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Copper Complexity for Health and Production in Sheep

Pankaj Kumar Rashmi R. Kumari Pallav Shekhar Archana Saxena
Vol 2(2), 42-47
DOI-

Mineral nutrition in sheep can be quite complicated. There are almost 15 minerals that have been demonstrated to be essential in sheep nutrition. Copper (Cu) requirements of sheep are dependent on dietary and genetic factors and therefore it is almost impossible to develop a set of well-defined requirements. Sheep accumulates copper in liver more readily than any other livestock and thus are highly susceptible to copper toxicity. In addition dietary requirement of copper is comparatively less in sheep and dietary copper utilization is highly variable in sheep depending on physiological state and age. It is essential for wool production and is involved in the animal’s immune response to disease challenges. Young sheep are more susceptible to Cu deficiency as milk is a poor source of copper. Placental transfer of Cu is less efficient in sheep because of low liver Cu reserves in ewe. Copper deficiencies in sheep can be either primary or secondary, depending on the nature of deficiency and involvement of other factors. In primary copper deficiency in sheep, enzootic ataxia is the major manifestation. Secondary copper deficiency in sheep is mainly associated with swayback, teart, reduced body growth, bone fragility and lameness due to spontaneous fractures.


Keywords : Copper Sheep Deficiency Health and production

Introduction:

A balanced feed ration is essential for normal health, growth and reproduction of animals. Nutrients in the feed are utilized by the sheep to meet their nutritional requirements. It is not the feed itself that meets these needs, but the components that make up the feed are essential. It occupies an important place in animal nutrition for production as well as health and is required for four basic functions i.e. structural, physiological, catalytic, and regulatory. As with vitamins and other essential food nutrients, mineral requirements vary with animal species. Mineral nutrition in sheep can be quite complicated. There are almost 15 minerals that have been demonstrated to be essential in sheep nutrition. They include sodium, chlorine, calcium, phosphorus, magnesium, potassium, sulfur, cobalt, copper, iodine, iron, manganese, molybdenum, selenium and zinc. Minerals are classified as macro or micro. The difference between the classifications reflect the amount needed in the diet and not there physical size. Although relatively precise requirements have been published for the different minerals, it should be recognized that in practice the true dietary requirements vary greatly depending on the nature and amount of these and associated minerals in the diet. The mineral content of feeds is direct reflection of the mineral content of the soil where cultivation was done. Thus, there are many regional differences in sheep mineral nutrition. A number of mineral balances (e.g. calcium and phosphorus, copper to molybdenum, selenium and vitamin E) must be considered when establishing the actual requirements under specific conditions. Most of these are met under normal grazing and feeding habits.

Copper is required for normal chemical and physical processes that occur in the body, normal iron metabolism, red blood cell formation and production of skin and hair pigments or melanin, formation of myelin, a substance that supports and protects the central nervous system and for cross-linking collagen and elastin which is required for normal bone formation (Sharma et al., 2005a). It is essential for wool production and is involved in the animal’s immune response to disease challenges (Underwood, 2001). Copper is essential component of numerous enzymes like superoxide dismutase (SOD), cytochrome oxidase, lysyl oxidase, ceruloplasmin (Pulina et al., 2005). Deficiency of copper has also been reported responsible for impaired fertility in livestock (Sharma et al., 2007).

Copper (Cu) requirements of sheep are dependent on dietary and genetic factors and therefore it is almost impossible to develop a set of well-defined requirements. In fact, it has been shown that dietary amounts of copper that are adequate in one situation may be deficient in another and possibly toxic in a third situation. Concentration of molybdenum is a major dietary factor affecting the ewes copper requirement. Molybdenum forms an insoluble complex with copper which reduces its absorption thus increasing the dietary levels needed to meet requirements. Also Merino breeds of sheep generally are less efficient in absorbing copper from feedstuffs than British breeds of sheep. Young animals are more susceptible to Cu deficiency as milk is a poor source of copper. Placental transfer of Cu is less efficient in sheep because of low liver Cu reserves in dam. There is a delicate balance between the copper requirement and copper toxicity in sheep. In most cases, sheep can meet or exceed their dietary requirements for copper from normal feeds and thus do not require additional copper. Sheep are more susceptible to copper toxicity problems than most other livestock species. Errors in feed mixing frequently result in death due to copper toxicity. Although it is impossible to give the exact requirements and toxic levels, the recommended copper allowance is 7 to 10 mg/kg DM when the molybdenum content in the diet is below 1.0 mg/kg and up to about 14-20 mg/kg when molybdenum content is above 3.0 mg/kg (Kott, 2006). It should be stressed that these are just guidelines and may vary drastically from situation to situation. When selecting a trace mineral mix for sheep, it is generally recommended to choose one that contains no or minimal copper. Supplementation in the form of mineral mixture @ exceeding over 4 mg of copper per ewe per day should be avoided.

Copper deficiencies can be classified into primary and secondary copper deficiencies depending on the nature of deficiency and involvement of other factors. Primary deficiency occurs as a result of low dietary intake of Cu that is when the forage is grown on deficient soils or on soils in which the copper is unavailable and no supplemental copper salt in feed.Secondary or conditioned copper deficiency occurs when the dietary intake of copper is adequate, but absorption and utilization of the copper are inadequate because of the presence of interfering substances in the diet. These interfering factors can be due to presence of molybdenum, sulphur, iron, cadmium and zinc. Copper, molybdenum and sulphur form thiomolybdates in rumen of all ruminants including sheep which reduce copper availability. Roughage grown on ‘improved pastures’ (fertilized, limed) are most likely to be Cu deficient as the liming reduces copper uptake by plants, and many fertilizers contain interfering factors like molybdenum. Good quality lush grass forages have less available copper than most hays, and legumes have more available copper than most grasses (Pugh et al., 2002).

Pathogenesis

The consequences of hypocuprosis include a failure of copper metalloenzymes (Copper Superoxide dismutase (SOD) and Ceruloplasmin (Cp)) which form part of the antioxidant   defence system resulting in oxidative damage to cellular components. The straightness and stringiness of wool is due to inadequate keratinisation probably due to imperfect oxidation of   free thiol groups due to deficiency of Cu. In the later stages of copper deficiency, the impairment of tissue oxidation causes interference with intermediary metabolism resulting in reduced bodyweight. Copper is necessary for the reutilization of iron liberated from the normal breakdown of haemoglobin, so deficiency may results in anemia. Microcytic hypochromic anemia is evident in copper deficiency. The osteoporosis which occurs in copper deficiency is caused by the depression of osteoblastic activity. Copper is a component of the enzyme lysyl oxidase which is having important functions in maintaining the integrity of tissues such as capillary beds, ligaments and tendon.Copper deficiency halts the formation of myelin and causes demyelination in lamb. Copper functions in the immune system through the energy production, neutrophil production and activity, antioxidant enzyme production, development of antibodies and lymphocyte replication (Sharma et al., 2005b). Low copper status has resulted in decreased humoral and cell-mediated immunity there by impair cell immune functions, affecting bactericidal capacity and making animals more susceptible to infection.

The major phases of copper deficiency include depletion, deficiency, dysfunction and disease (Radostits et al., 2007). During the depletion phase, there is loss of copper from any storage site, such as liver, but the plasma concentrations of copper may remain constant. With continued dietary deficiency, the concentrations of copper in the blood decline during the phase of marginal deficiency. The concentrations or activities of copper-containing enzymes in the tissues begin to decline during the phase of dysfunction. Further changes that occur in cellular function are manifested as clinical signs of disease.

Some Important Facts about Copper requirement in Small ruminants
Ø  Sheep should not be supplemented copper above 10ppm. Copper requirement for sheep was 5mg/kg dry matter of diet (NRC, 1975); latter was increased to 7-11 mg/kg dry matter (NRC, 1985). ARC (1980) estimated copper requirements from 1-8.6 mg/kg dry matter of diet depending on physiological state of animal.
Ø  Sheep accumulates copper in liver more readily than any other livestock and thus are highly susceptible to copper toxicity
Ø  Sheep has comparatively lower (5-10 ppm) requirement of dietary copper than goat (10-20 ppm)
Ø  Copper availability is reduced by other minerals like iron, sulphur, molybdenum, zinc (Davis and Mertz, 1987). The zinc-copper interaction is alleviated to a certain extent by maintaining the Zn: Cu between 3:1 and 5:1 ratio
Ø  Only a fraction (1.4-12.8% in adult (Underwood and Suttle, 1999) and may be up to 90% in young (ARC, 1980) ) of ingested copper is absorbed and is affected mainly by high level of molybdenum, which binds with copper to make it insoluble, as well as high levels of iron and zinc
Ø  Due to large number of interactions it is important to maintain a balance trace minerals without over supplementing trace minerals
Ø  Liver copper concentration is most reliable indicator of copper status in livestock

 

Clinical Diseases Associated With Copper Deficiency in Sheep

In primary copper deficiency in sheep enzootic ataxia is the major manifestation. The earliest sign of copper deprivation is loss of wool crimp (steely wool). Black wool shows depigmentation to gray or white. Anaemia may occur in the later stages of primary copper deficiency. Secondary copper deficiency in sheep is mainly associated with swayback, teart, reduced body growth, bone fragility and lameness due to spontaneous fractures. Swayback occurs in young lambs in severe copper deficiency of ewes during pregnancy. Hypocuprotic lambs are more susceptible to infections by common bacterial pathogens. Ill thrift is not a constant feature of copper deficiency in sheep.

Diagnosis

The diagnosis of copper deficiency in animals is based on a combination of collection and interpretation of the history, clinical examination of the affected animals, treatment response trial, laboratory tests of copper concentration in serum and liver biopsy samples and examination of the environment. The concentration of copper in serum is estimated using atomic absorption spectrophotometer after wet digestion (Kumar et al., 2007). The use of ceruloplasmin (Cp) to copper (Cu) ratios (Cp: Cu) have been suggested as a diagnostic test for copper deficiency (Telfer et al., 2004). Low copper and ceruloplasmin level (<5 U/l) in plasma indicate deficiency. The copper concentration in erythrocytes may better reflect   the   tissue   activities   of   copper   enzymes like copper superoxide dismutase.

Treatment and Prevention

Treatment of copper deficiency is normally achieved by injecting Cu chelated compounds like copper glycinate, copper heptonate @ dose rate of 1-2 mg/kg BW and the prognosis is often good. If the ewes are dosed throughout pregnancy with an oral dosing of one gram copper sulphate weekly will prevent the occurrence of swayback in lambs. Lambs can be protected after birth by dosing with 35 mg of copper sulphate twice a week. Dietary supplementation of at least 10 ppm of copper in the DM of the final ration and salt-licks containing 0.25-0.5% of copper sulphate ad lib are recommended for sheep. Copper sulphate at the rate of 10 kg/ha can be used for top dressing pastures, the amount required may vary widely with the soil type and the rainfall. Copper oxide needles or wire particles (fragments of oxidized copper wire up to 8 mm in length and 0.5 mm in diameter) are used for oral dosing dose of 0.1 g/kg live weight in sheep is found to be safe for treatment (Radostits et al., 2007).

References

Aitken, I.D. 2007. In: Diseases of sheep, 4th edition Blackwell publishing, pp. 382-386.

ARC. 1980. Nutrient requirements of ruminant livestock. (CAB: Slough)

Davis, G. K. and Mertz, W. 1987. Copper. In: Trace Elements in Human and Animal Nutrition (Mertz, W., ed.), 5th edn., Academic Press, San Diego, CA, pp. 301-364..

Kott, R. 2006. Montana Farm Flock Sheep Production Handbook, Animal & Range Sciences, Extension Service, Montana State University, Montana, USA. Retrieved 15 August 2011 from http://www.animalrangeextension.montana.edu

Kumar, Pankaj, Sharma, M. C. and Joshi, C. 2007. Effect on biochemical profile concurrent with micro-mineral deficiencies in buffaloes (Bubalus bubalis) of Eastern Uttar Pradesh. Indian Journal of Animal Science. 77: 84-89.

NRC. 1975. In: Nutrient requirement of sheep. Washington D C: National Academy Press.

NRC. 1985. In: Nutrient requirement of sheep. 6th Revised Edition. Washington D C: National Academy Press.

Pugh, D.G. 2002. In: Sheep and goat medicine, 1st edition Saunders, pp. 24-25.

Pulina, G. and Bencini, R. 2005. Dairy sheep nutrition: CAB International, 57, 187-188.

Radostits, O.M., Gay, C.C., Hinchcliff, K.W. and Constable, P.D. 2007. In: Veterinary medicine: A textbook of the diseases of cattle, horses, sheep, pigs and goats, 10th edition. Saunders Elsevier, pp. 1716-1722.

Sharma, M.C., Joshi, C. and Kumar, M. 2005a. Micro-minerals – their deficiency disorders and treatment: A review. Indian Journal of Animal Science. 75: 246-257.

Sharma M.C., Joshi, C., Pathak, N.N. and Kaur, H. 2005b. Copper status and enzyme, hormone, vitamin and immune function in heifers. Research in Veterinary Science, 79: 113-123.

Sharma M C, Joshi C, Das G and Hussain K. 2007. Mineral nutrition and reproductive performance of the dairy animals: a review. Indian Journal of Animal Science. 77: 599-608.

Telfer, S. B., Kendall, N.R., Illingworth, D. V., Mackenzie, A.M., (2004). Molybdenum toxicity in cattle: an underestimated problem. Cattle Practice. 12: 259-263.

Underwood, E. J., and N. F. Suttle. 1999. In: The Mineral Nutrition of Livestock. 3rd Edn. CABI Publishing, CAB International, Wallingford, Oxon, UK.

Underwood, E.J. and Suttle, N.F., 2001. Copper. In: The mineral nutrition of livestock. 3rd Edn. Wallingford, Oxon: CAB International 1999, pp. 283-342.

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