ABSTRACT Acinetobacter baumannii , a multidrug‐resistant opportunistic bacterium, poses a substantial hazard in hospital settings. The emergence of colistin‐ and tigecycline‐resistant strains further limits treatment options and necessitates detailed investigation of resistance mechanisms. A total of 144 clinical A. baumannii isolates from multiple hospitals in Iran were identified using standard microbiological and molecular techniques. Antimicrobial susceptibility was assessed using both disk diffusion and broth microdilution techniques. Biofilm formation was quantified by crystal violet staining. Resistance and biofilm‐related genes were detected by conventional polymerase chain reaction (PCR). The expression of key resistance genes ( pmrA , pmrB , adeB , adeJ , and adeG ) was evaluated by quantitative PCR (qPCR) in resistant isolates, and MLST was performed to determine the genetic relatedness among tigecycline‐ and colistin‐resistant isolates. Resistance to colistin and tigecycline was observed in 3 (2.08%) and 2 (1.4%) isolates, respectively, and 90.9% of the isolates were biofilm producers, with higher odds of strong biofilm formation significantly correlating with the presence of bla PER1 . All isolates carried pmrA and pmrB , but only colistin‐resistant isolates showed overexpression of these genes compared to susceptible ones. MLST revealed diverse sequence types among resistant isolates, including ST188, ST138, ST387, ST2288, and ST3337. This study highlights the complex interplay between the presence of genes, their expression, and the resistance phenotype in A. baumannii and underscores the importance of monitoring chromosomal resistance determinants for effective control and treatment strategies.
Hatem et al. (Mon,) studied this question.