Biofilm Formation and Antibiotic Resistance in Acinetobacter baumannii

Acinetobacter baumannii has emerged as a formidable nosocomial pathogen, notable for its capacity to form resilient biofilms on both biotic and abiotic surfaces and for its rapid acquisition of multidrug resistance. Biofilms comprise communities of cells enmeshed in a self-produced extracellular polymeric substance, which acts as a protective barrier against antimicrobial agents and host defences. Within these structures, regulatory networks—often centred on two-component systems, second messengers such as cyclic di-GMP and cyclic AMP, and surface appendages like Csu pili—coordinate the transition from planktonic growth to surface-associated communities. Biofilm formation not only shields A. baumannii from antibiotics by limiting penetration and fostering a localised high-density environment for horizontal gene transfer, but also promotes persistence on medical devices, thereby contributing to outbreaks in intensive care units worldwide. Concurrently, the pathogen’s arsenal of resistance mechanisms—including β-lactam-hydrolysing enzymes, efflux pumps and target-site mutations—synergises with biofilm-mediated tolerance to underpin treatment failures and high mortality rates. Recent efforts have focused on elucidating the genetic determinants of biofilm assembly, mapping signalling cascades that link environmental cues to adhesive phenotypes and identifying agents capable of disrupting established biofilms or sensitising cells to existing antibiotics. Together, these advances are directing novel therapeutic strategies, from inhibitors targeting key regulators to combination regimens that weaken the biofilm matrix and restore antibiotic efficacy.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Biofilm Formation and Antibiotic Resistance in Acinetobacter baumannii publication trend

The graph below shows the total number of articles in biofilm formation and antibiotic resistance in acinetobacter baumannii across all publications each year (not limited to Nature Index journals).

Technical terms

Biofilm: Surface-attached microbial community encased in a self-produced matrix that impedes antibiotic penetration.

Extracellular polymeric substance (EPS): Mixture of polysaccharides, proteins and nucleic acids forming the structural scaffold of a biofilm.

Pili: Hair-like appendages on bacterial surfaces mediating adhesion to host tissues and abiotic surfaces.

Two-component system: Regulatory cascade comprising a sensor kinase and response regulator that governs gene expression in response to stimuli.

Second messengers: Intracellular signalling molecules (e.g. cyclic di-GMP, cyclic AMP) that regulate biofilm formation and virulence traits.

Minimal inhibitory concentration (MIC): Lowest concentration of an antimicrobial that prevents visible growth of a bacterium.

References

1. Csu pili dependent biofilm formation and virulence of Acinetobacter baumannii. npj Biofilms and Microbiomes (2023).
2. Discovery of novel BfmR inhibitors restoring carbapenem susceptibility against carbapenem-resistant Acinetobacter baumannii by structure-based virtual screening and biological evaluation. Emerging Microbes & Infections (2024).
3. Cyclic AMP is a global virulence regulator governing inter and intrabacterial signalling in Acinetobacter baumannii. PLOS Pathogens (2024).