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Published on: September 5, 2011
Discordant fetal infection for parvovirus B19 in a dichorionic twin pregnancy
Jan E Dickinson1, Anthony D Keil, Adrian K Charles
1School of Women's and Infants' Health, The University of Western Australia, Perth. Jan.Dickinson@uwa.edu.au
There are only a few reports of fetal parvovirus infection in the circumstance of a twin pregnancy. We report a case of differential fetal infection following maternal parvovirus B19 infection in a dichorionic twin pregnancy culminating in a dual live-birth. A 32-year-old woman was diagnosed with parvovirus infection following exposure to her infected child at 19 weeks' gestation in a dichorionic twin gestation. Maternal IgG seroconversion was documented and maternal blood parvovirus B19 DNA was detected by PCR testing. Fetal monitoring with serial ultrasound assessment was instituted. At 25 weeks' gestation Twin I (male) displayed minor ascites, small pericardial effusion, placentomegaly and oligohydramnios. Middle cerebral artery peak systolic velocity (MCA PSV) studies were abnormal. Twin II (female) was sonographically unremarkable. A single fetal intravascular transfusion for Twin I was performed (pretransfusion Hb 80 g/L). Twin I fetal blood parvovirus B19 DNA was detected by polymerase chain reaction (PCR) and serum demonstrated both B19 IgG and IgM. Following fetal transfusion the hydrops resolved, although the placentomegaly persisted. Two live infants were delivered at 37 weeks' gestation. Individual neonatal venepuncture detected B19 DNA by PCR in Twin I but not in Twin II. B19 IgM was present in Twin I but not Twin II. Both neonates had B19 IgG antibodies. Placental histopathology demonstrated mild edema for Twin I but no inclusion cells. The placenta of Twin II was unremarkable. This case demonstrates the ability for differential transplacental infection of this virus and the assistance of fetal MCA flow studies to guide therapy in a multiple pregnancy at risk of parvovirus infection.
There are only a few reports of fetal parvovirus infection in the circumstance of a twin pregnancy. We report a case of differential fetal infection following maternal parvovirus B19 infection in a dichorionic twin pregnancy culminating in a dual live-birth. A 32-year-old woman was diagnosed with parvovirus infection following exposure to her infected child at 19 weeks' gestation in a dichorionic twin gestation. Maternal IgG seroconversion was documented and maternal blood parvovirus B19 DNA was detected by PCR testing. Fetal monitoring with serial ultrasound assessment was instituted. At 25 weeks' gestation Twin I (male) displayed minor ascites, small pericardial effusion, placentomegaly and oligohydramnios. Middle cerebral artery peak systolic velocity (MCA PSV) studies were abnormal. Twin II (female) was sonographically unremarkable. A single fetal intravascular transfusion for Twin I was performed (pretransfusion Hb 80 g/L). Twin I fetal blood parvovirus B19 DNA was detected by polymerase chain reaction (PCR) and serum demonstrated both B19 IgG and IgM. Following fetal transfusion the hydrops resolved, although the placentomegaly persisted. Two live infants were delivered at 37 weeks' gestation. Individual neonatal venepuncture detected B19 DNA by PCR in Twin I but not in Twin II. B19 IgM was present in Twin I but not Twin II. Both neonates had B19 IgG antibodies. Placental histopathology demonstrated mild edema for Twin I but no inclusion cells. The placenta of Twin II was unremarkable. This case demonstrates the ability for differential transplacental infection of this virus and the assistance of fetal MCA flow studies to guide therapy in a multiple pregnancy at risk of parvovirus infection.
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