Fetal parvovirus B19 infection

Abstract

Parvovirus B19 infection during pregnancy causes up to 27% cases of non-immune hydrops in anatomically normal fetuses. The virus is believed to cause arrest of maturation of red blood cell precursors at the late normoblast stage and also causes a decrease in the number of platelets. Fetal anemia is presently thought to be responsible for the development of skin edema and effusions. Myocarditis leading to heart failure may contribute to the development of fetal hydrops. We reviewed the literature regarding prevalence, transmission rates, clinical presentation, diagnostic techniques, current invasive vs. conservative management options, outcome and postmortem findings in a total of 82 studies involving 230 invasively and 435 conservatively managed pregnancies. In this non-selected population, the proportion of seronegative susceptible mothers ranged from 19 to 65%, seroconversion with an incubation time of up to 20 days occurred in 5.7-12.1%, and 188/230 (82%) who were transfused infected fetuses had a normal outcome as opposed to only 239/435 (55%) in the conservatively managed group. The average time from diagnosis to resolution in both groups was 6 weeks (range, 3-12 and 2-12 weeks, respectively). The most promising diagnostic techniques were PCR of amniotic fluid or fetal blood and electron microscopy. There are some reports of fetal abnormalities occurring (probably coincidentally) in cases of parvovirus, but the majority of postmortem findings were infection-related, in particular myocarditis and hepatic abnormalities. Although management guidelines cannot be derived from this study due to the variable degree of hydrops in the analyzed studies, the present data suggest a benefit of transfusion therapy over conservative management in infected fetuses. The only study which was corrected for severity of hydrops using ultrasound criteria showed a clear benefit of intrauterine transfusion.