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United Suffolk Sheep Association |
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Copper Poisoning Paul G. Eness, DVM Considerations in the occurrence, recognition and control of copper poisoning in sheep. As with many of the trace minerals, a deficiency of dietary copper may occasionally cause health problems in sheep. Copper excess leading to signs of toxicity is more likely to be a problem than is deficiency. Sheep are far more susceptible to the toxic effects of copper than are other farm animals. Cattle can tolerate 10 times the level of copper which may be toxic to sheep. Growing swine are often fed copper at levels of up to 250 parts per million (ppm) to enhance performance. As little as 12 ppm may cause serious problems in sheep. The widespread use of copper compounds in swine and poultry rations is one common source of problems for sheep producers. Operator error in the custom feed mill may lead to the inadvertent inclusion of excess levels of copper in a delivery of feed. These problems may occur as a result of incomplete emptying and cleaning of storage bins, augers or delivery trucks between a batch of feed intended for swine or poultry and one going to a sheep operation. Mixing errors of a similar nature have also caused death losses in sheep following accidental inclusion of monensin and other ration constituents at toxic levels. Other sources of toxic levels of copper include poultry and swine manure when applied to pastures being grazed by sheep. Occasional poisonings have occurred with the use of copper sulfate in foot baths. In some western states some plants, such as lupine, contain substances which may damage the liver rendering animals more subject to poisoning from copper. There are a number of complicating factors involved in the metabolism of copper by sheep. These factors are frequently involved in cases of copper toxicosis. The dietary ratio of copper to molybdenum, another trace mineral, is extremely important. Molybdenum and also sulfur act to neutralize the toxic effects of copper. If molybdenum levels are extremely low, part of this neutralizing potential is lost and poisoning may occur even with normal copper levels in the ration. Copper toxicosis occurs as an acute or, more often, chronic form. The acute form is seen shortly after the consumption of large amounts of copper. The clinical signs lead quickly to death of the animal. The chronic form is more insidious and is seen after animals have been fed rations marginally high in copper or very low in molybdenum or sulfur (the copper antagonists). This diet may have been fed for weeks or months with no evidence of copper poisoning. During this time excess copper is stored in the liver. Eventually the high levels of liver copper may damage this organ causing a sudden release of the stored copper. This release may also be observed following stress as from transport, showing, shearing, or extreme heat. The large amounts of circulating copper cause destruction of red blood cells leading to anemia, weakness, and loss of appetite. Death occurs in one to several days. The most obvious clinical sign in the living animal is icterus, which is an obvious yellowing of body tissues, especially evident in the whites of the eyes. Very few other conditions of sheep will cause this degree of icterus. The urine of these animals is dark brown. Post mortem examination reveals bright yellow fat deposits, very dark watery blood and dark gun metal gray colored liver and kidneys. In a recent case a number of near term abortions and still births occurred in a group of ewe lambs. No evidence of any infectious agent was detected in fetuses or placentas from aborting animals, but elevated copper levels were detected in the livers of stillborn lams. Several ewes died following lambing. Typical signs of copper toxicity were seen in these animals. Toxic levels (60 ppm) were found in a batch of feed delivered one month before abortions started. It was possible to define the source of the problem because feed samples were still available. This stresses the importance of keeping and labeling a small sample of feed from every batch fed. This is especially important with chronic copper poisoning as the source of feed may very well all be fed by the time clinical signs appear. Treatment of this condition in often unrewarding, but may be indicated when valuable breeding stock are affected. Treatment consists of daily drenching with ammonium molybdate and sodium sulfate for a period of several weeks. As appetite returns the feeding of these compounds may replace drenching. Another, more expensive, treatment involves daily use of penicillamine. Factors in prevention and diagnosis of copper toxicity in sheep: 1. Provide sheep with no mineral other than that specified for sheep. This will insure safe copper levels and the proper copper molybdenum ratio (10:1). 2. Do not fertilize sheep pastures with hog or poultry manure 3. Exercise extreme care in preparing sheep rations especially if equipment is also used for processing poultry or swine rations. 4. Retain samples from every batch of feed.
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