Thioridazine, a tricyclic drug, is known to have a direct effect on Trypano
soma cruzi, disrupting the parasites' mitochondria and kinetoplasts. In the
present study, the drug was used orally, at 80 mg/kg.day for 3 days, to tr
eat mice inoculated with low numbers of T. cruzi. The drug caused no appare
nt toxicity in the host. It cleared trypomastigotes from the bloodstream, p
revented the histological and functional alterations of the heart normally
observed in the chronic phase of the experimental disease, and greatly redu
ced the mortality rate compared with that in untreated, infected controls.
When checked 135 days post-infection, the density of cardiac beta receptors
and the cardiac histology of the treated mice were indistinguishable from
those of uninfected, untreated controls. The drug is already used to treat
humans, as a neuroleptic drug. It appears to be able to prevent acute infec
tion with T. cruzi evolving into chronic disease, at least in mice, and may
be a useful base from which to design new agents for the treatment of Chag
as disease.