Primary Copper Poisoning in Two Flocks of First Cross Ewes

Bruce Watt, District Veterinarian, Bathurst, Tablelands LHPA and Tristan Maugauret, Veterinary Intern, The University of Sydney

Posted Flock & Herd August 2009


Copper from the maladministration of copper supplements and copper containing agricultural chemicals can poison sheep. However, in southeastern Australia the most common source is copper accumulated in plants. Plant associated copper poisoning can be either primary (phytogenous) or secondary to liver damage (hepatogenous). Sheep are the most susceptible species of livestock and British breed sheep and their crosses are more susceptible than merinos.

Sheep can be poisoned with chronic intakes of 25 ppm and even lower concentrations are toxic in the face of relative deficiencies of molybdenum and sulphur (Radostits et al, 2007). Seawright (1982) claimed, 'the successful elucidation of the aetiology' of what was previously known as the toxaemic jaundice syndrome, 'stands as one of the great achievements of Australian veterinary science.' It is of interest that the then Stock Inspector with the Corowa Pastures Protection Board, Mac Anderson, played a significant role in that achievement. Copper poisoning was diagnosed on two properties running first cross ewes on improved pastures on high rainfall, basalt country south of Orange on the NSW central tablelands. Both properties are within 10 km of large open cut gold and copper mine and it is reputed that soils in the region are inherently high in copper.


Property 1 Six of 1700 first cross ewes died within a week before and during crutching in early December 2007. The owner had also noticed several weak ewes. The ewes were mostly in fat condition and were grazing abundant improved (predominantly phalaris and ryegrass) pastures with no supplementary feeding. Molybdenum enriched super phosphate had previously been applied to pastures but not within the past ten years. The owner in response to the deaths drenched the mob with Paramectin plus selenium and vaccinated them with 5:1.

Property 2 1600 first cross ewes. In late January 2008, the owner noticed that while almost all of the ewes in a mob of 250, 5-year-old ewes were in fat condition, one was dead and another was dull and sick. The owner noticed the sick ewe had grey skin and gums. She died within two hours. The ewes were running on a paddock of regrowth oats with some ryegrass and subterranean clover. He recalled that he similarly lost three ewes over two days in early January 2008 after he moved a mob of 180, three-year-old ewes.


Three ewes from Property 1 were examined. Two were presented alive. Ewe 1 was alert and responsive but weak. Her mucous membranes were pale and jaundiced and the urine was dark red. Ewe 2 was bright and alert, but in poor body condition. Her mucous membranes were normal; however, her respiratory rate was increased. Ewe 1 was euthanased, as was a third ewe (ewe 3) that had died earlier.

Ewe 1 showing haemoglobinuria


Both ewe 1 and ewe 3 from property 1 were markedly jaundiced, had dark red watery blood, swollen black kidneys and tan livers. A single ewe from property 2 was presented for post-mortem. The ewe was five years old and in fat condition. The tissues were jaundiced and the kidneys were black. The liver appeared relatively normal but the urine in the bladder was very dark red.

Case 1 showing icterus and black kidneys


Copper levels were elevated in the liver, kidneys and blood. Liver enzymes and bilirubin were elevated indicating liver pathology. The PCV in ewe two was very low as expected subsequent to a haemolytic crisis. Both ewes also had a marked neutrophilia presumably in response to liver necrosis.


Both cases showed evidence of diffuse periacinar loss and coagulative necrosis of hepatocytes. These signs of advanced hepatopathy are probably due to haemolytic anaemia, which is consistent with the clinical findings. Furthermore, the detection of scattered single cell necrosis amongst the remaining hepatocytes and copper pigment containing macrophages is evidence of copper toxicity. Large amounts of bile pigment were also seen in the canaliculi, hepatocytes and bile ductules.

Histopathological examination of the kidney of Ewe 3 was confounded by advanced autolysis; however, haemoglobin casts were still recognized. Examination of the kidney of Ewe 2 revealed haemoglobin droplets within tubular epithelial cells and many tubules containing proteinaceous casts and sometimes necrotic epithelial cells. These findings are consistent with haemoglobinuric nephrosis, following haemolysis.


The owner of property 1 elected to treat these ewes using a loose mix rather than to drench them with a molybdenum and sulphate solution. The mix he provided is as recommended by Radostits et al (2007) but is not currently registered in NSW. It consists of 86 kg of salt, 63kg of gypsum and 450g of sodium molybdate. The owner reported that the ewes readily consumed the loose mix and no subsequent losses occurred. The owner of property 2 also elected to treat the mob in which the recent deaths had occurred with a loose mix. He used the same mix as property 1 and fed it out in ten containers in the paddock. He reported that he did not lose any ewes subsequent to feeding the mix.


This case is consistent with primary (phytogenous), chronic copper intoxication. The soils in this area are considered to be high in copper and low in molybdenum. At least on property 1, the pastures are well managed and dominant in phalaris and ryegrass. They contain very few plants know to produce pyrrolizidine alkaloids (PA) but have short periods of subterranean clover proliferation.

The pathology report from ewes on property 1 indicates an absence of the changes consistent with PA damage. However it should be borne in mind that prime lamb producers often source ewes from western NSW were plants high in PAs most notably heliotrope (Heliotropum europaeum) and Paterson's curse (Echium plantagineum) are abundant. These ewes were Border Leicester cross Merino, known to be more susceptible to primary and secondary copper poisoning than Merinos.


  1. Hays, Virgil W and Swenson, Melvin J. Minerals in Duke's Physiology of Domestic Animals, 9th edition (Cornell University Press, New York, 1977) pp 403-405
  2. Radostits OM, Gay CC, Hinchcliff KW and Constable PD. (2007). Veterinary Medicine, 10th Edition, pp 1740- 1741
  3. Seawright AA, Chemical and Plant Poisons, in Animal Health in Australia, Volume 2, p 158


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