Government of Western Australia
(Previously published online: Agriculture and Food, Department of Primary Industries and Regional Development)
Yes, you read the title correctly. Contrary to common belief, sheep do have a requirement for copper. Although their requirement for supplemental copper may be lower than other ruminant species, excluding this mineral from the ration of a sheep diet can result in serious health issues.
Copper is an essential trace element for animals needed for body, bone and wool growth, pigmentation, healthy nerve fibers, and white blood cell function.
There are two main causes of copper deficiency in sheep
and cattle: low copper levels in plants due to a lack of copper fertilizer in naturally copper-deficient soils; and an induced deficiency caused by ingestion of excessive levels of molybdenum and sulphur in pasture or feed supplements.
When does copper deficiency occur?
In Western Australia, naturally occurring copper deficiency is uncommon, because most farmers have applied enough copper as fertilizer to ensure an adequate supply for grazing livestock. Recent increases in liming of properties may lead to an increase in cases of induced copper deficiency. As the soil pH rises, molybdenum is released from the soil leading to higher levels of molybdenum. Excess molybdenum in the diet leads to the formation of thiomolybdates. These can then react with copper-containing enzymes in the bloodstream resulting in signs which are the same as primary copper deficiency.
Rapid pasture growth after good winter rains reduces the concentration of copper in pasture. Seasonal variation in the availability of copper from pastures makes sheep and cattle most at risk of a deficiency during late winter and spring.
Plants have a differential uptake of copper, with legumes and clovers taking up more copper than grasses.
Copper deficiency is often seen in late winter or spring on rapidly growing grassy pastures.
What are the signs of copper deficiency?
- loss of pigment from colored 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
- 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 fetus 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 Western Australia.
- non-speciﬁc signs are ill-thrift, scouring, rough dull coat, anemia, 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.
Which animals are most at risk?
- newborn or young lambs
- pregnant, lactating and growing sheep and cattle
- sheep and cattle that have been grazed at excessive stocking rates
- cattle with heavy worm (Ostertagia) infestations
- cattle are more susceptible than sheep to a copper deficiency.
What are the causes of copper deficiency?
Soils containing little plant-available copper:
Soils that were originally copper-deficient occur throughout all farming districts. Where no copper fertilizer has been applied on deficient soils in the last seven or eight years, pastures often contain less than 2.5 parts per million (ppm) copper in spring, which may not be enough for the needs of animals.
Excessive intakes of molybdenum and sulphur:
Molybdenum reduces the availability of dietary copper in the rumen by forming copper-molybdenum-sulphur compounds in the rumen called thiomolybdates. These thiomolybdates can cross into the bloodstream and can cause disease signs very similar to copper deficiency.
In Western Australia, unlike many other parts of the world, the naturally occurring levels of molybdenum are rarely high enough to cause copper deficiency. However, excessive applications of molybdenum fertilizers have caused signs of copper deficiency in sheep and cattle.
Liming soils increases molybdenum availability, which can reduce copper availability and induce a copper deficiency when copper levels are marginal.
How is copper deficiency diagnosed?
If the soil provides enough copper for wheat, pasture grown on the same area will have sufficient copper for sheep and cattle, unless molybdenum levels in the soil are very high.
Swayback in lambs and falling disease in cows are strongly suggestive of copper deficiency.
While de-pigmentation of the hair around the eyes in cattle and of black wool in sheep indicates copper deficiency is likely, it is not certain as similar signs occasionally result from other causes. Use as many other indicators as possible to make sure of your diagnosis.
Liver copper concentration is one of the best indicators of copper status, although this is still not guaranteed. One cause for uncertainty is that individual sheep or cattle develop copper deficiency with different levels of copper in their livers. Another limitation can be the difficulty and cost of obtaining a liver sample by biopsy from live animals. It is the most useful test when done at post-mortem.
Where there is swayback in lambs, samples of brain and spinal cord are needed to confirm the diagnosis.
The concentration of copper in the blood is an unreliable guide to copper status if it is a molybdenum-induced deficiency. Caeruloplasmin activity in plasma or comparing different plasma inorganic copper fractions (TCA-soluble versus TCA insoluble) can indicate if molybdenum is involved.
Pasture analyses for copper and molybdenum concentrations provide only a rough guide to the copper status of sheep and cattle grazing them.
Pastures with less than 2.5 ppm copper are sometimes deficient for sheep and cattle. Above 4 ppm copper, they are not deficient, provided molybdenum levels are less than 1.5 ppm (normal for Western Australia agricultural areas). The likelihood of copper deficiency can be assessed using levels of copper, molybdenum and sulphur in plants.
Pasture with copper levels between 3 ppm and 4 ppm have seldom caused copper deficiency in stock in WA. However, with higher pasture molybdenum and sulphur levels, the copper concentration needed to give an adequate supply to sheep and cattle rises. For example, in other parts of the world, animals grazing pastures that have 5 ppm molybdenum and higher have still responded to copper even though the pasture contains as much as 10 ppm copper.
Copper treatment response trial
In the absence of clear-cut clinical signs, the most convincing evidence of a copper deficiency is a response to treatment with copper. Treat some stock with injectable copper supplement and compare body weight changes with untreated animals from the same flock or herd over two months.
Both groups must be run together under identical conditions. A minimum of 25 animals in each group is usually needed to detect small but economically important differences in live weight.
Multi-mineral supplements (salt blocks and licks)
Multi-mineral supplements are available in a loose granular or block form and are useful when individual animal treatment is impractical. Loose minerals are preferred and should be put in a covered feeder to keep rain out so they do not cake and become hard. While blocks and licks are a very practical supplement, some animals may fail to lick the block which reduces its efficacy or they may consume too much and risk toxicity. Recommended concentrations are 0.5% – 1.9% copper sulphate for cattle and 0.25% – 0.5% for sheep.
Give adequate copper nutrition to pregnant ewes at least six weeks before lambing to prevent swayback in lambs. In known deficient areas, strategic treatment can be given to cover sheep and cattle during winter and spring when copper deficiency is more likely to occur.
Sheep are highly susceptible to copper toxicity and should not be supplemented with copper unless there is an established diagnosis of copper deficiency.
Warning: Many liver toxins will cause copper to accumulate in the liver and can lead to secondary copper toxicity. Do not use copper supplements if there is a risk that liver damage has previously occurred.