Scarlet Fever



  • Scarlet fever or “scarlatina” is a manifestation of infection with Streptococcus pyogenes (group A β-hemolytic Streptococcus) that is characterized by an erythematous “sandpaper” rash. It results from infection with a strain of S. pyogenes that elaborates streptococcal pyrogenic exotoxin (SPE).
  • Typical presentation is in the setting of streptococcal pharyngitis but may occur with group A streptococcal skin or wound infections.
  • Disease is linked to SPE A, B, C, and F. SPE A is associated with more virulent disease.
  • A similar syndrome may also be seen in infection with certain enterotoxin-producing strains of Staphylococcus aureus, known as staphylococcal scarlet fever.



  • Disease is most common between ages 3 and 15 years.
  • Peak incidence is during the early school years.
  • There is little seasonal variation with slightly increased prevalence in winter and spring.
  • Recent studies have documented increasing incidence in certain parts of the world (e.g., United Kingdom, China, South Korea).
  • Incubation period is 2 to 5 days for strep pharyngitis and may be up to 10 days for strep skin infections.


  • Prevalence is equal in boys and girls.
  • By age 10 years, 80% of children have developed toxin-specific antibodies.

Risk Factors

  • Close contact with a case of scarlet fever
  • Crowded living conditions may contribute (schools, daycare centers, military training centers).
  • Prior sensitization to S. pyogenes is required.
  • Susceptible individuals may lack toxin-specific immunity.

General Prevention

  • Control measures were ineffective in a school outbreak. These included hygiene advice and exclusion of infected students for 24 hours while initiating penicillin treatment.
  • Prompt treatment of infection leads to fewer secondary cases of streptococcal disease.


  • Susceptible individuals are thought to lack toxin-specific immunity. This is supported by results of the now seldom-used Dick test, in which a small amount of toxin introduced intradermally produces local erythema in susceptible individuals but no reaction in those with toxin-specific immunity.
  • Rash and other toxic manifestations of scarlet fever have been attributed to the development of hypersensitivity to the toxin, which requires prior exposure to the toxin.
  • Toxin is produced when viral DNA is introduced into the streptococcal genome by a bacteriophage.
  • Histologic examination of affected skin shows dilated blood and lymphatic vessels and engorged capillaries, most prominently around hair follicles.
  • Acute, edematous polymorphonuclear inflammatory reaction is seen microscopically within affected tissues.
  • Epidermal inflammatory reaction is usually followed by hyperkeratosis, which accounts for scaling during defervescence.


Scarlet fever is a toxin-mediated consequence of infection with group A β-hemolytic Streptococcus.

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