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Editorial Information

Neil Sargison BA VetMB DSHP FRCVS

Copper Poisoning in Sheep

This bulletin was written between 2000-2006 and is currently being updated, you should be aware that some of the details may have changed since publishing

There were several NADIS reports of copper poisoning in sheep during the late summer.  Some outbreaks were seen in housed pet lambs, while others were seen in pedigree Bluefaced Leicester and Texel ram lambs and shearlings which were being fed substantial amounts of concentrates.

Copper is one of the most frequently diagnosed inorganic poisonings of domestic ruminants.  Two distinct syndromes are recognised: chronic copper toxicity which is commonly reported following long-term liver storage of dietary copper and acute copper toxicity which is occasionally reported following inaccurate administration of copper injections.



Chronic copper poisoning occurs after the sheep's liver capacity for copper storage has been exceeded.  This results in sudden release of copper into the circulation, causing liver damage, destruction of red blood cells and jaundice.

There is variation in breed susceptibility to copper toxicity related to ability to absorb dietary copper. North Ronaldsay, Texel, Suffolk and several continental short-wool breeds of sheep are relatively susceptible, when compared with, for example, Cheviots and Scottish Blackfaces.  Growing lambs are more susceptible than adult ewes.


Clinical signs

The clinical signs associated with chronic copper poisoning are sudden in onset and affected animals become increasingly weak.  Some sheep may spend time wandering aimlessly or head-pressing.  As the disease progresses, jaundice develops and breathing becomes shallow and rapid due in part to the development of anaemia.

1 Copper poisoning sheep black urine

Fig 1 Urine often appeasrs black due to red blood cell breakdown

2 Copper poisoning sheep jaundice of the gums

Fig 2 Jaundice of the gums

3 Copper poisoning sheep jaundice of the conjunctivae

Fig 3 Jaundice of the conjunctivae and third eyelid

4 Copper poisoning sheep jaundice of the sclera

Fig 4 Jaundice of the sclera of the eye

5 Copper poisoning sheep death yellow skin

Fig 5 Most animals die following a short period of recumbency.  Note yellow coloured skin

The diagnosis of copper poisoning is based on the housing and feeding history, clinical signs and post-mortem findings of a pale tan to bronze-coloured liver and dark red or black kidneys.  The diagnosis can be confirmed by laboratory identification of high kidney copper concentrations.

6 Copper poisoning sheep bronze coloured liver

Fig 6 Bronze coloured liver

7 Copper poisoning sheep gun metal kidneys

'Fig 7 'Gun Metal' appearance of the kidneys


Management of outbreaks of chronic copper poisoning

The treatment response to supportive therapy in animals showing clinical signs is poor.  Resources should be directed towards identification of the underlying causes of the problem and the prevention of clinical disease in the remaining at-risk animals.  This can be achieved by a programme of oral dosing or subcutaneous injection of ammonium tetrathiomolybdate to effectively 'strip' copper from the liver, although in recent months this has become prohibitively expensive other than for very valuable animals. Copper antagonists such as molybdenum or sulphur can be added to the ration to prevent further liver accumulation of copper.  Your vet can provide more precise information about the management of copper poisoning in sheep.


Prevention of copper poisoning

Poisoning results from a combination of efficient absorption and high dietary availability of copper. Prevention depends on avoiding the feeding of copper-rich diets to susceptible animals.  Sheep breed, age (young animals absorb copper very efficiently) and the presence of dietary copper antagonists such as iron, sulphur and molybdenum all influence the efficiency of absorption.  The availability of dietary copper varies between different feeds.  Feeds with high concentrations of available copper include -

  • Pasture, silage and root crops grown on ground to which large quantities of pig or poultry manure has been applied.
  • Distillery by-product feeds such as distiller's dark grains produced from copper stills. Concentrate feeds containing palm oil or molassed sugarbeet pulp.  (Whole grain cereals are relatively poor sources of copper.)
  • Other potential sources of copper include; access to cattle minerals; copper sulphate foot baths; and fungicide-treated timber.

In the highly susceptible North Ronaldsay breed of sheep, or in intensively-managed housed sheep, poisoning can result from prolonged feeding of diets with relatively low copper concentrations.  Housed sheep should, therefore, not receive any form of copper supplementation before or during housing.



Acute copper poisoning occurs sporadically, usually following gross over dosage of injectable copper preparations used for prevention of deficiency syndromes.  Stressful management or concurrent administration of other remedies may influence the animal's ability to remove copper from the circulation.  Clinical signs are sudden in onset and non-specific and include depression, rapid heart and respiratory rates and subnormal rectal temperature.  Blue/green-coloured diarrhoea is frequently present.  Collapse and death usually follow within 24 hours.

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