Nutritional Myopathy of Calves and Lambs

(White muscle disease, Stiff lamb disease, Enzootic muscular dystrophy)

Etiology Clinical Findings

Lesions

Diagnosis Prevention Treatment

A myodegeneration frequently develops in calves and lambs of dams that received selenium-deficient feed during or before gestation. Legume forages grown in certain areas where selenium is either deficient or unavailable in the soil seem to be particularly involved and appear to be less effective in taking up selenium from the soil than are grasses. When the diet is restricted to such feeds, as in range cattle or sheep production, the cows and ewes may receive inadequate selenium. This condition has been recorded in many countries and has been produced experimentally in several species by restricting intake of selenium and vitamin E. A similar myopathy is seen naturally in yearling and young adult cattle, goats, deer, foals, adult horses, dogs, rabbits, poultry, fish, and various laboratory and wild animals.

Etiology:
Some myopathies (especially in herbivores) and some of the related conditions listed above have been attributed to a deficiency of vitamin E, which may be caused by large amounts of unsaturated fatty acids and other peroxide-forming substances in the diet. For example, continuous supplementation with cod liver oil has induced cases of vitamin E deficiency. White muscle disease in pastured cattle after spring turnout has been attributed to absorption of the portion of polyunsaturated fatty acids in lush grasses that escapes ruminal hydrogenation. In many cases of nutritional myopathy, selenium deficiency is present. This may be a simple deficiency caused by animals eating forage grown on selenium-deficient soils, or it may be precipitated by antagonistic effects of various metals (eg, silver, copper, cobalt, cadmium, mercury, tin). High dietary intake of phosphorus has enhanced the severity of the disease and resulted in decreased hepatic

selenium content in sheep. Application of sulfur to pasture soils, as elemental sulfur or gypsum, may interfere with uptake of selenium by forage plants and precipitate the disease in grazing ruminants. Some myopathies and related conditions respond only to selenium, some only to vitamin E, others to either. While vitamin E cannot completely satisfy the need for selenium, it can reduce the amount required to protect against exudative diathesis. The converse is also true. A vitamin E deficiency in chicks ( Vitamin E Deficiency) apparently leads to development of encephalomalacia and muscular dystrophy even in the presence of selenium sufficient to protect against exudative diathesis (on a low-methionine, lowcystine diet). Similarly, selenium cannot replace vitamin E to prevent the sterility and myopathy in some experimental animals (rabbits) or encephalomalacia in chicks produced by diets deficient in vitamin E. Conversely, a naturally occurring infertility in ewes, apparently related to fetal deaths and sometimes associated with a high incidence of white muscle disease in lambs receiving adequate vitamin E, responds remarkably to minute supplements of selenium, as does alopecia in rats and primates. The hepatic necrosis seen in rats and pigs appears to respond to either nutrient.

Clinical Findings:
The congenital type of white muscle disease may result in sudden death within 2-3 days of birth, usually with involvement of the myocardium. The delayed type is associated with cardiac or skeletal muscle involvement and may be precipitated by vigorous exercise. Affected animals may move stiffly with an arched back and frequently become recumbent. If the condition is severe enough to prevent nursing, either from dysfunction of the muscles of the legs or the tongue, death may result from starvation. Sometimes, there is profuse diarrhea. In chronic cases, there may be relaxation of the shoulder girdle and splaying of the toes. In progressive cardiac failure, dyspnea results. Signs vary with dietary selenium status; in some areas, general unthriftiness may be the only sign associated with selenium deficiency. Lesions:

White muscle disease

Generally, skeletal muscle lesions are bilaterally symmetric and may affect one or more muscle groups. Grossly, the affected muscle is pale and dry. It usually shows distinct longitudinal striations or a pronounced chalky whiteness due to abnormal calcium deposition, but sometimes the involvement may be diffuse. Cardiac lesions are welldefined subendocardial plaques that often are more pronounced in the right ventricle in lambs and in the left ventricle in calves. Microscopically, evidence has been established for sequential changes in damaged muscle progressing from mitochondrial swelling and myofibrillar lysis to either hyaline or granular necrosis. When the heart is involved, cardiac muscle cells and Purkinje fibers may be damaged. Pleural, pericardial, and peritoneal effusions with pulmonary congestion and edema are not uncommon.

Diagnosis:
In lambs, outbreaks of infectious, nonsuppurative arthritis result in a clinical syndrome similar to that of white muscle disease, and sudden deaths from heart failure might be confused with enterotoxemia. The history and necropsy findings, however, are usually characteristic. In mild cases and in very young lambs, laboratory studies such as histologic examination and levels of glutathione peroxidase, AST, and CK may be necessary. In calves, the typical syndrome and lesions are reasonably definitive. In mild cases and particularly in older animalsdiagnosis can be difficult, and laboratory studies (as with lambs) may be necessary.

Prevention:
To prevent white muscle disease within 4 wk after birth, ewes are given 5 mg and cows 15 mg of selenium, PO or SC, usually as sodium selenite 4 wk before expected parturition. To prevent the delayed type, lambs are given 0.5 mg and calves 5 mg of selenium at 2-4 wk of age and twice more at monthly intervals. A selenium and vitamin E mixture is advocated in some areas. Other procedures for selenium supplementation include administration of intraruminal selenium pellets, use of selenium-fortified salt or mineral mixtures, SC implantation of selenium pellets, or soil application of selenium at 4 g/acre (10 g/hectare) in fertilizer. Adding selenium to feed for breeding animals or their young is useful in areas of known deficiency. The recommended supplemental level is 0.3 ppm selenium, calculated on the basis of total dry-matter intake. It is added as sodium selenite, which contains 45.65% selenium. Because of the minute quantities involved and the toxicity of excess intake, premixing and thorough subsequent mixing is necessary. In some countries, including the USA, addition of selenium to feeds is controlled by law, and appropriate authorities should be consulted; in all areas, caution in the use of selenium is indicated.

Treatment:

Lambs and calves may be given sodium selenite and vitamin E in sterile emulsion, SC or IM, at 1 mg selenium and 50 mg (68 IU) of vitamin E per 18 kg (40 lb) body wt. This may be repeated after 2 wk, but no more than 4 doses should be given. Larger dosages are sometimes advocated, but caution is advised because they approach the toxic level. In practice, several products are available for use with designated animal species. When simple vitamin E deficiency is apparent, dietary supplementation with -tocopherol or substances rich in vitamin E should be instituted. Minimum dosages have not been established. However, cures have been reported after daily doses of 5 mg of -tocopherol to rabbits; 500 mg initially, followed by 100 mg on alternate days to lambs; and 600 mg initially, followed by daily doses of 200 mg to calves. When the causative diet contains substances antagonistic to vitamin E, such as unprotected, polyunsaturated fats, these must be removed or stabilized by addition of an appropriate antioxidant. Dry concentrates of vitamins A and D may substitute for cod-liver oil, thus removing a potential source of oxidative damage.