Acinetobacter baumannii: Mechanisms of antibiotic resistance, quorum sensing regulation, and current therapeutic strategies
Abstract
Acinetobacter baumannii has emerged as a major global pathogen due to extensive resistance to last-resort antimicrobials, a high burden of nosocomial infections, and increasing community-acquired cases. Its adaptability is driven by diverse resistance mechanisms, including β-lactamase production, aminoglycoside-modifying enzymes, efflux pump overexpression, target-site mutations, and lipid A remodeling, all of which limit treatment options and worsen clinical outcomes. Pathogenicity is further enhanced by quorum-sensing systems, particularly AbaI/AbaR, which regulate biofilm formation, virulence, and antimicrobial tolerance. Despite extensive research, resistance, quorum sensing, and therapeutic strategies are often examined separately, limiting mechanistic understanding. This review integrates current evidence on the interplay between resistance evolution, quorum sensing, and biofilm persistence, linking these to therapeutic vulnerabilities. It further evaluates emerging interventions, including optimized antibiotic combinations, immunomodulation, drug repurposing, bacteriophage therapy, and alternative approaches, such as antimicrobial peptides, phytochemicals, nanotechnology, and photodynamic therapy to inform improved treatment strategies.
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