Abstract

The infective trypomastigote form of Trypanosoma cruzi, the causative agent of Chagas’disease, is able to penetrate a large number of cells through an endocytic process with formation of a parasitophorous vacuole. A few hours after penetration the trypomastigote form gradually transfomiates into the spherical amastigote form (Review in De Souza 1974). During this process a porin-like macro- molecule is released by the parasite (Andrewset al. 1990) gradually lysing the membrane lining the vacuole so that af­ter a few hours the amastigote form is in direct contact with the structures and or­gandíes of the host cell (De Carvalhoand De Souza 1994). There are very few in­formation on the changes which take place in the host cell cytoplasm during the evolution of the inlracellular parasitism. Here I report observations made on the distribution of glycogen partióles of heart muscle cells infected with T. cruzi.