PubMed1992
Human parvovirus B19 is a recently recognized cause of hydrops fetalis. It is a small, single-stranded DNA virus, which preferentially infects late erythroid precursors and produces red blood cell (RBC) aplasia, fetal anemia, and cardiac failure. Infection is accompanied by characteristic intranuclear inclusions in fixed and circulating RBC precursors. These inclusions have been shown to contain virus particles by electron microscopy and in situ hybridization. Infection of the fetus, mother, and newborn infant can be diagnosed by serological and molecular methods selected to match the stage of the infection. Recent work has shown that parvovirus B19 can infect cells other than erythroid precursors, and that additional mechanisms such as myocarditis may contribute to hydrops fetalis in some cases. Infected fetuses are not always hydropic. Maternal infection results in increased abortion and stillbirth even in the absence of transplacental transmission, which occurs in approximately one third of infected mothers. The overall risk of fetal loss following maternal exposure is much less than previously thought, and may be less than 3% in the first 20 weeks of gestation or approximately 10% if the mother is actually infected. Although parvoviruses are teratogenic in animals, there is no evidence that B19 is a significant teratogen in man. The long-term outlook of survivors of intrauterine infection, including those successfully treated by intrauterine blood transfusion, appears to be good, but requires further study.