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Antibiotics
Special Issues
Genetic Mechanisms of Bacterial Survival: Antibiotic Resistance and Defense Strategies
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Genetic Mechanisms of Bacterial Survival: Antibiotic Resistance and Defense Strategies

A special issue of Antibiotics (ISSN 2079-6382). This special issue belongs to the section "Mechanism and Evolution of Antibiotic Resistance".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 3667

Special Issue Editors

Dr. Caio Augusto Martins Aires

E-Mail Website
Guest Editor
Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal 59078 970, RN, Brazil
Interests: carbapenemases; gram-negative bacilli; ESBL; one health approach
Dr. Thiago Pavoni Gomes Chagas

E-Mail Website
Guest Editor
1. Department of Pathology, School of Medicine, Universidade Federal Fluminense, Niterói, RJ, Brazil
2. Molecular Epidemiology and Biotechnology Laboratory (LEMB), Faculty of Pharmacy, Universidade Federal Fluminense, Niterói, RJ, Brazil
Interests: antimicrobial resistance; one health; genetics of microorganisms

Special Issue Information

Dear Colleagues,

Bacteria have developed diverse genetic mechanisms that enhance their survival in hostile environments, particularly against antibiotics. These strategies, such as mutations, horizontal gene transfer, efflux pumps, enzymatic degradation, and biofilm formation, enable bacteria to resist not only antibiotics but also other antimicrobial agents like disinfectants, biocides, antiseptics, and heavy metals. Antibiotic resistance, driven by these mechanisms, poses a significant threat to global health. Rapid resistance spread through horizontal gene transfer emphasizes the need for constant vigilance. Early detection of resistance genes and robust surveillance systems are crucial for controlling the rise of resistant infections. Advanced“omics”technologies offer deeper insights into these mechanisms, aiding in developing new treatments. This Special Issue encourages submissions that expand our understanding of bacterial survival strategies, particularly against a wide range of antimicrobial agents.

Dr. Caio Augusto Martins Aires
Dr. Thiago Pavoni Gomes Chagas
Guest Editors

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. 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

  • antimicrobial resistance mechanisms
  • disinfectant and antiseptic resistance
  • biofilm formation
  • genomic insights
  • horizontal gene transfer

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Published Papers (2 papers)

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Research

18 pages, 1834 KB  
Article
Imipenem-Induced Transcriptional Responses of Porin, Efflux Pumps, and Carbapenemase Genes in Clinical Carbapenem-Resistant Acinetobacter baumannii
by Suna Sibel Rizvanoglu, Basar Karaca and Mujde Eryilmaz
Antibiotics 2026, 15(3), 299; https://doi.org/10.3390/antibiotics15030299 - 15 Mar 2026
Viewed by 605
Abstract
Background/Objectives: Carbapenem-resistant Acinetobacter baumannii poses a critical threat due to its ability to acquire multiple resistance mechanisms and persist under antibiotic pressure. This study aimed to elucidate the molecular basis of imipenem resistance in clinical A. baumannii isolates by integrating phenotypic, molecular, [...] Read more.
Background/Objectives: Carbapenem-resistant Acinetobacter baumannii poses a critical threat due to its ability to acquire multiple resistance mechanisms and persist under antibiotic pressure. This study aimed to elucidate the molecular basis of imipenem resistance in clinical A. baumannii isolates by integrating phenotypic, molecular, transcriptional, and clonal analyses. Methods: Eleven A. baumannii isolates identified by MALDI-TOF MS (matrix-assisted laser desorption ionization time-of-flight mass spectrometry) were investigated. Antimicrobial susceptibility to imipenem and meropenem was assessed, followed by polymerase chain reaction (PCR) detection of Ade efflux pump, outer membrane porin, and OXA-type carbapenemase genes. Transcriptional responses to sub-inhibitory imipenem exposure were evaluated using quantitative real-time PCR, and clonal relatedness was assessed by arbitrarily primed PCR. Results: All isolates were carbapenem-resistant, with blaOXA-23 detected in all isolates and blaOXA-24 absent in one isolate. Transcriptional analysis revealed isolate-specific responses to imipenem exposure. Among Ade efflux pump components, only adeR exhibited expression changes, displaying either downregulation or upregulation depending on the isolate, whereas adeA, adeB, adeC, and adeS transcripts were not detected under the tested conditions. Outer membrane porin genes showed heterogeneous regulation, with ompA and carO downregulated, while some isolates showed increased expression. Expression of oprD varied among isolates, and omp33–36 transcripts were detected in a single isolate and were reduced after exposure. Clonal analysis identified nine distinct genotypes, indicating genetic diversity and the absence of clonal dominance. Conclusions: These findings highlight the multifactorial and heterogeneous nature of carbapenem resistance in A. baumannii, emphasizing the interplay between regulatory efflux mechanisms, porin modulation, and carbapenemase carriage. Full article
(This article belongs to the Special Issue Genetic Mechanisms of Bacterial Survival: Antibiotic Resistance and Defense Strategies)
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13 pages, 556 KB  
Article
Prevalence and Variability of Helicobacter pylori Clarithromycin Resistance Mutations in Pediatric Patients in Poland: A Genotypic Analysis Using the Bosphore Genotyping Kit
by Tomasz Bogiel, Anna Szaflarska-Popławska and Agnieszka Krawczyk
Antibiotics 2025, 14(4), 352; https://doi.org/10.3390/antibiotics14040352 - 31 Mar 2025
Cited by 1 | Viewed by 2474
Abstract
Background: Helicobacter pylori is a Gram-negative bacterium responsible for various gastrointestinal diseases, including peptic ulcers and gastric cancer. Despite available antibiotic therapies, increasing resistance to clarithromycin—a key antibiotic in eradication regimens—poses a significant challenge. This resistance is primarily linked to point mutations in [...] Read more.
Background: Helicobacter pylori is a Gram-negative bacterium responsible for various gastrointestinal diseases, including peptic ulcers and gastric cancer. Despite available antibiotic therapies, increasing resistance to clarithromycin—a key antibiotic in eradication regimens—poses a significant challenge. This resistance is primarily linked to point mutations in the 23S rRNA gene, particularly A2143G, A2142G, and A2142C, which hinder clarithromycin binding, reducing its bacteriostatic efficacy. This study aimed to assess the prevalence and variability of clarithromycin resistance mutations in pediatric patients from Bydgoszcz, Poland. Methods: A total of 45 gastric biopsy samples from pediatric patients were analyzed using the Bosphore® Helicobacter pylori Genotyping Kit v1 to detect clarithromycin resistance-associated mutations. Results: Among the 45 tested samples, 30 were classified as wild-type, while 12 contained resistance-associated mutations. The most frequently detected mutation was A2143G (58.3%), followed by A2142G (33.3%). One sample exhibited both A2142G and A2143G mutations, and another contained a mixture of wild-type and mutant strains. The A2142C mutation was not detected in any sample. Conclusions: Our findings confirm the predominance of A2143G among clarithromycin-resistant H. pylori strains, consistent with global trends. The detection of both mutant and wild-type strains in a single patient highlights potential co-infections or subpopulations with varying resistance profiles. Continuous surveillance and improved diagnostic tools are crucial for optimizing treatment strategies. Tailored eradication protocols based on resistance profiling are necessary to enhance treatment efficacy and mitigate the spread of resistant strains. Further research is needed to understand the clinical implications of mixed infections and double mutations in H. pylori resistance development. Full article
(This article belongs to the Special Issue Genetic Mechanisms of Bacterial Survival: Antibiotic Resistance and Defense Strategies)
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