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Nutritional Myopathies in Ruminants and Pigs

By

Geof W. Smith

, DVM, PhD, Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University

Last full review/revision Mar 2021 | Content last modified Mar 2021
Topic Resources

Nutritional Myodegeneration

Nutritional myodegeneration (NMD) is an acute, degenerative disease of cardiac and skeletal muscle caused by a dietary deficiency of selenium or vitamin E in young, rapidly growing calves, lambs, and kids. Dams have usually consumed selenium-deficient diets during gestation. Selenium deficiency appears to be more important than vitamin E in causing NMD. NMD occurs worldwide in areas where the soil (and therefore the derived grains and forage) is deficient in selenium, and storage conditions do not preserve vitamin E in forages. Soil in the northeastern and eastern seaboards and northwestern regions of the USA are particularly deficient in selenium. Vitamin E deficiency occurs most commonly when animals are fed poor-quality hay, straw, or root crops.

Both vitamin E and selenium have an important antioxidant function and protect cell membranes against damage from free radicals. Selenium is an essential component of five antioxidant selenoproteins, including glutathione peroxidase, and vitamin E acts as an antioxidant within lipid bilayers. Muscle degeneration is the result of oxidant damage to cell membranes and proteins, leading to a loss of cellular integrity. Young, rapidly growing animals usually are affected, although the disease has also been reported in yearling and adult cattle.

When cardiac muscle is primarily affected, animals may be found in respiratory distress, have cardiac arrhythmias, or be found dead. In such cases, the clinical course is frequently short, with death occurring commonly in <24 hours despite medical therapy. When skeletal muscle is primarily affected, signs of muscle weakness, stiffness, and difficulty rising are seen. Most affected animals are able to remain standing only for short periods, and locomotor muscles may be firm and painful on palpation. If the respiratory muscles are affected, the animal may show respiratory distress and evidence of increased abdominal effort when breathing. The muscles of the tongue may be involved, resulting in dysphagia. Animals with skeletal NMD often respond favorably to treatment and rest. Improvement is evident after a few days; within 3–5 days, animals can often stand and walk.

Differential diagnoses include:

Supportive evidence of NMD includes increased levels of CK, AST, and LDH. Definitive diagnosis is based on demonstration of low whole blood selenium (normal range >0.1 ppm) or liver content (normal cattle 0.9–1.75 mcg/g of dry matter, sheep 0.9–3.5 mcg/g dry matter). The critical concentration of vitamin E (alpha-tocopherol) in plasma is 1.1–2 ppm in large animals. Vitamin E deteriorates rapidly in plasma samples. Therefore, plasma samples for alpha-tocopherol analysis should be put on ice immediately, protected from light by wrapping in foil, and stored at –21°F (–29°C) if analysis is to be delayed.

Bilaterally symmetric myodegeneration is a consistent finding in NMD. Skeletal muscle degeneration is characterized by pale discoloration and a dry appearance of affected muscle, white streaks in muscle bundles, calcification, and intramuscular edema. The white streaks seen in cardiac and skeletal muscle bundles represent bands of coagulation necrosis or, in chronic cases, fibrosis and calcification. In calves, the left ventricle and septum are most frequently involved, but both ventricles are usually involved in lambs. Histologically, affected muscle fibers may be hypercontracted and fragmented, with some mineralization of muscle fibers and others undergoing macrophage infiltration.

The cardiac form of NMD is often acutely fatal, whereas the skeletal form may respond to injectable selenium products. The label dosage for selenium is 0.055–0.067 mg/kg (2.5–3 mg/45 kg), IM or SC. Dosage of these injectable products should not be greatly increased above that on the label to prevent an inadvertent selenium toxicosis. When using vitamin E/selenium combinations, the amount of vitamin E is insufficient for supplementation; it is present only as a preservative for the solution. Injectable vitamin E products that contain 300 and 500 IU vitamin E per mL as d-alpha-tocopherol are available. Oral supplementation is the general approach to provide additional dietary levels of vitamin E. Recommended levels of supplementation for calves range from 15 to 60 mg of dl-alpha-tocopherol acetate per kg of dry feed. Antibiotics may be indicated to combat secondary pneumonia. Provision of adequate energy intake and attention to the fluid and electrolyte balance are critical if recovery is to be successful.

Under current federal regulations in the USA, selenium can be incorporated into the total ration of ruminants and other species to a level of 0.3 ppm. In salt/mineral mixtures formulated for free-choice feeding, selenium can be incorporated at 90 ppm for sheep and 120 ppm for cattle. In certain areas or in herds, levels as high as 200 ppm selenium in salt/mineral mixtures may be necessary to maintain adequate selenium levels. Federal regulations limit the intake of supplemental selenium to 0.7 mg/head/day in sheep and 3 mg/head/day in cattle.

The use in ruminants of rumenoreticular boluses, which release a precise amount of selenium daily, is common in many countries. These slow-release boluses can replace supplementation by salt mixtures or by injections and are valuable in extensive grazing systems. Alternatively, individual animals can be supplemented by periodic (30- to 60-day intervals) injections of selenium/vitamin E preparations to help maintain body concentrations and assist in transplacental transfer of selenium.

Regardless of the method of supplementation, periodic blood (or tissue) sampling of animals at risk is recommended to ensure desired levels of selenium. Feeding animals properly prepared and stored hay and grain or allowing access to high-quality, green forage should ensure adequate vitamin E intake.

Hypokalemic Myopathy

Hypokalemic myopathy in dairy cattle occurs when serum potassium concentrations are <2.0 mmol/L, producing severe signs of muscle weakness. Anorexia and enhanced potassium excretion due to the administration of one or more doses of isoflupredone acetate to ketotic cows are common causes of hypokalemia. Isoflupredone acetate has both glucocorticoid and mineralocorticoid activity, resulting in a decrease in mean plasma potassium concentration by 25% 2 days after a single injection (20 mg) and 46% in cows 3 days after two injections.

Clinical signs of hypokalemic myopathy include severe weakness, recumbency, abnormal position of the head and neck, rumen hypomotility or atony, abnormal feces, anorexia, and tachycardia. Cardiac arrhythmias are also common. Diagnosis is based on clinical signs combined with serum potassium of <2.0 mmol/L. Other common clinical chemistry abnormalities include ketosis, metabolic alkalosis, and increased serum CK and AST activities. Muscle biopsies reveal a vacuolar myopathy.

Restoration of whole-body potassium balance can be difficult, and serum potassium concentrations do not necessarily reflect muscle potassium concentrations. Recommended supplementation includes potassium chloride given IV (16 g/l00 kg) and PO (26 g/100 kg) for approximately 5 days. Treatment should also be directed at resolving the primary cause of ketosis and anorexia as well as providing supportive care. Survival has been reported to be 22%–79%.

Nutritional Myopathy of Pigs

There are several specific diseases of pigs in which muscle degeneration may be extensive (eg, mulberry heart disease) and others in which the degeneration is frequently less conspicuous (eg, hepatosis dietetica). Yellow fat disease Yellow Fat Disease in Cats and Other Animals Yellow fat disease is characterized by a marked inflammation of adipose tissue and deposition of “ceroid” pigment in fat cells. It may be seen alone in cats or with accompanying myopathy in... read more may be seen with accompanying myopathy.

Etiology of Nutritional Myopathy of Pigs

Mulberry heart disease and hepatosis dietetica are associated with diets low in selenium or vitamin E. Administration of iron dextran to piglets having low vitamin E status may precipitate a severe myopathy (See also Iron Toxicity in Newborn Pigs Iron Toxicity in Newborn Pigs read more ) with lesions identical to those of selenium or vitamin E deficiency. Other factors that may increase the selenium requirement include diets with low concentrations of protein (especially sulfur-containing amino acids), diets with an excess of selenium antagonistic compounds, and possibly genetic influences on selenium metabolism. Vitamin E may be less available in diets with high concentrations of polyunsaturated fatty acids, vitamin A, or mycotoxins.

Clinical Findings of Nutritional Myopathy of Pigs

Nutritional myopathy conditions have certain characteristics in common. Losses tend to occur sporadically, and rapidly growing pigs 2–16 weeks old are affected. Death almost invariably occurs suddenly and is often precipitated by exercise.

Lesions

In mulberry heart disease, the characteristic lesions are a pericardial sac grossly distended with straw-colored fluid that contains fibrin strands, and extensive hemorrhage throughout the epicardium and myocardium. Microscopically, the heart shows both vascular and myocyte lesions; in addition to interstitial hemorrhage, there is usually extensive myocardial necrosis together with fibrin thrombi in capillaries. If pigs survive for a few days, nervous signs may be seen as a result of focal encephalomalacia.

In hepatosis dietetica, there is often subcutaneous edema and varying amounts of transudate in serous cavities. Fibrin strands adhere to the liver, which has a characteristic mottled appearance caused by irregular foci of parenchymal necrosis and hemorrhage. Acute lesions may appear as scattered, red, swollen lobules and edema of the gallbladder wall. Focal lesions of myocardial necrosis and, less frequently, skeletal myonecrosis may be apparent.

Many pigs that die with selenium or vitamin E deficiency have esophagogastric ulceration or preulcerative changes.

Diagnosis of Nutritional Myopathy of Pigs

  • History, clinical signs, and necropsy findings

Diagnosis of nutritional myopathy is typically made via history, clinical signs and necropsy findings. The history and gross necropsy findings may be distinctive, but histology to demonstrate specific cardiac and skeletal muscle lesions is necessary.

Differential diagnoses for mulberry heart disease include:

Differential diagnoses for hepatosis dietetica include:

Cases of selenium or vitamin E deficiency in pigs can be identified, as in other species, by decreased levels of selenium, vitamin E, and glutathione peroxidase in the serum and tissues and by increased levels of CK and AST in the serum.

Prevention and Treatment of Nutritional Myopathy of Pigs

  • Supplementation with selenium/vitamin E

Treatment for nutritional myopathy is primarily by supplementing rations with additional selenium or vitamin E, or both (as for ruminants). Additionally, affected pigs and their herdmates may be given injections of selenium/vitamin E to increase tissue levels rapidly. Injection of sows in late gestation increases tissue levels in newborn piglets.

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