Experimental copper poisoning in the camel (Camelus dromedarius).

Copper sulphate was administered by the oral or intravenous route to five dromedary camels. Two camels (1 and 2) receiving copper sulphate at 200 mg per kg per day by drench died within 8 days and camel 3, receiving 100 mg per kg per day by the same route, was slaughtered on day 172. Intravenous injection of 2 mg per kg per day caused the death of camel 4 on day 95 and camel 5, treated similarly, was slaughtered on day 138. Anorexia, dullness, diarrhoea, dehydration and recumbency in camels 1 and 2 were probably clinical signs of copper toxicity. Camels 3, 4 and 5 lost weight. Jaundice was not a prominent clinical sign. The main lesions in camels 1 and 2 were fatty change and necrosis of the liver cells, dilatation and necrosis of kidney tubules, catarrhal abomasitis, enteritis and congestion of the blood vessels of the heart. In camels 3, 4 and 5 the hepatic lesions were mild, with leucocytic infiltration and gastrointestinal and heart lesions were either mild (camel 3) or absent (camels 4 and 5). Cytoplasmic copper granules in hepatic cells were generalized in distribution but more concentrated in the centrilobular zone. In the kidney these granules were confined to the cells of the proximal convoluted tubules. Copper accumulated in the liver and kidneys of all the camels and zinc accumulated in the liver and kidneys of those receiving copper sulphate intravenously. Macrocytic hypochromic anaemia developed in camels 3, 4 and 5 and haemoconcentration in camels 1 and 2. The concentration of serum copper, zinc and iron increased in animals 1, 2 and 4, and unbound iron binding capacity decreased in four camels. There was a rise in the activity of gamma GT, GOT, LDH and CPK in the serum of all the animals. Serum ALP activity, however, increased in camels 1 and 2 and decreased in camels 3, 4 and 5.