Tribasic copper chloride toxicosis in commercial broiler chicks.

Abstract

Two broiler chicken houses containing 17,500 chicks each experienced an extreme elevation in chick mortality beginning on day 3 after placement. Clinical signs observed upon farm visit included numerous small chicks for their age; depressed, lethargic, and comatose chicks; and chicks huddling near feed pans and under heaters. Necropsied chicks were markedly pale and had atrophy of the thymus and bursa, swollen and edematous proventriculus, erosions in the koilin and in the proventricular-ventricular junction, pale kidneys, and yellowish to brownish-orange liver often with linear pale areas. The chicks had watery blood and hematocrits measured from 9.5% to 18%. Chicken infectious anemia was initially suspected based on the clinical signs and gross lesions. Histopathology revealed multifocal acute hepatic degeneration and necrosis with golden-brown pigment in the cytoplasm of hepatocytes and Kupffer cells, moderate to severe koilin degeneration and fragmentation, multifocal mild to moderate proventricular necrosis, mild to moderate necrosis and loss of enterocytes, blunting of small intestinal villi, lymphoid depletion in the thymus and bursa, erythrophagocytosis in the liver and spleen, and acute renal tubular degeneration and necrosis. Special stains revealed mild to abundant accumulation of copper pigment in the cytoplasm of hepatocytes and iron pigment in the cytoplasm of Kupffer cells. Feed analysis revealed 2140 to 2393 parts per million of copper in the starter ration, and heavy metal analysis detected markedly elevated copper levels in formalin-fixed samples of the liver. Excessive amounts of tribasic copper chloride in the starter ration caused copper toxicosis in these chicks. Similar clinical signs and lesions were reproduced when the suspect feed was used in an experimental pen trial.