Parvovirus B19 Infection in Pregnancy: What is the Risk to the Fetus?
ABSTRACT & COMMENTARY
Synopsis: The risk of fetal death after intrauterine parvovirus B19 infection was found to be between 0% and 8.6%.
Source: Harger JH, et al. Prospective evaluation of 618 pregnant women exposed to parvovirus B19: Risks and symptoms. Obstet Gynecol 1998;91:413-420.
Harger and colleagues in pittsburgh, beginning in 1990, prospectively evaluated 618 women exposed to human parvovirus B19 infection. Of the total, 23% were exposed during their first trimester, 49% during their second, and 28% in their third trimester. Forty-three percent were exposed before or at 20 weeks of pregnancy.
Serological testing of blood obtained 10-14 days after first exposure revealed that 307 (49.7%) had been immune to infection. Of the remaining 311 who were susceptible at the time of exposure, 52 (16.7% of susceptibles, 8.4% of the total) developed infection, as determined by the presence of IgM antibody to the virus, while the rest remained susceptible. One-third of maternal B19 infections were asymptomatic.
Logistic regression analysis found that the only significant predictor of maternal infection was exposure to her own child as the source. Occupations such as being an elementary school teacher, health care worker, or day care worker were not significantly associated with prior infection.
The 52 women with evidence of parvovirus B19 infection were advised to undergo weekly fetal ultrasound examinations for 12 weeks. No cases of hydrops fetalis were detected and no fetal or neonatal morbidity could be attributed to infection with this virus. The 95% Confidence Interval for the risk of developing hydrops fetalis after human parvovirus B19 infection in pregnancy was 0-8.6%.
COMMENT BY STAN DERESINSKI, MD, FACP
Parvovirus B19 is a nonenveloped, single-stranded DNA virus that requires actively dividing target cells for its replication. The major target of infection is the erythroid precursor cell (hence the genus name, Erythrovirus), which it enters by endocytosis after attachment to P antigen on the cell surface. Individuals with p red blood cell phenotype, lacking P antigen, are resistant to infection.1 The virus dramatically interferes with hematopoiesis, and reticulocytopenia is universally present after infection. Patients with pre-existing chronic hemolytic disease who undergo parvovirus B19 infection develop, as a consequence, aplastic crisis that persists for 7-10 days and resolves upon clearance of viremia associated with the appearance of antibody to the virus. Chronic viremia, which may be seen in the immunodeficient patient incapable of clearing the virus, may result in persistent red cell aplasia.
The fetus combines the need for rapid expansion of its erythrocyte compartment with an immature immune system. Vertical transmission of parvovirus B19, particularly during the first one-half of gestation may, as a consequence, result in severe persistent fetal anemia with resultant high output cardiac failure, sometimes complicated by viral myocarditis, recognized as hydrops. Hydrops may take 1-2 weeks to develop, with death following within days to weeks.
Earlier studies have found, as did the one reviewed here, that approximately 50% of women of childbearing age in the United States are seronegative and, thus, are susceptible to infection with parvovirus B19. Harger and colleagues found that 16.7% of susceptible exposed pregnant women became infected. Previous estimates have indicated that approximately one-third of maternal infections result in infection of the fetus and also that 2-10% of maternal infections lead to fetal death.2 Harger et al, using frequent fetal ultrasound examinations, calculated a 95% Confidence Interval for the development of hydrops, with an upper estimate of 8.6%.
Given the low rates of fetal hydrops and death, as well as the absence of known associated congenital abnormalities in affected fetuses, the value of repeated fetal ultrasound can be questioned. Harger et al suggest that performing limited ultrasound examinations aimed only at detection of hydrops may be more cost-effective. That, of course, assumes that intervention in the form of fetal blood transfusion improves the outcome, since hydrops may resolve spontaneously and intrauterine transfusion is not without risk, including the potential for causing fetal death.3 While, to my knowledge, no randomized trial has been published, a retrospective observational study does suggest that transfusion improves fetal outcome.4 In this report, three (25%) of 12 who were transfused died, while 13 (50%) of 26 who did not receive blood transfusion did so. These data can, however, be taken as suggestive, but not definitive. An alternative therapeutic approach-intravenous administration of immunoglobulin-has been attempted, but its value remains unknown.4
References
1. Brown KE, et al. Resistance to parvovirus B19 infection due to lack of virus receptor (erythrocyte P antigen). N Engl J Med 1994;330:1192-1196.
2. Anderson LJ. Human parvovirus B19. In: Richman DD, Whitley RJ, Hayden FG, eds. Clinical Virology New York: Churchill Livingstone; 1997:613-631.
3. Bhal PS, et al. Spontaneous resolution of non-immune hydrops fetalis secondary to transplacental parvovirus B19 infection. Ultrasound Obstet Gynecol 1996;7: 55-57.
4. Fairley CK, et al. Observational study of effect of intrauterine transfusions on outcome of fetal hydrops after parvovirus B19 infection. Lancet 1995;346: 1335-1337.
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