Acinetobacter baumannii is a Gram-negative, non-motile pathogen commonly associated with healthcare settings. It is capable of causing severe infections, particularly in immunocompromised and critically ill individuals, and is linked to poor clinical outcomes. Infections caused by carbapenem-resistant A. baumannii (CRAB) represent a major public health concern due to limited treatment options and high resistance rates. Several virulence determinants contribute to CRAB’s pathogenicity, including capsular exopolysaccharide (CPS), lipopolysaccharide (LPS), lipooligosaccharide (LOS), efflux pumps, outer membrane proteins (OMPs), pili, metal acquisition systems, two-component regulatory systems (TCSs), and secretion systems (SSs). The dominant resistance mechanism in CRAB involves the production of carbapenemases, most notably oxacillinase-23 (OXA-23) and metallo-β-lactamases (MBLs) such as Verona integron-encoded MBL (VIM) and New Delhi MBL (NDM). Accurate identification of these resistance mechanisms is crucial for guiding effective antimicrobial therapy. Potential treatment options include older agents like polymyxins, ampicillin–sulbactam, high-dose carbapenems, tigecycline, and minocycline, along with newer antimicrobials such as eravacycline, cefiderocol, and aztreonam–avibactam. This review aims to explore the virulence mechanisms and molecular pathogenesis of CRAB, while also presenting recent developments in its epidemiology and available antimicrobial therapies.
Karampatakis et al. (2025) studied this question.