Sheep and goats are more susceptible to copper poisoning than cattle.
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 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.
British breeds and crosses are more susceptible to copper accumulation than pure merinos. Goats are more resistant to copper accumulation than sheep.
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 live export process.
Conditions of risk in the live 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 feed 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 carcass, orange liver, 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 in sheep and Bacillary Haemoglobinuria 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 (redwater 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.
Drench with 100mg ammonium molybdate and 1g sodium sulphate daily for a few days, then administer on hay for a few weeks. Survivors may suffer permanent illthrift from liver and kidney damage.
Avoid feedstuffs and mineral supplements with extra copper and treatments for copper deficiency unless copper deficiency is confirmed. Ensure molybdenum concentrations are adequate in formulated rations. Handle and manage animals in ways that minimise stress.