Formulating pig diets: Selenium toxicity, deficiency

Pig diets need extreme care to avoid overdosing of selenium, however, feedstuffs from deficient soil should receive extra consideration in feed formulation.

Selenium is an essential trace mineral that is routinely added in all swine diets via trace-mineral premixes. Pigs require selenium as a component of an enzyme (glutathione peroxidase) that protects membranes at the cellular and subcellular level against lipid peroxide damage. Selenium also has been shown to be involved in the metabolism of thyroid hormones, which play a central role in the regulation and coordination of metabolism.

Selenium is a unique trace element in that toxicity can occur at concentrations only slightly higher than those required for normal metabolism. The current dietary requirements for pigs, as established by the National Research Committee on Swine Nutrition (2012), range from 0.3 mg/kg in nursery pigs to 0.15 mg/kg in finishing pigs and breeding sows. The Food and Drug Administration strictly regulates dietary additions of selenium in pig diets in the U.S. Current regulations allow up to 0.3 mg/kg of added selenium in the diets of all classes of swine. The same is true for the European Union, where total maximum levels of dietary selenium are 0.5 mg/kg.

Concerns about selenium supplements

The greatest concern in using selenium supplements is that in growing pigs, toxicity can be induced easily by feeding as little as 5 to 10 mg/kg of diet. Signs of toxicity include anorexia, hair loss, liver and kidney damage, edema, hoof loss and nervous system disorders. Also, selenium excesses interfere with zinc absorption and utilization, reduce tissue iron stores and increase tissue copper levels.

Commercial supplements of selenium include inorganic (selenite and selenate) and organic (selenocysteine and selenomethionine) forms. Selenium from these compounds is reduced to a common intermediate, selenide, which is further methylated to mono-, di-, and trimethylselenoium ions, and then excreted via urine. Selenomethionine can enter the amino acid pool as is and be incorporated into body proteins, without being distinguished from methionine.

The most common cause of selenium toxicosis in swine production is overdose. Most commercial trace-mineral premixes contain inorganic and (or) organic selenium compounds that furnish elemental selenium as part of a nutritional supplement. Toxicosis results from high selenium concentrations in the premix (error in manufacturing process) or incorrect inclusion rate of the premix in the final diet (error in feed mixing).

In a recently reported case, excessive selenium in a premix resulted in selenium concentrations in final diets that ranged from 10 to 27 mg/kg and caused fatal paralytic disease in a group of growing pigs. The pigs were exposed to the toxic diets for a period of 60 days before diagnosis was made. In another incident, selenium was incorporated into a diet at a rate that was 1,000 times higher than recommended. A group of finishing pigs was exposed to final diets containing 300 mg/kg selenium as opposed to 0.3 mg/kg. Depression, anorexia and nervous system aberrations were followed by 89 percent mortality. Kidneys from these intoxicated pigs were found to have the highest selenium concentration among the organs examined.

The practice of administering selenium and vitamin E preparations via intramuscular injection in baby pigs can be the cause of another form of toxicosis. This is a routine farm practice in areas where grain is grown in soils poor in selenium. In an incident where nursing pigs deficient in selenium and vitamin E where administered an intramuscular injection of a selenium-vitamin E preparation, pigs experienced vomiting, anorexia, depression, dyspnea and coma. Death occurred within 24 to 48 hours. Liver necrosis and degeneration was the main pathological alteration. The liver was found to be the organ with the highest concentration of selenium.

Interestingly, injection of the same preparation at the same dosage to selenium-vitamin E non-deficient piglets did not induce toxicosis of the same magnitude.

Bioavailability of selenium

Apart from incidental cases of selenium overdose that cause acute toxicosis, other forms of milder toxicity can occur as a result of wide variations in bioavailability of selenium in natural ingredients and inorganic or organic compounds that are used in premixes. In general, plant ingredients have a higher bioavailability of selenium than animal ingredients. In contrast, selenized yeast appears to have a higher selenium bioavailability than sodium selenite.

The need for supplemental selenium in U.S. pig diets is largely dependent on the soil type in which the corn and soybeans are grown for inclusion in pig diets. The heaviest concentration of both corn and soybean production in the U.S. occurs in the Midwestern states, and virtually all of the soils in this area are very low in selenium. Thus, most of the corn and soybean meal sourced from the U.S. should be considered as deficient in selenium.

In contrast, most soils in Europe, including Russia, appear to be marginally sufficient in selenium, with Germany and Ireland having the highest levels. In contrast, countries like Poland, France, and most of the Balkans appear to suffer from selenium deficient soils.

Page 1 of 51
Next Page