Swayback in lambs and falling disease in cows are strongly suggestive of copper deficiency.
Copper is necessary for the metabolism of iron. Copper deficiency may occur secondary to high dietary molybdenum or sulfate in cattle and can develop in pigs fed whey diets.
Although it can occur as a primary deficiency on copper deficient pastures, secondary copper deficiency is more common due to antagonism by sulphur, iron and especially molybdenum in the rumen.
Copper is an essential trace element for animals needed for body, bone and wool growth, pigmentation, healthy nerve fibres and white blood cell function.
and an induced deficiency caused by ingestion of excessive levels of molybdenum and sulphur in pasture or feed supplements.
Molybdenum reduces the availability of dietary copper in the rumen by forming copper-molybdenum-sulphur compounds in the rumen called thiomolybdates.
Clinical signs
Cattle
loss of pigment from coloured hair especially around the eyes, giving the animal a bespectacled appearance (not visible in cattle with white hair around the eyes)
falling disease – sudden heart failure causing sudden death
lameness.
Sheep
swayback or enzootic ataxia of lambs. Lambs with this condition cannot coordinate their legs. They may be severely affected at birth and may be unable to stand; some may be born dead. Other lambs appear normal at birth but between one and six months they develop an uncoordinated gait. This condition is caused by impaired development of the central nervous system in the foetus and cannot be reversed by copper treatment once signs appear
loss of pigmentation in black-woolled sheep. Because there is usually a wide variation in susceptibility to copper deficiency between individuals within any flock, normal pigmentation in one or two black sheep does not guarantee copper sufficiency among the white-woolled individuals. Other conditions can occasionally cause loss of pigmentation
increased incidence in fractures of the long bones and rib bones in lambs.
Loss of crimp, secondary crimping and steeliness of wool are poor guides to copper deficiency in sheep because they are not solely caused by lack of copper and experts cannot consistently differentiate between steely and doggy wool. Copper deficiency is rarely the cause of the poorly crimped wool often seen in WA.
Goats
non-specific signs are ill-thrift, scouring, rough dull coat, anaemia and poor fertility
Angoras may have harsh mohair
swayback in kids. Affected kids are usually weak and in poor condition, due to either an inability to suckle or keep up with their mother. Paralysis develops in the hindlimbs and kids are unable to stand. Kids can be born with a degree of swayback but more commonly develop the condition after 4–6 weeks of age.
Overview
Copper is an essential trace element for animals needed for body, bone and wool growth, pigmentation, healthy nerve fibres and white blood cell function.
Copper is involved in the formation of red blood cells, the absorption and utilization of iron, the metabolism of cholesterol and glucose, and the synthesis and release of life-sustaining proteins and enzymes. … Copper also helps to neutralize “free-radicals”, which can cause severe damage to cells.
Copper is an essential cofactor for a wide variety of enzymatic reactions, and copper deficiency produces a constellation of clinical signs related to impairment of these reactions. Copper plays an important role in iron transport from the gut to the marrow and in the incorporation of iron into the heme moiety. The anemia produced by copper deficiency is generally moderate and slowly progressive. It closely resembles iron deficiency in that it is usually a microcytic, hypochromic anemia.
There are two main causes of copper deficiency in sheep and cattle: low copper levels in plants due to a lack of copper fertiliser in naturally copper-deficient soils; and an induced deficiency caused by ingestion of excessive levels of molybdenum and sulphur in pasture or feed supplements.
Copper deficiency occurring during gestation in sheep may manifest as congenital*enzootic*ataxia, or ‘swayback’, and may be due to a primary deficiency due to low soil copper levels (as occurs on volcanic red soils after rain), or secondary to impaired gut absorption, usually from the presence of antagonists such as molybdenum. Copper is important for coenzyme for metabolic functions, and inadequate levels impede cellular respiration leading to energy deprivation.
Copper deficiency in Goats - it may cause locomotor difficulties in goats in two distinct ways. Abnormal bone growth with increased bone fragility can predispose to fractures of long bones. Independently, a neurologic condition known as enzootic ataxia or swayback develops, in which copper deficiency of kids in utero or after birth results in permanent myelin degeneration in the spinal cord, leading to progressive incoordination and paralysis with failure of mobility. Clinically, this appears similar to the neurologic form of caprine arthritis-encephalitis virus (see Caprine Arthritis and Encephalitis) infection in young kids. Copper status of the ration needs to be evaluated, and copper supplementation provided as necessary.
Copper deficiency causes a condition in newborn lambs known as enzootic swayback. Lambs are typically normal at birth but develop hindlimb paresis or paralysis within a few weeks. The neurologic deficits are caused by a dystrophic demyelination of the white matter in the spinal cord.
Infertility problems also have been blamed on copper deficiencies. Impaired fertility is associated with secondary copper deficiency due to high molybdenum intakes rather than primary copper deficiency.
Clinical signs
loss of pigment from coloured hair especially around the eyes, giving the animal a bespectacled appearance (not visible in cattle with white hair around the eyes)
falling disease – sudden heart failure causing sudden death
lameness.
Diagnosis and differentials
Liver Copper levels less than 32 ppm are deficient. 16-32
Normal 32 - 600
The concentration of copper in the blood is an unreliable guide to copper status if it is a molybdenum-induced deficiency.
Pastures with less than 2.5ppm copper are sometimes deficient for sheep and cattle. Above 4ppm copper, they are not deficient, provided molybdenum levels are less than 1.5ppm (normal for WA agricultural areas).
Treatment and control
Oral or injectable Cu supplementation is indicated as treatment for Cu deficiency. Copper status of the ration needs to be evaluated, and copper supplementation provided as necessary.
The minimum recommended dietary copper concentration (dry matter basis) is 4 to 10 ppm (mg/kg) for cattle, 5 ppm for sheep
One application of 0.8–2.5 kilograms per hectare of copper (3.3–10kg/ha copper sulphate), according to soil type and locality, will supply adequate copper to sheep and cattle for at least eight years.
A second application of 0.5kg/ha copper (2kg/ha copper sulphate) 10 years after the first is generally adequate.
Summary
Copper is an essential trace element for animals needed for body, bone and wool growth, pigmentation, healthy nerve fibres and white blood cell function.
Pregnant ewes require ~5 mg of copper (Cu) daily, which is the amount provided when the forage contains ≥5 ppm. However, the amount of copper in the diet necessary to prevent copper deficiency is influenced by the intake of other dietary constituents, notably molybdenum (Mo), inorganic sulfate, and iron. High intake of molybdenum in the presence of adequate sulfate increases copper requirements. Because sheep are more susceptible than cattle to copper toxicity, care must be taken to avoid excessive copper intake (see Copper Poisoning). Toxicity may be produced in lambs being fed diets with 10–20 ppm of copper, particularly if the Cu:Mo ratio is >10:1. The Cu:Mo ratio should be maintained between 5:1 and 10:1.