Feeds high in the concentration of polyunsaturated fatty acids, copper, vitamin A or mycotoxins can either destroy vitamin E or make it less bioavailable. Grains from soils deficient in selenium, or selenium antagonists in mixed feeds, can result in feeds low in selenium. Both vitamin E and selenium work as antioxidants.
There are three closely related, overlapping syndromes associated with vitamin E and/or selenium deficiency. The most common is mulberry heart disease (MHD). The true causal mechanism is not known but the condition can usually be prevented with additional vitamin E supplementation. MHD usually occurs when vitamin E is low but is also seen in the face of seemingly adequate levels of vitamin E in tissue or serum. MHD is manifested by sudden death in pigs a few weeks to four months of age that were believed to be in excellent health. The condition was named after the mottled appearance of the heart muscle in affected pigs. Typically, there are alternating areas of necrosis and hemorrhage throughout the myocardium. The pericardial sac is distended with fluid and fibrin strands. Straw-colored fluid is often present in the pleural cavity and lungs are edematous. Microscopically there are degenerative changes in arteriole walls at many sites. Supplementation with vitamin E, either parenterally or orally, will prevent deaths from this disease.
Hepatosis dietetica (HD) is a much more rarely encountered presentation of vitamin E and/or selenium deficiency since legal levels of selenium supplementation in livestock feed were raised to 0.3 ppm. Clinically, HD presents as sudden deaths with few or no preceding signs. This syndrome was named on the basis of hepatic lesions and the belief that they are related to the pig’s diet. There are irregular focal to large areas of hepatic necrosis and hemorrhage; some lobules are distended and reddened. The gall bladder often is edematous. Myocardial necrosis and pulmonary edema may be present. Supplementation with selenium will ameliorate HD.
White muscle disease (WMD) is a presentation of vitamin E and/or selenium deficiency that is much more common in lambs, calves and chickens rather than swine. Skeletal muscle pallor or streaks of white, gritty mineralization are observed, particularly in the longissimus dorsi muscle. Microscopically, characteristic necrosis and/or mineralization of individual muscle fibers are observed.
Since these deficiencies are similar, it is not surprising that lesions of the syndromes sometimes overlap. Diagnosis can often be made on the basis of gross lesions, microscopic lesions in heart, liver, or muscles, and analysis for vitamin E/selenium levels in the liver or serum.
For prevention or treatment of a deficiency, pigs can be injected with vitamin E and/or selenium and tissue levels will be increased rapidly. Also, prevention is possible through supplementation of feed or drinking water. Sows injected in late gestation give birth to pigs with increased levels of both compounds. The syndromes described above may not always be responsive to supplemental vitamin E and selenium. MHD is more responsive to vitamin E; HD more so to selenium.
Pigs on pasture usually get enough vitamin E and selenium unless the soil is deficient in selenium. In outbreaks, feed content and quality as well as feed storage conditions should be examined carefully to determine why the feed is deficient. Improper feed storage, high copper levels, high fat levels, and poor quality feed constituents can result in destruction of vitamin E in a feed otherwise formulated adequately.
Pigs deficient in vitamin E and/or selenium may be more susceptible to other diseases. Also, deficient small piglets are quite susceptible to iron toxicity. If treated with iron dextran for anemia prevention, many deaths may occur. Myocardial lesions will closely resemble those of mulberry heart disease (MHD).