Nutritional myopathy in chickens, turkeys, waterfowl, and ostriches is attributed to vitamin E/selenium deficiency. As in mammals, selenium deficiency is the most common cause. Vitamin E deficiency, when accompanied by a sulfur amino acid deficiency, causes nutritional myopathy in chicks by approximately 4 weeks of age.
Lesions of vitamin E/selenium deficiency have been reported in the skeletal (especially breast), cardiac, and smooth (gizzard and intestine) muscle of ducks, turkeys, and chickens. Arsenic, zinc, copper, and other metals are antagonistic to selenium, and exposure to these other metals can precipitate outbreaks of nutritional myopathy.
Nutritional myopathy is usually subclinical but can result in decreased meat quality. Locomotor difficulties can be observed. Dyspnea and sudden death can occur when severe myopathy affects the respiratory or cardiac musculature.
Gross lesions of nutritional myopathies in poultry are similar to those of nutritional myopathies in mammals, with pale foci or streaking of the muscle. Microscopic changes include focal or widespread myofiber swelling, edema, hyalinization, mineralization, degeneration, and lysis, with infiltration of macrophages and heterophils.
Hypercellularity from proliferation of satellite cells (mononuclear stem cells located between the basement and plasma membranes of the muscle fiber) can be prominent with nutritional myopathy in poultry, if regeneration is occurring.
In many parts of the world, poultry feeds contain added selenium at 0.1–0.3 ppm to prevent selenium deficiency and subsequent nutritional myopathy.
For More Information
Klasing KC, Korver DR. Nutritional diseases. In: Swayne DE, ed. Boulianne M, Logue CM, McDougald LR, Nair V, Suarez DL, associate eds. Diseases of Poultry. 14th ed. Wiley Blackwell; 2020:1255-1385.
