title: Prevalence of internalisation-associated gene, prtF1, among persisting group-A streptococcus strains isolated from asymptomatic carriers.
abstract: BACKGROUND
  The failure of antibiotic treatment to eradicate group-A streptococci in up to 30% of patients with pharyngotonsillitis is unexplained. Some strains of group-A streptococci can enter respiratory epithelial cells, where they would be inaccessible to antibiotics unable to penetrate the cell membrane, such as penicillins. The fibronectin-binding proteins, F1 and SfbI, are needed for this process. We hypothesised, therefore, that an intracellular reservoir of group-A streptococci could account, at least partly, for failure to eradicate throat carriage, and that the presence of the gene for fibronectin-binding protein (F1) might be linked to the ability of a strain to persist in the throat after therapy.
  
  
  METHODS
  We investigated the frequency of prtF1-containing strains among 67 patients with pharyngotonsillitis. All patients were clinically cured, although 13 of them continued to carry group-A streptococci in the throat during or after therapy. To distinguish between persisting and recolonising strains, isolates from the 13 patients were serologically tested and compared by polymorphic DNA-amplification technique.
  
  
  RESULTS
  12 (92%) of the 13 patients with symptomless carriage had prtF1-containing strains in the throat, compared with 16 (30%) of the 54 patients with successful eradication (p=0.0001). Three of the 13 eradication-failure patients were recolonised with strains that differed from the pretreatment strains. Nine of the ten (90%) persisting strains carried prtF1 (p=0.0009).
  
  
  CONCLUSIONS
  Our findings suggest that protein-F1-mediated entry to cells is involved in the causative process of the carriage state.
authors.affiliation: Department of Human Microbiology, Sackler School of Medicine, Tel-Aviv University, Israel.
authors.forename: R
authors.initials: R
authors.lastname: Neeman
authors.forename: N
authors.initials: N
authors.lastname: Keller
authors.forename: A
authors.initials: A
authors.lastname: Barzilai
authors.forename: Z
authors.initials: Z
authors.lastname: Korenman
authors.forename: S
authors.initials: S
authors.lastname: Sela
mesh_terms: D018829:Adhesins, Bacterial / Q000235:genetics* / Q000302:isolation & purification; D000293:Adolescent; D000658:Amoxicillin / Q000627:therapeutic use; D002353:Carrier State / Q000188:drug therapy / Q000382:microbiology*; D000077722:Ceftibuten; D002511:Cephalosporins / Q000627:therapeutic use; D002648:Child; D002675:Child, Preschool; D004311:Double-Blind Method; D005784:Gene Amplification; D006801:Humans; D010406:Penicillins / Q000627:therapeutic use; D010612:Pharyngitis / Q000188:drug therapy / Q000382:microbiology*; D015995:Prevalence; D012703:Serotyping; D013290:Streptococcal Infections / Q000188:drug therapy / Q000382:microbiology*; D013297:Streptococcus pyogenes / Q000145:classification / Q000187:drug effects / Q000235:genetics* / Q000302:isolation & purification; D014069:Tonsillitis / Q000188:drug therapy / Q000382:microbiology*
chemical_list: D018829:Adhesins, Bacterial; D002511:Cephalosporins; D010406:Penicillins; C078635:fibronectin-binding proteins, bacterial; D000658:Amoxicillin; D000077722:Ceftibuten