Abstract
BackgroundThere is concern about the development of anemia-associated fetal hydrops associated with maternal parvovirus B19 infection. Parvovirus B19 infection occurs via the globoside (P antigen) receptor, the main glycolipid of erythroid cells, which induces apoptosis. Similar findings have been reported for the P antigen of globoside-containing placental trophoblast cells.Case descriptionA 32-year-old woman was infected with human parvovirus B19 at week 32 of pregnancy, and had severe anemia at week 34. At week 37, an emergency cesarean section was performed because of sudden abdominal pain and fetal bradycardia; placental abruption was found. A live male infant was delivered with no sign of fetal hydrops or fetal infection. Placental tissue was positive for parvovirus B19 according to polymerase chain reaction. Immunohistochemical analysis using caspase-related M30 CytoDEATH monoclonal antibody revealed M30 staining of the placental villous trophoblasts.Discussion and evaluationPlacental trophoblasts and erythroid precursor cells have been reported to express globoside (P antigen), which is necessary for parvovirus B19 infectivity, and to show apoptotic activity as a result of infection. Placentas from three other pregnancies with documented abruption showed no M30 staining.ConclusionThe present case strongly suggests an association between placental abruption and apoptosis resulting from parvovirus B19 infection.
Highlights
Discussion and evaluationPlacental trophoblasts and erythroid precursor cells have been reported to express globoside (P antigen), which is necessary for parvovirus B19 infectivity, and to show apoptotic activity as a result of infection
There is concern about the development of anemia-associated fetal hydrops associated with maternal parvovirus B19 infection
The present case strongly suggests an association between placental abruption and apoptosis resulting from parvovirus B19 infection
Summary
Histlogical findings of placenta suggested that PB19-specific DNA were present and apoptosis was almost exclusively observed to a greater extent in the chorionic and decidual cells. Case 1 was an adult with an initial PB19 infection, no fetal disorder was found; the mother exhibited severe anemia and slightly decreased blood platelets, but her anemia did not worsen after transfusion She developed placental abruption during hospitalization, she had no risk factors for abruption (Cunningham et al 2014; Oyelese and Ananth 2006). Detection of apoptosis using immunostaining with M30 Mab should be performed as much as possible in women potentially infected with PB19, including those who have experienced miscarriage or stillbirth We anticipate comparing these PB19-related cases with or without placental abruption, and will perform further studies to determine the differences in histologic findings of the placenta in order to clarify the cause and course of placental abruption. With the assumption that placental abruption may be caused by apoptosis in the chorion in mothers with severe PB19 infection, clinical management may require high-level intervention equivalent to that for preterm premature rupture of the membranes and chorioamnionitis
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