Molecular characterisation of quinolone-resistance in erythromycin-resistant Streptococcus agalactiae clinical isolates

Abstract number: P1239

Llaneza M.E., Seral C., Pardos M., Durán E., Castillo F.J., Rubio M.C., Gómez-Lus R.

Objectives:Streptococcus agalactiae (GBS) remains susceptible to penicillin; nevertheless, an increase in the resistance to other antimicrobial families, such as macrolides and more rarely fluoroquinolones, has been described. The purpose of the study was to surveillance the fluoroquinolone resistance in GBS isolated from blood cultures, in erythromycin-resistant GBS isolated from vaginal colonisation and characterise the molecular mechanisms of resistance implicated and their genetic similarity.

Methods: Antimicrobial susceptibility (according to CLSI guidelines) of 153 erythromycin-resistant GBS from vaginal colonisation (2002–2004) and 28 GBS from blood cultures (1994–2004) were recorded by our Clinical Laboratory (Hospital Lozano Blesa, Zaragoza, Spain). Levofloxacin and ciprofloxacin resistance in GBS was identified by disk diffusion and broth microdilution methodology in all the isolates. Therefore, we determined the nucleotide sequences and deduced amino acid sequences of gyrA and parC genes including QRDRs in 5 isolates with low-level susceptibility to levofloxacin. These sequences were compared with those of susceptible strains. Pulsed-field gel electrophoresis (PFGE) analysis was performed on the 5 GBS isolates following Sma1 digestion.

Results: Five low-level fluoroquinolone-resistant GBS strains were detected (MICs range were 0.5–2 mg/l) but no high-level fluoroquinolone-resistant GBS (MICs >8 mg/l) were found in the GBS isolates. Of these, in 3 isolates no mutations in the QRDR of parC were found, in a blood isolate collected from a patient previously treated with norfloxacin the sequence analysis of the parC gene showed a base pair chain TCT/CCT at position 238 that resulted in an aminoacid substitution Ser80Pro and in a vaginal isolate three parC silent mutations were found and their implications in quinolone resistance remains unclear. No mutations in the QRDRs of gyrA were detected. The PFGE pattern study did not suggest genetic relation of these five isolates.

Conclusion: Low-level fluoroquinolone-resistant GBS were recovered from 5 patients and we found that one contained an aminoacid substitution in the topoisomerase IV gene (Ser80Pro). This mutation was described previously only in Streptococcus pyogenes. It seems that parC is the primary target of the quinolones in S. agalactiae. These findings emphasise the importance of monitoring antibiotic susceptibility to quinolones antibiotics.

Session Details

Date: 19/04/2008
Time: 00:00-00:00
Session name: 18th European Congress of Clinical Microbiology and Infectious Diseases
Location: Barcelona, Spain
Presentation type:
Back to top