Acinetobacter baumannii, a bacterial strain which demonstrates an elevated wide range multidrug resistance to commonly prescribed antibiotics, has been linked to recent major global outbreaks, raising a major clinical concern. Its reduced antibiotic susceptibility is closely related to the acquisition of a potent carbapenemase and/or intrinsic gene "over expression" through insertion sequences. Hence, this study aimed at investigating the antimicrobial susceptibility and molecular mechanisms underlying β-lactam resistance in A. baumannii, isolated at an academic medical centre. To understand the basis of resistance, 103 multidrug-resistant (MDR) A. baumannii isolates were collected, their antibiotic susceptibility was tested phenotypically, and then molecular analyses were performed, by testing a range of commonly encountered carbapenemases-OXA-51, OXA-23, NDM, VIM, and KPC. All strains demonstrated pan-resistance to most of the advanced antibiotics tested, including piperacillin/tazobactam, ceftazidime, cefepime, and ciprofloxacin. Moreover, majority of isolates exhibited resistance to imipenem (98.1%) and trimethoprim (90.3%). Approximately 50% of the strains showed meropenem, amikacin, and gentamycin resistance; however, lower resistance rate to tigecycline (4.9%) was noted. Moreover, isolates contained potent carbapenemases such as the intrinsic OXA-51 (89.3%), as well as the acquired resistant genes OXA-23 (68.9%), NDM (84.5%), and VIM (88.3%). The insertion sequence element ISAba1 was only detected in 35.9% of the strains. Potent resistant genes known to be carried on mobile genetic elements that aid the spread of highly resistant phenotypes were observed in a majority of isolates. These findings enforce the need for vigilant infection control measures and continuous surveillance.