Truyens Carine, Mjihdi Karim, Lambot Marie-Alexandra, Rivera Maria Teresa, Noël Jean-Christophe, Carlier Yves
Laboratoire de Parasitologie, Faculté de Médecine, Université Libre de Bruxelles, Belgium.
Rev Soc Bras Med Trop. 2005;38 Suppl 2:68-72.
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.
病原体可能与先天性感染相关或不相关地损害生殖功能。我们研究了恰加斯病的原生动物病原体克氏锥虫急性感染对雌性小鼠生殖的影响。在感染的急性、寄生虫血症阶段,雌性小鼠完全无法繁殖。其中大多数(80%)不育,未出现任何妊娠情况。在少数怀孕的感染小鼠中,着床数量与未感染的对照小鼠相同。然而,与未感染雌性小鼠的胎儿相比,它们的胎儿平均体重降低了40%,并且所有胎儿在妊娠期或出生后48小时内死亡。这种大量死亡并非由先天性感染导致,因为并未发生先天性感染。妊娠早期出现的不育和胎儿死亡(吸收)与母体高寄生虫血症显著相关,而后期胎儿死亡与子宫 - 胎盘单位中细胞内寄生虫的存在有关。蜕膜对克氏锥虫的增殖特别敏感,因为该组织中无鞭毛体的数量比母体心脏或其他胎盘组织多125倍。此外,死胎的胎盘出现了组织病理学病变(炎性浸润、纤维蛋白沉积和缺血性坏死)。当雌性小鼠处于感染的慢性期时,未观察到急性感染的这种有害影响,因为它们能正常繁殖。它们的胎儿仅遭受中度且可逆的生长迟缓。这些结果表明,根据母体寄生虫负荷情况,克氏锥虫感染可能对妊娠产生非常有害的影响。