Efflux-Mediated Antibiotic Resistance in Acinetobacter baumannii

Acinetobacter baumannii is a Gram-negative opportunistic pathogen responsible for severe hospital-acquired infections worldwide. Its ability to survive desiccation and adhere to medical devices contributes to persistent outbreaks in intensive-care settings. A. baumannii has evolved multiple strategies to resist antibiotics, among which active efflux of drugs is a central mechanism. Efflux pumps belonging to the resistance-nodulation-division (RND) family, notably AdeABC, AdeIJK and AdeFGH, export a broad spectrum of antimicrobial agents, including carbapenems, fluoroquinolones and tigecycline. Overexpression of these transporters is frequently driven by mutations in two-component regulatory systems such as AdeRS or BaeSR, resulting in multidrug resistance that compromises last-line therapies. Efflux-mediated resistance also interacts with biofilm formation, as pump activity can influence cell aggregation and horizontal gene transfer. Global surveillance has revealed the widespread distribution of efflux variants, underscoring their clinical significance. Efflux pump inhibitors and novel compounds targeting regulatory pathways are under investigation to restore antibiotic efficacy. Improved understanding of pump structure, substrate specificity and regulatory networks is critical for guiding stewardship and designing next-generation therapeutics against this high-priority pathogen.

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Efflux-Mediated Antibiotic Resistance in Acinetobacter baumannii publication trend

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

Technical terms

Efflux pump: membrane protein complex that exports antibiotics and toxins out of bacterial cells.

Resistance-nodulation-division (RND) family: a major class of tripartite efflux systems in Gram-negative bacteria.

Minimum inhibitory concentration (MIC): the lowest antibiotic concentration that prevents visible bacterial growth.

Sub-minimal inhibitory concentration (sub-MIC): antibiotic concentration below the MIC that may induce resistance mechanisms.

References

1. The Mechanism of Tigecycline Resistance in Acinetobacter baumannii under Sub-Minimal Inhibitory Concentrations of Tigecycline. International Journal of Molecular Sciences (2024).
2. Resistance mechanisms of tigecycline in Acinetobacter baumannii. Frontiers in Cellular and Infection Microbiology (2023).
3. The RND Efflux Pump Gene Expression in the Biofilm Formation of Acinetobacter baumannii. Antibiotics (2023).
4. Global genomic epidemiology of chromosomally mediated non-enzymatic carbapenem resistance in Acinetobacter baumannii: on the way to predict and modify resistance. Frontiers in Microbiology (2023).
5. The Acinetobacter baumannii Two-Component System AdeRS Regulates Genes Required for Multidrug Efflux, Biofilm Formation, and Virulence in a Strain-Specific Manner. mBio (2016).
6. Role of the BaeSR two-component system in the regulation of Acinetobacter baumannii adeAB genes and its correlation with tigecycline susceptibility. BMC Microbiology (2014).