Context.–Case reports and rare case series have demonstrated variable placental pathology in the setting of maternal severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In rare small studies demonstrating infection of the placental parenchyma, histologic manifestations have included variable degrees of histiocytic intervillositis, perivillous fibrin deposition, and syncytiotrophoblast necrosis.
Objective.–To characterize the placental pathological features of SARS-CoV-2 infected placentas, irrespective of fetal-maternal transmission, and to examine the frequency of C4d activation in such cases.
Design.–Retrospective study of seven placentas from mothers with active SARS-CoV-2 infection and placental infection as demonstrated by RNA in situ hybridization.
Results.–Six placentas were from live-born neonates (5 singletons, 1 non-fused diamniotic-dichorionic twin placenta), and one was from a stillbirth. Five of the eight neonates (including the stillbirth) tested negative for SARS-CoV-2, and all were negative for neonatal infection. The remaining three neonates were well at time of discharge. All placentas were positive for SARS-CoV-2 infection by RNA in situ hybridization and demonstrated variable degrees of histiocytic intervillositis, perivillous fibrin deposition, and trophoblast necrosis. Three cases demonstrated features of fetal vascular malperfusion. CD68 highlighted intervillous histiocytes. C4d expression was present along the villous borders in 6 of 7 cases.
Conclusions.–SARS-CoV-2 placentitis is defined by the triad of histiocytic intervillositis, perivillous fibrin deposition, and trophoblast necrosis. The features may occur in cases without confirmed transplacental transmission. The damage caused by SARS-CoV-2 placentitis is likely mediated by complement activation.