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Antibiotics
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Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination
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Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination

A Special Issue of Antibiotics (ISSN 2079-6382) belonging to the section "Mechanism and Evolution of Antibiotic Resistance".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 6048

Editors

Dr. Ivo Nikolaev Sirakov

E-Mail Website
Guest Editor
Department of Medical Microbiology, Faculty of Medicine, Medical University of Sofia, 1431 Sofia, Bulgaria
Interests: molecular virology; sequencing; phylogenetic; diagnosis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Slawomir Ciesielski

E-Mail Website
Guest Editor
Department of Environmental Biotechnology, University of Warmia and Mazury in Olsztyn, 10-907 Olsztyn, Poland
Interests: antimicrobial agents; gut microbiome; metaomics; microbial biopolymers; microbial diversity; prokaryotic gene regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Antibiotic resistance develops through various well-known mechanisms, such as enzymatic degradation or modification of antimicrobial agents, alteration of target sites, reduced membrane permeability, and active efflux of drugs. These mechanisms have made infection control increasingly challenging worldwide. One main question remains unanswered: “Where do antibiotic resistance genes come from, and how is resistance acquired?”. Do they derive from the microbiome of humans and animals, from microorganisms in the environment, from the adaptation of the pathogens themselves (mutations in certain genes), a combination of these factors, or for another reason?

This Special Issue welcomes collaborative proposals across different research fields, inviting original scientific articles and reviews related to antibiotic resistance and the future consequences of its development. Research areas may include (but are not limited to) the following:

- Bacterial resistance;

- Viral resistance;

- Fungal resistance;

- Resistance gene transfer;

- Mutations in the genome of microorganisms;

- Evolution and adaptation of microorganisms;

- Mechanisms of resistance;

- Diagnostics of resistance;

- Therapy.

Dr. Ivo Nikolaev Sirakov
Prof. Dr. Slawomir Ciesielski
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-anonymized 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

  • antibiotic resistance genes
  • transposons
  • integrons
  • gene transfer
  • therapy

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Published Papers (7 papers)

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14 pages, 740 KB  
Article
Molecular Characterization of Colistin Resistance Acinetobacter baumannii Isolates and Identification of Mutations in pmrA and lpxA Genes from a Tertiary Care Hospital in South India
by MuthuLakshmi BackiaSubramanian, Madhumala Shanmugasundaram, Shanthi Mariappan, Uma Sekar, Renuka M K and Thyagarajan Ravinder
Antibiotics 2026, 15(9), 846; https://doi.org/10.3390/antibiotics15090846 - 31 Aug 2026
Viewed by 176
Abstract
Background/Objectives: Acinetobacter baumannii is a multidrug-resistant (MDR) nosocomial pathogen associated with significant morbidity and mortality. The emergence of strains resistant to multiple antibiotics has markedly reduced available treatment options. A. baumannii now demonstrates resistance to most first-line antibiotics, resulting in the extensive [...] Read more.
Background/Objectives: Acinetobacter baumannii is a multidrug-resistant (MDR) nosocomial pathogen associated with significant morbidity and mortality. The emergence of strains resistant to multiple antibiotics has markedly reduced available treatment options. A. baumannii now demonstrates resistance to most first-line antibiotics, resulting in the extensive use of colistin, which in turn has led to the emergence of colistin-resistant strains. There are very limited studies from India on the mechanisms of colistin resistance. In this study, we focused on the molecular mechanisms leading to colistin resistance. Methods: A total of 225 clinical isolates of Acinetobacter baumannii were analyzed in this study. Antimicrobial susceptibility testing was done using the disk diffusion method for various classes of antimicrobial agents as per the Clinical Laboratory Standards Institute (CLSI M100 Ed 35,2025). Susceptibility to colistin was tested by the Microbroth dilution method. Colistin resistance mediated by the mcr gene and alterations in the pmrAB and lpxACD genes were investigated using conventional PCR followed by mutational analysis. Results: Among the 225 isolates, 4 isolates were found to be colistin resistant. All the resistant isolates had an MIC ≥ 16 mcg/mL. Mutations were found in lpxA and pmrB (c.391T > C, c.495T > C, c.516A > G, c.732A > G and c.966T > C). Mutations in pmrA, lpxC, and lpxD were not detected in this study. Mcr-1 gene was not detected in this study. Conclusions: Colistin is the last resort for the treatment of MDR strains, and the increase in resistance to colistin has become a huge concern among the medical community as it reduces the options available for treatment. This is the first report on the molecular mechanisms of colistin resistance in South India using PCR. The study is also the first to report four novel mutations in the genes that may be responsible for resistance. Early detection of resistance and swift control measures can help curb the morbidity and mortality rate among such A. baumannii strains. Full article
(This article belongs to the Special Issue Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination)
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14 pages, 1997 KB  
Article
Molecular Detection of Linezolid Resistance Determinants and Identification of a Novel C2626T Mutation in Clinical Isolates of Enterococcus Species from India
by Madhumala Shanmugasundaram, MuthuLakshmi BackiaSubramanian, Shanthi Mariappan, Uma Sekar, Kennedy Kumar Palraj, Binesh Lal Yesudhason and Rhea Michelle J. Khodabux
Antibiotics 2026, 15(9), 841; https://doi.org/10.3390/antibiotics15090841 - 31 Aug 2026
Viewed by 162
Abstract
Background: Enterococcus species have emerged as significant multidrug-resistant nosocomial pathogens. Linezolid remains a vital last-resort therapeutic option for the management of severe infections caused by vancomycin-resistant Enterococci. However, resistance to linezolid occurs through several mechanisms, including the presence of the cfr [...] Read more.
Background: Enterococcus species have emerged as significant multidrug-resistant nosocomial pathogens. Linezolid remains a vital last-resort therapeutic option for the management of severe infections caused by vancomycin-resistant Enterococci. However, resistance to linezolid occurs through several mechanisms, including the presence of the cfr, cfr(D), and optrA genes, as well as mutations in domain V region of the 23S ribosomal RNA gene. This study aimed to detect and characterize linezolid resistance in clinical Enterococcus species. Methodology: A total of 266 clinical isolates belonging to the Enterococcus species were analyzed in this study. Antimicrobial susceptibility testing was performed using the disc diffusion method. The Minimum Inhibitory Concentration (MIC) of linezolid was determined by the agar dilution technique. PCR was performed to detect the presence of cfr, cfr(D), and optrA genes, along with mutations in domain V of the 23S rRNA gene. Results: Among the 266 isolates analyzed, 25 (9.4%) were found to be resistant to linezolid, with MIC values ≥ 8 µg/mL. Of these resistant isolates, the cfr gene was detected in one isolate, cfr(D) in sixteen isolates, and optrA in nine isolates. Notably, four isolates carried mutations in the domain V region of the 23S rRNA gene, including a novel C2626T mutation (in India) along with the previously reported G2592T mutation. Conclusions: This study reports the detection of cfr- and cfr(D)-mediated linezolid resistance among Enterococcus species in India. Furthermore, the presence of optrA and a novel C2626T mutation, alongside the G2592T mutation, was identified among resistant isolates. These findings underscore the urgent need for molecular surveillance to prevent further dissemination of these multidrug-resistant pathogens. Full article
(This article belongs to the Special Issue Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination)
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13 pages, 1982 KB  
Article
Multiple Independent Origins of Tn916-Mediated Tetracycline Resistance in Clostridium tetani from a Confined Geographic Area
by Chie Shitada, Motohide Takahashi and Makoto Kuroda
Antibiotics 2026, 15(8), 745; https://doi.org/10.3390/antibiotics15080745 - 31 Jul 2026
Viewed by 272
Abstract
Background/Objectives: Tetracycline resistance in Gram-positive bacteria has increased globally through horizontal gene transfer. Antimicrobial resistance genes in Clostridium tetani, the causative agent of tetanus, are rarely reported. Previously, we identified tetracycline resistance gene tet(M)-positive C. tetani strains in Japan, but their [...] Read more.
Background/Objectives: Tetracycline resistance in Gram-positive bacteria has increased globally through horizontal gene transfer. Antimicrobial resistance genes in Clostridium tetani, the causative agent of tetanus, are rarely reported. Previously, we identified tetracycline resistance gene tet(M)-positive C. tetani strains in Japan, but their evolutionary origin and acquisition mechanism remain unclear. This study aimed to elucidate the evolutionary origin of tet(M)-positive C. tetani and clarify the mechanism of horizontal resistance gene acquisition. Methods: Complete genome sequences of six tet(M)-positive C. tetani strains were determined using hybrid assembly of short-read (Illumina) and long-read (Oxford Nanopore) sequencing. Core genome single-nucleotide variant (SNV) analysis was performed to determine phylogenetic relationships. Tn916 element analysis of the tet(M) gene identified the origin of resistance genes and potential donor bacteria. Results: Based on core genome SNV analysis, all six tet(M)-positive strains belonged to Clade 1-2. The Tn916 element was approximately 18 kb and highly conserved; however, insertion sites differed significantly among strains. Phylogenetic analysis of the tet(M) gene revealed at least three distinct variants with different origins. Conclusions: Multiple independent acquisitions of Tn916-mediated tet(M), rather than clonal propagation, drove resistance emergence in geographically confined C. tetani populations. These findings support the notion that tetracycline resistance emerged through multiple independent horizontal transfer events involving Tn916. This pattern suggests that persistent environmental selective pressure, rather than clonal expansion, has shaped resistance dissemination, highlighting the importance of genomic surveillance and systematic monitoring to track the emergence of antimicrobial resistance in environmental and clinical settings. Full article
(This article belongs to the Special Issue Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination)
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17 pages, 1971 KB  
Article
Staphylococcal Cassette Chromosome mec (SCCmec) Natural Excision Frequencies and Its Contributing Factors in Variant SCCmec Type Prototypic Strains
by Salman Mirza, Laura Fine, Jo-Ann McClure, Joseph Kim, John M. Conly and Kunyan Zhang
Antibiotics 2026, 15(6), 555; https://doi.org/10.3390/antibiotics15060555 - 30 May 2026
Viewed by 888
Abstract
Background: Staphylococcus aureus acquires methicillin resistance genes through the SCCmec element. Although spontaneous SCCmec excision has been observed, its frequency, type-specific variation, and responsiveness to environmental conditions remain undefined. Here, we systematically quantified SCCmec excision across diverse prototypic types/subtypes and [...] Read more.
Background: Staphylococcus aureus acquires methicillin resistance genes through the SCCmec element. Although spontaneous SCCmec excision has been observed, its frequency, type-specific variation, and responsiveness to environmental conditions remain undefined. Here, we systematically quantified SCCmec excision across diverse prototypic types/subtypes and evaluated the factors that contribute to excision variability. Methods: Twenty five prototypic MRSA strains (SCCmec types I–VIII, XI–XIII and defined subtypes) were examined under standard growth temperature (37 °C), elevated temperature (42 °C), desiccation, prolonged continuous culture (30 days), and sub-lethal oxacillin pressure. Excision frequencies were quantified using qPCR, normalized to the gyrB housekeeping gene using the formula: 10−((Ct,orfX−Ct,gyrB)/3.32). Statistical analyses included one-way ANOVA, t-tests, and OLS regression for time-dependent trends. Results: At 37 °C, excision frequencies ranged from 2.40 × 10−6 to 1.32 × 10−3 and varied among representative SCCmec types/subtypes but were unrelated to SCCmec size (R2 = 0.027, p = 0.44). Type I showed no detectable excision due to a truncated ccrB gene. At 42 °C, excision increased in 14 of 24 types (median +11.2%; eight significant) and decreased in 10 (median −7.4%; four significant). Desiccation produced similar effects, with nine types increasing (median +7.1%; four significant), 14 decreasing (median −8.2%; five significant), and one unchanged. Continuous culture exhibited progressive increases in excision across multiple types (R2 = 0.3–0.94), whereas sub-lethal oxacillin uniformly maintained low detectable excision frequencies across all SCCmec types. Conclusions: Excision varied among representative SCCmec types and was influenced heterogeneously by distinct stress conditions. Continuous culture promoted excision, whereas oxacillin exposure maintained low detectable excision. This work quantitatively confirms spontaneous SCCmec excision and provides new insights into MRSA genome plasticity. Full article
(This article belongs to the Special Issue Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination)
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21 pages, 2188 KB  
Article
High-Resolution Genomic Surveillance of Carbapenem-Resistant Acinetobacter baumannii: IC-2 Clonal Diversity, Resistance Determinants, and Virulence Signatures
by Arianna Basile, Valentina Antonelli, Claudia Rotondo, Michele Properzi, Francesco Messina, Silvia D’Arezzo, Valentina Dimartino, Ivano Petriccione, Laura Loiacono, Maria Grazia Bocci, Giulia Capecchi, Alessia Arcangeli, Alessandra Marani, Filippo Pasquale Riggio, Massimiliano Lucidi, Francesco Imperi, Paolo Visca and Carla Fontana
Antibiotics 2026, 15(5), 464; https://doi.org/10.3390/antibiotics15050464 - 4 May 2026
Viewed by 1515
Abstract
Background/Objectives: Acinetobacter baumannii is a critical opportunistic pathogen causing severe healthcare-associated infections, particularly in intensive care units. The global dissemination of carbapenem-resistant A. baumannii (CRAB) and its environmental persistence necessitate continuous genomic surveillance to monitor high-risk clones. Methods: We conducted whole-genome sequencing [...] Read more.
Background/Objectives: Acinetobacter baumannii is a critical opportunistic pathogen causing severe healthcare-associated infections, particularly in intensive care units. The global dissemination of carbapenem-resistant A. baumannii (CRAB) and its environmental persistence necessitate continuous genomic surveillance to monitor high-risk clones. Methods: We conducted whole-genome sequencing (WGS), core genome multi-locus sequence typing (cgMLST), and phylogenomic analyses on 26 CRAB isolates collected at the National Institute for Infectious Diseases (INMI) “Lazzaro Spallanzani” IRCCS (September 2023–September 2024). Antimicrobial resistance determinants, virulence-related genes, and capsular (KL) and lipooligosaccharide outer core (OCL) loci were characterized by interrogation of comprehensive bioinformatic pipelines. Results: All CRAB isolates displayed an extensively drug-resistant (XDR) phenotype, with a shared resistance pattern to carbapenems, aminoglycosides, fluoroquinolones, fosfomycin, and sulfonamides, while being susceptible only to colistin and cefiderocol. The carbapenemase gene blaOXA-23 was detected in all CRAB isolates, together with clone-specific blaOXA-51-like variants. For all isolates, the resistome profile fully matched the observed resistance phenotype. All isolates belonged to the International Clonal Lineage II (ICL II), Pasteur Sequence Type (ST) 2, and Oxford ST369, ST208, and ST455. Integration of cgMLST data with phylogenomic analyses and genome-based classification of KL and OCL loci revealed five distinct clusters, each one including nearly identical isolates, indicating both intra-hospital dissemination and possible inter-hospital transmission. Virulome profiling revealed heterogeneous repertoires of virulence-associated genes, resulting in cluster-specific patterns, while patristic analysis identified phylogenetic clusters linking the study isolates to other Italian and other European lineages. Conclusions: This study underscores the complex genomic landscape of CRAB in our setting, driven by the circulation of different ICL II clonal types, and reinforces the urgency of integrated genomic surveillance and robust antimicrobial stewardship to mitigate the spread of high-risk XDR A. baumannii clones. Full article
(This article belongs to the Special Issue Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination)
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18 pages, 2621 KB  
Article
Genetic and Phenotypic Characterization of a Salmonella Enteritidis ST11 Clinical Isolate Carrying blaNDM-13 in Jiaxing City, China
by Ping Li, Weiming Yang, Zhongwen Chen, Henghui Wang, Miaomiao Jia, Xuejuan Liu, Yong Yan and Guoying Zhu
Antibiotics 2026, 15(4), 381; https://doi.org/10.3390/antibiotics15040381 - 9 Apr 2026
Cited by 1 | Viewed by 908
Abstract
Background/Objectives: Multidrug-resistant Salmonella enterica serovar Enteritidis, especially those isolated from humans, remains a public concern. In the present study, S. Enteritidis strain 31404 was obtained clinically from a fecal sample of a fifteen-year-old girl, who was positive for blaNDM-13. [...] Read more.
Background/Objectives: Multidrug-resistant Salmonella enterica serovar Enteritidis, especially those isolated from humans, remains a public concern. In the present study, S. Enteritidis strain 31404 was obtained clinically from a fecal sample of a fifteen-year-old girl, who was positive for blaNDM-13. Methods: Antibiotic susceptibility testing and whole genome sequencing were performed. Core genome MLST and hierarchical clustering (HierCC) were performed using EnteroBase. Population structure analysis of 57 S. Enteritidis isolates collected between 2023 and 2025 in Jiaxing city was conducted. A comparative structure analysis of blaNDM-13-positive plasmids was also performed. Results: S. Enteritidis strain 31404 was resistant to 13 antimicrobial agents. We found that strain 31404 belonged to ST11 and carried resistance genes, such as blaNDM-13, blaCTX-M-14, bleMBL, fosA3, qnrS, and tet (A). blaNDM-13 was located on an IncI1-I (α) plasmid designated as p31404-NDM13. S. Enteritidis isolate 31404 was closely related to PNUSAS514422, which was isolated from the United States in 2025. Comparative genetic environment related to blaNDM-13-positive plasmids available in the NCBI database indicates that ΔTn125-mediated contexts were commonly associated with blaNDM-13. IS1294 (IS91 family), which replaces ISAba125, is likely to mobilize blaNDM-13. Conclusions: The findings in this study provide insights into the molecular characterization and diversification of blaNDM-13. The identification of blaNDM-13-containing transferable plasmids in different serotypes of Salmonella isolates (such as S. Rissen, S. Typhimurium, and S. Enteritidis) in different cities in China highlights the risk of the spread of carbapenem-resistant genes among Salmonella isolates. Full article
(This article belongs to the Special Issue Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination)
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27 pages, 2459 KB  
Systematic Review
Mobile Genetic Elements Associated with Antimicrobial Resistance Across One Health Interfaces in Africa: A Systematic Review and Meta-Analysis
by Kedir A. Hassen, Jose Fafetine, Laurinda Augusto, Inacio Mandomando, Marcelino Garrine, Rogerio Marcos and Gudeta W. Sileshi
Antibiotics 2026, 15(5), 456; https://doi.org/10.3390/antibiotics15050456 - 30 Apr 2026
Cited by 1 | Viewed by 1307
Abstract
Background: High infectious disease burden and uncontrolled antibiotic usage across human, animal, and environmental contaminants make antimicrobial resistance (AMR) a growing public health problem in Africa. Mobile genetic elements (MGEs) such plasmids, transposons, integrons, conjugative elements, and phages help spread AMR via horizontal [...] Read more.
Background: High infectious disease burden and uncontrolled antibiotic usage across human, animal, and environmental contaminants make antimicrobial resistance (AMR) a growing public health problem in Africa. Mobile genetic elements (MGEs) such plasmids, transposons, integrons, conjugative elements, and phages help spread AMR via horizontal gene transfer (HGT) across human, animal, food, and environmental sources. Despite growing evidence for antibiotic resistance genes (ARGs), Africa lacks a one-health-focused synthesis of mobile genetic element-mediated AMR. Objective: This systematic review and meta-analysis aimed to consolidate information on MGEs and ARGs in AMR dissemination throughout Africa’s one health interface. Methods: The literature was searched using PubMed, Scopus, and ScienceDirect. Observational. molecular epidemiology, whole genome sequencing (WGS), and metagenomic investigations of MGE-associated AMR in Africa were eligible. The study selection, data extraction, and quality assessment were performed by two independent reviewer and quality was graded using ROBVIS 2 utilizing Rayyan software. Narrative synthesis, random-effect meta-analysis, subgroup analysis, and meta-regression were utilized. Results: A total of 109 studies were included, with 91 studies contributing to the meta-analysis. MGEs reported were plasmids (71.7%) and integrons (54.8%). ARGs carried by MGEs were blaCTMX-M-15 (78.6%), Sul2 (69.6%), blaTEM (59.1%), and tetA (49.9%). Horizontal gene transfer was seen in 259 instances; however, transmission was unclear. In 442 observations, transmission pathways across human, animal, and environmental interfaces showed AMR prevalence of 75.1% in human, 98.0% in human–animal, and 61.3% in one health interface. Whole-genome sequencing was the most frequently used method for detecting MGEsThe pooled pathogen and AMR prevalence rates were 73.3% (95% CI: 60.5–83.7%) and 94% (95% CI: 85–98%), with significant heterogeneity (I2 = 97.8% and 97.4%, respectively). The prevalence of Escherichia coli was 93% and Salmonella enterica 85% in subgroup analysis. Fluoroquinolones, aminoglycosides, and beta-lactams were prevalent in humans (89.7%) and human–animal interactions (98.0%) according to AMR Class. Conclusions: Horizontal gene transfer has propagated MGE-mediated antimicrobial resistance across human, animal, and environmental interfaces in Africa. To combat AMR in Africa, coordinated, genomics-informed One Health surveillance and antibiotic stewardship are needed. Due to variability and publication bias, these data should be considered cautiously. Pooled data may only show descriptive patterns, and not necessarily precise continent-wide prevalence estimates. Full article
(This article belongs to the Special Issue Antibiotic Resistance Genes: Mechanisms, Evolution and Dissemination)
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