Prevalence of internalisation-associated gene, prtF1, among persisting group-A streptococcus strains isolated from asymptomatic carriers.

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. 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. 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). Our findings suggest that protein-F1-mediated entry to cells is involved in the causative process of the carriage state.