title: Strain prevalence, rather than innate virulence potential, is the major factor responsible for an increase in serious group A streptococcus infections.
abstract: BACKGROUND
  It is postulated that the surge in incidence and severity of group A streptococcus (GAS) infections since the 1980s is due to the emergence of strains of GAS with increased virulence. We used active, population-based surveillance of invasive GAS disease, serologically confirmed pharyngitis, and carriage to determine whether particular strains were associated with invasive disease.
  
  
  METHODS
  Two hundred twenty GAS isolates were collected--78 invasive, 34 pharyngitis, and 108 carriage. Isolates were characterized using emm typing, random amplification of polymorphic DNA (RAPD) profiling, and superantigen genotyping.
  
  
  RESULTS
  emm1, emm12, and emm28 predominated in invasive disease and accounted for 30.8%, 12.8%, and 12.8% of all isolates, respectively. emm1, emm75, emm28, and emm4 were the most frequently isolated emm types in pharyngitis, and emm12 and emm1 predominated in carriage. emm12 was significantly associated with carriage rather than disease. There were no other significant associations between emm type and disease or carriage. There were no associations between any RAPD profile or superantigen genotype and invasive disease, pharyngitis, or carriage. One RAPD profile accounted for most cases of necrotizing fasciitis, which suggests that this strain might have particular features promoting connective-tissue infection.
  
  
  CONCLUSIONS
  These data suggest that the emergence of GAS strains with increased virulence is not the main factor responsible for the surge in GAS-related infections. The prevalence of particular emm types, RAPD profiles, or superantigen genes in invasive disease may simply indicate widespread transmission of these strains in the population, rather than a particular ability to cause disease.
authors.affiliation: Department of Paediatrics, University of Melbourne, Melbourne, Australia.
authors.forename: Susan
authors.initials: S
authors.lastname: Rogers
authors.forename: Robert
authors.initials: R
authors.lastname: Commons
authors.forename: Margaret H
authors.initials: MH
authors.lastname: Danchin
authors.forename: Gowri
authors.initials: G
authors.lastname: Selvaraj
authors.forename: Loraine
authors.initials: L
authors.lastname: Kelpie
authors.forename: Nigel
authors.initials: N
authors.lastname: Curtis
authors.forename: Roy
authors.initials: R
authors.lastname: Robins-Browne
authors.forename: Jonathan R
authors.initials: JR
authors.lastname: Carapetis
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000942:Antigens, Bacterial / Q000145:classification / Q000235:genetics; D001425:Bacterial Outer Membrane Proteins / Q000145:classification / Q000235:genetics; D002352:Carrier Proteins / Q000145:classification / Q000235:genetics; D002353:Carrier State / Q000453:epidemiology* / Q000382:microbiology; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D008875:Middle Aged; D010612:Pharyngitis / Q000453:epidemiology* / Q000382:microbiology; D011159:Population Surveillance; D015995:Prevalence; D019105:Random Amplified Polymorphic DNA Technique; D013290:Streptococcal Infections / Q000453:epidemiology* / Q000382:microbiology; D013297:Streptococcus pyogenes / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity*; D018089:Superantigens / Q000145:classification / Q000235:genetics; D014774:Virulence
chemical_list: D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins; D002352:Carrier Proteins; D018089:Superantigens; C014689:streptococcal M protein