Molecular and bacteriological characterization of colistin and carbapenem-resistant nosocomial isolates of Acinetobacter baumannii isolated from different Iraqi hospitals
Dhuha A. Abbas, Mushtak T.S. Al-Ouqaili, Mohammed J. Alfeehan
Abstract
Colistin- and carbapenem-resistant Acinetobacter (A.) baumannii pose a global health threat in healthcare settings due to difficult-to-treat infections. This study investigates their prevalence, resistance mechanisms, and the role of biofilm formation in persistence and pathogenicity. This cross-sectional observational study was conducted on 335 clinical specimens, specifically isolates of A. baumannii , during the period from December to July 2025. Bacteriological investigation was confirmed using the automated Vitek 2 compact system, and antimicrobial susceptibility was determined using the AST 419 card, in accordance with the CLSI 2025 guidelines. Biofilm formation was assessed using the microtiter plate method. PCR detection for carbapenem and colistin-resistant genes ( bla NDM , bla NDM-1 , bla VIM , bla IMP , bla OXA-48 ) and ( mcr-1 , mcr-5 , pmrA , and pmrB ), respectively, has been done. A total of 335 clinical study specimens were analyzed, with 222 (66.2%) representing bacterial growth. Of these, 64 (28.8%) were well bacteriologically identified as A. baumannii . Out of these isolates, 50 were multidrug resistant, classified into 31 (62%) as extensively drug resistant (XDR) and 19 (38%) as Pan-drug resistant. Biofilm formation was distributed as strong biofilm formation in sputum (31.2%), wound swabs (25%), urine (7.1%), and vaginal swabs (100%). Molecular analysis revealed that bla NDM-1 (18%) was the most common carbapenemase-resistant gene, followed by blaVIM (16%), bla IMP-1 (12%), bla NDM (4%), and bla OXA-48 (2%) . For colistin resistance, pmrB ( 54%) and pmrA (40%) were predominant, while mcr-1 was (4%). Notably, mcr-5 was not detected in all colistin-resistant genes. Most A. baumannii isolates were extensively drug-resistant or pan-drug-resistant and exhibited variable biofilm formation, likely enhancing persistence in hospital environments. High prevalence of bla NDM-1 and bla VIM carbapenem resistance genes, along with pmrB and pmrA colistin resistance genes, complicates treatment and diagnostics. Prompt detection, effective infection control, and continuous surveillance are urgently needed to limit the spread of these highly resistant strains.