Emergence of mcr- and fosA3-mediated colistin and fosfomycin resistance among carbapenem-resistant Acinetobacter baumannii in Iraq

Abstract

IntroductionAcinetobacter baumannii infections have spread in healthcare and community settings with extensive drug-resistance in various locations. Considering importance of source tracking, our aim was molecular characterization and genetic analysis of fosfomycin- and colistin-resistant A. baumannii. MethodsIn this study, 205 A. baumannii were identified from hospital settings during 2014–2018. Their drug resistance pattern was assessed using disk diffusion method as per clinical and laboratory standards institute (CLSI). The colistin, imipenem and meropenem minimum inhibitory concentrations (MICs) were determined using broth microdilution method. Among multidrug-resistant strains, colistin and fosfomycin resistance genes (mcr1-mcr4 and fosA3, respectively) were screened by polymerase chain reaction (PCR) technique. Genetic relation of isolates was evaluated using pulsed field gel electrophoresis (PFGE) method. ResultsOf 205 A. baumannii, the resistance rate against carbapenems, fosfomycin and colistin included 95%, 30% and 32%, respectively. The colistin MIC≥4 μg/ml was observed among 26.34% of them. The fosA3 and mcr-1 genes were detected in 7% (n = 15) and 11% (n = 22) of them, but mcr-2, mcr-3 and mcr-4 were not detected. The strains exhibited 13 pulsotypes (A-M). Hence, the genotypic patterns were different in each hospital of Baghdad city. ConclusionIn this study, we observed an increase in the rate of fosfomycin- and colistin-resistant A. baumannii in Baghdad, Iraq during 2014–2018. The fosA3 and mcr-1 participated in fosfomycin and colistin resistance, respectively. Major risk factors for isolation of colistin-resistant A. baumannii included prior six months consumption of cephalosporins and carbapenems and previous two months of hospitalization. PFGE results unraveled 13 pulsotypes (A-M) without genetic relation.