Ruminants: Vitamin E

Vitamin E displays a wide variety of deficiency signs, more than any other vitamin. Deficiency signs differ among species and even within species. Blaxter (1962) reported that muscle degeneration and muscular dystrophy appear to be the one vitamin E deficiency syndrome common to all species. White muscle disease (WMD), also known as nutritional muscular dystrophy or nutritional myodegeneration (NMD), is the major clinical manifestation of a vitamin E or selenium deficiency in newborn calves, lambs and kids. Cardiac white muscle disease, the equivalent of Mulberry heart disease in pigs, is a common deficiency lesion in calves and lambs born to vitamin E-deficient dams. The young also tend to lack a normal suckling reflex and may be unable to stand or walk. White muscle disease occurs in all laboratory and farm animals, as well as camels, buffalo, rhinos and kangaroos. Muscular dystrophy is reported in a number of wild animals, the condition in antelope, for example, being indistinguishable from WMD in cattle or sheep (NRC, 1983).

Fundamentally, WMD is a Zenker’s degeneration of both skeletal and cardiac muscle fibers. Damaged muscle is replaced by connective tissue that is observable as gross white striations in the muscle fiber bundles (Smith, 1970). Lesions are usually symmetrical and bilateral (Blaxter, 1962), and affected muscles may tear easily and appear edematous. Necropsy may reveal generalized edema of the abdominal cavity and the lungs (Morrill and Reddy, 1987). Serum glutamic-oxaloacetic transaminase (SGOT), lactic dehydrogenase (LDH) and creatinine phosphokinase (CPK) are elevated in vitamin E-deficient calves (Cipriano et al., 1982; Reddy et al., 1987b) and yearling cattle (Allen et al., 1975). Osmotic fragility of erythrocytes has been reported to increase in some instances of vitamin E deficiency (McDowell, 2000).

Nutritional muscular dystrophy of ruminants occurs worldwide, but its incidence or at least diagnosis, particularly in a mild or subclinical form, varies widely between and even within countries (McDowell et al., 1985). The incidence of WMD in certain world regions is sporadic, with less than 1% of livestock herds affected. In other areas, such as Turkey and New Zealand, a 20% to 30% incidence of WMD may occur regularly. Considerable research has revealed an inverse relationship between the selenium content of soil and the geographic occurrence of vitamin E-selenium responsive muscular dystrophy. Similarly, signs of vitamin E deficiency have been observed in zoo animals fed diets devoid of their natural forage or browse.

White muscle disease occurs with two clinical patterns. The first is a congenital type of muscular dystrophy in which calves, lambs or kids may be born dead or die within a few days of birth, following sudden physical exertion such as nursing or running. The second clinical pattern ("delayed white muscle disease") develops after birth; it is observed most frequently in lambs within three to six weeks of birth but may occur as late as four months after birth. The condition in calves is generally manifested at one to four months of age. A vitamin E-responsive white muscle disease has been observed in four- to six-month-old lambs that are kept on dry, poor quality, late-season pasture.

Godwin (1975) reported that the electrocardiogram of WMD-affected animals shows progressive development of a characteristic abnormality accompanied by a fall in blood pressure. Therefore, a fundamental change occurring in vitamin E-selenium deficiency is circulatory failure, linked to cardiac muscle degeneration and possibly also to loss of blood vessel integrity.

Muscle damage resulting from vitamin E and (or) selenium deficiencies causes leakage of cell contents into the bloodstream. Thus, elevated levels of selected enzymes, above normal ranges, serve as diagnostic aids in detecting tissue degeneration. Serum enzyme concentrations used to monitor the incidence of nutritional muscular dystrophy include SGOT, LDH, CPK, aspartate amino transferase (AST) and malic dehydrogenase (MDH). These enzymes may also be elevated by liver damage. An elevation of enzyme activity in serum usually precedes any gross pathological changes or clinical signs (Tollersrud, 1973). In addition to elevation of selected enzymes, serum and tissue concentrations of vitamin E and selenium decrease as a result of deficiencies and may be used to monitor the nutritional status of livestock at high risk of developing WMD (McDowell, 1992, 2000).

Typically, WMD in calves is characterized by generalized leg weakness, stiffness of gait and myodegeneration ( Illus. 1). Affected animals have difficulty standing, exhibit crossover walking and have impaired suckling reflex and ability (Muth, 1955). In calves, the tongue musculature may be affected, explaining the impaired suckling response (NRC, 1996). Calves may display a repeated extension and curling of the tongue (Morrill and Reddy, 1987). Death often occurs suddenly during exertion, from heart failure as a result of severe damage to heart muscle. Calves with WMD have chalky white striations, degeneration, and necrosis in the skeletal muscles and heart ( Illus. 2). In milder cases with calves, where the chief clinical signs are stiffness and difficulty standing, dramatic, rapid recovery can be achieved with vitamin E-selenium injection followed by dietary fortification with vitamin E and selenium.

Acute, chronic and peracute forms of the disease can be distinguished in older calves, usually during the latter growth or early finishing period. Sudden stressors such as transport, regrouping, disease exposure, multiple vaccinations, severe weather or abrupt changes in feed composition are generally considered precipitating factors. Sudden death without previous clinical signs of WMD is the main feature of the peracute condition. The cause is usually found by necropsy as advanced degeneration of the myocardium, with possible lesions of skeletal muscle. In acute cases, motor disturbances, such as an unsteady gait or stiff-calf disease, stiffened muscles in the lumbar region, neck, and forelimb muscles, muscle tremors, perspiration and sudden collapse known as "buckling," are encountered. Chronic marginal vitamin E deficiency is characterized by reduced disease resistance, reduced feed-to-gain ratio and generally poor performance, especially under stress conditions.

Feeder calves display also the vitamin E deficiency symptom known as buckling, in which a stress, such as unloading at the feedlot or passage through the processing chute, triggers weakness of rear legs, buckling of fetlocks and, frequently, shaking or quivering of muscles ( Illus. 3). In many cases, calves become progressively worse until they are unable to rise and may appear to be paralyzed. Frequently, affected calves will be down or continue to buckle for extended periods, and death loss is high in severe cases. Calves (breeds) with excitable temperaments appear to be most affected. Postmortem examination reveals pale, chalky streaks in muscles of the hamstring and back, often with damage to the heart, rib (intercostal) muscles and diaphragm (McDowell, 2000).

Calves with experimentally induced vitamin E deficiencies have exhibited clinical signs of nutritional muscular dystrophy similar to those observed in calves under field conditions (Safford et al., 1954). The same symptoms also appeared in calves fed milk containing high levels of polyunsaturated oils, but not in calves fed milk containing high levels of hydrogenated (saturated) oils (Adams et al., 1959).

WMD can be easily induced in preruminant calves by feeding polyunsaturated oils. Originally, it was thought that ruminating calves would be protected from the vitamin E-depleting effect of PUFA because of the apparent near 100% hydrogenation of all unsaturated fatty acids by the rumen microflora (Noble et al., 1974). However, more recent research indicates that unsaturated fatty acids in grasses can produce oxidative damage and nutritional muscular dystrophy (NMD) in ruminating calves (McMurray and Rice, 1984). Nutritional muscular dystrophy (degenerative myopathy) in older calves occurs most frequently at turnout to spring pasture (Anderson et al., 1976). McMurray et al. (1980) showed that polyunsaturated fatty acids escape ruminal hydrogenation, resulting in a threefold increase of plasma linolenic acid within three days after turnout. Rice et al. (1981) showed that linolenic acid, if protected from ruminal hydrogenation, rapidly reaches high levels in blood and is associated with a rise in plasma creatine phosphokinase, indicating degenerative myopathy (muscle damage). Likewise, Walsh et al. (1993a) reported that ruminating calves fed diets deficient in either vitamin E or both vitamin E and selenium had increased lipid peroxidation products in muscle tissue. Feeding rumen-protected linseed oil to vitamin E-selenium deficient calves further increased the level of lipid peroxidation in muscle.

Although most cases of WMD involve younger animals, degenerative myopathy has been reported in adult cattle (Van Vleet et al., 1977; Gitter and Bradley, 1978; Hutchinson et al., 1982). Yearling Chianina heifers exhibited abortion, stillbirth and periparturient recumbency (downer cow syndrome) (Hutchinson et al., 1982). Necropsy and tissue analysis revealed myodegeneration and a combined deficiency of vitamin E and selenium. Rapid growth in these heifers, coupled with the stresses of late pregnancy and parturition, may have contributed to this form of vitamin E deficiency. Marginal selenium status would be a predisposing factor. A myopathic condition affecting yearling cattle was reported by Barton and Allen (1973) and was associated with animals fed grains treated with propionic acid, which is known to destroy vitamin E. Depletion/repletion studies indicate that feedlot cattle require 50 to 100 IU per day supplemental vitamin E (Hutcheson and Cole, 1985; NRC, 1996). The NRC (1996) states that receiving and starting feedlot cattle should be supplemented with 400 to 500 IU of vitamin E per day to optimize performance and health.

The common factors in development of vitamin E-related WMD appear to be marginal vitamin E and selenium status; sudden change of diet to one high in polyunsaturated fatty acids; and sudden stress of the animal. These factors in combination can precipitate vitamin E responsive myopathy. Vitamin E should be supplemented at levels that ensure protection against marginal or outright deficiency. Optimal levels of supplementation will be discussed below.

Vitamin E Deficiency in Sheep and Goats

In lambs, white muscle disease (WMD, also known as stiff-lamb disease) takes a course similar to that observed in calves. Motor disturbances such as unsteady gait (Illus. 4), stiffness of the muscles of the hindquarters, neck and forelimbs, arched back, muscle tremors and perspiration are encountered in the acute form. On necropsy, white striations in cardiac muscle and bilateral lesions in skeletal muscles characterize the disease. A gradual but progressive swelling of the muscles, particularly in the lumbar region and rear legs, gives the erroneous impression of muscular development. In similarity to the peracute deficiency encountered in calves (changes occur primarily in the myocardium), chronic cardiac muscle degeneration also occurs in the lamb. Affected lambs appear normal at birth, but quickly lose weight after the third week of life. They also show aversion to social stress and may stand apart from the flock. Cardiac arrhythmia and increased heart rate can result even after slight exercise. In the advanced stage, animals consume little if any feed and rapid wasting occurs. Symptoms can be reversed by prompt administration of vitamin E and selenium.

For dystrophic lambs, an oral therapeutic dose of 500 IU dl-alpha-tocopheryl acetate followed by 100 IU on alternate days until recovery is successful (Rumsey, 1975). Vitamin E-selenium responsive conditions are not restricted to young animals and are manifested as lack of thrift, occurring in lambs at pasture (Underwood, 1981). Marginal vitamin E deficiency of yearling sheep can progress to WMD. In sheep of nine to 12 months of age, the disease is frequently observed following driving of the flock with the rapid onset of listlessness, muscle stiffness, inability to stand, prostration and, in severe acute cases, death within 24 hours (Andrews et al., 1968). Hartley and Grant (1961) reported the incidence of WMD in barren ewes was reduced from over 30% to 5% with selenium administration. Farms in New Zealand have had lamb losses as high as 40% to 50%. In these regions, the syndrome may respond to vitamin E, selenium or both. Maas et al. (1984) described nutritional myodegeneration in lambs and yearling ewes with normal selenium status but deficiency of vitamin E.

Deficiency of vitamin E and (or) selenium in the goat, as in other ruminants, results mainly in WMD. Goat kids are born with little or no reserves of the fat-soluble vitamins A, D, and E. Sudden death of young kids under two weeks of age may reveal postmortem evidence of muscle disease and degeneration in the heart muscle or the diaphragm. In older kids and mature animals, deficiency can occur after sudden exertion and stress. Affected animals exhibit bilateral stiffness, usually in the hind legs. In high-producing dairy goats, deficiency manifests itself in poor involution of the uterus, accompanied by retained placenta and metritis following kidding (Guss, 1977). Goat kids four to five weeks of age that were diagnosed with nutritional muscular dystrophy (myodegeneration, NMD) had lower concentrations of both vitamin E and selenium in the liver, skeletal muscle and myocardium (Rammell et al., 1989). Vitamin E concentrations in the liver, skeletal muscle and myocardium in NMD cases averaged 40%, 43% and 30% of those in healthy goat kids, clearly indicating vitamin E depletion.

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