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  • Author: Chang Hong-Yue x
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Abstract

NiC21H22O6N6, orthorhombic, Pnma, a = 18.214(3) Å, b = 20.934(3) Å, c = 5.5296(8) Å, V = 2108.3(5) Å3, Z = 4, R gt(F) = 0.0279, wR ref(F 2) = 0.798, T = 296(2) K.

Abstract

Objective To identify the risk factors for imipenem resistance development and transmission of clinical Pseudomonas aeruginosa isolates.

Methods Thirty-seven imipenem unsusceptible Pseudomonas aeruginosa isolates collected from patients in absence of carbapenem treatment were characterized by antimicrobial susceptibility test, pulsed field gel electrophoresis (PFGE) and carbapenem resistant mechanism analysis.

Results Before the collection of imipenem unsusceptible Pseudomonas aeruginosa isolates, the average time of patients treated with more than one antimicrobial (20.0 ± 9.5 days, n = 16) was significantly longer than those treated with only one antimicrobial (12.6 ± 4.4 days, n = 21; t-test, Welch, t = -2.9004, P < 0.01). And 32 isolates showed resistance to more than 3 classes of antimicrobials. Six PFGE clusters were identified and 26 isolates were grouped into one dominant cluster (C2). An ISpa1328 sequence insertion in oprD was detected in 33 isolates and the function of efflux was observed in all 37 isolates in the presence of a wide spectrum efflux inhibitor.

Conclusions Our data demonstrated that exposure to non-carbapenem drug classes, especially fluoroquinolones and β-lactams, may be important risk factors for the spread of carbapenem resistant Pseudomonas aeruginosa.