Las lesiones placentarias en la infección humana por Trypanosoma cruzi / Placental lesions in human Trypanosoma cruzi infection

This histopathological study analyzes placentas of babies congenitally infected with T. cruzi (M+B+), or babies not infected but born from infected- (M+B-), or non infected-mothers (M-B-). Placentas M+B+ showed lesions of chorionitis, chorioamnionitis and cord edema with lymphocyte infiltration, whereas such lesions were infiltrated only with polymorphonuclear cells in M+B- and M-B- placentas. Parasites were found in M+B+ placentas, in fibroblasts and macrophages of chorion, membranes, chorionic plate, mainly in the area of membrane insertion, as well as in cells of Wharton jelly and myocytes of umbilical cord vessels. These results suggest that the materno-fetal transmission of parasites occurs mainly through the marginal sinus, spreading into the chorionic plate infecting fibroblasts and macrophages so far as to found a fetal vessel, inducing a fetal infection by hematogenous route.

Efectos de la infección aguda y crónica por Trypanosoma cruzi en la gestación de los ratones / Effects of acute and chronic Trypanosoma cruzi infection in pregnant mice

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, on reproduction of female mice. In the acute, parasitemic, phase of the infection, female mice were totally unable to reproduce. Most of them (80%) were infertiles and did not develop any gestation. In the few gravid infected mice, implantation numbers were as in uninfected control mice. However, their fetuses presented a weight meanly reduced by 40% as compared to those of uninfected females, and all of them died during the gestation or whithin 48 h after birth. Such massive mortality did not result from congenital infection, which did not occur. The infertility and the fetal mortality occuring early in gestation (resorptions) were significantly correlated with a high maternal parasitemia, whereas later fetal mortality was associated with the presence of intracellular parasites in the utero-placental unit. The decidua was particularly receptive to T. cruzi multiplication, since this tissue harboured 125 fold more amastigotes than the maternal heart or other placental tissues. In addition, placentas of dead fetuses presented histopathological lesions (inflammatory infiltrates, fibrine deposits and ischemic necrosis). Such harmfull effects of acute infection were not observed when female mice were in the chronic phase of the infection, since these reproduce normally. Their fetuses only suffered from moderate and reversible growth retardation. These results indicate that, following the maternal parasite burden, T. cruzi infection may induce very deleterious effects on gestation.