Objectives: Pseudomonas aeruginosa is one of the most common pathogens causing nosocomial pneumonia. The aim of this study was to investigate the epidemiology and resistance of P. aeruginosa isolated from hospitalised patients in the respiratory department of a hospital in China.
Methods: Clinical isolates were collected from the respiratory department of Southwest Hospital (Chongqing, China) from January 2013 to December 2014. Patients' social and demographic information was obtained from the hospital's information system. Antimicrobial susceptibility was assessed using the agar dilution method. Screening for carbapenemase production among carbapenem-resistant P. aeruginosa was performed using the modified Hodge test and MBL Etest, and carbapenemase-encoding genes were amplified by PCR. Amplification and sequencing of the oprD gene were performed for carbapenem-resistant P. aeruginosa. Sequence types were determined by multilocus sequence typing (MLST).
Results: A total of 92 P. aeruginosa isolates were collected from patients in the respiratory department, and piperacillin/tazobactam was the most effective antibiotic against these isolates. Multivariate analysis revealed that antibiotic use prior to admission was an independent risk factor for P. aeruginosa infection. The isolates comprised 25 genotypes, the most common of which were ST235 and ST111. The blaIMP-4 gene was present in 4 isolates and blaVIM-2 in 1 isolate among the 24 carbapenem-resistant isolates. Most of the carbapenem-resistant isolates contained mutational inactivation of the oprD gene.
Conclusions: These results suggested that patients and the hospital environment were sources of P. aeruginosa in nosocomial infections. Mutational inactivation of the oprD gene might be the main mechanism of carbapenem resistance.
Keywords: Epidemiology; Multilocus sequence typing; Nosocomial infection; Pseudomonas aeruginosa; Resistance.
Copyright © 2017 International Society for Chemotherapy of Infection and Cancer. Published by Elsevier Ltd. All rights reserved.