Roseola Infantum Clinical Presentation

  • Author: Stephen W White, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jan 26, 2012
 

History

  • The classic roseola infantum patient is a 9- to 12-month-old infant in previously good health and who has an abrupt onset of high fever (40°C), which lasts for 3 days with nonspecific complaints. A febrile seizure occurs in 15% of patients. Rapid defervescence is striking with the onset of a mild, pink, morbilliform exanthem.
  • In roseola infantum patients who are immunocompromised, the onset of symptoms is usually abrupt, with fever, malaise, and CNS and other organ system involvement.
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Physical

  • Despite the high fever, few clinical findings are observed early in the course of roseola infantum. The lack of upper respiratory tract infection is notable, and meningeal signs and encephalopathy are not present. Gastrointestinal symptoms, signs of electrolyte imbalance, or evidence of dehydration are rarely present.
  • A febrile seizure, with no residual findings, may have occurred.
  • After an abrupt loss of fever, the characteristic rash appears.
    • The eruption is generalized and subtle.
    • It is composed of either discrete, small, pale pink papules or a blanchable, maculopapular exanthem that is 1-5 mm in diameter. This rash may last 2 days.
  • The characteristic enanthem (Nagayama spots) consists of erythematous papules on the mucosa of the soft palate and the base of the uvula. The enanthem may be present on the fourth day in two thirds of patients with roseola.
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Causes

  • The causative agent of roseola infantum was discovered in 1986. The Roseolovirus genus of the beta herpes virus hominis subfamily contains human herpesvirus (HHV)–6 and HHV-7. HHV-6 has 2 variants: HHV-6A and HHV-6B. Their major differences are cellular tropism. Debate has existed whether they represent 2 species.
    • HHV-6A infection is rarely associated with roseola infantum. HHV-6A is associated with infection in adults who are immunocompromised. HHV-6A infection occurs later in life, and details are lacking.
    • HHV-6B is the cause of roseola in infants. Because seropositivity is nearly 100% in older children, most primary infections with HHV-6B are asymptomatic.
    • HHV-7 has been identified in a few cases of roseola infantum.
  • Recurrences of roseola infantum are not common. A well-documented case of a 13-month-old child who had a second episode of roseola exists. In the acute phase of the second episode, HHV-7 was identified and excreted in the saliva. This was followed by excretion of HHV-6.
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Contributor Information and Disclosures
Author

Stephen W White, MD  Clinical Assistant Professor, Department of Dermatology, George Washington University Hospital; Chief, Sub-section of Dermatology, Suburban Hospital

Stephen W White, MD is a member of the following medical societies: American Academy of Dermatology, International Society of Dermatology, Society for Investigative Dermatology, and Society for Pediatric Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher R Gorman, MD  Bethesda Dermatology, Private Practice; Assistant Clinical Professor, George Washington University School of Medicine and Health Sciences; Staff Dermatologist, National Naval Medical Center

Christopher R Gorman, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Specialty Editor Board

Franklin Flowers, MD  Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, Affiliate Associate Professor of Pediatrics and Pathology, University of Florida College of Medicine

Franklin Flowers, MD, is a member of the following medical societies: American College of Mohs Micrographic Surgery and Cutaneous Oncology

Disclosure: Nothing to disclose.

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Paul Krusinski, MD  Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

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