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

Citation
R. Neeman et al., Prevalence of internalisation-associated gene, prtF1, among persisting group-A streptococcus strains isolated from asymptomatic carriers, LANCET, 352(9145), 1998, pp. 1974-1977
Citations number
27
Language
INGLESE
art.tipo
Article
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
LANCET
ISSN journal
0140-6736 → ACNP
Volume
352
Issue
9145
Year of publication
1998
Pages
1974 - 1977
Database
ISI
SICI code
0140-6736(199812)352:9145<1974:POIGPA>2.0.ZU;2-G
Abstract
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.