The protozoan parasite Entamoeba histolytica is the causative agent of amoebiasis, a human disease characterized by dysentery and liver abscess. The physiopathology of hepatic lesions can be satisfactorily reproduced in the hamster animal model by the administration of trophozoites through the portal vein route. Hamsters were infected with radioactively labeled amoebas for analysis of liver abscess establishment and progression. The radioimaging of material from parasite origin and quantification of the number inflammation foci, with or without amoebas, described here provides the first detailed assessment of trophozoite survival and death during liver infection by E. histolytica. The massive death of trophozoites observed in the first hours postinfection correlates with the presence of a majority of inflammatory foci without parasites. A critical point for success of infection is reached after 12 h when the lowest number of trophozoites is observed. The process then enters a commitment phase during which parasites multiply and the size of the infection foci increases fast. The liver shows extensive areas of dead hepatocytes that are surrounded by a peripheral layer of parasites facing inflammatory cells leading to acute inflammation. Our results show that the host response promotes massive parasite death but also suggest also that this is a major contributor to the establishment of inflammation during development of liver abscess.Amoebiasis is a widespread human parasitic disease caused by the protozoan Entamoeba histolytica. The two major clinical manifestations of E. histolytica infection are amoebic colitis and liver amoebic abscess. Yearly, 50 million people develop intestinal amoebiasis and it is estimated that 10% of individuals with amebic colitis will develop an amebic liver abscess. Amoeba infection causes 100,000 deaths per year, ranking, second after malaria, among the most deadly human parasitic diseases caused by a protozoan (6).During invasive amoebiasis, highly motile trophozoites invade the intestinal epithelium, causing extensive tissue damage characterized by acute inflammation and ulceration with necrosis and hemorrhage. In contrast to intestinal amoebiasis, invasion of the liver is characterized by the presence of nonmotile E. histolytica trophozoites that cause an acute inflammatory reaction. Well-individualized infection foci contain mostly dead hepatocytes, polymorphonuclear leukocytes (PMN), macrophages, and parasites. Differences in pathology between amoebic colitis and amoebic liver abscess (ALA) likely result from a variation of the E. histolytica virulence repertoire in the two organs and from different responses of these organs to amoeba infection (11). Understanding the physiopathology of amoebiasis thus requires the development of new experimental strategies that take into account the multifactorial cross talk between the amoeba and the host cells during invasion of a specific human organ.Our current knowledge of ALA development is essentially derived from studies with rodent mode...