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Effect of Aflatoxin Induced Immunosuppression on Pathogenesis of H9N2 Avian Influenza Virus
Hala MF El Miniawy1, Kawkab A Ahmed1, Ahmed A El-Sanousi2 and Marwa M Salah Khattab1
1Department of Pathology; 2Department of Virology, Faculty of Veterinary Medicine, Cairo University, El Giza Square, Giza, Egypt. *Corresponding author:


The study was performed to investigate the immunosuppressive effect of aflatoxin on the pathogenesis of H9N2 AI virus in SPF chickens. The experiment was carried out on 110 unvaccinated day old SPF chicks. They were divided into four groups of 25 birds each. Group I was kept as a non-treated and non-infected control; group II was intranasally infected with H9N2 AI virus at the 4th week of age; group III was fed on a diet containing 0.75 ppm aflatoxin from day one through the entire experiment period and group IV was fed on diet containing 0.75 ppm aflatoxin as group III and infected intranasally with H9N2 AI virus at the 4th week of age. Five chicks were kept as contact control (without infection) to group II and group IV. Five chickens from each group were slaughtered at 4th, 9th, 14th, 20th and 27th DPI Serum was collected from all slaughtered birds (5 serum samples/group/slaughter time) for serology (HI). Specimens from nasal conchae, trachea, lungs, liver, kidneys, bursa of Fabricius, thymus, spleen, pancreas and brain were collected from slaughtered birds for histopathology and immunohistochemistry. The histopatholo- gical lesions were more severe and persist till the end of the experiment in group IV. Using immunoperoxidase technique viral antigens were detected in the nasal conchae, trachea, lungs, thymus, kidneys and brain in group II while in group IV it extended further to the pancreas and bursa of Fabricius. In conclusion, the immunosuppression caused by aflatoxin increased the severity of lesions and allowed the virus to be disseminated to more organs.

Key words: Avian influenza virus (H9N2), Aflatoxin, Pathology, Immunoperioxidase, Chickens


ISSN 0253-8318 (Print)
ISSN 2074-7764 (Online)