High Level Aminoglycoside Resistance in Clinical Isolates of Enterococci

Introduction: Enterococci though being intestinal commensal flora have gained significance as a serious nosocomial pathogen owing to their exceptional ability to survive in the harsh environments and increasing high level resistance to antibiotics. The emergence of high level aminoglycoside resistant (HLAR) clinical enterococcal isolates is of serious concern worldwide and thwarts the available therapeutic options.

Materials and Method: A total of 25 non-repetitive isolates of Enterococci (E. faecalis (n = 15), E. faecium (n= 10)) recovered various clinical samples were screened for HLAR among the isolates was performed by disk diffusion method using High Level Gentamicin and High Level Streptomycin disks. The isolates were further confirmed as HLGR and HLSR by agar dilution method. Genes encoding Aminoglycoside Modifying Enzymes (AGMEs) were detected by multiplex PCR. Susceptibility to linezolid was determined by Kirby Bauer disk diffusion method.

Results: All the 25 isolates of enterococci exhibited HLAR phenotype (resistant to HLG and/or HLS). Majority (96%) of the isolates were resistant to HLG and 64% were resistant to HLS. MIC of gentamicin was >500 μg/mL for HLG^R isolates and MIC of streptomycin was MIC > 2000 cg/mL for HLS^R isolates. In our study, 92% of the enterococci harbored aac(6’)-Ie-aph(2’’)-Ia and/or aph(3’)-IIIa. Of note, 15(60%) of the enterococci exhibited dual resistance to gentamicin and streptomycin (HLG^RHLS^R). Nevertheless, 92% of the isolates were found to be susceptible to linezolid.

Conclusion: Prompt detection and characterization of HLAR among clinical strains of Enterococci within our setting is very essential as few of them exhibit co-resistance to glycopeptides and have lost synergism with the cell wall active agents