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Nutritional Myopathy in Poultry


Arnaud J. Van Wettere

, DVM, MS, PhD, DACVP, Utah Veterinary Diagnostic Laboratory, School of Veterinary Medicine, Utah State University

Last full review/revision Feb 2020 | Content last modified Mar 2020

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 ~4 weeks of age. Lesions of vitamin E/selenium deficiency have been reported in skeletal (especially breast muscle), cardiac, and smooth muscle (gizzard and intestine) of ducks, turkeys, and chickens. Arsenic, zinc, copper, and other metals are antagonistic to selenium, and exposure to these other metals may precipitate outbreaks.

Gross lesions are similar to those of nutritional myopathies in mammals, with pale foci or streaking of the musculature. 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 may be prominent if regeneration is occurring. Poultry feeds in many parts of the world contain added selenium at 0.1–0.4 ppm to prevent this myopathy.

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