Accumulative Copper Poisoning in Sheep in Northeastern Brazil

Resumo

Background: Despite the proven copper deficiency in several parts of Brazil, reports of acute and accumulative copper poisoning are increasing in ruminants. Sheep are known to be far more sensible to copper toxicity than cattle, but the sensibility of goats is not quite known. The present paper aimed to describe the epidemiological, clinical, laboratorial and pathological findings of two outbreaks of accumulative copper poisoning in sheep fed poultry litter in Ceará and Rio Grande do Norte, Northeastern Brazil, and to compare these findings with national outbreaks.

Cases: Two outbreaks of copper poisoning occurred in the municipalities of Mossoró, Rio Grande do Norte [outbreak 1], and Icapuí, Ceará [outbreak 2], Brazil. A total of 35 sheep [outbreak 1] and 190 small ruminants (175 sheep and 15 goats) [outbreak 2] were fed poultry litter. First clinical signs of poisoning started after two months of litter consumption. Main clinical signs were apathy, jaundice, hepatomegaly, abdominal pain, diarrhea, and dark urine. Clinical evolution varied between one and eight days. Laboratorial findings in ill animals consisted of anemia, highly increased serum AST and GGT activities and urea and creatinine levels; whilst in the non symptomatic sheep and one goat revealed high and light GGT increase, respectively. Poultry litter analysis revealed levels of 449, 2610, 414 and 333 mg/kg of copper, iron, manganese and zinc, respectively. Analysis of copper levels by atomic absorption spectrometry in two sheep showed 730.1 and 1526.5 mg/kg in liver and 485.1 and 519.4 mg/kg in the kidneys. Treatment consisted of oral administration of 100 mg ammonium molibdate and 1 g sodium sulphate for five days. A total of 32 sheep died and necropsy of five animals showed deep jaundice, livers presenting a yellow to orange coloration, splenomegaly, hepatomegaly, blackish kidneys and dark urine. The microscopic examination of liver and kidneys showed degenerative and necrotic lesions.

Discussion: This is the first report of copper poisoning in sheep from Rio Grande do Norte and Ceará, Northeastern Brazil. Even though it is not allowed in Brazil, the use of poultry litter for animal feeding still occurs and represents a great risk for copper poisoning in ruminants, especially sheep. The use of poultry litter should be discouraged to producers for feeding ruminants and requires more awareness of them that the use of this product is prohibited for this purpose. Clinical signs were typical of accumulative copper poisoning and the most evident changes in the serum biochemistry analyses were anemia and increased serum AST and GGT activities and urea and creatinine levels. Serum activity of GGT in a non symptomatic goat was slight increased, which is suggestive of an initial liver damage promoted by copper accumulation. Main pathological changes are associated to liver and kidney damage. Measurement of copper levels in liver and kidney fragments by atomic absorption spectrometry confirmed the diagnosis of poisoning by this element. Oral administration of ammonium molibdate associated to sodium sulphate was efficient for the treatment of poisoned sheep because both compounds reduce digestive absorption and increase excretion of copper. The absence of poisoning in goats fed the same poultry litter confirms that this species is more resistant than sheep to copper toxicity. Nevertheless further research must be carried out to test this sensibility. The use of poultry litter should be discouraged to producers for feeding ruminants and requires more awareness of them that the use of this product is prohibited for this purpose.

Keywords: jaundice, hemoglobinuric nephrosis, poultry litter, small ruminants.