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Advanced Strategies in Bacterial Antibiotic Resistance
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Advanced Strategies in Bacterial Antibiotic Resistance

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 20 August 2026 | Viewed by 1040

Special Issue Editor

Dr. Xuemei Yang

E-Mail Website
Guest Editor
Department of Food Science and Nutrition, The Hong Kong Polytechnic University, Hong Kong
Interests: bacterial pathogens; antimicrobial resistance; virulence factors; molecular epidemiology; transmission; vaccines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The relentless evolution of bacterial antibiotic resistance (AMR) constitutes a global health emergency, threatening modern medicine. They deploy sophisticated tactics—genetic mutations, adaptive evolution, and exploitation of mobile genetic elements (MGEs) like plasmids, transposons, and integrons—to acquire, optimize, and spread resistance. Understanding these bacterium-deployed tactics—their emergence, regulation, spread, and evolution—is fundamental to designing effective, next-generation countermeasures before our antimicrobial arsenal is rendered obsolete.

This Special Issue aims to gather cutting-edge research and comprehensive reviews that explores the novel and evolving tactics employed by bacteria to survive antibiotic pressure. It focuses on the molecular, genetic, and ecological strategies bacteria use to achieve and enhance resistance.

Suitable topics include, but are not limited to, the following:

  1. Novel resistance mechanisms (enzymatic inactivation pathways, efflux pump variants, target site mutations, and permeability barriers).
  2. Emerging vectors (plasmids, ICEs, phages) and conditions facilitating the accelerated spread of resistance genes.
  3. Strategies like persister cell formation, transient tolerance induction, and population heterogeneity enabling survival under fluctuating antibiotic exposure.
  4. Global regulators, stress responses, metabolic adaptations, epistasis, and compensatory evolution fine-tune resistance and fitness.
  5. Enhanced resistance mechanisms unique to or amplified within biofilm communities.

Dr. Xuemei Yang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • antibiotic resistance
  • resistance mechanisms
  • antibiotic resistance genes (ARGs)
  • antibiotic tolerance
  • heteroresistance
  • horizontal gene transfer (HGT)
  • compensatory evolution

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Published Papers (2 papers)

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21 pages, 3450 KB  
Article
The Synergistic Armory: A Global Genome-Wide Association Study Reveals the Integrated Mechanisms of Azithromycin Resistance in Neisseria gonorrhoeae
by Boris Shaskolskiy, Konstantin Tutaev, Dmitry Kravtsov, Ilya Kandinov and Dmitry Gryadunov
Int. J. Mol. Sci. 2026, 27(5), 2258; https://doi.org/10.3390/ijms27052258 - 27 Feb 2026
Viewed by 435
Abstract
Azithromycin remains an important agent in gonorrhea treatment, yet resistance is a growing global threat. To comprehensively define its genetic basis, we performed a large-scale genome-wide association study of 14,727 Neisseria gonorrhoeae genomes with linked azithromycin MICs from 66 countries. We identified 113 [...] Read more.
Azithromycin remains an important agent in gonorrhea treatment, yet resistance is a growing global threat. To comprehensively define its genetic basis, we performed a large-scale genome-wide association study of 14,727 Neisseria gonorrhoeae genomes with linked azithromycin MICs from 66 countries. We identified 113 genetic variants significantly associated with elevated MICs. Beyond well-known mutations in 23S rRNA (A2059G, C2611T) and mtrCDE operon, we uncovered a broad repertoire of potential resistance determinants, including multiple amino acid substitutions in 16 ribosomal proteins (e.g., L2, L4, L13, L23) forming the nascent peptide exit tunnel (NPET), and porin PorB alterations (G120K, A121D/N). Systematic pairwise analysis revealed extensive synergistic interactions, particularly between variants affecting drug influx/efflux (PorB, MtrCDE) and ribosomal target affinity. Phylogenetic analysis identified successful, globally circulating lineages employing distinct resistance strategies: NPET-dominated, 23S rRNA-associated, and porin/efflux-mediated. Our findings demonstrate that azithromycin resistance is a polygenic trait shaped by functional complementarity and epistasis between target modification, membrane permeability, and efflux. This integrated model is essential for accurate resistance prediction from genomic data and highlights key lineages for focused surveillance. Full article
(This article belongs to the Special Issue Advanced Strategies in Bacterial Antibiotic Resistance)
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15 pages, 2579 KB  
Article
Sublethal Antibiotic Exposure Induces Microevolution of Quinolone Resistance in Pathogenic Vibrio parahaemolyticus
by Qian Wu, Han Yang, Tianming Xu, Pradeep K. Malakar, Huan Li and Yong Zhao
Int. J. Mol. Sci. 2026, 27(3), 1416; https://doi.org/10.3390/ijms27031416 - 30 Jan 2026
Viewed by 331
Abstract
The microevolutionary pathways and molecular mechanisms by which the important pathogen Vibrio parahaemolyticus acquires resistance in the aquatic environment under continuous selective pressure from quinolone antibiotic residues are still unknown. Here, the study successfully simulated the long-term pressure of antibiotic residues in aquaculture [...] Read more.
The microevolutionary pathways and molecular mechanisms by which the important pathogen Vibrio parahaemolyticus acquires resistance in the aquatic environment under continuous selective pressure from quinolone antibiotic residues are still unknown. Here, the study successfully simulated the long-term pressure of antibiotic residues in aquaculture by susceptible V. parahaemolyticus (VPD14) which was isolated from seafood, to a 30-day in vitro induction with sublethal concentrations of levofloxacin, which yielded the mutants (VPD14M). A phenotypic analysis revealed that VPD14M exhibited resistance to ampicillin, levofloxacin and ciprofloxacin, compared to VPD14. These changes were accompanied by adaptations, including a decreased growth rate and an enhanced biofilm formation capacity. Whole-Genome Sequencing identified that the acquired resistance was primarily attributable to key point mutations in three Quinolone Resistance-Determining Regions (QRDRs). Specifically, a G → T substitution at nucleotide position 248 in the gyrA gene, leading to a serine-to-isoleucine substitution at the 83rd amino acid position (Ser83Ile) of the DNA gyrase subunit A; a C → T substitution at position 254 in the parC gene, resulting in a serine-to-phenylalanine substitution at position 85 (Ser85Phe) of the topoisomerase IV subunit A; and a C → T substitution at position 2242 in the gyrB gene, causing a proline-to-serine substitution at position 748 (Pro748Ser) of the DNA gyrase subunit B. Collectively, the study demonstrated that sublethal antibiotic levels rapidly drive quinolone resistance in V. parahaemolyticus, and the specific mutations identified offer critical support for resistance monitoring and seafood safety alerts. Full article
(This article belongs to the Special Issue Advanced Strategies in Bacterial Antibiotic Resistance)
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