Identification, resistance mechanisms, and innovative therapeutic approaches against Acinetobacter baumannii–calcoaceticus complex

Le résumé fourni par la source

Acinetobacter baumannii–calcoaceticus complex (ABC complex) is recognized as one of the most critical multidrug drugs resistant (MDR) pathogens worldwide and remains a major cause of hospital-acquired infections, particularly in intensive care settings. Members of this complex are associated with ventilator-associated pneumonia, bloodstream infections, wound infections, urinary tract infections, and meningitis, often affecting critically ill and immunocompromised patients. Their clinical importance is primarily driven by their remarkable ability to acquire, accumulate, and maintain resistance determinants against multiple classes of antimicrobial agents. The ABC complex acquires resistance through diverse and coordinated mechanisms, including the production of β -lactamases, target-site alterations, efflux pump overexpression, reduced membrane permeability, horizontal gene transfer (HGT), and the mobilization of insertion sequences and other genetic elements that modulate intrinsic and acquired resistance genes. The rapid dissemination of these determinants has significantly limited therapeutic options and contributed to global outbreaks. Accurate identification of individual members within the complex is essential, as closely related species may differ in epidemiology and resistance profiles. A comprehensive understanding of molecular resistance mechanisms, reliable diagnostic approaches, and evolving treatment strategies, including combination therapies and novel agents, is crucial. This review summarizes current knowledge on resistance mechanisms, identification methods, and innovative therapeutic strategies, highlighting the need for integrated clinical and microbiological efforts to combat ABC complex infections.

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