作者: Yanpeng Zhang , Zhuocheng Li , Xiaolong He , Fanglin Ding , Weiqing Wu
DOI: 10.2147/IDR.S151423
关键词:
摘要: Purpose Acinetobacter baumannii is an important pathogen in the nosocomial infections worldwide. Combining with carbapenemases, efflux pumps and outer membrane proteins (OMPs) have been thought to affect development of carbapenem resistance A. baumannii. This study aimed investigate contributions different OMPs developing a clinical isolate reveal possible mechanism overproduction main pumps. Patients methods In this study, imipenem-susceptible was identified as named SZE. Several common carbapenemases were detected by polymerase chain reaction (PCR). Imipenem-selected mutants selected from SZE serial subcultivations on Mueller-Hinton agar, minimum inhibitory concentration (MIC) detected. Gene expressions four families pumps, five OMPs, blaOXA-51 determined reverse transcription quantitative PCR, comparisons made between strain imipenem-selected mutants. The adeRS system its mutant sequenced aligned. Results Under consecutive stress, MIC imipenem increased gradually 0.125 μg/mL 8 μg/mL. effect inducement almost neutralized when treated pump inhibitor. expression adeB, adeG, adeJ, 6.9-, 4.0-, 2.1-fold mutants, respectively, compared A single mutation (G A) at position 58 regulatory possibly upregulated adeB expression, then affected strains. Conclusion conclusion, under stress vitro, evolved ability reduce susceptibility variety antimicrobials Especially, resistance-nodulation-cell division super family nucleotide regulating caused overexpression adeABC.