Fluoroquinolone resistance conferred by gyrA, parC mutations, and AbaQ efflux pump among Acinetobacter baumannii clinical isolates causing ventilator-associated pneumonia.

Acinetobacter baumannii has emerged as an important nosocomial pathogen due to its ability to survive in hospital settings and its antimicrobial resistance. It is one of the key pathogens in ventilator-associated pneumonia (VAP). The aim of this study was to characterize the mechanisms of quinolone resistance among A. baumannii isolates causing VAP and to investigate the presence of the novel abaQ gene among them. Quinolone-resistant A. baumannii isolates causing VAP were collected over a period of 4 months. Mutations within gyrA and parC were analyzed and the presence of qnrA, qnrB, qnrS, and abaQ was investigated genotypically. Twenty-one A. baumannii isolates were collected, most of them (76.2%) were extensively drug-resistant (XDR) and only one isolate (4.8%) was pandrug-resistant (PDR). All isolates showed high level of resistance to ciprofloxacin, while qnrA, qnrB and qnrS were absent among our isolates. This is the first report of A. baumannii isolates co-harboring Ser81Leu in gyrA and Ser84Leu in parC together with the novel abaQ gene. Interestingly, a new mutation in gyrA quinolone resistance-determining region Arg89Cys was detected among two of our isolates. The emergence of XDR and PDR isolates among A. baumannii causing VAP is an alarming threat.