Page 27

4—
Nutrition Disorders

Enterotoxemia

Enterotoxemia (overeating disease, pulpy kidney disease) is a feed-related malady that causes sudden death in sheep due to a toxin produced by the bacterium Clostridium perfringens type D (although occasionally type C also occurs, particularly in 2- to 4-week-old suckling lambs). The organism appears to be widespread in nature and has been isolated from pastures, manure, and the gastrointestinal tract of healthy sheep (Jensen, 1974; Buxton, 1983).

Under conditions of high carbohydrate intake (high-grain diet; high milk intake; and rarely, high intake of immature forage) the causative bacteria multiply rapidly and produce a toxin. Thus, it is a disease that afflicts suckling lambs, creep-fed lambs, growing-finishing lambs, and ewes fed high levels of grain. Anything that interferes with the normal passage of feed through the gut, such as a heavy burden of parasites, exacerbates the situation (Jensen, 1974; Buxton, 1983).

Protection of lambs against enterotoxemia can be achieved by vaccinating twice (at least 10 days apart) with Clostridium perfringens type D toxoid. Approximately 2 to 4 weeks is required for the development of immunity after vaccination. Vaccinating pregnant ewes 2 to 4 weeks before parturition will transfer sufficient passive immunity to their lambs to protect them for the first 4 to 6 weeks postpartum. Lambs should receive a protective dose of antiserum at this age to protect them until market (Oxer et al., 1971; Jensen, 1974).

Polioencephalomalacia

Polioencephalomalacia (PEM), first described in the United States by Jensen et al. (1956), and cerebrocortical necrosis (CCN), first described in England by Terlecki and Markson (1959, 1961), are now considered synonymous terms for the same disease (Loew, 1972; Edwin and Jackman, 1982). Polioencephalomalacia has since been reported in most areas of the world and affects both cattle and sheep (Loew, 1972; Edwin, 1975). Clinical signs include disorientation, dullness, aimless wandering, loss of appetite, circling, progressive blindness, extensor spasms, and occasionally head pressing (Loew, 1972; Edwin, 1975; Edwin and Jackman, 1982). Final diagnosis is dependent on histopathological examination (Loew, 1972; Edwin et al., 1979; Spicer and Horton, 1981).

Following the finding that thiamin therapy could be used with marked success (Davies et al., 1965), it was established that affected animals were indeed thiamin deficient (Pill, 1967; Edwin, 1970). Although the precise etiology of the disease is still not known, it is now accepted that the thiamin deficiency, probably associated with cofactors and antimetabolites, is initiated by rumenproduced thiaminases (Roberts and Boyde, 1974; Mueller and Asplund, 1981; Edwin and Jackman, 1982; Edwin et al., 1982). The disease has been reported in most ages and classes of sheep, but it occurs most often in feedlot lambs (Loew, 1972; Mueller and Asplund, 1981). Animals affected with PEM can be successfully treated with 200 to 500 mg of thiamin injected intravenously, intramuscularly, or subcutaneously (McKenzie and Steele, 1980; Chick et al., 1981; Spicer and Horton, 1981; Edwin and Jackman, 1982). Although response is often dramatic, if significant brain damage has occurred the recovered animals rarely regain satisfactory levels of productivity. Therefore, very early treatment is critical. The thiamin injection can also be used to protect sheep at risk—for example, the remainder of a group in which PEM has been diagnosed (McKenzie and Steele, 1980; Chick et al., 1981).



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Page 27 4— Nutrition Disorders Enterotoxemia Enterotoxemia (overeating disease, pulpy kidney disease) is a feed-related malady that causes sudden death in sheep due to a toxin produced by the bacterium Clostridium perfringens type D (although occasionally type C also occurs, particularly in 2- to 4-week-old suckling lambs). The organism appears to be widespread in nature and has been isolated from pastures, manure, and the gastrointestinal tract of healthy sheep (Jensen, 1974; Buxton, 1983). Under conditions of high carbohydrate intake (high-grain diet; high milk intake; and rarely, high intake of immature forage) the causative bacteria multiply rapidly and produce a toxin. Thus, it is a disease that afflicts suckling lambs, creep-fed lambs, growing-finishing lambs, and ewes fed high levels of grain. Anything that interferes with the normal passage of feed through the gut, such as a heavy burden of parasites, exacerbates the situation (Jensen, 1974; Buxton, 1983). Protection of lambs against enterotoxemia can be achieved by vaccinating twice (at least 10 days apart) with Clostridium perfringens type D toxoid. Approximately 2 to 4 weeks is required for the development of immunity after vaccination. Vaccinating pregnant ewes 2 to 4 weeks before parturition will transfer sufficient passive immunity to their lambs to protect them for the first 4 to 6 weeks postpartum. Lambs should receive a protective dose of antiserum at this age to protect them until market (Oxer et al., 1971; Jensen, 1974). Polioencephalomalacia Polioencephalomalacia (PEM), first described in the United States by Jensen et al. (1956), and cerebrocortical necrosis (CCN), first described in England by Terlecki and Markson (1959, 1961), are now considered synonymous terms for the same disease (Loew, 1972; Edwin and Jackman, 1982). Polioencephalomalacia has since been reported in most areas of the world and affects both cattle and sheep (Loew, 1972; Edwin, 1975). Clinical signs include disorientation, dullness, aimless wandering, loss of appetite, circling, progressive blindness, extensor spasms, and occasionally head pressing (Loew, 1972; Edwin, 1975; Edwin and Jackman, 1982). Final diagnosis is dependent on histopathological examination (Loew, 1972; Edwin et al., 1979; Spicer and Horton, 1981). Following the finding that thiamin therapy could be used with marked success (Davies et al., 1965), it was established that affected animals were indeed thiamin deficient (Pill, 1967; Edwin, 1970). Although the precise etiology of the disease is still not known, it is now accepted that the thiamin deficiency, probably associated with cofactors and antimetabolites, is initiated by rumenproduced thiaminases (Roberts and Boyde, 1974; Mueller and Asplund, 1981; Edwin and Jackman, 1982; Edwin et al., 1982). The disease has been reported in most ages and classes of sheep, but it occurs most often in feedlot lambs (Loew, 1972; Mueller and Asplund, 1981). Animals affected with PEM can be successfully treated with 200 to 500 mg of thiamin injected intravenously, intramuscularly, or subcutaneously (McKenzie and Steele, 1980; Chick et al., 1981; Spicer and Horton, 1981; Edwin and Jackman, 1982). Although response is often dramatic, if significant brain damage has occurred the recovered animals rarely regain satisfactory levels of productivity. Therefore, very early treatment is critical. The thiamin injection can also be used to protect sheep at risk—for example, the remainder of a group in which PEM has been diagnosed (McKenzie and Steele, 1980; Chick et al., 1981).

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Page 28 Pregnancy Disease Pregnancy disease, also referred to as ketosis, acetonemia, and pregnancy toxemia, is associated with undernourishment and particularly with over-fat condition among ewes. It occurs in ewes in late pregnancy and usually is restricted to those carrying multiple fetuses. Stress factors such as shearing, transporting, severe weather exposure, and predator attacks, in addition to undernourishment, can precipitate outbreaks of the disease. Clinical features of the disease include high blood levels of ketone bodies and hypoglycemia. The affected animals appear depressed, lack appetite, have a staggering gait, separate from the flock, and exhibit nervousness (Reid, 1968). In the final stages of the disease (prior to death), vision is impaired and ewes are unable to rise or stand because of weakness, stiffness, or partial paralysis. Ewes that give birth during the early stages of the syndrome usually recover. During late pregnancy there are high glucose demands (about 1.5 times maintenance levels) placed on the ewe by the rapidly developing fetuses. With reduced rumen capacity due to increasing fetal size, feed intake is impaired. The ewe mobilizes adipose tissue in an attempt to meet glucose needs, the liver produces less glucose, a metabolic acidosis develops, and ketone bodies accumulate in the blood. The disease is not related to lack of exercise. It can be prevented by ensuring adequate nutrient intake in late pregnancy so that increases in weight occur. A drench of 200 to 300 ml of propylene glycol or glycerol can be used when signs first appear, as an energy source for ewes refusing to eat sufficient feed. Urinary Calculi Urinary calculi (uroliths) are mineral deposits occurring in the urinary tract (Field, 1969). Although these deposits form in all breeds and sexes of sheep, blockage of the flow of urine generally only occurs in intact or castrated male sheep. The blockage may rupture the urinary bladder, resulting in a condition commonly called water belly, and cause death. Difficult or painful urination as evidenced by straining, slow urination, stomping of the feet, and kicking at the area of the penis are signs of calculi problems (Jensen, 1974). Under feedlot conditions, this disease appears to have a nutritional or metabolic origin; affected animals excrete an alkaline urine that has a high phosphorus content (Crookshank, 1968; Jensen, 1974). Dietary intakes of calcium, phosphorus, magnesium, and potassium appear to play a major role in the incidence of calculosis in feedlot lambs, and an equation that uses intakes of these four minerals has been used to predict calculi formation in wethers (Lamprecht et al., 1969). The incidence of urinary calculi in growing-finishing lambs can be greatly reduced by preventing an excessive intake of phosphorus and by maintaining a calcium-to-phosphorus ratio greater than 2:1 (Emerick and Embry, 1963). Reducing the alkalinity of the urine by feeding acid-forming salts is also effective (Crookshank, 1968, 1970). Ammonium chloride or ammonium sulfate added to the complete diet at 0.5 percent has been used successfully; ammonium chloride appears to be more effective than ammonium sulfate (Crookshank, 1970). Ammonium chloride has also been used to drench sheep at a level of 7 to 14 g per sheep per day for 3 to 5 days. Reasonable success has been achieved with this procedure so long as animals were still able to pass a small amount of urine. Injection with a smooth muscle relaxant is helpful in these cases. In range sheep, the disease is associated with the consumption of forages having a high silica content (Emerick et al., 1959; Bailey, 1978). Sodium chloride, fed at a level of 4 percent or more of the total diet, helps prevent urinary calculi, especially in range animals. Sodium chloride increases consumption of water and the amount of urine produced. It may be fed to range animals as a part of the protein supplement, provided adequate water is available. Availability of a plentiful supply of clean water is important in minimizing calculi problems under range and feedlot conditions.