Diverse populations of fluoroquinolone nonsusceptible groupA streptococci recovered from colonisation and infections in Portugal (19992006)
Abstract number: P1726
Pires R., Ardanuy C., Oliveira V., Rolo D., Almeida J.F., Brito-Avô A., Morais A., Gonçalo-Marques J., Liñares J., Santos-Sanches I.
Objectives: To examine ciprofloxacin nonsusceptible (Cip-NS) Group A streptococci (GAS) isolated from clinical origins and asymptomatic colonisation, and to explore the associated clones and mechanisms of resistance.
Methods: A total of 1,541 GAS collected from oropharyngeal colonisation (n = 938), tonsillitis (n = 487), skin/soft tissue infections (n = 72) and invasive disease (n = 44) were studied. Susceptibility to ciprofloxacin was evaluated by disk diffusion and by microdilution methods. Point mutations in the parC-quinolone resistance determining region (QRDR) were identified by sequencing and by restriction of PCR amplicons with HinfI and LweI. Cip-NS isolates were characterised by emm-typing, pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST) to assign sequence types (ST).
Results: Eighty-one (5%) isolates were Cip-NS showing a MIC range between 2 and 8 mg/L. This rate was higher among skin/soft tissue infection isolates (15%, n = 11/72). All but three strains had ParC changes: S79F (n = 73), D83N (n = 4) and D83Y (n = 1). Seven ST or lineages, of diverse emm and PFGE types, were found among 81 Cip-NS isolates. A major lineage ST382/emm6;others/PFGE.AD;DX;DY;AM;DW (n = 73 isolates from different origins) showed the ParC-S79F change. Other Cip-NS strains were (all n = 1): ST52/emm28/PFGE.AC ParC-D83N, ST52/emm28/PFGE.BT ParC-D83Y, ST46/emm22/PFGE.B ParC-D83N, ST99/emm5/PFGE.BB ParC-D83N, ST-unassigned/emm5/PFGE.K ParC-D83N. The remaining 3 strains with no ParC changes were: ST36/emm12/PFGE.AP, ST39/emm4/PFGE.CH and ST39/emm89/PFGE.CZ. Lineages ST36 and ST-unassigned were associated with oropharyngeal colonisation isolates, ST39 and ST46 with tonsillitis and ST52 and ST99 with skin/soft tissue infections.
Conclusions: Nonsusceptibility to Cip among GAS in Portugal was similar to the one reported in European surveys. The majority of Cip-NS isolates belonged to emm6 (ST382) with S79F mutation however other different types emm28 (ST52), emm22 (ST46) or emm5 (ST99) found among colonisation and/or clinical isolates showed different ParC changes (D83N/Y). The absence of point mutations in the parC-QRDR region of emm4/89 (ST39) and emm12 (ST36) isolates suggests mechanism(s) of fluoroquinolone resistance other than point mutations in the parC-QRDR region (e.g., single parE mutations and/or efflux pumps).
|Session name:||19th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Helsinki, Finland, 16 - 19 May 2009|
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