Special Veterinary Pathology

COPPER

• Copper is an essential component of the animal system and plays an important physiological role in haematopoiesis, myelin formation, phospholipids formation, connective tissue metabolism and enzyme systems.
• Copper toxicity has been encountered in most parts of the world. Sheep are affected most often, although other species are also susceptible.
• Acute poisoning is usually seen after intake of excessive copper salts being employed in agriculture and veterinary practice.

Sources of  poisoning

• Toxicity may occur due to copper sulphate, copper subacetate, copper chloride, oxychloride and carbonate and copper edentate.
• Cases of acute poisoning occur when animals have mistakenly been given too large a therapeutic dose and occasionally, when they get access to food contaminated with copper salts.
• Losses in lambs occur after treatment for foot-rot, either from contamination of ewes udder or from drinking of foot-rot bath water.
• Copper edentate use in the treatment of swayback disease in lambs has been reported to cause fatalities in undersized animals even at recommended dose levels (50 mg/ kg).
• Chronic copper poisoning occurs due to intake of successive non-toxic doses of copper.
• Grazing of animals in orchard sprayed with copper salts (copper sulphate), salt-licks and copper-supplemented diets result in chronic toxicity.
• Ponds treated with copper sulphate for algicidal effect, chicken manure (being a good source of non-protein nitrogen) mixed with silage or other feed and contaminated forage in the vicinity of mines or smelters could be other sources that could result in chronic toxicity.
• Damage to liver by grazing plants like Heliotropium europium or Senecio sp. can lead to abnormal accumulation of copper and cause haemolytic crisis in chronic copper poisoning.
• In certain areas, soil may be normal in copper contents but special climatic conditions may favour either the growth of non-graminous plants like Trifolium subterraneum which accumulate copper.
• Development of a high copper molybdenum ratio within plants is considered to be involved in chronic copper poisoning since it is well established that a low molybdenum intake enhances the storage of copper in liver.

Clinical signs

• Symptoms of acute copper poisoning are nausea, vomition (in capable species), salivation, purgation, violent abdominal pain, dehydration, tachycardia, shock and collapse, ending in death.
• The faeces of affected animals contain mucus and are of deep green colour due to the presence of a copper-chlorophyll compound.
• Chronic copper poisoning takes places in three stages.
• In the first stage, which may last for 2 to 3 months, there are no apparent clinical signs except a decrease in ruminal fermentation and ruminal stasis.
• In the second stage which may last for 14 -25 days, there is impairment of liver function which is characterized by symptoms of anorexia, depression, weakness, thirst and diarrhoea.
• In the third (haemolytic crisis) stage lasting for 2-5 days, there is generalized icterus, haemoglobinemia, haemoglobinuria and recumbency.
• Severe hepatic insufficiency is responsible for deaths.
• Animals that survive acute episode may die of subsequent renal failure.
• Herd mortality is often <5% though more than 75% of the affected animals die.
• Losses may continue for upto two months after dietary problem has been rectified.

Post mortem lesions

• Acute Copper Poisoning
• Severe gastroenteritis with erosions and ulcerations in the abomasums of ruminants.
• A characteristic feature is that blood is found to have coagulated at the time of death.
• Icterus develops in animals that survive beyond 24hrs.
• Chronic Copper Poisoning
• Generalized icterus is the main lesion
• The liver is enlarged, yellow in colour and friable.
• Gall bladder is distended with thick greenish – brown bile.
• Swollen gunmetal coloured kidneys (showing haemorrhagic mottling when capsule is removed)
• Port wine-coloured urine
• Enlarged spleen with dark, brown-black (black berry jam) parenchyma
• Histologically, there is centrilobular hepatic and renal tubular necrosis and the brain may manifest spongy degeneration and astrocyte damage.

Diagnosis

• Copper is a normal constituent of tissues and blood.
• The diagnosis of chronic copper poisoning would, therefore, depend upon finding markedly elevated concentrations of copper in the tissues of animals having history, clinical signs and lesions of copper toxicosis.
• Blood and liver copper concentrations are increased during the period of haemolytic crisis.
• Blood levels often rise to 5-20 µg/ml compared to the normal level of almost 1 µg/ml. Liver concentrations of > 150ppm (wet weight) are significant in sheep.

Evidence of blue-green ingesta, deep green-coloured faeces and increased faecal (8000-10000 ppm) and kidney (> 15ppm, wet weight) levels of copper are considered significant in acute copper toxicosis.