adeabc efflux pump genes in multidrug resistant acinetobacter baumannii isolates

conclusions adeabc efflux system plays a vital role in multidrug resistance in clinical a. baumannii isolates. it was noted that the most important gene responsible for multidrug resistance within this system was the adeb gene especially in carbapenems resistance. methods this study was conducted on 84 multidrug resistant and 13 carbapenem-susceptible a. baumannii isolates obtained from burn and wound infections in baghdad hospitals, iraq. the adeabc genes were detected by polymerase chain reaction (pcr) assay. phe-arg-beta-naphthylamide (paβn)-based method was used for determination of efflux pump activity. results this study showed high prevalence of efflux pump genes in our local isolates. the adeb gene was present in all multidrug resistant isolates (100%) while aders gene was found in 95.2%, adec gene in 83.3% and adea gene in 77.4%. by comparing the prevalence of these gene in carbapenem-susceptible isolates, it was demonstrated that the gene adeb was absent in all susceptible isolates, also the regulatory gene aders was not found in most of these isolates, while the other genes (adea and adec) were detected in most carbapenem- susceptible isolates. susceptibility of isolates to amikacin, gentamicin, ciprofloxacin, levofloxacin, tetracycline and tigecycline was highly increased in the presence of efflux pump inhibitor, so that, paβn reduced the minimum inhibitory concentrations (mics) by 4 to 32 folds. also, mics of carbapenems were reduced in the presence of the inhibitor by two to eight folds, while the mics of colistin were not affected. objectives acinetobacter baumannii is an opportunistic nosocomial pathogen and a cause of severe infections in hospitalized patients, owing to its ability to acquire drug resistance by the efflux pump mechanism. the current study investigated the detection and prevalence of efflux pump genes (adeabc) in multidrug resistant a. baumannii isolates and the role of these genes in multidrug and carbapenems resistance.