Parvovirus B19 causes prolonged epidemics of erythema infectiosum. Infection causes clinically significant anemia in individuals with high red cell turnover, including the fetus. Transmission can occur via the respiratory route, hand-tomouth contact, blood products, and vertically from mother to the fetus. The virus replicates in rapidly proliferating cells, such as erythroblast precursors. In healthy hosts, the virus can cause a range of clinical manifestations, including erythema infectiosum (ie, fifth disease), transient aplastic crisis, chronic red cell aplasia, myocarditis, arthropathy, and nonimmune hydrops fetalis. Approximately 40% women of childbearing age are susceptible, and annual seroconversion rates vary from 1.5% during endemic periods to 10-15% during epidemics. Infection occurs in around 50% of susceptible women exposed at home and 20-30% following occupational exposure (for example, at a primary school). Maternal infection in the first half of pregnancy is associated with a 10% excess fetal loss and hydrops fetalis in 3% of cases (of which up to 60% resolve spontaneously or with appropriate management). No congenital abnormalities or long-term sequelae have been attributed to parvovirus B19 infection. The overall risk of serious adverse outcome of occupational exposure to parvovirus B19 infection during pregnancy is low (excess early fetal loss in 2-6/1,000 pregnancies and fetal death from hydrops in 2-5/10,000 pregnancies). It is not recommended that, susceptible pregnant women be excluded routinely from working with children during epidemics.