Nutritional Myopathy in Poultry
- Myopathies
- Exertional Myopathy in Poultry
- Mechanically Induced Myopathy in Poultry
- Nutritional Myopathy in Poultry
- Toxic Myopathy in Poultry
- Injection Site Injury in Poultry
- Minimal Myopathy in Poultry
- Genetic Myopathy in Poultry
Nutritional myopathy in chickens, turkeys, waterfowl, and ostriches is attributed to vitamin E/selenium deficiency. However, as in mammals, selenium deficiency is most often the main cause of the myopathy. Vitamin E deficiency, when accompanied by a sulfur amino acid deficiency, causes nutritional myopathy in chicks by ~4 wk of age. Lesions of vitamin E/selenium deficiency have been reported in skeletal (especially breast muscle), heart, 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, with pale foci or streaking, are similar to those of nutritional myopathies in mammals. 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.
- Myopathies
- Exertional Myopathy in Poultry
- Mechanically Induced Myopathy in Poultry
- Nutritional Myopathy in Poultry
- Toxic Myopathy in Poultry
- Injection Site Injury in Poultry
- Minimal Myopathy in Poultry
- Genetic Myopathy in Poultry