Priyanka Paul Biswas1 , Anamika Singh2 , Mohammad Intekhab Alam Chand3 , Sangeeta Dey4 , Aninda Sen5
BACKGROUND We wanted to determine the frequency of occurrence of HLAR, HLGR, and HLSR phenotypes among Enterococcus species isolated from clinical specimens and determine their susceptibility to different groups of antibiotics. METHODS Enterococci were isolated from various clinical samples, and identification to species level was done using standard methods. High level resistance to gentamicin and streptomycin was done by high potency disc diffusion method [HPDDM]. Biofilm production was seen by microtiter assay and slime layer formation and gelatinase production. Minimum inhibitory concentrations [MIC] to vancomycin, ampicillin, gentamicin, streptomycin and teicoplanin were determined by agar dilution method. Multiplex PCR was used to detect the presence of AME genes. RESULTS Strains showing combined resistance [HLAR] were recovered from the age group 51 - 60 years (75%). Enterococcus faecalis, that carried aph (3”)-IIIa gene 7.6% [1/3] exhibited complete resistance to vancomycin with MIC of 32-64 μg/mL. 7.6% [1/6] unusual species that expressed both [aac (6 ′ )-ie-aph (2 ′′)-Ia + aph(3”)-IIIa] genes was also resistant to vancomycin. VR Enterococcus faecium that showed high level resistance to streptomycin [HLSR] 10.0% [1/10] also exhibited resistance to linezolid. The differences in antibiotic resistance pattern to ampicillin, penicillin, piperacillin, tetracycline, erythromycin, ciprofloxacin and imipenem amongst Enterococcus faecalis, Enterococcus faecium and unusual strains were statistically significant [P=0.05, P= 0.01, P=0.000]. Resistance to piperacillin amongst the HLGR strains was also significant [P= 0.001]. Biofilm formation was seen in 79.3% [23/29] of Enterococcus species resistant to streptomycin followed by 50.0% of HLAR strains and 45.7% of HLGR strains. CONCLUSIONS This study showed the slowly increasing prevalence of HLAR and resistance to other antibiotics. Much more extensive synergism studies of cell wall–active agents combined with various aminoglycosides against enterococci that possess different combinations of aminoglycoside resistance genes must be conducted.
