Pathomechanism of cerebral hypoplasia in experimental toxoplasmosis in murine fetuses

Abstract

In order to elucidate the pathological mechanism of cerebral hypoplasia in congenital toxoplasmosis, fetal toxoplasmosis was induced by intraperitoneal injection of Toxoplasma gondii into five pregnant mice on embryonal Day 5 (E5). The maternal and fetal brains were examined histologically and immunohistochemically; six fetuses were examined on E16 and 21 on E18. T. gondii organisms were immunohistochemically detected in the maternal brains, placentas and the ventricular zone of the fetal cerebrum. In none of the fetal brains was any gross deformity observed, except for cerebral hypoplasia. On E16 and E18, the cerebral cortices were seen to consist of immature laminations, and the cells had less cytoplasm and rounder hyperchromatic nuclei than those in the control mice. The cerebral walls and the cortical layers, except in the ventricular zone, were thinner than in the controls (P < 0.01 in each case). On E18, the proliferating cell nuclear antigen immunolabeling index was higher, and the cytoplasm of more cells in the cortical plate was immunoreactive with anti-beta-tubulin antibody compared with control mice. Using an in situ end-labeling technique, apoptotic cells were not observed in the cortices in mice of both groups. It is suggested that the cerebral hypoplasia following Toxoplasma infection is related to delayed maturation.