Scarlet Fever in Emergency Medicine 

  • Author: Jerry Balentine, DO; Chief Editor: Robert E O'Connor, MD, MPH   more...
 
Updated: Mar 19, 2010
 

Background

Scarlet fever (known as scarlatina in older literature references) is an exotoxin-mediated disease arising from group A beta-hemolytic streptococcal infection. Ordinarily, scarlet fever evolves from a tonsillar/pharyngeal focus, although the rash develops in fewer than 10% of cases of "strep throat." The site of bacterial replication tends to be inconspicuous compared to the possible dramatic effects of released toxins. Exotoxin-mediated streptococcal infections range from localized skin disorders (eg, bullous impetigo) to the systemic rash of scarlet fever to the uncommon but highly lethal streptococcal toxic shock syndrome.

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Pathophysiology

Usually, the sites of group A beta-hemolytic streptococcal replication in scarlet fever are the tonsils and pharynx. Clinically indistinguishable, scarlet fever may follow streptococcal infection of the skin and soft tissue, surgical wounds (ie, surgical scarlet fever), or the uterus (ie, puerperal scarlet fever).

Group A beta-hemolytic streptococci secrete a number of toxins, enzymes, and erythrogenic toxins. Release of erythrogenic toxin causes the pathognomonic rash of scarlet fever. Local lesions reveal a characteristic inflammatory reaction, specifically hyperemia, edema, and polymorphonuclear cell infiltration.

The organism is able to survive extremes of temperature and humidity, which allows spread by fomites. Geographic distribution of skin infections tends to favor warmer or tropical climates and occurs mainly in summer or early fall in temperate climates.

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Epidemiology

Frequency

United States

In the past century, the number of cases of scarlet fever has remained high, with marked decrease in case-mortality rates secondary to widespread use of antibiotics. Transmission usually occurs via airborne respiratory particles that can be spread from infected patients and asymptomatic carriers. The infection rate increases in overcrowded situations (eg, schools, institutional settings). Immunity, which is type specific, may be induced by a carrier state or overt infection. In adulthood, incidence decreases markedly as immunity develops to the most prevalent serotypes. Complications (eg, rheumatic fever) are more common in recent immigrants to the United States.

Mortality/Morbidity

Scarlet fever is no longer associated with the deadly epidemics that made it so feared in the 1800s.

  • Today, scarlet fever infection usually follows a benign course, and any undue morbidity and mortality are more likely to arise from suppurative complications, such as peritonsillar abscess, sinusitis, bronchopneumonia, and meningitis, or problems associated with immune-mediated sequelae, rheumatic fever, or glomerulonephritis. Very rare complications, such as septic shock with multisystem organ failure, have been reported.[1]
  • Risk of acute rheumatic fever following an untreated streptococcal infection has been estimated at 3% in epidemic situations and approximately 0.3% in endemic scenarios.
  • If a nephritogenic strain of group A beta-hemolytic streptococci causes infection, the individual has a 10-15% chance of developing glomerulonephritis. A lethal form of streptococcal infection is capable of producing the toxic streptococcal syndrome.

Sex

  • Males and females are affected equally.

Age

  • Peak incidence of scarlet fever occurs in children aged 4-8 years.
  • By the time children are 10-years-old, 80% have developed lifelong protective antibodies against streptococcal pyrogenic exotoxins.
  • Scarlet fever is rare in children younger than 2 years because of the presence of maternal antiexotoxin antibodies and lack of prior sensitization.
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Contributor Information and Disclosures
Author

Jerry Balentine, DO  Professor of Emergency Medicine, New York College of Osteopathic Medicine; Executive Vice President, Chief Medical Officer, Attending Physician in Department of Emergency Medicine, St. Barnabas Hospital

Jerry Balentine, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American College of Physician Executives, American Osteopathic Association, and New York Academy of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Daniel P Lombardi, DO  Clinical Assistant Professor, New York College of Osteopathic Medicine and Clinical Instructor, Albert Einstein College of Medicine of Yeshiva University; Attending Physician and Program Director, Department of Emergency Medicine, Saint Barnabas Hospital

Daniel P Lombardi, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Joseph A Salomone III, MD  Associate Professor and Attending Staff, Truman Medical Centers, University of Missouri-Kansas City School of Medicine; EMS Medical Director, Kansas City, Missouri

Joseph A Salomone III, MD is a member of the following medical societies: American Academy of Emergency Medicine, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Eric L Weiss, MD, DTM&H  Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

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

Robert E O'Connor, MD, MPH  Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

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The exudative pharyngitis typical of scarlet fever. Although the tongue is somewhat out of focus, the whitish coating observed early in scarlet fever is visible.
Desquamation of the palms is a frequently observed self-limited manifestation of scarlet fever present in the healing period following resolution of the infection and acute eruption.
 
 
 
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