Special Issue "Bacterial Resistance to Antibiotics: Experimental and Epidemiological Evolution"

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

Deadline for manuscript submissions: 30 November 2023 | Viewed by 1554

Special Issue Editor

Univ. Grenoble Alpes, CNRS, Grenoble INP, CHU Grenoble Alpes, TIMC-IMAG, 38000 Grenoble, France
Interests: bacterial zoonoses; clinical microbiology; epidemiology; Francisella tularensis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Antibiotic resistance is a major threat to human health and a worldwide public health priority. Almost all bacterial species causing human infections have developed resistance to one or several antibiotic classes. Antibiotic resistance mechanisms are complex and associated with phenotypic and genetic changes. In addition to the classical resistance mechanisms (i.e., modification of the antibiotic bacterial targets, inactivation of the antibiotic, reduction in antibiotic penetration, and antibiotic efflux), bacteria can develop many other resistance pathways (including metabolism reduction, persisters, and other physiological changes). Understanding the evolutionary mechanisms leading to these resistances remains a challenge. Experimental models have allowed researchers to address several issues, including the speed, frequency, reproducibility, and conditions of resistance selection as well as the phenotypic and genetic changes, molecular mechanisms, evolution pathways, and fitness costs associated with antibiotic resistance. Strategies to combat antibiotic resistance have also been evaluated experimentally, and include preventing or delaying evolution to antibiotic resistance, reverting antibiotic resistance to susceptibility, restoring antibiotic-susceptible populations, and increasing the bacterial fitness cost of antibiotic resistance. The Special Issue focuses on all these aspects of experimental evaluation of bacterial evolution to antibiotic resistance using axenic media, cell cultures, or animal models.

Dr. Max Maurin
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.


  • antibiotic resistance
  • experimental models
  • antibiotic resistance selection
  • antibiotic resistance evolution pathways
  • antibiotic resistance phenotypes
  • antibiotic resistance genotypes
  • antibiotic resistance mechanisms
  • antibiotic resistance cost
  • antibiotic resistance prevention and control
  • antibiotic resistance reversion

Published Papers (1 paper)

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Progressive Sub-MIC Exposure of Klebsiella pneumoniae 43816 to Cephalothin Induces the Evolution of Beta-Lactam Resistance without Acquisition of Beta-Lactamase Genes
Antibiotics 2023, 12(5), 887; https://doi.org/10.3390/antibiotics12050887 - 10 May 2023
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Bacterial exposure to antibiotic concentrations below the minimum inhibitory concentration (MIC) may result in a selection window allowing for the rapid evolution of resistance. These sub-MIC concentrations are commonly found in soils and water supplies in the greater environment. This study aimed to [...] Read more.
Bacterial exposure to antibiotic concentrations below the minimum inhibitory concentration (MIC) may result in a selection window allowing for the rapid evolution of resistance. These sub-MIC concentrations are commonly found in soils and water supplies in the greater environment. This study aimed to evaluate the adaptive genetic changes in Klebsiella pneumoniae 43816 after prolonged but increasing sub-MIC levels of the common antibiotic cephalothin over a fourteen-day period. Over the course of the experiment, antibiotic concentrations increased from 0.5 μg/mL to 7.5 μg/mL. At the end of this extended exposure, the final adapted bacterial culture exhibited clinical resistance to both cephalothin and tetracycline, altered cellular and colony morphology, and a highly mucoid phenotype. Cephalothin resistance exceeded 125 μg/mL without the acquisition of beta-lactamase genes. Whole genome sequencing identified a series of genetic changes that could be mapped over the fourteen-day exposure period to the onset of antibiotic resistance. Specifically, mutations in the rpoB subunit of RNA Polymerase, the tetR/acrR regulator, and the wcaJ sugar transferase each fix at specific timepoints in the exposure regimen where the MIC susceptibility dramatically increased. These mutations indicate that alterations in the secretion of colanic acid and attachment of colonic acid to LPS may contribute to the resistant phenotype. These data demonstrate that very low sub-MIC concentrations of antibiotics can have dramatic impacts on the bacterial evolution of resistance. Additionally, this study demonstrates that beta-lactam resistance can be achieved through sequential accumulation of specific mutations without the acquisition of a beta-lactamase gene. Full article
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