Altered placental development in pregnancies resulting in sudden infant death syndrome (SIDS).

BACKGROUND: Sudden infant death syndrome (SIDS) is postulated to be a developmental disorder originating during fetal life in utero. Knowledge regarding the intrauterine environment in which SIDS infants develop is, however, inadequate and how the placenta develops prior to a SIDS event has not been studied. AIM: To investigate the morphological development of the placenta obtained from full-term infants who subsequently succumbed to SIDS. STUDY DESIGN: To estimate the percentage and total volumes of the chorionic villi and villous trophoblast membrane using stereological techniques. SUBJECTS: Placentas were obtained retrospectively from normal birthweight (SIDS-NBW n=18) and small-for-gestational age (SIDS-SGA, n=14) infants who had succumbed to SIDS, and compared to either control (n=8) or SGA placentas (n=7), respectively. RESULTS: SIDS-NBW placentas displayed evidence of augmented villous growth shown by significantly greater volumes of placental chorionic villi (gas-exchanging (GE) villi) in comparison to controls; this was not observed for SIDS-SGA placentas. However, both SIDS-NBW and SIDS-SGA placentas displayed significantly greater volumes of the cytotrophoblast (CT) (SIDS-NBW only), syncytiotrophoblast (SIDS-SGA only) and syncytial knots (SCT-K) and those displaying apoptotic syncytial nuclei (AP SCT-K). In contrast, SGA placentas displayed significantly reduced volumes of chorionic villi, GE villi and the villous trophoblast indicating a SIDS-specific effect associated with augmented placental growth. CONCLUSIONS: Our findings provide initial evidence that placental abnormality, although not necessarily causative, may precede a subset of SIDS cases supporting the hypothesis that the origins of SIDS begin during fetal life in utero.

Parvovirus infects cardiac myocytes in hydrops fetalis.

Parvovirus infection during pregnancy is an important cause of hydrops fetalis. It is attributed to anemia caused by viral-induced destruction of red blood cells. Infection of other organs has been reported including the heart, liver, and lungs. Few of these reports, however, convincingly demonstrate virions within the functional parenchyma of the tissue. This is of particular concern regarding myocardium in the context of hydrops fetalis which is, in part, due to cardiac failure. The problem in routine pathology practice is that most fetuses with the infection are macerated. This, in part, probably explains the paucity of published information on cardiac involvement. This study examined five cases of fatal hydrops fetalis with variable maceration with serologically proven parvovirus B19 infection. Transmission electron microscopy of cardiac tissue demonstrated intranuclear virions in both erythroid precursor cells and in cardiac myocytes in three of these cases. In each of these, immuno-gold electron microscopy provided confirmatory evidence of parvovirus infection. Virions were not identifiable where maceration had caused disintegration of nuclei in the myocytes. In addition, virions were absent in the three negative control cases where retroplacental hemorrhage was confirmed as the cause of death. This study suggests that parvovirus infection of cardiac myocytes may play a more important role in causing hydrops fetalis than previously realized. It also demonstrates that maceration should not discourage the use of electron microscopy.