The macrophage function was investigated in mice infected with Trypanosoma cruzi. Two subpopulations of the parasite were utilized, RA and K98. Strain RA is efficiently internalized by macrophages and is lethal for mice, and clone K98 is poorly phagocytosed by macrophages and is not lethal. Treatment with silica enhanced parasitemia and mortality in mice infected with both parasite subpopulations. Parasitemia kinetics, however, were affected only in mice infected with RA, which suggests that macrophage effector mechanisms may play a more relevant role in this experimental group than in mice infected with K98. Resistance to Salmonella typhimurium infection and bactericidal activity of macrophages depended upon the T. cruzi subpopulation utilized and the infection period. Infection with K98 induced only a trend towards enhanced resistance to bacterial challenge during both the acute and chronic phases, whereas a significantly enhanced bactericidal activity of spleen and liver phagocytes was observed. Mice acutely infected with RA showed significantly enhanced susceptibility to S. typhimurium infection and lower bactericidal activity. Mice surviving infection with this aggressive strain, however, showed significantly enhanced resistance and bactericidal activities. Mice acutely infected with the RA strain displayed a dissociation between macrophage capacities to control S. typhimurium and T. cruzi. A similar phenomenon was also observed in other parasitoses (schistosomiasis, African trypanosomiasis). This fact may be due to differences in the lethal mechanisms through which macrophages control these parasites and S. typhimurium.