Copper toxicity in sheep and goats (Proceedings)

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Copper toxicity in sheep and goats (Proceedings)

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Aug 01, 2009

Acute copper toxicity results from ingestion of high copper feeds, copper salts, pesticides, poultry litter and other high copper substances. Acute copper poisoning can occur at copper intakes of 20-100 mg/kg in sheep and young calves, and 200-800 mg/kg in adult cattle. Chronic copper toxicity occurs when high levels of copper are ingested over a period of time, but at doses below the acutely toxic level. Sheep are the most susceptible species to chronic copper toxicity, because their liver cells have a high affinity for copper and they excrete copper into the bile at a very low rate, leading to a build-up of liver copper concentration over time. One of the most common causes of toxicity in sheep is the accidental feeding of feedstuffs intended for other livestock. Molybdenum reduces the accumulation of copper in the liver. The ratio of copper to molybdenum in the feed is, therefore, an important factor determining the risk of copper poisoning. Chronic copper toxicity typically involves the ingestion of feeds that have a high copper : molybdenum ratio. Any feed which tests to have copper levels > 25 ppm or has a copper : molybdenum ratio of >10:1 is considered potentially toxic for sheep.

Copper is a strong oxidizing agent. It binds to proteins in the liver cells and is stored in lysosomes within hepatocytes. As long as the copper remains stored in lysosomes it does not cause tissue damage. Copper can, however, be spontaneously released or released at times of stress, including shearing, weather extremes or transport. Chronic copper poisoning is, therefore, often described as a stress-related disease. When copper enters the blood it partitions into red cells, elevating red cell copper levels 15-20 times, while plasma copper levels only increase 2-3 times. It causes oxidative injury to hemoglobin, inducing Heinz-body formation and converting it to methemoglobin, which cannot bind O2 or CO2. The sulfhydryl groups of the red blood cell membrane also undergo oxidative change, resulting in significant hemolysis and anemia. Finally, this massive release of hemoglobin can result in hemoglobinuric nephrosis and renal failure.

Many animals affected by copper toxicity are simply found dead. Necropsy findings will include icterus and "gun metal blue" kidneys. In the live animal, icterus, red or brown urine, anorexia, pallor, weakness and recumbency are common signs. Brown blood or pink serum may be noted on blood collection and processing; anemia and, in some cases, evidence of red blood cell regeneration, will be present on blood work. Elevations in creatinine are expected in animals with renal involvement. Hepatocellular injury and bile duct occlusion occur as the copper release and the enzymes AST and GGT have been shown to be elevated as far as 9 weeks prior to the development of clinical signs.

Once these clinical signs are recognized, the current feed for the flock should be withdrawn pending testing for both copper and molybdenum. Because copper may be stored in the liver for up to 18 months, it is common to find that the current feed is not the source. On necropsy, fresh samples of liver and kidney should be submitted to a diagnostic laboratory for copper levels. Serum copper levels are unreliable in live animals due to the primary storage in liver. If serum copper levels are elevated (> 2.0 ppm), this is diagnostic. If the levels are below this level, copper toxicity cannot be excluded because the elevation in serum copper concentration is often transient. Liver copper levels should also be interpreted with caution, because the release of copper from the liver during the disease process can significantly reduce liver copper concentrations.