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Parvovirus B19 infection can be fatal to a fetus if maternal exposure is not diagnosed and treated during pregnancy. An algorithm tells how.
Parvovirus B19 infection, usually less serious in children and healthy adults, can be fatal to a fetus. The infection, caused by a single-stranded DNA virus, can also lead to other serious fetal complications during pregnancy, such as anemia and hydrops. Fortunately, in utero diagnosis and treatment of fetal infection can prevent complications from the virus, and if a fetus is anemic, in utero blood transfusion can be lifesaving.
But what's the first diagnostic step you should take when you suspect B19 infection in your pregnant patient?
Infections from parvovirus B19, first identified in 1975, can occur worldwide and often occur in childhood.1 The prevalence of parvovirus B19-specific IgG is 2% to 15% in children ages 1 to 5, and 30% to 60% in adults. The infection peaks in late winter and early spring, and epidemics occur every 4 years (the last epidemic reported was in 2001). Among reproductive-aged women, the seroconversion rate is 1.5% per year. Parvovirus B19 infection affects 1% to 5% of pregnant women, with seroconversion rates as high as 20% during epidemics. You cannot acquire parvovirus B19 infection through casual contact; it's transmitted through respiratory droplets and by blood products, especially pooled factor XIII and IX.2,3
Parvovirus B19 is a potent inhibitor of hematopoiesis by direct cytotoxic effects on erythroprogenitor cells. The cellular receptor for parvovirus B19 is globoside (P antigen), which is found on erythroprogenitor cells, endothelial cells, fetal myocardium, and placental cells.4,5 The presence of globoside on the surface of erythrocyte precursors, placenta, and fetal myocardium is consistent with the clinical effects of parvovirus B19 infection.6
Clinical infection in fetuses, children, and adults
The most common clinical manifestation of parvovirus B19 infection in children is erythema infectiosum (fifth disease), which produces a characteristic facial rash. After infection, a prodromal period of up to 2 weeks occurs, which is often asymptomatic but can be associated with upper respiratory or gastrointestinal symptoms; this coincides with virus excretion from the respiratory tract. You can expect parvovirus B19-specific IgM levels to rise 7 to 10 days after infection, and antibody levels peak when the viral load reaches its peak at roughly 10 to 14 days. IgM can persist for up to 3 months after the primary infection.3
A second phase of clinical symptoms, which occurs 17 to 18 days after primary infection, involves rash, itching, or arthropathy. Believed to be due to immune complex deposition, the rash is usually characterized by "slapped cheeks" (red cheeks with circumoral pallor), but can also extend to the trunk and limbs and may include vesicles. Parvovirus B19-specific IgG rises slowly, reaches a plateau 4 weeks after infection, and persists for life. The period of infectivity (when the virus is present in and excreted from the respiratory tract) occurs 2 to 3 weeks before the onset of clinical symptoms.