Background The failure of antibiotic treatment to eradicate group-A strepto
cocci in up to 30% of patients with pharyngotonsillitis is unexplained. Som
e strains of group-A streptococci can enter respiratory epithelial cells, w
here they would be inaccessible to antibiotics unable to penetrate the cell
membrane, such as penicillins. The fibronectin-binding proteins, F1 and Sf
bI, are needed for this process. We hypothesised, therefore, that an intrac
ellular reservoir of group-A streptococci could account, at least partly, f
or 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 st
rain 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, alth
ough 13 of them continued to carry group-A streptococci in the throat durin
g or after therapy, To distinguish between persisting and recolonising stra
ins, isolates from the 13 patients were serologically tested and compared b
y polymorphic DNA-amplification technique.
Findings 12 (92%) of the 13 patients with symptomless carriage had prfF1-co
ntaining strains in the throat, compared with 16 (30%) of the 54 patients w
ith 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).
Interpretation Our findings suggest that protein-F1-mediated entry to cells
is involved in the causative process of the carriage stale.