COPPER DEFICIENCY (Enzootic ataxia, sway back)

Copper is an essential trace element for animals needed for body, bone and wool growth, pigmentation, healthy nerve fibers and white blood cell function. Copper deficiency is a disease of grazing animals. It mostly surfaces when serum copper levels of the females (cows, does, ewe etc.) are low during pregnancy and may give birth to young ones with copper deficiency. Although it can occur as a primary deficiency on copper deficient pastures caused by low levels of copper in the soil, conditioned or secondary copper deficiency is more common due to antagonism (opposition) by Sulphur, iron and especially molybdenum in the rumen. Two or more of these elements will act synergistically to reduce available copper in the diet. Hence what may be considered a ‘normal’ concentration of these, acting together, can produce signs of copper deficiency. Copper deficient areas in Botswana include Letlhakane, Molepolole, Selebi-Phikwe and Francistown veterinary districts (Mushi et al, 1999).


Animals mostly at risk are:

  • Newborn or young lambs
  • Pregnant, lactating and growing sheep, goats and cattle
  • Sheep, goats and cattle that have been grazed at excessive stocking rates
  • Cattle with heavy worm (Ostertagia) infestations
  • Cattle are more susceptible than sheep and goats to copper deficiency.


Generally symptoms may appear in animals in two forms with the general signs being:

Congenital form

  • Young ones may not survive at birth.
  • They may die from cold without any signs of the disease.

Delayed form

Signs may appear several weeks after birth.

  • Animal eats and drinks well
  • Young ones may be stunted
  • Weak bones which fractures easily
  • Muscle tremors
  • Head shaking
  • Hind legs are unsteady, eventually become paralyzed
  • Some animals may have pale mucous membranes
  • Poor/ dull hair coat
  • Reduced fertility
  • Decreased immune resistance
  • Diarrhoea
  • General ill-health
  • Some may die

Some specific symptoms for livestock are as follows:


  • 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.
  • Lameness.


  • 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 1-6 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-woolen 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-woolen 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 (the waviness of wool fibers as naturally grown on sheep), 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.


  • 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 hind limbs 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.


  • No abnormalities can be seen with the naked eye during slaughter.
  • Degenerative changes in the brain and nerves.
  • Brittle bones
  • 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.


  • There is essentially only one way to treat a copper deficiency – increase copper intake! In more severe cases, copper solutions can be injected to rapidly raise blood plasma Cu levels. In most cases however, a commercially available dietary copper supplement can be added to the feed. This will ensure the animals are meeting their required daily intake of dietary copper.
  • Treatment is not useful in prolonged cases.
  • Liaise with your district veterinary officer.
  • Oral drench (Copper oxide tablets).

Note: obey instructions given by manufacturer for too much copper is toxic!


  • To prevent future instances of copper deficiency, you could either choose to continue supplementing the poor quality feed with a copper supplement or increase the quality of feed.
  • Submit soil and forage to National Veterinary Laboratory to determine the levels of copper and also the substances which bind copper e.g. Sulphur, molybdenum and iron.
  • Supplement females during pregnancy, make enquiries at the Livestock Advisory Centre. Oral drenches and injectable preparations of copper supplements are available. Consult your veterinarian.

There are several methods of supplementing copper that you may also consider including the following:

  • Mineral or salt mix. This is an economical means of providing supplemental copper. The rate of consumption can be controlled. If animals are eating more salt than expected, switching to a copper-free salt can be fed for a time. Copper-supplemented protein blocks can also give good control. Diagnosed copper deficient herds are supplemented with 0.2% to 0.5% copper, for cows consuming 30g of the product per head per day.
  • Injection. These subcutaneous injections are hard on cows, marginally effective, and last for 4-6 months or less.
  • Bolus. Copper boluses are given orally and persist in the reticulum-rumen. They contain a measured amount of copper oxide in the form of small needle particles which results in slow release of copper over a prolonged period of time. The copper bolus may take more time to raise blood copper levels than other methods; a problem if animals are already deficient. Copper boluses may also contribute to lower forage fiber digestibility and poorer cow and calf performance in cattle.
  • Foliar Applied. Applying copper directly to pasture plants is a method of supplementation. With this method, the copper sulfate is applied directly on the pasture grass.