Session: Poster Session: Antimicrobial Susceptibility Testing 2008
Monday, October 27, 2008: 12:00 AM
Room: Hall C
Background: Detection of high level gentamicin resistance (HLGR) is important to evaluate the use of beta lactam and aminoglycoside combination for treatment. Most common mechanism of HLGR is due to aac-aph gene. Methods: 27 vancomycin resistant strains were tested for gentamicin susceptibility by using VITEK2 and PHOENIX systems, agar dilution MICs, E test and disk diffusion using 0.120 mg disks. Clonality of strains were tested by PFGE and presence of resistance genes by PCR . Results: All isolates tested carried vanA and aac-aph genes. No inhibition zone was obtained with highly charged gentamicin disks as well as E tests. Agar dilution MICs showed that 5, 3 and 19 strains had MIC 256, 512 and >1024 mg/L, respectively. Four of 5 isolates with gentamicin MICs 256 were susceptible by both VITEK 2 and PHOENIX, and the remaining one was susceptible by PHOENIX and resistant by VITEK 2. 3 isolates with MICs 512 mg/L were reported resistant by both systems. 1 isolate with MIC >1024 were reported susceptible by both automates. PFGE indicated presence of 3 pulsotypes with their variants among 27 VRE. Conclusion: Gentamicin breakpoints determined by CA-SFM, EUCAST, BSAC and CLSI have some differences for E. faecium. EUCAST has no breakpoint but indicates that there is no synergie between beta-lactams and aminoglycosides for strains with MICs >128mg/L. CA-SFM accepts <256 mg/L as susceptible while for BSAC and CLSI < 512 mg/L is susceptible. For Enterococci gentamicin susceptibility testing is useful only to evaluate presence of beta lactam-aminoglicoside synergie and the synergie is broken for isolates with MIC >128 mg/L. Our study showed that some of the strains with aac-aph gene were reported as susceptible by VITEK and PHOENIX. We believe that larger studies should be done to re-evaluate gentamicin breakpoints for Enterococci.