Novel Antimicrobial Strategies to Combat Multidrug-Resistant (MDR) Gram-Negative Bacteria, 2nd Edition

A special issue of Antibiotics (ISSN 2079-6382).

Deadline for manuscript submissions: 31 October 2025 | Viewed by 198

Special Issue Editor


E-Mail Website
Guest Editor
Department of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ, USA
Interests: antibiotic resistance; multidrug resistance; lysine acetylation; KAT; KDAC; histone-like proteins; post-translational modifications; mass spectrometry; proteomics; antimicrobial peptides; biofilm
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Infections and mortality caused by Gram-negative bacteria (GNBs) are increasing all over the world. Moreover, these types of infections are becoming increasingly difficult to treat, given the concurrent increase in the prevalence of antibiotic-resistant bacteria. Further compounding this problem, GNBs tend to become resistant to multiple drug classes and are referred to as multidrug-resistant (MDR) GNBs, which often leaves physicians with few or no treatment options. In fact, the 2024 World Health Organization priority pathogens list predominantly comprises GNBs, including all those in the critical category. GNBs possess a plethora of resistance strategies, either intrinsic or acquired, to avoid antibiotic-mediated cell death. Resistance genes and determinants rapidly spread among bacterial populations, which contributes to the rapid emergence of MDR strains. Intrinsically, the main weapon of GNBs is their cell wall, specifically the outer membrane, which serves as an excellent permeability barrier to drugs and environmental insults. Bacteria can also acquire or evolve resistance to common skin antiseptics and disinfectants, which contributes to hospital outbreaks of MDR bacteria. Novel strategies to treat and limit the spread of drug-resistant GNBs are imperative and will serve as the primary focus of the second edition of this Special Issue. This research topic focuses on studies (including original research, methods, perspectives, reviews, and commentaries) that explore and discuss the following topics:

  • New insights into the mechanisms of antibiotic or antiseptic resistance;
  • Determination of novel combinations of drugs to eliminate MDR bacteria;
  • Discovery of novel drug targets for antibiotic development;
  • Development of novel in vitro or animal models of infection;
  • Discovery and evaluation of new beta-lacatamase, aminoglycoside-modifying enzyme, or efflux pump inhibitors;
  • Evaluation of the potency of new antibiotics on MDR bacteria;
  • Emergence of new resistance determinants in hospital populations.

Dr. Valerie Carabetta
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Antibiotics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • gram negative
  • antibiotic resistance
  • antiseptic resistance
  • multidrug resistant
  • extensively drug resistant
  • pandrug resistant
  • MDR
  • XDR
  • PDR
  • efflux pumps
  • mechanisms of resistance
  • beta-lactamase
  • outer membrane

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

11 pages, 370 KiB  
Article
Description of Two Resistance-Nodulation-Cell Division Efflux Systems Involved in Acquired Antibiotic Resistance: AxySUV in Achromobacter xylosoxidans and AinCDJ in Achromobacter insuavis
by Arnaud Magallon, Julien Bador, Thomas Garrigos, Caroline Demeule, Anaïs Chapelle, Véronique Varin, Catherine Neuwirth and Lucie Amoureux
Antibiotics 2025, 14(6), 536; https://doi.org/10.3390/antibiotics14060536 - 23 May 2025
Viewed by 73
Abstract
Background/Objectives: Achromobacter xylosoxidans and Achromobacter insuavis are emerging opportunistic pathogens. Several Resistance-Nodulation-cell Division (RND) efflux systems are involved in intrinsic or acquired antibiotic resistance (AxyABM, AxyXY-OprZ, and AxyEF-OprN). The aim of this study was to explore the resistance mechanisms in one-step mutants in [...] Read more.
Background/Objectives: Achromobacter xylosoxidans and Achromobacter insuavis are emerging opportunistic pathogens. Several Resistance-Nodulation-cell Division (RND) efflux systems are involved in intrinsic or acquired antibiotic resistance (AxyABM, AxyXY-OprZ, and AxyEF-OprN). The aim of this study was to explore the resistance mechanisms in one-step mutants in which the efflux systems described to date are not involved: one mutant of A. insuavis AXX-A (AXX-A-Do1) and two mutants of A. xylosoxidans CIP102236 (CIP102236-El9 and CIP102236-Eo4) selected on fluoroquinolones. Methods: In vitro mutants were compared to parental isolates by WGS. RT–qPCR and gene inactivation were used to explore the role of the new efflux systems detected. Results: In the A. insuavis AXX-A mutant (AXX-A-Do1), WGS showed a substitution in the putative regulator of the new RND efflux system AinCDJ. The transporter gene ainD was 79-fold overexpressed in AXX-A-Do1, compared to its parental strain. The inactivation of ainD in AXX-A-Do1 led to a decrease in MICs of (8-fold), levofloxacin (8-fold), cefepime (≥8-fold), meropenem (4-fold), doripenem (4-fold), doxycycline (4-fold), minocycline (4-fold), tigecycline (4-fold) and chloramphenicol (≥8-fold). The MICs values obtained were similar to those of the parental strain AXX-A. The same approach allowed the detection of the new efflux system AxySUV in A. xylosoxidans CIP102236 mutants, in which substitutions in the putative AxySUV regulator were associated with the overexpression of the transporter gene axyU. axyU inactivation in the mutants led to a decrease in MICs of ciprofloxacin (8- to 16-fold), levofloxacin (4- to 8-fold), doripenem (4-fold), doxycycline (4-fold), minocycline (4-fold), and chloramphenicol (≥4-fold). Interestingly, axySUV is present in only about 50% of available A. xylosoxidans genomes, whereas ainCDJ is detected in all A. insuavis genomes. Conclusions: This study demonstrated that AinCDJ overproduction is involved in the acquired resistance of A. insuavis to cefepime, meropenem, doripenem, fluoroquinolones, minocycline, doxycycline, tigecycline, and chloramphenicol and that AxySUV overproduction is involved in the acquired resistance of A. xylosoxidans to meropenem, fluoroquinolones, minocycline, doxycycline, and chloramphenicol. Full article
Show Figures

Figure 1

Back to TopTop