Fifth Disease or Erythema Infectiosum 

  • Author: Kenneth T Kwon, MD; Chief Editor: Richard G Bachur, MD   more...
 
Updated: Apr 18, 2012
 

Background

Erythema infectiosum is usually a benign childhood condition characterized by a classic slapped-cheek and lacy exanthem. It is an infection caused by human parvovirus (HPV) B19. Human parvovirus B19 also is associated with other hematologic, rheumatologic, and neurologic conditions, including polyarthropathy, aplastic anemia, and hydrops fetalis.

Classic slapped-cheek appearance of fifth disease.Classic slapped-cheek appearance of fifth disease.
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Pathophysiology

Human parvovirus B19, a member of the family Parvoviridae, is a heat-stable, single-stranded DNA virus. Human parvovirus B19 was accidentally discovered in 1975.[1] It is the only parvovirus known to cause disease in humans. Transmission occurs through respiratory secretions, possibly through fomites, and parenterally via vertical transmission from mother to fetus and by transfusion of blood or blood products.

Anderson et al described the pathophysiology of the virus by studying human volunteers who had been inoculated with the virus.[2]

The incubation period is usually 7-10 days, but it can be 4-21 days. The mechanism producing the dermatologic and rheumatologic features is unknown but thought to represent antigen-antibody (Ag-Ab) complexes in the skin and joints.

Arthropathy is observed most commonly in adult women and occurs in fewer than 10% of children. It is a symmetric polyarthritis, usually involving finger joints. The onset of joint symptoms occurs 2-3 weeks after exposure.

The association of human parvovirus B19 and aplastic anemia is thought to be due to the affinity and cytotoxicity of the virus for erythroid progenitor cells. This complication is primarily observed in patients with underlying hemolytic anemias (eg, sickle cell disease, thalassemia) or immunodeficiency states (eg, leukemia, HIV). These disease states depend on high red-cell production, due to shortened cell life span. The hematocrit of these patients may drop as much as 10-15% per day during acute infection. Most patients have a human parvovirus B19 aplastic crisis only once, and a rash following aplastic crisis is rare.

Previously healthy patients also develop transient (and usually clinically insignificant) bone marrow suppression and reticulocytopenia. In rare cases, mild lymphopenia, neutropenia, and thrombocytopenia also may occur.

Fetal transmission may result in severe anemia with resultant congestive heart failure and fetal hydrops. This occurs in fewer than 10% of primary maternal infections. Recent studies report 1-9% risk of fetal death in pregnant women exposed to active human parvovirus infection, with greater risk of fetal loss in early pregnancy. Approximately one half of women of childbearing age are seropositive; therefore, they are immune and are of no risk to the fetus. No evidence suggests specific congenital malformations due to in-utero exposure to human parvovirus B19.

An association between human parvovirus B19 infection and encephalitis, neuropathies, myocarditis, nephritis, systemic lupus erythematosus (SLE), Henoch-Schönlein purpura (HSP), and rheumatoid arthritis has been described. Many of these associations have not been validated.

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Epidemiology

Frequency

United States

Sporadic cases occur, but outbreaks are more common. Up to 60% of the population is seropositive for anti-HPV B19 immunoglobulin G (IgG) by age 20 years. The incidence peaks in winter and early spring.[3] Human parvovirus B19 epidemics appear to occur in cyclical fashion every 4-7 years and are estimated to affect 30-50% of US households. Community epidemics usually last 3-6 months. Subclinical infections are common.

International

The disease occurs worldwide, especially in temperate climates. Anti-parvovirus IgG is found equally among Americans, Asians, and Europeans.[4]

Mortality/Morbidity

Arthropathy is observed in fewer than 10% of children with fifth disease. Incidence of human parvovirus B19-induced aplastic crisis in patients with chronic hemolytic anemia is 2-5% per year. Very rarely, children may develop elevated liver transaminases or self-limited hepatitis.[4]

Sex

Females are affected slightly more often than males.

Age

Approximately 70% of total cases occur in children aged 5-15 years. Infants and adults are affected infrequently.

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Contributor Information and Disclosures
Author

Kenneth T Kwon, MD  Director of Pediatric Emergency Medicine, Associate Clinical Professor, Department of Emergency Medicine, University of California at Irvine Medical Center, Co-Director, Pediatric Emergency Services, Mission Regional Medical Center/Children's Hospital of Orange County at Mission

Kenneth T Kwon, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Megan Boysen, MD  Resident Physician, Department of Emergency Medicine, University of California Irvine Medical Center

Megan Boysen, MD, is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Debra Slapper, MD  Consulting Staff, Department of Emergency Medicine, St Anthony's Hospital

Debra Slapper, MD is a member of the following medical societies: American Academy of Emergency Medicine

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.

Wayne Wolfram, MD, MPH  Associate Professor, Department of Emergency Medicine, Mercy St Vincent Medical Center

Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Richard G Bachur, MD  Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston

Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research

Disclosure: Nothing to disclose.

References
  1. Cossart YE, Field AM, Cant B, Widdows D. Parvovirus-like particles in human sera. Lancet. Jan 11 1975;1(7898):72-3. [Medline].

  2. Anderson MJ, Higgins PG, Davis LR, Willman JS, Jones SE, Kidd IM. Experimental parvoviral infection in humans. J Infect Dis. Aug 1985;152(2):257-65. [Medline].

  3. American Academy of Pediatrics. Red Book: 2006 Report on the Committee of Infectious Diseases. 2006:484-487.

  4. Young NS, Brown KE. Parvovirus B19. N Engl J Med. Feb 5 2004;350(6):586-97. [Medline].

  5. Servey JT, Reamy BV, Hodge J. Clinical presentations of parvovirus B19 infection. Am Fam Physician. Feb 1 2007;75(3):373-6. [Medline].

  6. B-19 Parvovirus Vaccine Study. ClinicalTrials.gov. Available at http://clinicaltrials.gov/ct2/show/results/NCT00379938. Accessed 05/23/2010.

  7. Anderson LJ. Human parvovirus. In: Richman DD, Whitley RJ, Hayden FG, eds. Clinical Virology. New York: Churchill Livingston Inc; 1997:613-31.

  8. Cherry JD. Parvoviruses. In: Feigin RD, Cherry JD, eds. Textbook of Pediatric Infectious Diseases. Philadelphia: WB Saunders Co; 1992:1626-33.

  9. Cohen B. Parvovirus B19: an expanding spectrum of disease. BMJ. Dec 9 1995;311(7019):1549-52. [Medline].

  10. Feder HM Jr, Anderson I. Fifth disease. A brief review of infections in childhood, in adulthood, and pregnancy. Arch Intern Med. Oct 1989;149(10):2176-8. [Medline].

  11. Hall CJ. Parvovirus B19 infection in pregnancy. Arch Dis Child Fetal Neonatal Ed. Jul 1994;71(1):F4-5. [Medline].

  12. Hammond GW. Parvovirus. In: Long SS, Pickering LK, Prober CG, eds. Principles and Practice of Pediatric Infectious Diseases. New York: Churchill Livingston Inc; 1997:1205-9.

  13. Heegaard ED, Hornsleth A. Parvovirus: the expanding spectrum of disease. Acta Paediatr. Feb 1995;84(2):109-17. [Medline].

  14. Jones MF, Wold AD, Espy MJ, Smith TF. Serologic diagnosis of parvovirus B19 infections. Mayo Clin Proc. Nov 1993;68(11):1107-8. [Medline].

  15. Keeler ML. Human parvovirus B-19: not just a pediatric problem. J Emerg Med. Jan-Feb 1992;10(1):39-44. [Medline].

  16. Kirchner JT. Erythema infectiosum and other parvovirus B19 infections. Am Fam Physician. Aug 1994;50(2):335-41. [Medline].

  17. Qari M, Qadri SM. Parvovirus B19 infection. Associated diseases, common and uncommon. Postgrad Med. Jul 1996;100(1):239-43, 246, 252. [Medline].

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Classic slapped-cheek appearance of fifth disease.
Pathognomonic reticulated lacy-appearing eruption of fifth disease.
 
 
 
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