Abstract
Carbapenem- and colistin-resistant Acinetobacter baumannii pose a serious global health threat due to limited therapeutic options and rapid dissemination of resistance determinants. This cross-sectional study investigated known carbapenemase and colistin resistance genes among clinical A. baumannii isolates from hospitalized patients in Chattogram, Bangladesh. A total of 325 clinical specimens (urine, wound swab, sputum, blood, and endotracheal aspirate) were processed by standard microbiological methods. Species confirmation was performed by 16S rRNA gene amplification. Antimicrobial susceptibility was determined by the Kirby-Bauer method, and colistin MICs were measured by broth microdilution. Among 239 bacterial isolates, 26 (10.9%) were confirmed as A. baumannii. High resistance rates were observed for ciprofloxacin (65.4%), cefepime (65.4%), meropenem (53.9%), and imipenem (46.2%). Four isolates (15.4%) were colistin-resistant, with MICs ranging from ≤0.5 to 64 µg/mL. Carbapenemase genes were detected in 16 (61.5%) isolates, predominantly blaNDM-1 (50%), followed by blaVIM (7.7%) and blaOXA-48 (3.8%), showing a strong association with carbapenem resistance (P = 0.0000124). The phoQ gene was identified in 7 (26.9%) isolates, with co-existence of pmrC in 2; four of these were colistin-resistant (P = 0.0023). Sequencing of phoQ revealed point mutations consistent with known resistance-associated variants. The predominance of blaNDM-1 & phoQ-mediated resistance highlights the urgent need for molecular surveillance and stringent antimicrobial stewardship to curb the spread of multidrug-resistant A. baumannii in Bangladeshi hospitals. IMPORTANCE: Antibiotic-resistant Acinetobacter baumannii is a serious threat to patient health worldwide because it can resist many of the strongest available antibiotics, making infections difficult to treat. This study identifies the genes that allow these bacteria to survive last-resort drugs such as carbapenems and colistin in hospitals in Chattogram, Bangladesh. By pinpointing the common carbapenem-resistance gene (blaNDM-1) and colistin-resistance mutations (phoQ), the research shows how these bacteria evade treatment and highlights the risk of their spread in healthcare settings. Understanding these resistance mechanisms helps doctors choose effective therapies and informs hospital policies to prevent outbreaks. The findings underscore the urgent need for ongoing monitoring of antibiotic resistance and stronger stewardship of antibiotic use to protect patients and curb the rise of these dangerous "superbugs."