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Copper Poisoning, a Deadly Hazard for Sheep

Journal

ANIMALS
Volume 12, Issue 18, Pages -

Publisher

MDPI
DOI: 10.3390/ani12182388

Keywords

chronic copper poisoning; acute copper poisoning; copper toxicity; hepatic copper accumulation; sheep; lamb; anaemia

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Sheep are highly susceptible to copper intoxication, which is a deadly disease causing significant economic losses worldwide. Depending on the duration of exposure, two types of copper poisoning can occur in sheep. Chronic toxicosis is the most common form and develops after a long subclinical period of copper accumulation in the liver. Acute copper poisoning, although less frequent, results from accidental administration or ingestion of toxic amounts of copper.
Simple Summary Sheep are very susceptible to copper intoxication, a deadly disease that causes significant economic losses worldwide. Two types of copper poisoning can occur depending on the chronic or acute exposure to copper. Chronic toxicosis is the most common form and is developed after a long subclinical period of copper accumulation in the liver. When the capacity of the liver for copper storage is exceeded, a sudden release of copper into the blood causes severe haemolysis and the death of the animals. Acute copper poisoning is much less frequent and appears following the accidental administration or ingestion of toxic amounts of copper. Collapse and death occur shortly after parenteral administration, whereas acute oral exposure to copper causes severe gastroenteritis followed by shock and death. In this review, we summarise the available information on the aetiology, epidemiology, pathogenesis, clinical features, diagnosis, treatment and prevention of sheep copper poisoning. Copper (Cu) is an essential microelement for animals. However, sheep are particularly susceptible to Cu intoxication, a deadly disease reported worldwide. The risk of developing this poisoning is higher in vulnerable breeds and in intensively managed lambs or milk sheep. Two types of Cu intoxication can occur depending on the chronic or acute exposure to Cu. In chronic Cu poisoning (CCP), the most common form, Cu is accumulated in the liver during a subclinical period. A low intake of Cu antagonists (molybdenum, sulphur, iron, or zinc) favours Cu accumulation. The sudden release of Cu into the blood causes acute haemolysis with anaemia, haemoglobinuria, jaundice and death within 1-2 days. Acute Cu poisoning is related to the accidental administration or ingestion of toxic amounts of Cu. Acute oral exposure to Cu causes severe gastroenteritis, shock and death. Collapse and death occur shortly after parenteral administration. The diagnosis is based on history, clinical, gross pathological, histological and toxicological findings. Treatment of sheep with severe clinical signs often has poor success but is very effective during the Cu accumulation phase. Different therapies, based on either chelating agents or Cu antagonists, have been used to treat and prevent CCP.

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