Wei Feng1, Qing Huang2, Yu Wang1, Qian Yuan1, Xiaoyu Li3, Peiyuan Xia4, Fengjun Sun5. 1. Department of Pharmacy, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China. 2. Department of Laboratory Medicine, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China. 3. Department of Pharmacy, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; Department of Pharmacy, Handan Branch of Chinese PLA 980 Hospital, Handan, Hebei province, China. 4. Department of Pharmacy, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China. Electronic address: peiyuan_xia2013@163.com. 5. Department of Pharmacy, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China. Electronic address: fengj_sun@163.com.
Abstract
PURPOSE: The aim of this study was to investigate the changes over a ten-year period in the resistance and epidemiological characteristics of Pseudomonas aeruginosa strains isolated from the Department of Respiratory in Southwest Hospital. METHODS: Antimicrobial resistance was detected using the plate double dilution method. PCR amplification and sequencing were performed to evaluate the carbapenemase genes and the oprD gene. Bacterial genotypes were analyzed by multilocus sequence typing (MLST). Quantitative real-time PCR experiments were performed to assess the expression of efflux pump (mexA and mexX) and ampC gene. RESULTS: We collected 233 P. aeruginosa isolates in 2006-2007 and 128 isolates in 2016-2017. The resistance rate of P. aeruginosa strains to the tested antibiotics was significantly lower in 2016-2017 than in 2006-2007. The MLST results showed 27 genotypes in 2006-2007 and 18 genotypes in 2016-2017. ST235 was the most prevalent sequence type, and there was no significant change in the genotypes over the ten-year period. Both VIM-2 and IMP-4 genes were found in 2006-2007, whereas only IMP-4 was found in 2016-2017. The oprD mutational inactivation was the main factor responsible for carbapenem resistance, and the overexpression of mexX had a good correlation with aminoglycoside resistance. CONCLUSION: These results indicated that the antibiotic resistance of P. aeruginosa in our respiratory department decreased. The loss of oprD gene was the main mechanism of carbapenem resistance, and mexX overexpression was the major contributing factor to aminoglycoside resistance.
PURPOSE: The aim of this study was to investigate the changes over a ten-year period in the resistance and epidemiological characteristics of Pseudomonas aeruginosa strains isolated from the Department of Respiratory in Southwest Hospital. METHODS: Antimicrobial resistance was detected using the plate double dilution method. PCR amplification and sequencing were performed to evaluate the carbapenemase genes and the oprD gene. Bacterial genotypes were analyzed by multilocus sequence typing (MLST). Quantitative real-time PCR experiments were performed to assess the expression of efflux pump (mexA and mexX) and ampC gene. RESULTS: We collected 233 P. aeruginosa isolates in 2006-2007 and 128 isolates in 2016-2017. The resistance rate of P. aeruginosa strains to the tested antibiotics was significantly lower in 2016-2017 than in 2006-2007. The MLST results showed 27 genotypes in 2006-2007 and 18 genotypes in 2016-2017. ST235 was the most prevalent sequence type, and there was no significant change in the genotypes over the ten-year period. Both VIM-2 and IMP-4 genes were found in 2006-2007, whereas only IMP-4 was found in 2016-2017. The oprD mutational inactivation was the main factor responsible for carbapenem resistance, and the overexpression of mexX had a good correlation with aminoglycoside resistance. CONCLUSION: These results indicated that the antibiotic resistance of P. aeruginosa in our respiratory department decreased. The loss of oprD gene was the main mechanism of carbapenem resistance, and mexX overexpression was the major contributing factor to aminoglycoside resistance.