OBJECTIVE: To investigate the antibiotics resistance of Enterococcus, the aminoglycoside-modifying enzymes (AME) and homology of high-level gentamicin resistant (HLGR) Enterococcus in clinical specimens for the implementation of effective infection control measures. METHODS: The resistance of 13 antimicrobial agents was determined by Kirby-Bauer (K-B) or agar dilution method. And the HLGR and high-level streptomycin resistant (HLSR) isolates were screened by agar screen. Production of beta-lactamases was tested by the nitrocefin disc method. The aminoglycoside-modifying enzyme genes were detected by polymerase chain reaction (PCR). Pulsed-field gel electrophoresis (PFGE) was used to analyze the homology of HLGR isolates from in-patients. RESULTS: No isolates resistant to linezolid, vancomycin and teicoplanin were found. Ampicillin-resistant isolates did not produce beta-lactamases and 68 HLGR isolates were screened at the rate of 64.2%. The positive rate of aac(6')-Ie-aph(2'')-Ia was 86.8% and 3 isolates had the new AME gene designated aph(2'')-Ie mostly similar to aph(2'')-Id. Among 51 HLGR isolates from in-patients, PFGE grouped 17 Enterococcus faecalis (E. faecalis) isolates into 4 clusters (A-D), and 33 Enterococcus faecium (E. faecium) isolates into 8 clusters (A-H), of which the A cluster is the main. CONCLUSIONS: HLGR has become the important antibiotic resistance pathogen causing nocosomial infection. And the aac(6')-Ie-aph(2'')-Ia gene was the main aminoglycoside-modifying enzyme gene leading to HLGR.
OBJECTIVE: To investigate the antibiotics resistance of Enterococcus, the aminoglycoside-modifying enzymes (AME) and homology of high-level gentamicin resistant (HLGR) Enterococcus in clinical specimens for the implementation of effective infection control measures. METHODS: The resistance of 13 antimicrobial agents was determined by Kirby-Bauer (K-B) or agar dilution method. And the HLGR and high-level streptomycin resistant (HLSR) isolates were screened by agar screen. Production of beta-lactamases was tested by the nitrocefin disc method. The aminoglycoside-modifying enzyme genes were detected by polymerase chain reaction (PCR). Pulsed-field gel electrophoresis (PFGE) was used to analyze the homology of HLGR isolates from in-patients. RESULTS:No isolates resistant to linezolid, vancomycin and teicoplanin were found. Ampicillin-resistant isolates did not produce beta-lactamases and 68 HLGR isolates were screened at the rate of 64.2%. The positive rate of aac(6')-Ie-aph(2'')-Ia was 86.8% and 3 isolates had the new AME gene designated aph(2'')-Ie mostly similar to aph(2'')-Id. Among 51 HLGR isolates from in-patients, PFGE grouped 17 Enterococcus faecalis (E. faecalis) isolates into 4 clusters (A-D), and 33 Enterococcus faecium (E. faecium) isolates into 8 clusters (A-H), of which the A cluster is the main. CONCLUSIONS: HLGR has become the important antibiotic resistance pathogen causing nocosomial infection. And the aac(6')-Ie-aph(2'')-Ia gene was the main aminoglycoside-modifying enzyme gene leading to HLGR.