Copper Nutrition in Farm Animals (Cows, Sheep, Goats)
Evidence that copper is a dietary essential was obtained in 1924, when experiments with rats showed that copper was necessary for haemoglobin formation. Although copper is not actually a constituent of haemoglobin, it is present in certain other plasma proteins, such as ceruloplasmin, concerned with the release of iron from the cells into the plasma. A deficiency of copper impairs the animal’s ability to absorb iron, mobilise it from the tissues and utilise it in haemoglobin synthesis.
Copper is also a component of other proteins in blood. One of these, erythrocuprein, occurs in erythrocytes, where it plays a role in oxygen metabolism. The element is also known to play a vital role in many enzyme systems; for example, copper is a component of cytochrome oxidase, which is important in oxidative phosphorylation.
It is also a component of superoxide dismutase, which forms part of the cell’s antioxidant system. The element also occurs in certain pigments, notably turacin, a pigment of feathers. Copper is necessary for the normal pigmentation of hair, fur and wool. It is thought to be present in all body cells, being particularly concentrated in the liver, which acts as the main copper storage organ of the body. Copper has been shown to reduce the susceptibility to infection in lambs directly.
Since copper performs many functions in the animal body, there are a variety of deficiency symptoms. These include anaemia, poor growth, bone disorders, scouring, infertility, depigmentation of hair and wool, gastrointestinal disturbances, and lesions in the brain stem and spinal cord.
The lesions are associated with muscular incoordination and occur, especially, in young lambs. A copper deficiency condition known as ‘enzootic ataxia’ has been known for some time in Australia; the disorder there is associated with pastures low in copper content (2–4 mg/kg DM) and can be prevented by feeding with a copper salt.
A similar condition that affects lambs occurs in the UK and is known as ‘swayback’. The signs of swayback range from complete paralysis of the newborn lamb to a swaying staggering gait that affects, in particular, the hind limbs. The condition can occur in two forms, one congenital, in which the signs are apparent at birth and are due to the failure of the myelin sheath of nerves to develop, and the other in which the onset of the clinical disease is delayed for several weeks. The congenital form of the condition is irreversible and can be prevented only by ensuring that the ewe receives an adequate level of copper in her diet. Delayed swayback can be prevented or retarded in copper-deficient lambs by parenteral injection of small doses of copper complexes.
Although the dietary level of copper is an important factor in the aetiology of swayback, the condition does not appear to be invariably caused by a simple dietary deficiency of the element. Swayback has been reported to occur on pastures apparently normal or even high (7–15 mg/kg DM) in copper content. One important factor is that the efficiency of absorption of dietary copper is very variable. For example, there is about a tenfold variation in the efficiency with which Scottish Blackface ewes absorb copper from autumn pasture (1.2 per cent) and from leafy brassicas (13.2 percent). It is also known that genetic factors influence the concentration of copper in the blood, liver and brain of the sheep, and hence the incidence of swayback can be affected by genotype. Blackface lambs given a copper-supplemented barley and fishmeal diet retained 6 per cent of the dietary copper in the liver, whereas Texel lambs retained 13 per cent. Finnish Landrace and Suffolk lambs were intermediate, at 8–9 per cent retention.
Copper plays an important role in the production of ‘crimp’ in wool. The element is present in an enzyme that is responsible for the disulphide bridge in two adjacent cysteine molecules. In the absence of the enzyme, the protein molecules of the wool do not form their bridge and the wool, which lacks crimp, is referred to as ‘stringy’ or ‘steely’.
Nutritional anaemia resulting from copper deficiency has been produced experimentally in young pigs by diets very low in the element, and this type of anaemia could easily arise in such animals fed solely on milk. In older animals, copper deficiency is unlikely to occur and copper supplementation of practical rations is generally considered unnecessary. There are, however, certain areas in the world where copper deficiency in cattle occurs. A condition in Australia known locally as ‘falling disease’ was found to be related to a progressive degeneration of the myocardium of animals grazing on copper-deficient pastures.
Certain pastures on calcareous soils in parts of England and Wales have been known for over 100 years to be associated with a condition in cattle known as ‘teart’, which is characterised by unthriftiness and scouring. A similar disorder occurs on reclaimed peat lands in New Zealand, where it is known as ‘peat scours’. Molybdenum levels in teart pasture are of the order of 20–100 mg/kg DM compared with 0.5–3.0 mg/kg DM in normal pastures, and teart was originally regarded as being a straightforward molybdenosis. In the late 1930s, however, it was demonstrated that feeding with copper sulphate controlled the scouring and hence a molybdenum–copper relationship was established.
It is now known that the effect of molybdenum is complex, and it is considered that the element exerts its limiting effect on copper retention in the animal only in the presence of sulphur. Sulphide is formed by ruminal microorganisms from dietary sulphate or organic sulphur compounds; the sulphide then reacts with molybdate to form thiomolybdate, which in turn combines with copper to form an insoluble copper thiomolybdate (CuMoS4), thereby limiting the absorption of dietary copper. In addition, it is considered likely that if thiomolybdate is formed in excess, it may be absorbed from the digestive tract and exert a systemic effect on copper metabolism in the animal.
It has long been known that copper salts given in excess to animals are toxic. Continuous ingestion of copper in excess of nutritional requirements leads to an accumulation of the element in the body tissues, especially in the liver. Copper can be regarded as a cumulative poison, so that considerable care is required in administering copper salts to animals. The tolerance to copper varies considerably between species. Pigs are highly tolerant and cattle relatively so. On the other hand, sheep are particularly susceptible and chronic copper poisoning has been encountered in housed sheep on concentrate diets. There is a gradual accumulation of copper in the liver of sheep until the danger level of about 1000 mg/kg fat-free DM is reached. Poisoning has been known to occur in areas where the herbage contains copper of the order of 10–20 mg/kg DM and low levels of molybdenum.
Chronic copper poisoning results in necrosis of the liver cells, jaundice, loss of appetite and death from hepatic coma. The slow accumulation of copper in the liver causes damage to the organ without overt symptoms. There is leakage of enzymes from the damaged cells into the blood. Eventually there is a sudden release of copper and haemolysis, which can occur spontaneously or as a result of stressors such as parturition or infection. There is a genetic variation in animals’ susceptibility to copper poisoning related to the efficiency of retention. The EU maximum permitted level for copper in sheep diets is 15 mg/kg – this should not be exceeded if toxicity is to be avoided. For susceptible breeds, a dietary level of 10 mg/kg can be excessive. It is unwise to administer copper supplements to sheep unless deficiency conditions are liable to occur – many cases of death due to copper poisoning caused by the indiscriminate use of copper-fortified diets have been reported. Chronic copper poisoning in sheep has occurred under natural conditions in parts of Australia where the copper content of the pasture is high. Care should be taken when sheep are given antiprotozoal compounds such as monensin, which may eliminate the protozoa that produce the sulphide that normally reduces copper availability.