Placental pathology in malaria: A histological, immunohistochemical, and quantitative study

To characterize the histological changes in malarial placentas and their re lationship with parity and maternal and cord parasitemias, we conducted a h istological study on 1,179 placentas from Ifakara, Tanzania, an area with i ntense and perennial malaria transmission. Immunohistochemical and quantita tive studies for CD45, fibrin, and villous area were performed in 60 cases. Four hundred fifteen placentas (35.2%) showed parasites (active infections ); in 303 of them, parasites co-existed with pigment covered by fibrin (chr onic infections), and in 112 only parasites were detected (acute infections ). Four hundred seventy-five cases (40.3%) showed hemozoin deposition witho ut parasites (past infections). Of women with parasitized placentas, 46.3% did not show parasites in the peripheral blood. Basal membrane thickening ( P =.002), fibrinoid necrosis (P =.004), and prominence of syncytial knots ( P =.031) were associated with active malarial infection. No quantitative di fferences for perivillous fibrin deposition or villous area were found. The most significant association with active malarial infection was intervillo us infiltration by mononuclear inflammatory cells (P <.001). Chronic infect ions were associated with the most severe changes, particularly intervillou s mononuclear inflammation (OR, 28.7; 95% CI=16.0 to 51.5, P<.001). Past in fections showed only minimal differences with noninfected placentas. Primip aras showed chronic infections more frequently than multiparas (52% v 15%, P <.001). They also showed significantly higher placental parasitemias and intervillous inflammatory infiltrate. In conclusion, placental histology is more sensitive than peripheral blood examination in detecting malarial inf ection during pregnancy. Most malarial infections recover during pregnancy, leaving few residual changes in the placenta. Intervillous inflammation is the most frequent finding associated with malaria and is especially severe in primiparas, suggesting that mechanisms other than immunosuppression are responsible for the high susceptibility in this group. HUM PATHOL 31:85-93 . Copyright (C) 2000 by W.B. Saunders Company.