Acute Trypanosoma cruzi infection in mouse induces infertility or placental parasite invasion and ischemic necrosis associated with massive fetal loss.

Pathogens may impair reproduction in association or not with congenital infections. We have investigated the effect of acute infection with Trypanosoma cruzi, the protozoan agent of Chagas' disease in Latin America, on reproduction of mice. Although mating of infected mice occurred at a normal rate, 80% of them did not become gravid. In the few gravid infected mice, implantation numbers were as in uninfected control mice, but 28% of fetuses resorbed. Such infertility and early fetal losses were significantly associated with high maternal parasitemia. The remaining fetuses presented with reduced weights and all died later in gestation or within 48 hours after birth. Several organs of these fetuses were infiltrated by polynuclear cells and presented ischemic necrosis but did not harbor T. cruzi parasites, discarding congenital infection as the cause of mortality. However, surprisingly, the deciduas were massively invaded by T. cruzi parasites, harboring 125-fold more amastigotes than the maternal heart or other placental tissues. Parasites were significantly more numerous in the placentas of dead fetuses. In addition, placentas contained inflammatory infiltrates and displayed ischemic necrosis, fibrin deposits, and vascular thromboses. These results show that acute T. cruzi infection totally impairs reproduction in mice through inducing infertility or fetal-neonatal losses in association with placental parasite invasion and ischemic necrosis.