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A study was conducted to evaluate the effects of ochratoxin A (OA) on Escherichia coli -challenged broiler chickens. One hundred and eighty-four one-day-old broiler chicks were divided into two groups of 92 chicks each, with one group fed a control mash diet and the other fed a mash diet containing 2 parts/10 6 OA. On day 14, each group was further subdivided into two groups with one group inoculated with E. coli O78 (1/10 7 colony-forming units/0.5 ml) by the intraperitoneal route, whereas the other group was not inoculated with E. coli. Four birds from each group were sacrificed at 1, 2, 3, 5, 7, 10, 14 and 21 days post-inoculation to record pathological changes in the liver, kidneys, heart, lungs, bursa, spleen and thymus. E. coli infection induced perihepatitis and pericarditis in the liver and heart, respectively, in chickens infected with E. coli alone or in OAfed birds from 1 day post-infection (DPI) onwards. At 1 DPI, a thin fibrin layer covered the liver and heart; however, at subsequent days, the layer became thicker. E. coli infection did not produce appreciable changes in the kidneys, bursa or thymus. However, there was congestion of the lungs along with mononuclear cell infiltration. Ochratoxin feeding induced changes from 10 DPI onwards in chicks fed OA alone and those infected with E. coli. The changes in kidneys included swollen proximal convoluted tubules, degeneration of tubular epithelium and interstitial nephritis. Degenerative changes and mononuclear cell infiltration were recorded in the liver. There was atrophy of the lymphoid organs along with depletion of lymphocytes. Gross and histopathological changes were more severe in chickens fed OA and inoculated with E. coli than the chickens fed OA alone or those infected with E. coli, indicating combined action of these two.

FIG 1: Intracytoplasmic neuronal immunolabelling localised in the thalamic area of the brain by immunohistochemical detection using 3F4 monoclonal antibody (x 1000) FIG 2: Protease resistant prion protein (PrP res) demonstrated by Western blotting of samples from brains of cheetah (1, 2), sheep (3), cow (4) or BSE-infected mouse (5), with spongiform encephalopathy, using RS1 antiserum (2-5) or 3F4 monoclonal antibody (1)

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