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When copper becomes toxic

A sheep farm was visited where copper (Cu) toxicity was suspected. Several lambs appeared lethargic and anaemic. The farmer had purchased lambs from a farm that had been feeding poultry litter (manure is usually treated with copper sulphate to reduce the bacterial level).

Mature ewes of British breed origin appear to be the most vulnerable and there is evidence to suggest that Finn Sheep and Texels also have a tendency to accumulate more Cu in the liver than other breeds.

Copper is essential for life. It is required for normal iron metabolism, synthesis of elastin and collagen, melanin production, and integrity of the central nervous system. It is essential in keratin (wool) production. More recently, it has been shown that copper is one of the key trace minerals required for an effective immune response.

Signs of Cu deficiency also include brittle or fragile bones, loss of hair or wool pigmentation and poor wool growth. In sheep, “hairy wool” and “swayback” are common. Affected sheep may also grind their teeth incessantly and experience extreme thirst. Membranes are very pale and may appear yellow, as jaundice sets in. Urine is a bloody color. Death usually occurs one to two days after the onset of clinical symptoms. At post-mortem, tissues are pale to dark yellow, and the kidneys are a very dark color.

Generally, sheep require about 5 ppm (parts per million or mg/kg) of Cu in their total diet. Toxicity can occur at levels above 25 ppm. However, dietary molybdenum (Mo) levels also affect copper requirements, as Mo forms an insoluble complex with Cu to prevent copper absorption. If molybdenum levels are low (less than 1 ppm), sheep are more susceptible to Cu toxicity. If Mo intakes exceed 10 ppm, Cu deficiency may occur on diets that would normally be adequate. Sulfur (S) further complicates the Cu:Mo relationship by binding with the Mo.

Copper toxicity in sheep usually results from the accumulation of excess Cu 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 Cu stores to cause toxicity (rapid breakdown of red blood cells). In these situations, chronic Cu poisoning may result from excessive Cu intakes or from low intakes of Mo, S, zinc, calcium or following liver damage. Stresses, such as weather, environment, facial eczema, poor nutrition, transportation, and handling, can also cause the liver cells to die and release the stored copper into the bloodstream.

Talk to us if you suspect Cu problems.

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