FieldDxSecondary copper poisoningClinical signs, differential diagnosis, treatment and prevention in cattle and sheep.
Overview
Chronic copper toxicosis in sheep and cattle stays hidden in the liver until a sudden release of stored copper triggers a haemolytic crisis. Copper builds up in the liver from prolonged excess dietary copper, or secondarily from liver disease that impairs copper sequestration and biliary excretion.
Clinical signs
- Subclinical until a haemolytic crisis.
- Crisis: depression, weakness, recumbency, rumen stasis, pale mucous membranes, jaundice and haemoglobinuria.
- Liver enzyme rises may appear days before the crisis.
- Sheep kidneys may look dark and swollen; cattle often do not show this.
- Secondary photosensitisation can follow liver injury.
Predisposing factors
- Prolonged excess dietary copper, especially from feeds not formulated for sheep.
- Low dietary molybdenum relative to copper, which favours copper retention.
- Secondary liver damage, such as from chronic pyrrolizidine alkaloid plant ingestion in sheep.
- Stressors that trigger release: transport, handling, bad weather, pregnancy, lactation, exercise and poor nutrition.
Treatment
- Supportive care once clinical signs appear has a poor response; effort is better directed at identifying and correcting the underlying dietary copper:molybdenum:sulfur imbalance in at-risk animals.
- Subcutaneous ammonium tetrathiomolybdate (repeated doses) has been used to control outbreaks in sheep flocks.
Prevention
1. Avoid over-supplementing copper; use mineral packs and feeds formulated for sheep. 2. In flocks, stop copper supplementation and adjust the copper to molybdenum ratio (ideal about 6:1, tolerable 10:1). 3. Add molybdenum and thiosulphate to reduce copper absorption during outbreaks. 4. Test rations, mineral supplements and water for copper and molybdenum. 5.
Source
MSD Veterinary Manual — Copper Toxicosis in Animals (accessed 2026-08-12)
MSD Veterinary Manual — Copper Toxicosis in Animals (accessed 2026-10-29)
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