Parvovirus B19 Infection

Parvovirus B19 Infection is a topic covered in the 5-Minute Clinical Consult.

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  • Human parvovirus B19 is the primary cause of acute erythema infectiosum (EI, or fifth disease).
  • Individuals with increased RBC turnover (e.g., sickle cell anemia [SS]) are more susceptible to transient aplastic crisis (TAC). In immunocompromised individuals, pure red cell aplasia (PRCA) and chronic anemia are significant complications. In normal hosts, arthritis and arthralgias are common complications.
  • System(s) affected: hematologic/lymphatic/immunologic, musculoskeletal, skin/exocrine, possibly central nervous system (CNS), cardiac, renal

Pregnancy Considerations
A documented acute infection during pregnancy should prompt referral to a maternal–fetal medicine specialist. Maternal parvovirus B19 infection between 9 and 20 weeks’ gestation has the highest fetal risk.


  • Parvovirus infection is common in childhood.
  • EI has an extremely low mortality rate.
  • Peak age for EI is 4 to 12 years.
  • Males and females are equally affected.
  • Women more likely to develop postinfectious arthritis
  • No known racial predilection
  • In temperate climates, infections often occur from late winter to early summer.
  • Local outbreaks may occur every 2 to 4 years.


Extremely common in the United States. Based on IgG serology:

  • 1 to 5 years of age: 2–15% seropositive
  • 6 to 15 years of age: 20–40% seropositive
  • 16 to 40 years of age: 50–60% seropositive
  • >40 years of age: 70–85% seropositive

Etiology and Pathophysiology

  • Small (20 to 25 mm), nonenveloped, single-stranded DNA virus in Parvoviridae family
    • Only known parvovirus to infect humans
  • Natural host of B19 is human erythroid progenitor.
  • Respiratory, hematogenous, and vertical transmission are sources of human spread.
  • 4- to 14-day incubation. Rash and joint symptoms occur 2 to 3 weeks after initial infection.
  • Most contagious 5 to 10 days after exposure
  • EI rash thought to be autoimmune due to IgM complexes concurrent with viral clearance
  • Cytotoxic infection of proerythroblasts reduces RBC production.

Erythrocyte P antigen–negative individuals are resistant to infection.

Risk Factors

  • School-related epidemic and nonimmune household contacts have a secondary attack rate of 20–50%.
  • Highest secondary attack rates are for daycare providers and school personnel in contact with affected children.
  • Increased cell turnover (e.g., hemoglobinopathy, SS, thalassemia) increases risk for TAC.
  • Immunodeficiency (e.g., HIV, congenital) increases risk of PRAC and chronic anemia.
  • As many as 40% of pregnant women are not immune; 1.5% seroconversion rate per year

General Prevention

  • Respiratory spread; hand washing and barrier precautions
  • Droplet precautions are recommended around patients with TAC, chronic infection, or anemia.
  • Difficult to eliminate exposure because the period of maximal contagion occurs prior to the onset of clinical symptoms (rash)
  • Pregnant health care workers should not care for patients with TAC.
  • No significant risk of infection based on occupational exposure. Exclusion from the workplace is neither necessary nor recommended.
  • No preventive vaccine is available.

Commonly Associated Conditions

  • Nondegenerative arthritis
    • In adults, 80% of patients may manifest polyarthritis and/or arthralgia (female > male).
    • In children, joint symptoms are less common.
    • Knees, hands, wrists, and ankles (frequently symmetric) are most commonly involved.
    • Joint symptoms usually subside within 3 weeks but may persist for months. Routine radiography is not necessary.
  • TAC
    • Involves patients with increased RBC turnover (SS, spherocytosis, thalassemia) or decreased RBC production (iron deficiency anemia)
    • Presents with fatigue, weakness, lethargy, and pallor (anemia)
    • Aplastic event may be life-threatening but is typically self-limited. Reticulocytes typically reappear in 7 to 10 days with full recovery in 2 to 3 weeks.
    • In children with sickle cell hemoglobinopathies and heredity spherocytosis, fever is the most common symptom (73%); rash uncommon in these patients
  • Chronic anemia
    • Seen in immunocompromised individuals (HIV, cancer, transplant) with poor IgM response
    • Usually no clinical manifestations (fever, rash, or joint symptoms)
  • Fetal/neonatal infection (1)
    • Risk of transplacental spread of virus is ~33% in infected mothers.
    • Test pregnant women with a rash or arthralgias consistent with parvovirus B19.
    • Clinical manifestations vary. Many patients seroconvert without symptoms and have a normal pregnancy. Other patients develop variable degrees of fetal hydrops. 2nd- and 3rd-trimester pregnancy loss can occur without hydrops.
    • Suspect B19 infection in cases of nonimmune fetal hydrops.
    • Fetal bone marrow is primarily impacted. RBC survival is shortened resulting in anemia and (potentially) high-output cardiac failure.
    • >95% of fetal complications (fetal hydrops and death) occur within 12 weeks of acute maternal parvovirus B19 infection.
    • Risk of fetal loss is highest (2–5%) in the 1st trimester.
    • Infants requiring intrauterine transfusions due to parvovirus B19 infection are at risk for long-term neurodevelopmental impairment.
  • Papular purpuric gloves and socks syndrome (PPGSS) is an uncommon dermatosis associated with parvovirus B19 infection. It results in a petechial and ecchymotic rash of the hands and feet associated with febrile tonsillopharyngitis and oral ulcerations (2).

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