Epidemiology: The lifetime seroconversion rate for Parvovirus B19 is in excess of 90%, with half of all children converting by age 15. Similar trends are seen worldwide, except in rare isolated populations. In the U.S., child-bearing age women seroconvert at the rate of 1.5%. Viremia, however, is rare in asymptomatic individuals.

Clinical manifestations and pathogenesis: Parvovirus B19 infection causes a wide spectrum of disease including the childhood exanthematous rash known as Fifth disease, polyarthropathy, transient aplastic crisis, pure red cell aplasia in immunocompromised patients, and rarely aseptic meningitis and myocarditis. Exposure of pregnant women to the virus, particularly during the first 20 weeks of gestation, provides the opportunity for transplacental transmission to the fetus. Infection of red cell precursors in the hematopoietically active fetal liver results in fetal anemia, with the potential for high output cardiac failure. The flow abnormalities result in fluid accumulation within the pericardial, pleural and abdominal spaces (hence the name, hydrops, which means "edema"). Excess amniotic fluid often accumulates as well. As a result, stillbirth may occur.

Diagnosis: Parvovirus B19 is a relatively rare cause of hydrops fetalis (1 in 3000 live births), therefore other causes must be ruled out. Roughly 25% of cases are caused by red blood cell alloimmunization, which can be assessed by testing for maternal serum for red cell antibodies. Of the non-immune causes, Parvovirus B19 accounts for approximately 10-15%. Non-immune causes include structural cardiac anomalies, lymphatic anomalies such as cystic hygroma, pulmonary malformations, fetomaternal or twin-twin transfusion, obstructive urologic anomalies, and others. Thorough fetal anatomic survey, and fetal echocardiography are therefore critical. Acute maternal infection with toxoplasma and syphilis are assessed with repeat serologic tests and comparison with prenatal results. Fluid obtained by amniocentesis is useful for karyotype analysis and PCR amplification of CMV and Parvovirus B19 DNA. The Parvovirus B19-specific PCR amplifies the coding region of the VP1 capsid proteins. There are reports that direct tests for Parvovirus B19 capsid antigens in amniotic fluid are sensitive and more rapid than PCR. Serologic testing of the mother may also be useful to document seroconversion.

Treatment: The majority of cases of hydrops fetalis due to Parvovirus B19 gradually resolve without specific therapy. Excess rates of fetal loss are roughly 10%, with decreasing risk of loss after 20 weeks of gestation. Serial sonographic observations are therefore indicated. In some studies, persistent hydrops treated with intrauterine fetal blood transfusions improved survival. However, the role of this treatment remains controversial. Several studies have shown no acute or long-term disease in children who survive a hydropic pregnancy due to Parvovirus B19.

Follow-up: Sonograms were performed weekly with complete resolution of hydrops within 2 weeks.