Parvovirus B19

A single-stranded DNA virus belonging to the family Parvoviridae; the cause of erythema infectiosum (fifth disease) and aplastic crises.P. (B19V) was first isolated in 1975 from a specimen of healthy donor blood. In 1983 it was linked to erythema infectiosum, also called fifth disease, a generally benign febrile exanthem of children. B19V infection occurs worldwide and can attack persons of any age. It is most often contracted in childhood; 30–60% of adults have protective IgG antibody to the virus. Infection is asymptomatic in 20–50% of persons who acquire it. Transmission is usually by respiratory secretions. The virus replicates in bone marrow. Classical erythema infectiosum typically occurs in children 4–15 years of age. Sporadic outbreaks are common, and the peak incidence is during the winter and spring. After an incubation period of 4–14 days, the child develops prodromal symptoms, usually mild, consisting of headache, fever, chills, joint pains, and malaise. About 1 week later, a bright red “slapped cheek” rash appears on the face, and over the next 3–4 days the rash spreads to the rest of the body (proximal extremities, then trunk and distal extremities, including palms and soles), where it has a reticular or maculopapular appearance. Itching, if any, is slight. The rash is an immune response, heralding the appearance of IgM antibody and the end of the period of communicability. The disease typically runs a benign course, and treatment is purely symptomatic. (Like certain other viruses, B19V also occasionally causes a benign exanthem known as papular-purpuric gloves-and-socks syndrome.) Infection in adults follows a different pattern : the “slapped cheek” appearance does not occur, and the rash on the trunk and limbs tends to be milder and more subtle, but 15–20% of adult patients, virtually all of them women, develop significant joint involvement. Deposition of immune complexes in joint membranes leads to sudden onset of symmetric polyarthritis, affecting particularly the metacarpophalangeal and proximal interphalangeal joints, the wrists, and the knees. Swelling may or may not occur. Pain and disability can be severe, and symptoms can persist for weeks or months, although eventual spontaneous resolution is the rule. Because B19V infects the bone marrow, most patients experience a transient decline in red blood cells, white blood cells, and platelets. Generally this is of no consequence, but occasionally it progresses to a transient aplastic crisis (TAC), in which red blood cell production virtually stops and the red blood cell count falls rapidly. The risk of this complication is much greater in sickle cell anemia, autoimmune hemolytic anemias, immunodeficiency, and pregnancy. With the formation of IgG antibody by the immune system, red blood cell formation resumes and the anemia resolves. In patients with congenital or acquired immune deficiency, however, failure to form antibody can lead to prolonged anemia. Infection in a pregnant woman has about 1 chance in 3 of being passed to the fetus and inducing a fetal aplastic crisis. This in turn can result in congestive heart failure and fetal hydrops. Spontaneous recovery is typical, but fetal death occurs in as many as 10% of cases. Fetal infection with B19V apparently does not cause congenital anomalies. Acute B19V infection can be confirmed by a rapid rise and fall of IgM antibody. Diagnosis can also be established by culturing the virus from bone marrow or by ELISA detection of the antigen in serum. The treatment of all forms of B19V infection is purely symptomatic and supportive, since specific antiviral therapy is not available. Hospitalized patients with B19V are isolated, and pregnant workers are advised to avoid contact with them. Severe anemia may require blood transfusions. When prolonged anemia results from inability to form IgM antibody, intravenous immune globulin may help.