Copper deficiency

Copper deficiency may be primary or secondary (conditional). Primary copper deficiency occurs due to its inadequate dietary intake; whereas secondary copper deficiency occurs due to its impaired absorption and utilization, even though dietary copper intake is sufficient. The deficiency of copper is clinically marked by unthriftiness, discolouration of hair, chronic diarrhoea, neonatal ataxia and anaemia in the later stage.

Aetiology: Inadequate amount of copper in the diet causes primary copper deficiency. Enzootic ataxia of sheep in Australia, New Zealand and USA, falling disease of cattle in Australia and licking disease of cattle in Holland are caused by primary copper deficiency. Concurrent deficiency of cobalt and copper, characterized by deficiencies of both minerals, is also reported in Australia (Cost disease) and USA (Salt sickness) Composition of plants and soil characteristics can contribute to primary copper deficiency.

Secondary copper deficiency is associated due to impaired copper utilization, even through diet contains adequate level of copper. Various conditioning factors are suggested to interfere gut absorption of copper. Excess molybdenum is the best known conditioning factor. Molybdenum content in diet reduces copper absorption to below normal levels. Teart disease of sheep and cattle in Britain and Peat scours of cattle in Canada are associated with secondary copper deficiency due to excess molybdenum. Zinc, iron, lead, calcium carbonate and inorganic sulphate are also conditioning factors, which interfere with the absorption of copper. Presence of inorganic sulphates and molybdenum has significant effect on absorption of copper. An increase in sulphate  content potentiates effects of molybdenum and copper deficiency. Copper, molybdenum and sulphate tend to form an insoluble-un-absorbable triple complex copper- tetrathiomolybdate and depletes tissue copper level.

Clinical findings: Copper is an important component of metallo-enzymes such as copper-zinc superoxide dismutase (Cu-Zn SOD) and ceruloplasmin. Copper also affects activities of antioxidant enzymes glutathione peroxidase and cytochrome oxidase. The deficiency of copper therefore, inhibits activities of these enzymes resulting in faulty tissue oxidation and associated signs such as changes in wool of sheep. Impaired tissue oxidation also causes loss of condition and retarded growth. Copper is necessary for reutilization of iron released during heme metabolism. This may be responsible for anaemia in copper deficiency. Impaired collagen formation and significant increase  osteoporotic activity with osteoporosis, degenerative diseases of cartilage and other changes in bones and joints are also seen in copper deficiency. Copper deficiency also affects function of immune cells, heart, nervous system, and reproductive system. In general, the clinical findings are the outcome of malfunction of these metabolic processes and may vary widely with severity of condition, species involved and climatic conditions.

Abnormal hair pigmentation is a consistent clinical finding in copper deficiency in cattle. The change in hair coat colour are particularly prominent around eyes (be- spectacled appearance), on the tips of ears and on the flanks. The hair coat is rough and staring. Calves show slow growth with an increased tendency of bone fracture. Young calves show incoordination, stiff gait and opisthotonous. Ataxia may occur after exercise with sudden loss in control of hind limbs resulting in falling or o sitting posture position.Secondary copper deficiency in cattle is manifested by the clinical signs similar to primary deficiency, but anaemia is not a consistent finding. Persistent diarrhoea is more common in copper deficiency associated with molybdenum excess and in peat scour (teart). Watery, yellow-green to black and foul smelling faeces, debility and depigmentation of hair coat are characteristic signs in peat scour. ‘Falling disease’ is characterized by head throwing, bellowing, and falling followed by death.

Pine disease or unthriftiness of calves is manifested by stiffness of gait, unthriftiness, and painful enlarged distal ends of metacarpal and metatarsal bones. Depigmentation around eyes is apparent and few calves show diarrhoea.Abnormalities of wool are important clinical findings in of primary copper deficiency in sheep. Wool becomes straight, glossy, and steely in appearance ( steely wool disease). Anaemia, scouring, unthriftiness, infertility are common signs of extreme primary copper deficiency in sheep. Retarded growth, diarrhoea and osteoporosis are also seen. Sway back in sheep is reported from UK. The congenital form occurs in extreme primary copper deficiency. The lambs are born week and are unable to stand. They show incoordination, erratic movements and spastic paralysis. Delayed spinal swayback develops after few weeks of birth. Postnatal acute fatal swayback may develop suddenly with death occurring within 1-2 days.Enzootic ataxia occurs only in unweaned lambs, generally at 1-2 month age. The  disease may last for 3-4 weeks in older lambs with more chances of survival. Incoordination of hind limbs is the first sign of enzootic ataxia. Excessive flexion of joints, knuckling over fetlocks, and wobbling of hind quarters and finally falling are important clinical findings. Lambs kick vigorously even in recumbency. Enzootic ataxia has also been reported in goats due to primary copper deficiency in India. The clinical findings are similar to those observed in sheep. Adult horses seldom suffer from copper deficiency, but foals thriving in copper-deficient areas may show unthriftiness and retarded growth, stiffness of limbs and enlargement of joints. Naturally occurring enzootic ataxia is also reported in piglets with signs of posterior paresis, ataxia, nystagmus, inability to stand, paddling movements of the limbs and death.

Diagnosis: Copper deficiency can be diagnosed on the basis of history, physical examination of the affected animals, serum biochemistry, and estimation of copper in liver, feed, soil and water, and presence of other predisposing factors. Plasma copper level below 19 mg/dl represents functional copper deficiency in cattle and sheep. The copper concentration below 200 mg/kg in sheep and 100 mg/kg in cattle are indicative of copper deficiency.

Treatment and Prevention: Copper deficiency can be treated by oral dosing with copper sulphate given @ 5 g to 2-6 months old calves, 8-10 g for mature cattle and buffaloes at weekly intervals for 3-5 weeks. Copper glycinate can also be given parenterally.  In copper deficient areas, ration should be supplemented with copper sulphate (5-10 mg copper per kg DM) to provide minimum dietary requirement. Copper sulphate is a better choice than copper oxide or injectable copper for cattle consuming excess molybdenum and sulphur. Area specific mineral mixture technology has been developed by the Indian Veterinary Research Institute and farmer can choose a copper rich mineral mixture as dietary supplement for preventing copper deficiency in the copper deficient geographical areas. Providing free access to  salt-licks, containing
0.25-0.5% copper sulphate for sheep and 2% for cattle, and top dressing of pasture with copper sulphate (10 kg/ha) can also be practiced to prevent occurrence of copper deficiency.