Session: Poster Session: Streptocci and Enterococci
Monday, October 27, 2008: 12:00 AM
Room: Hall C
Background: FQ resistance in Sag was only reported in few countries. Through the National Surveillance (WHO-Arg Network, 70 Hosp) the FQ resistance was evaluated in 1128 Sag between 2005 and 2007. Ten (0.9%) Sag isolates displayed no inhibition zone to levofloxacin (LEV), and 9 of them were submitted to the National Reference Laboratory (INEI) for further characterization. The aim was to characterize the mechanisms involved in FQ-resistant Sag and to determine the genetic relationship between them. Methods: Nine Sag, 7 from urine and 2 from vaginal screening culture, (5 Hosp, 5 cities) were studied. MIC to FQs was performed by agar dilution. QRDRs of parC and gyrA genes were sequenced. Reserpine (20 mg/L) was used for efflux inhibition assays. Detection of mefA and ermB genes was carried out by PCR. Molecular typing was assessed by ApaI-PFGE. Results: All Sag were susceptible to penicillin (0.06 mg/L) and resistant (MIC range mg/L) to ciprofloxacin (32-64), LEV (16-32), ofloxacin (32-64), norfloxacin (32-64), gatifloxacin (4) and moxifloxacin (2). No inhibitory effect was observed when MIC to ciprofloxacin plus reserpine was evaluated. Three Sag were also resistant to macrolides due to ermB gene. All strains contained the same mutations, Ser79Phe in ParC and Ser81Leu in GyrA. Clone A (6 strains; subtypes A1 to A4) was detected in all the 5 Hosp, and B (3 strains) only in one Hosp. Conclusions: Mutations in parC (S79F) and gyrA (S81L), were the mechanisms responsible of FQ resistance in the firsts Sag isolates from Latin-America. Two clones were distinguished, although the clone A was present in the five institutions. The prevalence of this mechanism is still low but the active surveillance become critical to detect the emergence of this phenotype in others cities.