Copper

 Copper poisoning is encountered in most parts of the world. Sheep are affected most often, although other species are also susceptible.

Sources :

• Cu salts are extensively use in the veterinary practice. CuSo₄ is frequently used as fungicide, destroying of intermediate host specially snail; treatment of foot rot.
• Cu naphthenate is used as wood preservations.
• Cu carbonates used as seed dressing.
• Copper sulphate also finds a place in the treatment of parasitic gastritis in sheep.
• Soils and plants fertilised using poultry litter and swine manure have more copper content. Soil also gets contaminated with copper by mining and smelting industries.

• The most common and serious problem in copper toxicosis is molybdenum deficiency in sheep, an acute syndrome which suddenly occurs after chronic dietary exposure to an excessive copper to molybdenum ratio.
• Genetic defects in some dog breeds (Bedlington terriors) cause excessive storage of copper in the liver.
• Phytogenous chronic poisoning is seen after ingestion of plants, such as subterranean clover (Trifolium subterraneum), that produce a mineral imbalance and result in excessive copper retention. The ingestion of plants such as Heliotropium europaeum or Senecio spp (Plants Poisonous to Animals) for several months may cause hepatogenous chronic copper poisoning .

Toxicokinetics:

Absotption :Copper after ingestion is absorbed from the intestine and then it enters the systemic circulation.

Distribution:  In blood it is present in the erythrocytes and also in the serum.

Metabolism:  Metabolished in the  liver and stored in the soft tissue .

Excretion : Copper is excreted by the bile.

Mechanism of action:

• It causes the inhibition of dihydropolydehydrogenase enzyme which causes the inhibition of pyruvic acid and alpha keto gluterate dehydrogenase. As a result, TCA cycle and enzymes systems are disrupted.
• Copper salts act as direct tissue irritants and oxidants and cause coagulative necrosis of the gastrointestinal mucosa.
• Copper accumulates in the liver and causes progressive hepatocyte organelle damage and cellular degeneration or necrosis.
• It inhibits the vital enzymes and as a consequence there will be elevated SGOT, lactic dehydrogenases, plasma arginase and plasma bilirubin.
• There will be sudden and massive lysis of erythrocytes called haemolytic crisis. This symptom is absent in non-ruminants, probably because they store less copper than ruminants.
•  Due to this crisis, the kidneys fail because the renal tubules get clogged with haemoglobin and necrosis of tubules and glomeruli due to excess copper in the kidneys.

Clinical symptoms :

• In acute poisoning the symptoms noticed are nausea, vomiting, salivation, purgation, violent abdominal pain, dehydration, tachycardia, shock and collapse, ending in death.
• The faeces of the affected animals contain mucous and are of deep green colour.
• In chronic poisoning there will be decreased ruminal fermentation and ruminal stasis initially.
• Later, there will be impairment of liver function characterised by anorexia, depression, thirst and diarrhoea.
• In the later stages there will be generalised icterus, haemoglobinaemia, haemoglobinuria and recumbency.

PM Lesions:

• In acute poisoning severe gastroenteritis with erosions and ulcerations are noticed in the abomasum of ruminants.
• A characteristic feature is that blood is found to be coagulated at the time of death.
• In chronic cases, generalised icterus, enlarged, yellow and fragile liver and enlarged spleen is noticed.
• Animal voids port wine coloured urine.
• The kidney is bluish black in colour and this is known as gun-metal kidney. This type of kidney is formed due to the haemolytic crisis with chronic copper poisoning.

Treatment:

Treatment is often unsuccessful.

• Gastrointestinal sedatives to reduce irritation and other symptomatic treatment is useful.
• Ammonium molydate 50-500mg/ Kg body weight orally.

NaSO₄ 300 mg/ Kg body weight orally.

• Penicillamine (50 mglkg, PO, sid, for 6 days) may be useful if administered in the early stages of disease.
• Ammonium tetrathiomolybdate (15 mg/kg, IV, on alternate days) is effective for the treatment and prevention of copper poisoning.