Nutritional myodegeneration

What it is

Nutritional myodegeneration (white muscle disease, nutritional muscular dystrophy) is a necrosis of muscle fibres caused by deficiency of selenium, vitamin E or both. Selenium is part of the enzyme glutathione peroxidase and vitamin E is a membrane antioxidant; together they protect cells from peroxide damage. When they are lacking, free radicals damage the membranes of muscle fibres, which necrose and mineralise, and the affected muscle looks pale, with white streaks and a chalky appearance.

Selenium deficiency occurs in areas with selenium-poor soils, whose forage is also poor in selenium; vitamin E deficiency, with poor-quality or long-stored conserved forage. Unaccustomed exercise (for example, turnout to pasture in spring), rapid growth and dietary polyunsaturated fatty acids, which increase oxidative stress, can trigger outbreaks.

Who it affects

Mainly calves from birth to a few months of age, born to deficient cows; also young cattle housed over winter when turned out to pasture. There is a congenital form in stillborn or weak calves. It affects beef and dairy herds in regions with deficient soils if they are not supplemented.

Anatomy involved

• Muscles of the rump and thigh: the large muscles of the pelvic limb, such as the semimembranosus and quadriceps femoris, are often affected, bilaterally and symmetrically; they are swollen and firm on palpation, with white streaks on cut section.
• Heart: in the cardiac form there are white plaques or streaks in the myocardium, preferentially in the left ventricle and papillary muscles; it causes acute heart failure and sudden death.
• Diaphragm: together with the intercostal muscles, its necrosis causes respiratory distress, which can be mistaken for pneumonia.
• The tongue (difficulty suckling), neck muscles and muscles of the shoulder can also be affected.

Clinical signs

• Cardiac form: calves that die suddenly, sometimes after handling or exercise, or that show weakness, tachycardia, arrhythmias and dyspnoea.
• Skeletal form: stiffness, a stiff gait, tremors, weakness and recumbency, with the animal still alert and willing to eat. The muscles are firm and painful. Urine may be dark from myoglobinuria.
• Respiratory form: tachypnoea and abdominal breathing from involvement of the diaphragm and intercostal muscles.
• In the congenital form, weak calves at birth that cannot stand or suckle.

Diagnosis

• Muscle enzymes: markedly raised creatine kinase (CK) indicates active muscle necrosis; aspartate aminotransferase (AST) stays raised for longer.
• Selenium and vitamin E status: whole-blood selenium or blood glutathione peroxidase activity, and serum α-tocopherol, in the affected animal and in other animals of the herd; liver selenium at necropsy.
• Necropsy and histopathology: pale muscles with white streaks, often symmetrical, and hyaline necrosis with mineralisation of the fibres.
• Differential diagnosis: pneumonia, trauma, neurological diseases and other causes of recumbency or sudden death in calves.

Treatment and prevention

• Parenteral selenium and vitamin E for affected animals and the other animals at risk in the group; rest, minimal stress and supportive care. The skeletal form responds well if treated early; the cardiac form has a poor prognosis.
• Prevention in deficient areas: supplementation of cows during pregnancy (minerals in the ration or in blocks, ruminal boluses, organic selenium or injections), and of calves at birth when the risk is high; vitamin E in diets poor in it.
• Selenium has a narrow safety margin and is toxic in excess: several sources of supplementation should not be stacked without checking the herd's status.
• Drug and supplement use in food-producing animals is subject to national regulations (including limits on selenium in feed) and to withdrawal periods for milk and meat.

Key studies

No controlled trials with clinical disease as the outcome were found; the evidence on prevention comes mainly from observational studies and from trials that measure selenium or vitamin E status.

• Kennedy et al. (1987), controlled experimental study of 14 calves fed a diet low in vitamin E and selenium and 10 supplemented controls. Depleted calves showed falling α-tocopherol and glutathione peroxidase and rising CK, with mild myopathic lesions in the 6 that were killed, but no clinical signs. Adding polyunsaturated fatty acids to the diet of 8 depleted calves produced cardiopulmonary and locomotor signs and myoglobinuria within 6–11 days, with severe skeletal myodegeneration in all 8 and myocardial lesions in 5, mainly in the left ventricle. Controls had no lesions. It is a small experimental study.
• Sanguinetti et al. (2023), systematic review of measures to reduce preweaning mortality in beef calves, with 11 studies (10 cross-sectional and 1 randomised trial). Injecting selenium and vitamin E at birth was one of the practices significantly associated with calf mortality; the abstract does not give the size of the effect and the evidence is mainly observational.
• Ceballos et al. (2009), systematic review and meta-analysis of 42 studies of oral selenium supplementation in cattle. Supplementation raised milk selenium by an average of 0.16 µmol/L (95% CI, 0.117–0.207), with large heterogeneity between studies; organic selenium (yeast) raised it more than inorganic forms. It measures selenium status, not disease.
• Swecker et al. (2008), three trials with 144 weaned steers given selenium, vitamin E or both subcutaneously. Selenium raised serum selenium, but injected vitamin E did not raise serum vitamin E in any of the trials, and no treatment improved weight gain.