DESCRIPTION

• Scarlet fever, also known as “scarlatina,” is an acute illness with a constellation of clinical symptoms caused by Streptococcus pyogenes, a type of group A β-hemolytic Streptococcus (GAS).
• Scarlet fever describes a clinical syndrome consisting of fever, pharyngitis, and an associated characteristic sandpaper rash. Contaminated wounds and burns infected with GAS may also cause scarlet fever in the absence of pharyngitis.
• S. pyogenes produces a variety of streptococcal pyrogenic exotoxins (SPEs—A, B, and C), antigens, and cell wall associated with M proteins that result in a wide range of virulence mechanisms.
• Scarlet fever results from local inflammatory response to exotoxins and superantigens produced by S. pyogenes.
• There are rare cases of staphylococcal scarlet fever, caused by Staphylococcus aureus, which causes a clinically mild staphylococcal scalded skin–like syndrome.

EPIDEMIOLOGY

• Peak incidence of GAS infections in school-aged children ages 5 to 15 years (15–30% when compared to 5–15% in adults)
• Low incidence in children <3 years of age
• There is a little seasonal variation with slightly increased prevalence in winter and spring.
• Incidence is higher in undeveloped nations.
• Short incubation period of 2 to 5 days for Streptococcal pharyngitis
• There is no significant difference in incidence among males and females.

ETIOLOGY

Scarlet fever is predominantly caused by transmission of GAS through large respiratory droplets (saliva, nasal discharge) and less frequently through contaminated objects, foods, or wounds.

RISK FACTORS

• Age
• Duration of exposure
• Environmental factors
  • Population density
  • Close contact (child care, schools, contact sports)
  • Crowded living conditions (military barracks, dormitories)

GENERAL PREVENTION

• Good hygiene practices and disinfection are recommended due to prolonged survival of S. pyogenes, although there is no evidence of direct transmission via fomites.
• Droplet/contact precautions, particularly in health care settings may reduce transmission of nosocomial infections.
• Early appropriate antibiotic treatment reduces spread of infection.

PATHOPHYSIOLOGY

• Although the pathogenesis of scarlet fever is not completely understood, the virulence of S. pyogenes has been linked to the organism’s capsule and expression of M protein types and exotoxins.
• The M protein in the cell wall of S. pyogenes is proinflammatory and facilitates mucosal adhesion in the absence of antibodies.
• Strains of S. pyogenes rich in M protein can evade phagocytosis and stimulate type-specific antibodies.
• In the absence of toxin-specific immunity, individuals are susceptible to infection as suggested by the Dick test (intradermal injection of toxin produces a blanching erythematous rash in naive individuals compared to those with prior history of scarlet fever and conferred immunity).
• S. pyogenes can produce a combination of 12 SPEs. SPEs A, B, and C are thought to be responsible for the distinct scarlet fever rash, which requires prior exposure to GAS.