Malaria causes major losses to human populations in the world. Experimental models are needed for a better understanding of the pathological mechanisms of the diseases and the development of new treatments. Chickens infected with Plasmodium gallinaceum constitute an adequate malaria model due to the phylogenetic proximity of this parasite to human Plasmodium as well as similarities in disease manifestation, as cerebral malaria. The aim of the present study was to investigate the role of nitric oxide in avian malaria development in chickens experimentally infected with P. gallinaceum, treated or not with aminoguanidine (AG - nitric oxide synthase inhibitor). Survival, classical hematology, serum biochemistry and pathology was assayed during the development of the disease. The greatest survival was observed in animals treated with AG that also presented higher parasitemia. Decrease in hematological parameters and Mean Corspucular Volume of erythrocytes increase was showed, indicating bone marrow response to anemia. Lymphopenia and thrombocytopenia were detected in infected animals, but not at the same proportion in treated animals. Monocytes, lymphocytes and heterophils showed an increase in size and changes that indicated activation. Thrombocytes were also higher with the infection and with atypical morphology. Treated animals showed fewer lesions in histological sections of brain, liver and spleen, and NO production decreased, principally during high parasitemia, compared to untreated animals. These results characterize the participation of the chemistry mediator nitric oxide in the pathogenesis of malaria in the avian model.
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