Parvovirus B19 Infection Workup

  • Author: David J Cennimo, MD, FACP, FAAP, AAHIVS; Chief Editor: Russell W Steele, MD   more...
 
Updated: Mar 30, 2012
 

Laboratory Studies

Most patients with parvovirus B19 (B19V) infection do not require laboratory studies because symptoms are mild and the illness resolves over 5-7 days.

  • Parvovirus serology (anti–parvovirus B19 immunoglobulin M [IgM] and immunoglobulin G [IgG] antibodies) can be determined using enzyme-linked immunoassay (ELISA), radioimmunoassay, or immunofluorescence. Results of IgM testing are particularly difficult to interpret. Standardization between laboratories is lacking. Even in a single laboratory, sensitivity and specificity are partly determined by operator skills. High-level viremia in acutely infected persons may cause virus-antibody complexes, which will result in a false-negative IgM test result.[30] In this setting, polymerase chain reaction (PCR) may be a better diagnostic modality.
  • PCR testing for parvovirus B19 is routinely available with increased sensitivity level. However, contamination and false-positive results are noted risks that lead to confusing interpretation. Low levels of B19 DNA may detectable for more than 4 months in serum after acute infection and for years in other tissues.[31, 32] . This test, a more useful clinical tool to diagnose chronic infection, detects viral DNA present in the blood or other tissues/fluids.[20] The interpretation, especially as it pertains to pregnant women is uncertain.[19, 23] The diagnosis of acute or chronic infection should be made on the basis of standard DNA hybridization or quantitative (real-time) PCR in combination with serologic assays for B19-specific IgG, IgM, or both.[8]
  • During experimental infection of volunteers, IgM antibodies were detected 10-12 days after inoculation, and IgG antibodies were detected at 2 weeks.[33] Ninety percent of patients with classic erythema infectiosum rash had IgM antibodies detected at initial presentation and IgG antibodies by day 7.[9] IgM remains detectable for months and IgG for life.[9, 8]
  • In patients with evidence of clinically significant anemia or transient aplastic crisis (TAC), obtain a CBC count with reticulocyte count.
    • Patients infected with parvovirus B19 have a low reticulocyte count (0-1%).
    • In an aplastic crisis, hemoglobin levels drop below the patient's baseline by at least 2 g/dL.
    • IgM antibodies are usually present by day 3 of illness or the time of hematopoietic nadir. IgG antibodies are detectable around the time of the recovery of erythrogenesis.[8, 9, 24, 18]
    • Parvovirus B19 PCR demonstrates high level viremia during TAC.[8]
  • Immunodeficient patients with chronic B19V infection and pure red cell anemia (PRAC) also have signs of anemia. In contrast to TAC, PRAC is characterized by very low or absent antibody levels. PCR is the diagnostic test of choice to demonstrate viremia.[5, 8]
  • If a pregnant woman is exposed to parvovirus B19, obtain IgG and IgM serology as soon as possible.[23, 20]
    • Positive IgG results and negative IgM results indicate past infection (no risk to fetus).
    • Positive IgG and IgM results indicate infection within the last 7-120 days (possible risk to fetus).
    • Negative IgG results and positive IgM results indicate acute infection (higher risk to fetus).
    • Negative IgG and IgM results indicate that the mother is not immune and that no evidence of acute infection is noted. In this case, repeat the tests in 3 weeks. Subsequent development of IgM indicates an acute infection.
    • No standards have been established to evaluate parvovirus B19 PCR on maternal blood; low levels may be detected long after clinical infection.[32] PCR may be performed on fetal serum of amniotic fluid to detect virus.[19]
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Imaging Studies

Routine imaging is not necessary.

Fetal ultrasonography may be useful in detecting hydrops. The timing and frequency of ultrasonography surveillance for infected pregnant women have not been conclusively determined.[20]

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Contributor Information and Disclosures
Author

David J Cennimo, MD, FACP, FAAP, AAHIVS  Assistant Professor of Medicine and Pediatrics, Adult and Pediatric Infectious Diseases, Co-Director Physician's Core, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

David J Cennimo, MD, FACP, FAAP, AAHIVS is a member of the following medical societies: American Academy of HIV Medicine, American Academy of Pediatrics, American College of Physicians, American Medical Association, HIV Medicine Association of America, Infectious Diseases Society of America, Medical Society of New Jersey, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Coauthor(s)

Arry Dieudonne, MD  Associate Professor of Pediatrics, Division of Pulmonology, Allergy, Immunology and Infectious Diseases, University of Medicine and Dentistry of New Jersey-New Jersey Medical School; Clinical Director, Francois-Xavier Bagnold Center for Children, University Hospital

Arry Dieudonne, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Glenn Fennelly, MD, MPH  Director, Division of Infectious Diseases, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center; Clinical Associate Professor of Pediatrics, Albert Einstein College of Medicine

Glenn Fennelly, MD, MPH is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Joseph Domachowske, MD  Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthor Dennis Cunningham, MD, to the original writing and development of this article.

References

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Note the right side of this boy's face displaying signs of erythema infectiosum, or Fifth disease. Image courtesy of CDC
Elementary school child with Fifth Disease. Image courtesy of CDC.
 
 
 
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