![]() In this article, we have reviewed the literature on Cu poisoning in sheep addressing the most relevant aspects of aetiology, epidemiology, pathogenesis, clinical features, diagnosis, treatment and prevention of this disease which allow a better understanding and more effective control of this deadly hazard for sheep. In this sense, in some countries the problem is particularly important and is considered one of the most important illnesses affecting the sheep industry. Although many factors can predispose sheep to Cu poisoning, there is evidence that the incidence of this disease is increasing as more intensive methods of sheep production are adopted, or susceptible breeds are used. The disease has been reported in many sheep-rearing areas of the world and can cause significant economic losses due to the high mortality rates in clinically affected animals. Because of this, Cu intoxication, also known as Cu poisoning or Cu toxicosis, is widespread in sheep flocks, mainly due to chronic exposure to Cu. Monogastrics seem to tolerate excess Cu much better than ruminants, and sheep are particularly susceptible to the effects of Cu toxicity because their Cu excretory mechanism is less efficient. Nevertheless, Cu in excess has been shown to cause toxicity in both humans and animals. Therefore, a low Cu status contributes to the development of a wide range of hepatic, neurological and other types of disorders, and dietary Cu additions are routinely used in livestock production. It is an essential component of several important enzymes involved in the formation of connective tissue, iron metabolism, cellular respiration, protection against oxidant stress, catecholamine biosynthetic pathway, formation of myelin, melanin pigment and keratin, and it is also a key trace mineral required for effective immune response. Different therapies, based on either chelating agents or Cu antagonists, have been used to treat and prevent CCP.Ĭopper (Cu) has been shown to be an essential microelement for animals and plays an important role in many biological processes. Treatment of sheep with severe clinical signs often has poor success but is very effective during the Cu accumulation phase. The diagnosis is based on history, clinical, gross pathological, histological and toxicological findings. Collapse and death occur shortly after parenteral administration. Acute oral exposure to Cu causes severe gastroenteritis, shock and death. Acute Cu poisoning is related to the accidental administration or ingestion of toxic amounts of Cu. The sudden release of Cu into the blood causes acute haemolysis with anaemia, haemoglobinuria, jaundice and death within 1–2 days. A low intake of Cu antagonists (molybdenum, sulphur, iron, or zinc) favours Cu accumulation. ![]() In chronic Cu poisoning (CCP), the most common form, Cu is accumulated in the liver during a subclinical period. Two types of Cu intoxication can occur depending on the chronic or acute exposure to Cu. The risk of developing this poisoning is higher in vulnerable breeds and in intensively managed lambs or milk sheep. However, sheep are particularly susceptible to Cu intoxication, a deadly disease reported worldwide. Copper (Cu) is an essential microelement for animals.
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