Copper Poisoning

Sheep and goats are more susceptible to copper poisoning than cattle, and sheep are more susceptible than goats. British breed sheep and crosses are more likely to suffer from copper accumulation than pure Merinos.

Copper poisoning occurs when copper accumulates to toxic levels in the liver, as a result of imbalance between uptake and excretion. Sudden death is usually the first indication. When copper accumulation reaches a critical level, liver cells degenerate and there is a sudden release of copper into the blood stream causing massive haemolysis (breakdown of red blood cells) and death.

There are several pathways by which copper toxicity can occur. Excessive intake or administration of copper can cause copper poisoning. Certain hepatotoxic plant and fungal toxins that cause chronic liver injury predispose to copper poisoning by reducing liver function. Diets low in copper antagonists, such as molybdenum and sulphate, can result in excessive copper accumulation over time even when diets do not have elevated copper levels. Copper antagonists such as molybdenum and sulphate would be expected to combine with copper to reduce copper availability.

Animals that have been grazing lupin stubbles that support growth of the fungus Diaporthetoxica or that have been grazing plants containing pyrrolizidine alkaloids such as heliotrope and Paterson's Curse (Salvation Jane) are especially at risk.

The trigger for release of accumulated copper from the liver is usually a stressor that interrupts food intake such as transport, yarding, strenuous exercise or heat and cold stress. Any of these stressors may occur at any stage of the export process.

Conditions of risk in the export process also include improper formulation of pellets such that dietary intake of copper is elevated or molybdenum reduced. This may be due to errors in combining feed ingredients or by incorporating ingredients such as chicken manure that may contain elevated copper levels. Misdiagnosis of copper deficiency may result in administration of copper to animals as mineral mixes or injections, and inadvertent exposure may occur if copper pipes are used to deliver water for livestock.

Sudden deaths with jaundice should raise strong suspicions of copper poisoning. Signs in sick animals include jaundice, red urine, depression and collapse. Necropsy findings include muddy yellowing of the carcase, orange liver, blue-green ingesta, black bile, grey to black kidneys and dark red urine.

Specimens required for laboratory confirmation include sections of liver and kidney in buffered formalin for histology, and 30 g of liver and kidney in separate yellow- top jars, submitted chilled and unpreserved for copper estimation.

Differential diagnoses include Eperythrozoonosis (Mycoplasma ovis) in sheep and Bacillary Haemoglobinuria (Red Water Disease) in cattle. Eperythrozoonosis will cause sudden deaths and occasionally cause haemolysis sufficient to produce red urine but is expected to affect younger sheep. Bacillary Haemaglobinuria (Red Water Disease) is an acute, sporadic disease of cattle caused by Clostridium novyi type D. It is a waterborne disease occurring in poorly drained areas and cases are more common in young or naïve cattle.