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  1. Definition. Human parvovirus B19 (PB19) is a small single-stranded, nonenveloped DNA virus.

  2. Incidence. An infection with PB19 is common worldwide. Infection occurs mostly among school-aged children where the major manifestation is erythema infectiosum (fifth disease). The prevalence of immunoglobulin G (IgG) antibodies directed against PB19 ranges from 15–60% in children 6–19 years old. About 35–45% of women of childbearing age do not possess protective IgG antibodies against PB19 and therefore are susceptible to primary infection. Annual seroconversion rates in pregnant women in the United States range from 1–1.5%.

  3. Pathophysiology. The only known natural host cell of PB19 is the human erythroid progenitor cells. PB19 is a potent inhibitor of hematopoiesis. The cellular receptor for PB19 is globoside or P-antigen, which is found on erythrocyte progenitor cells, synovium, placental tissue, fetal myocardium, and endothelial cells. Infection with PB19 is usually acquired through respiratory droplets, but the virus can also be transmitted by blood or blood products and vertically from mother to fetus. In children and adults, viremia develops 2 days after exposure and reaches its peak at ~1 week. During the phase of viral replication and shedding, the patient is generally asymptomatic. When the characteristic rash (also known as erythema infectiosum) or arthralgias develop, the patient is no longer infectious to others. Symptoms during pregnancy are nonspecific and include a flulike syndrome with a low-grade fever, sore throat, generalized malaise, and headache. The fetus may become infected during the maternal viremic stage. Because of active erythropoiesis in the fetus with a shortened red cell life span, marked fetal anemia, high-output cardiac failure, and fetal hydrops may develop. Myocarditis may be a contributing factor to fetal cardiac failure. PB19 is nonteratogenic with no congenital malformations syndromes attributed to this infection.

  4. Risk factors. For the pregnant woman, the risk of acquiring PB19 infection is highest in those who have school-aged children at home.

  5. Clinical presentation

      1. During pregnancy the mother may report a history of exposure to a child with erythema infectiosum. More commonly, the mother does not recall such exposure and the diagnosis is made based on ultrasound findings. Fortunately, most maternal infections are associated with normal pregnancy outcomes. The risk of adverse outcomes after primary infection is probably <5% despite transplacental transmission rate of 33–50%. Adverse outcomes include the following:

          1. Fetal death. Infection in the first trimester may result in fetal loss or miscarriage. Cases of fetal death due to PB19 infection have been described mostly between 20 and 24 weeks' gestation. Fetuses that die in the third trimester (stillborn) are usually nonhydropic.

          1. Nonimmune hydrops fetalis. The observed risk of PB19-induced hydrops fetalis is 3.9% after maternal infection throughout pregnancy, with a maximum of 7.1% when infection occurred between 13 and 20 weeks' gestation.

      1. Neonatal period. The newborn infant may present with anemia, especially if maternal infection occurred in the third trimester. Few cases of encephalopathy, meningitis, and severe central nervous system abnormalities following intrauterine PB19 infection have been reported.

  6. Diagnosis

      1. Laboratory studies

          1. Serologic tests. PB19 IgG and IgM antibodies are first ordered when PB19 infection is suspected. PB19-specific IgM ...

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