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Pediatrics, Roseola Infantum

Author: Lisa S Lewis, MD, Consulting Staff, Division of Emergency Medicine, Children's Hospital Medical Center of Cincinnati
Contributor Information and Disclosures

Updated: Jul 14, 2009

Introduction

Background

Roseola infantum is the sixth of the traditional exanthems of childhood. The condition is an acute benign disease of childhood characterized by a history of a prodromal febrile illness lasting approximately 3 days, followed by defervescence and the appearance of a faint pink maculopapular rash.

Since identification of the etiologic agent human herpesvirus type 6 (HHV-6), infection has been documented without the characteristic fever or rash. The virus may present as an acute febrile illness associated with respiratory or gastrointestinal symptomatology. In one prospective cohort, 93% of newly acquired infections were symptomatic, with fever, fussiness, diarrhea, and rash as the most distinguishing features.1

Newly recognized clinical manifestations of HHV-6 infection include hepatitis, encephalitis, myocarditis, hemophagocytic syndrome, and an adult mononucleosislike illness. The full spectrum of clinical manifestations of HHV-6 has not been elucidated.

Pathophysiology

Respiratory secretions of asymptomatic individuals probably transmit the virus. The child is most likely to spread the infection during the febrile and viremic phase of the illness.

Cell-associated viremia has been noted, usually on the third day of illness and immediately before rash appearance. By the eighth day of illness, antibody activity peaks and results in resolution of the viremia.

Children with the cell-free virus also have been noted. This likely represents a greater magnitude of viral dissemination because these children have more severe clinical manifestations.

Frequency

United States

Approximately 12-30% of children have clinical manifestations consistent with roseola. Eighty-six percent of children have acquired HHV-6 antibodies by age 1 year. By age 4 years, almost all children are seropositive. Roseola appears to peak in spring and fall.

International

A relationship seems to exist among prevalence, geographic location, and ethnicity. The prevalence of roseola is 92% in Ecuador, 60% in Japan, 20% in Morocco, and 49-76% in Malaysia. The disease is more prevalent among younger infants in Japan than in the United States or Europe.

Mortality/Morbidity

  • Roseola is usually a self-limited illness with no sequelae.
  • The major morbidity associated with roseola is seizures (6-15%) during the febrile phase of the illness.
  • Encephalitis, fulminant hepatitis, hemophagocytic syndrome, and disseminated infection with HHV-6 are extremely rare manifestations.

Sex

No predilection for roseola infantum exists.

Age

Most cases present within the first 2 years of life, with peak occurrence in infants aged 9-21 months.

Clinical

History

  • Roseola is typically characterized by a history of high fever followed by rapid defervescence and a characteristic rash.
  • Fever (often up to 40°C)
  • Rash (fades within a few hours to 2 d)
    • Maculopapular or erythematous
    • Typically beginning on the trunk and may spread to involve the neck and extremities
    • Nonpruritic
    • Blanches on pressure
  • Seizures (6-15%)
  • Diarrhea (68%)
  • Prodromal symptoms (14%)
    • Listlessness
    • Irritability
  • Cough (50%)

Physical

  • Alert, nontoxic appearance
  • Fever (98%)
  • Rash (98%)
    • Rose pink macules or maculopapules approximately 2-5 mm in diameter are present.
    • Lesions are characteristically discrete, rarely coalesce, and fade with blanching of the skin surface.
    • Typically, roseola infantum involves the trunk or back with minimal facial or proximal extremity involvement.
    • Some lesions may be surrounded by a halo of pale skin.
    • The rash typically evolves over 12 hours with a duration of 1-2 days.2
  • Bulging anterior fontanel (26%)
  • Nagayama spots (erythematous papules on the soft palate and uvula) (65%)
  • Periorbital edema, most common in the preexanthematous stage (30%); palpebral edema also common
  • Cervical, postauricular, and postoccipital lymphadenopathy (31%)
  • Splenomegaly
  • Encephalopathy
  • Conjunctival erythema

Causes

  • HHV-6 was identified as the etiologic agent in 1988.
    • This large, double-stranded deoxyribonucleic acid (DNA) virus is a member of the Herpesviridae family.
    • Two major strains, variants A and B, of this virus exist. HHV-6A appears to be more cytolytic and potentially more virulent. Strain B is responsible for most of the exanthem subitum infections in children.
    • The incubation period is approximately 9 days (range, 5-15 d).
  • HHV-6B is not believed to be the only causative agent of exanthem subitum. Primary infection with human herpesvirus type 7 (HHV-7) has also been implicated in exanthem subitum, but it is typically asymptomatic.
  • Transmission is likely horizontal via person-to-person oral secretions. Adult family members or older siblings appear to be the infective source. The virus has been found in the saliva of healthy adults.

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References

References

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  2. Stoeckle M. The spectrum of human herpesvirus 6 infection: from roseola infantum to adult disease. Annu Rev Med. 2000;51:423-430. [Medline].

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Further Reading

Keywords

roseola infantum, childhood exanthem, roseola, prodromal febrile illness, maculopapular rash, pink maculopapular rash, human herpesvirus type 6, HHV-6, hepatitis, encephalitis, hemophagocytic syndrome, mononucleosis-like illness, fulminant hepatitis, adult mononucleosislike illness, cell-associated viremia

febrile seizure, erythematous rash, bulging anterior fontanel, Nagayama spots, HHV-A, HHV6-B, palpebral edema, Herpesviridae, human herpesvirus type 7, HHV7, exanthem subitum, immunoglobulin M serology, IgM serology, HHV-6-specific immunoglobulin G, HHV-6-specific IgG

Contributor Information and Disclosures

Author

Lisa S Lewis, MD, Consulting Staff, Division of Emergency Medicine, Children's Hospital Medical Center of Cincinnati
Lisa S Lewis, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Garry Wilkes, MBBS, FACEM, Director of Emergency Medicine, Bunbury Hospital, Western Australia; Medical Director, St John Ambulance, WA Ambulance Service; Adjunct Associate Professor, Edith Cowan University; Clinical Associate Professor, Rural Clinical School, University of Western Australia, Australia.
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center
Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

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.

 
 
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