Experimental infection of Trypanosoma (Trypanozoon) evansi in Bandicota bengalensis produces an acute disease course leading to untimely death of the bandicoot rat. The sequential alteration of liver, spleen, lung, kidney, and heart was studied on the 5th, 8th, 12th, and 14th days postinoculation. The rats showed inflammatory, degenerative, and necrotic changes in these organs. In liver, pseudolobule formation, necrosis and hemorrhage within the sinusoids, and fatty degeneration of hepatic cells were the predominant histopathological changes. The changes were destructive and irreversible. In spleen giant cells aggregation and granulomatous lesion, i.e., accumulation of histiocytes, were the protective changes, whereas tissue and cell damage indicated irreversible degeneration. The gradual development of intrabronchus inflammation, aggregation of inflammatory cells around the alveoli, congestion of bronchioles, septal edema, atrophy of alveolar walls, migration of macrophages, and emphysema were the histopathological changes noticed in the lungs of the infected rats. The affected kidney showed infiltration of lymphocytes, hemorrhage in the interlobular space, and glomerulitis as the irreversible and destructive changes in the rats. There was degeneration of myocardium in the hearts of the rats. The histopathological changes in these organs are compared with those studied in surra, human sleeping sickness disease, and African trypanosomiasis. Possible mechanisms for these histological changes in the visceral organs are discussed. © 2001 Elsevier Science (USA).