by Larry L. Berger, Ph.D.
Professor, Animal Sciences
University of Illinois
Importance of Copper
Copper toxicity in sheep is more often a problem of nutritional management than it is excess copper intake. The purpose of this paper is to look at such factors as nutrient interactions, animal management, and environmental conditions that may increase the risk of copper toxicity and how the sheep producer can minimize these risks.
The importance of copper as an essential nutrient has been known since the 1920′s. Copper is required for normal iron metabolism, elastin and collagen synthesis, melanin production and integrity of the central nervous system. There are numerous metalloprotein enzymes, metalloporphyrin enzymes and non-enzyme metalloproteins in animals that require copper to be biologically active. More recently it has been shown that copper is one of the key trace minerals required for an effective immune response. The bottom line is that copper is essential for life. Consequently, most trace mineralized salt products contain 0.03 to 0.04% (300 to 400 ppm) of copper to prevent copper deficiency.
Sensitivity of Sheep
Like most nutrients, excessive concentrations can cause toxicity. However, sheep tend to be much more sensitive than other farm animals. For example, growing swine are often fed copper concentrations as high as 250 ppm in the diet to improve performance. Cattle can consume diets containing 100 ppm copper with no problem, while toxicities have occurred in sheep with concentrations as low as 10 ppm (Church and Pond 1988).
Copper toxicity in sheep usually results from the accumulation of copper in the liver over a period of a few weeks to more than a year with no clinical signs followed by a sudden release of liver copper stores to cause toxicity. In these situations, chronic copper poisoning may result from excessive copper intakes or from low intakes of molybdenum, sulfur, zinc, calcium or following liver damage (Kimberling, 1988). Sheep accumulate copper in the liver more readily than other farm animals and over a period of time, 1000 – 3000 ppm on a dry weight basis may be achieved. During the accumulation phase, blood copper levels are normal in the 0.10 to 0.20 mg/dl. Toxicity results when stress conditions cause the liver cells to die and release the stored copper into the blood. Plasma copper levels then increase 10 to 20 fold. These elevated blood copper levels (500-2000 mg/dl) usually precede clinical signs by 24 to 48 hours (Kimberling 1988). The most common symptoms are anorexia, excessive thirst and depression. These are accompanied by severe hemoglobinemia, anemia, icterus and methemoglobinemia. Most sheep will die within 1 to 2 days of the onset of these signs (Merck Veterinary Manual 1979).
The ratio of copper to molybdenum is the most important dietary factor affecting copper toxicity in sheep. Ratios of 10:1 or less will prevent toxicity in most cases. The exact mechanism by which molybdenum prevents copper toxicity is poorly understood. However, it is known that an insoluble complex, CuMo04, can be formed in the gastrointestinal tract thus reducing copper absorption. This theory is substantiated by the fact that increasing dietary copper is an effective treatment of molybdenum toxicity.
Molybdenum concentrations in most feeds are in the range of 1 to 3 ppm in the total diet. If molybdenum concentrations are low (less than 1 ppm), diets containing copper in the range of the normal requirement (8 – 11 ppm) have been known to produce toxicity (NRC 1975). Sheep producers who live in or buy feed from molybdenum deficient areas should pay close attention to dietary copper levels. Such feeds as distillers dried grains and soybean meal which are normally high in copper should be limited in the diet. Trace mineralized salt should not be removed from the diet because it contains zinc which also reduces copper absorption. Diets containing high concentrations (100 ppm) of zinc have been shown to reduce liver copper stores. In addition, eliminating all trace mineral supplementation may actually worsen the situation by creating an even greater mineral imbalance.
Although prevention is much preferred, there are times when mass treatment is indicated. The most common treatment is to give a drench daily containing 50 to 100 mg of ammonium molybdate and 0.5 to 1.0g of sodium sulfate per animal for three weeks. To reduce labor, an aqueous solution of the two salts can be sprayed onto the feed. This approach is recommended as a treatment procedure only if all animals are eating regularly.
Animal Management and Environment
Besides nutrition, animal management factors can affect the incidence of copper toxicity in sheep. For example, although this disease can occur in both sexes of all breeds, mature ewes of British breeds seem to be the most susceptible. In the United States this disease is most common in the western states of the intermountain region. Although the disease can occur anytime, peak incidence usually is in the fall and winter.
Environmental factors and stress can also affect the susceptibility of sheep to this disease. For example, grazing sheep in areas containing certain potentially toxic plants may predispose them to copper toxicity. Plants such as lupines, which contain toxic alkaloids, produce copper toxicity by impairing the liver’s ability to metabolize ingested copper. Chronic toxicity is also common in sheep grazing subterranean clover and is associated with normal levels of copper, low levels of molybdenum and no apparent liver damage. The stress associated with shipping ewes from mountain ranges to pastures some distance away appears to make ewes more susceptible.
In summary, sheep producers should become familiar with copper and molybdenum levels of feeds grown in their area. If the area is deficient in molybdenum or high in copper, feed samples should be analyzed routinely to monitor the copper: molybdenum ratio in the diet. Supplemental feeds which are known to be low in copper should be used whenever possible. Feeding a properly fortified trace mineralized salt is essential to the health and production of the sheep flock.
church, d.c. and w.g. pond, 1988. basic animal nutrition and feeding, 3rd edition. published by john wiley and sons, new york. pp. 196-199
Kimberling, C.V. 1988., Jensen and Swift’s Disease of Sheep, 3rd Edition. Published by Lea and Febiger, Philadelphia, PA. pp. 372-374. Merck Veterinary Manual, 1979. 5th Edition. Published by Merck and Company. Rahway NJ. pp. 977-978. NRC., 1975. Nutrient Requirements of Sheep. 5th Edition, National Academy Press. Washington DC.
Salt Institute, 1991