The parvovirus family includes many viruses that infect a variety of animal species. In humans, parvovirus B19 has the most clinical significance. It can cause a number of different disease states (see accompanying table), which Young and Brown detail in their review article.

Infection with parvovirus B19 is common across the globe. By 15 years of age, about one half of adolescents have detectable antibodies against the virus. Infection is spread by respiratory droplets and occurs most commonly in springtime. Parvoviruses are resistant to heat or solvent solutions.

The majority of children infected with parvovirus B19 are asymptomatic, but when detectable disease occurs, the presentation is known as erythema infectiosum or fifth disease. Fever and typical viral symptoms are followed about two weeks later by the characteristic “slapped cheek” rash. This rash may wax and wane, with exacerbations caused by sunlight exposure, heat, and exercise.

When parvovirus B19 infection occurs in adults, it is more symptomatic. An inflammatory arthritis occurs in about 50 percent of older persons who become infected. This arthropathy typically presents with symmetric involvement of the hands and, occasionally, the wrists, knees, and ankles. Rheumatoid factor testing during infection may be positive, but the arthritis caused by parvovirus B19 resolves over several weeks and does not cause joint destruction.

Patients with sickle cell or other hemolytic anemias have an increased demand for erythrocyte production. Parvovirus B19 infection suppresses red cell production and may lead to transient aplastic anemia in these patients. While the aplastic crisis is self-limited, the authors note that the severe anemia precipitated by parvovirus infection may be fatal without appropriate transfusion support. In addition to the severe anemia, aplastic crises also may lead to decreased white cell or platelet counts.

Immunocompromised persons (e.g., those with human immunodeficiency virus [HIV] infection) may not produce enough neutralizing antibodies to combat parvovirus B19 infection and may suffer from a prolonged, severe anemia. Fetal parvovirus infection also may lead to severe sequelae. Population-based studies indicate that about one half of pregnant women do not have protective antibodies from prior infection. If infection is acquired during pregnancy, the risk of transplacental spread to the fetus is estimated at about 30 percent, with a 5 to 9 percent risk of fetal loss.

Diagnosis of acute parvovirus B19 infection may be confirmed by elevated IgM antibody titers. IgG titers, on the other hand, vary widely after infection. According to the authors, chronic infection is diagnosed best by testing for the presence of parvovirus DNA and should not be inferred solely by the lack of virus-specific IgG antibodies.

Treatment usually is not necessary, because most infections are self-limited. Removing immunosuppressive therapy or starting highly active antiretroviral therapy in HIV-infected patients may be helpful when immunocompromise has led to chronic infection. Immune globulins that act against parvovirus are available and may be helpful in treating persistent infection. Effective vaccines exist for a number of animal parvoviruses. The authors note that lack of commercial interest, not efficacy or safety issues, has limited the development of a human vaccine for parvovirus B19.