Placental Malaria: A New Insight into the Pathophysiology

Abstract

Malaria in pregnancy poses a great health risk to mother and her fetus and results into complications, such as abortion, still birth, intra uterine growth retardation, and low birth weight. The heavy infiltration of Plasmodium falciparum-infected RBCs in the intervillous spaces of placenta seems to be responsible for all the complications observed. Infected RBCs in the placenta cause an inflammatory environment with increase in inflammatory cells and cytokines which is deleterious to the placenta. Increased inflammatory responses in the infected placenta result into oxidative stress that in turn causes oxidative stress-induced placental cell death. Moreover, heat shock proteins that are produced in high concentration in stressed cells to combat the stress have been reported in fewer concentrations in malaria-infected placenta. Pathologies associated with placental malaria seems to be the effect of a change in immune status from antibody-mediated immune response to cell-mediated immune response resulting into excess inflammation, oxidative stress, apoptosis, and decreased heat shock protein expression. However, we also need to study other aspects of pathologies so that better drugs can be designed with new molecular targets.

Keywords: intra uterine growth retardation; low birth weight; malaria; placenta; pregnancy.

Figure 1

Diagrammatic representation of the placental malaria and implications. Malarial infection during pregnancy results into infiltration of the parasite-infected RBCs to the intervillous space of placenta resulting into exacerbated inflammatory response. High inflammation causes oxidative stress-induced apoptotic cell death in the placenta. Decreased expressions of the heat shock protein genes in the infected placenta further contribute to the placental pathology. All these pathological alterations in the placenta contribute to the poor pregnancy outcomes associated with malarial infection.