect against toxicity of excess selenium. Selenium should not be added to diets in areas where excess selenium occurs. Selenium accumulates in the body, but mild chronic signs can be overcome readily. Selenium is eliminated rapidly from the body of the affected animal when the animal is fed selenium-low forage (155). Small amounts of arsenilic acids are effective in reducing the toxicity of selenium (155).
Selenium deficiencies have occurred throughout the United States and in all areas of the world. In the United States, selenium deficient areas have been found in 44 states. Feeds produced in selenium deficient states are shipped to other states and to many foreign countries. Therefore, selenium deficiencies are likely to occur almost anywhere. Countries that import U.S. produced grain and soybeans are likely to encounter selenium deficiencies, even though native soils may contain adequate levels of selenium. Taiwan is a typical example, because its swine industry imports grain and soybean meal from the United States.
Swine
Sudden death is a prominent feature of selenium deficiency. Gross necropsy lesions of a selenium deficiency are identical to those of a vitamin E deficiency (87). They include massive hepatic necrosis, and edema of the spiral colon, lungs, subcutaneous tissues, and submucosa of the stomach. Bilateral paleness and dystrophy of the skeletal muscles (white muscle disease) are often found. Occasionally, mottling and dystrophy of the myocardium (mulberry heart disease) are also observed. Mulberry heart disease in pigs is most common when cereal-based diets contain less than 0.05 ppm selenium. Recent research by Mahan showed that adding .15 or .30 ppm selenium from sodium selenite from late gestation through day 14 of lactation increased milk selenium content and serum selenium concentration in nursing pigs compared to the unsupplemented controls (271). Organic selenium sources (selenium yeast) did increase milk selenium 2.5 to 3.0 times higher than the sodium selenite. Selenium supplementation of the sow may reduce the incidence of mulberry heart disease in the young pig. The incidence and degree of selenium deficiency may be increased by environmental stress. Dietary arsenicals help to alleviate selenium toxicity (87, 92).
Poultry
The main symptom of selenium deficiency is exudative diathesis. This disease characterized by edema of the breast, wing and neck regions. This edema is caused by an abnormally high permeability of the capillary walls that allows fluid to accumulate between the muscle and skin. In broilers fed low-selenium grains, chicks between 3 and 6 weeks of age, begin to show signs of weight loss, leg weakness and eventual death. With severe selenium deficiency, the growth rate is reduced and mortality increased even in the presence of adequate vitamin E. Pancreatic fibrosis and a reduction in pancreatic output of lipase, trypsinogen, and chymotrypsinogen are associated with selenium deficiency. Pancreatic lesions can occur as early as 6 days of age and usually return to normal within two weeks of selenium supplementation. In laying hens egg hatchability is the most sensitive criteria of selenium deficiency. Selenium is also required to prevent myopathies of the gizzard and heart in turkeys and ducks. Encephalomalacia, membrane lipid peroxidation, erythrocyte hemolysis, and muscular dystrophy are benefited by selenium (95, 110, 141).
Dairy Cattle
A major symptom of selenium deficiency is white muscle disease, which usually occurs in young calves. This causes chalky white striations, degeneration, and necrosis in cardiac and skeletal muscles. Heart failure, paralysis (usually of the hind legs), a dystrophic tongue and elevated SGOT (serum glutamic oxaloacetic transaminase) values may also be evident. Smith (255) reported that selenium injections reduced the duration, but not the incidence of mastitis when dietary selenium was deficient. Other symptoms include unthriftiness, growth depression, diarrhea, retained placenta, and lower reproductive efficiency (which includes increased services per conception) and birth of premature, weak, and dead calves (91, 156). Harrison and Hancock (333) recently reviewed the role of selenium and vitamin E in reproductive diseases in dairy cows.
Part of the reason ruminants are susceptible to selenium deficiency is that absorption is less efficient and more variable than in non-ruminants (256). Most of the selenium that is ingested leaves the rumen attached to the cell membranes of bacterial. Part of these cell membranes passes through the small intestine unabsorbed. The true absorption of selenium from grass hay has ranged from 10 to 16% (257). Organic selenium in selenized yeast increases blood and milk selenium more than an equal amount of selenium from selenite (337).
Beef Cattle
Symptoms of selenium deficiency are white muscle disease, heart failure, and paralysis. Paralysis can range in severity from slight lameness to inability to stand. Hollow or swayed back is typical. A dystrophic tongue is often seen in selenium deficient animals. Cows grazing forages lacking in selenium tend to produce calves with nutritional muscular dystrophy or white muscle disease (85, 157). White muscle disease is a degenerative rather than a dystrophic disease of the striated muscles. Lesions are probably the result of free-radical damage (258). Affected calves have muscle stiffness, arrhythmia, tachycardia and abdominal breathing. A selenium-vitamin E mixture injected into cows one month before calving prevented losses from birth of premature, weak, or dead calves in parts of California (112), and greatly reduced the incidence of retained placenta in cows in Scotland (113). French researchers (274) looked at the effect of selenium supplementation before and after calving on selenium status in deficient cows and their calves. This study demonstrated that adding 13.0 to 45.5 mg of dietary selenium daily to beef cows for 15 days in late pregnancy produced satisfactory selenium status in cows and their calves for up to three months after the end of supplementation. However, a more dependable approach is to prevent the selenium deficiency from developing in the first place by feeding supplemental selenium throughout gestation.
Missouri researchers determined the selenium status of 532 feeder calves representing 178 herds from all nine agricultural districts of the state (331). Deficient status was defined as less than 70 ppb whole blood selenium wet weight. On average, 16.5% of the calves were deficient in selenium. By district the deficiency rate varied from 4.7% to 40.0%. The districts with the highest proportion of deficient calves have higher annual rainfall than the rest of the state.
In most cases salt and inorganic selenium will be adequate, however, in some cases a more available source of selenium may be beneficial. Florida researchers (361) showed that adding selenium-yeast to free-choice salt increased calf plasma selenium concentrations more than giving cows selenium injections. Nursing calves eat little salt and so depend primarily on milk and forage to meet their needs. Arkansas researchers showed that calves born to cows fed selenium-yeast had higher whole blood selenium concentrations and greater glutathione peroxidase activity than calves from cows fed sodium selenite (363). Previous research had shown that selenium yeast increased milk selenium concentrations more than feeding selenite or selenate (362).
Sheep
Selenium deficiency has serious effects on lamb production. The manifestations are reduced growth and white muscle disease, which affects lambs at two to eight weeks of age (155). New Zealand studies have shown that lack of selenium causes high embryonic mortality, infertility, and high lamb mortality (111). Selenium supplementation increased the number of lambs marketed per 100 ewes lambing from 43 to 93% in the selenium treated group. Neither vitamin E nor an antioxidant was of much benefit in this study, which indicated that selenium per se was primarily responsible.
Goats
Research information is lacking on selenium for goats. There is a good possibility, however, that they would respond similarly to sheep in deficiency symptoms and in the need for selenium. Research scientists in France (114) and Nigeria (115) recommend the use of 0.1 ppm selenium in goat diets.
Horses
White muscle disease in foals, which can be prevented by selenium injection, has occurred in several countries. At necropsy the affected foals have alopecia, degenerative skeletal muscle, yellow-brown fat, and many small hemorrhages (154). Selenium deficiency results in reduced blood serum selenium and elevated serum glutamic oxalacetic transaminase levels. White muscle disease in foals has occurred in a number of foreign countries in areas where cattle and sheep respond to selenium. The foals show muscular stiffness, difficulty in walking, and may be unable to nurse. In severe cases, foals have a dejected appearance, become prostate, and usually die in one to seven days. Some may excrete myoglobin, which gives the urine a peculiar brownish color. "Tying-up" in horses may respond to selenium and vitamin E injections. Sometimes a single dose of 25 mg of selenium and 250 mg of vitamin E cures horses of "tying-up." Some horses are cured immediately, whereas others respond only partially or take a longer time to respond (93, 98).
Selenium can be quite toxic to horses. In fact some have speculated that General Custer’s horses were lame in the Battle of the Little Big Horn from grazing forages containing high levels of selenium. Some selenium accumulator plants can contain 50-10,000 ppm selenium (298). Generally these plants are not very palatable for horses.
Other Animals
Small animals also need selenium in the diet and a level of 0.1 ppm can be added to their diets. In some instances where selenium deficiencies have been studied, the symptoms obtained show some similarity to those of domestic farm animals.
Optimal Selenium Levels
Evidence is accumulating to indicate that higher levels of selenium than now approved by the Food and Drug Administration may be beneficial. The 1984 National Research Council report, Nutritional Requirements of Poultry, recommended selenium levels of 0.15 ppm for chicks 0-6 weeks old; 0.15 ppm for broilers; 0.2 ppm for turkeys; 0.14 ppm for ducks; and 0.2 ppm for Japanese quail (141). Except for turkeys, all the selenium levels are higher than FDA has approved. The 1985 NRC report, Nutritional Requirements of Sheep, recommended a level of 0.1 to 0.2 ppm selenium sheep diets which is higher than the current FDA approved level of 0.1 ppm (155). The 1983 NRC report, Selenium in Nutrition, stated that dietary requirements of most animals for selenium appear to fall within the range of 0.05 to 0.30 ppm (148).
The National Research Committee on Selenium Nutrition has proposed a maximum tolerable level of selenium of 2 ppm in the diet (148). This is a safe level that should not cause harmful effects. It should not be confused with a level that causes toxic effects. The 2 ppm level would allow a reasonable safety factor between the nutritional requirement for selenium and the maximum tolerated level allowed in the diet.
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