Abstract
The effects of treatment of virulent blood forms of Trypanosoma cruzi with ethidium bromide (EtBr), an intercalating drug that inhibits DNA synthesis, on parasite association with (a term to mean surface binding plus internalization) and multiplication within different types of host cells were investigated. EtBr markedly reduced the extent of T. cruzi association with Vero cells or rat heart myoblasts (RHM) as evidenced by significant decreases in both the number of flagellates per cell and the percentage of infected cells with respect to control values obtained with organisms treated with medium alone. Treatment of Vero cells with EtBr had no significant consequence on the extent of cell-T. cruzi association and did not affect the capacity of the parasites to transform into amastigotes and multiply intracellularly. Very few organisms were able to gain access to the cytoplasms of the host cells after treated with 1 .times. 10-5 M EtBr but these were virtually unable to multiply intracellularly. Parasites treated with 1 .times. 10-6 M EtBr multiplied at a slower rate than medium-treated organisms. Unlike untreated trypomastigotes, parasites treated with 1 .times. 10-5 M EtBr were unable to transform into amastigotes in a cell-free medium that supported the growth of untreated organisms. A marked reduction in the rate of amastigote multiplication was seen in cells with an established infection when they were treated with EtBr. Apparently, ongoing DNA synthesis by T. cruzi is required for it to effectively bind and infect host cells. The known effect of EtBr against experimental T. cruzi infection may be underlaid by a reduction in the parasite ability to associate with and penetrate host cells, as well as by inhibition of intracellular parasite transformation and multiplication.

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