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Antibiotics
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Mechanisms of Bacterial Antibiotic Resistance and Interventions to Prevent Their...
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Mechanisms of Bacterial Antibiotic Resistance and Interventions to Prevent Their Spread

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: closed (31 December 2022) | Viewed by 8515

Special Issue Editors

Dr. Li Yang HSU

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Guest Editor
NUS Saw Swee Hock School of Public Health, Singapore City, Singapore
Interests: bacterial antibiotic resistance: epidemiology, mechanisms, and interventions; tuberculosis: epidemiology and drug resistance; global health
Dr. Rick Twee-Hee ONG

E-Mail Website
Guest Editor
NUS Saw Swee Hock School of Public Health, Singapore City, Singapore
Interests: bacterial antibiotic resistance: genomic epidemiology and genetic mechanisms; tuberculosis: genomic epidemiology and genetic mechanisms for antiTB drug resistance
Dr. Chongguang Yang

E-Mail Website
Guest Editor
School of Public Health (Shenzhen), Sun Yat-sen University, No. 135, Xingang Xi Road, Guangzhou 510275, China
Interests: antibiotic resistance; infectious diseases; tuberculosis; Mycobacterium tuberculosis; genome; bacterial; molecular epidemiology
Special Issues, Collections and Topics in MDPI journals
Dr. Antonio Russo

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Guest Editor
Department of Mental Health and Public Medicine–Infectious Diseases Unit, University of Campania Luigi Vanvitelli, 80138 Naples, Italy
Interests: HIV infection; HIV treatment; AIDS; meta-analysis; HBV infection; HCV infection; HBV/HDV infection; tuberculosis

Special Issue Information

Dear Colleagues,

Antimicrobial resistance (AMR), including bacterial antibiotic resistance, remains a global public health threat, causing over 700,000 deaths each year. In the November 2020 report published by the Wellcome Trust, it is clear that the trajectory and success of our response to AMR will depend on actions and policies of the next few years.Whereas the COVID-19 pandemic has surely slowed and diverted resources away from AMR research and control, our response to it has also shown new possibilities for innovation and collaboration that can potentially be employed for other causes, such as AMR.

In this Special Issue, we welcome the sharing of new insights into bacterial (including Mycobacterium tuberculosis) antibiotic resistance and control. We look forward to contributions in the form of original research or systematic reviews in the following areas:

  • Mechanisms of bacterial antibiotic resistance, in particular focusing on carbapenem and polymyxin resistance, as well as resistance to new antibiotics and new anti-tuberculosis drugs
  • Appropriate prescribing of antibiotics, particularly in the community setting
  • Novel infection prevention methods for preventing the spread of drug-resistant bacteria in the hospital setting and community setting
  • The role of the human and environmental microbiome on bacterial antibiotic resistance

Please contact us directly for other topics not listed above.

Dr. Li Yang HSU
Dr. Rick Twee-Hee ONG
Dr. Chongguang Yang
Dr. Antonio Russo
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 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

  • bacterial antibiotic resistance
  • antibiotic stewardship
  • microbiome
  • drug-resistant tuberculosis
  • infection prevention
  • novel antibiotics

Published Papers (4 papers)

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Research

19 pages, 5793 KiB  
Article
Discovery of Novel Resistance Mechanisms of Vibrio parahaemolyticus Biofilm against Aminoglycoside Antibiotics
by Cuifang Tian, Mengqi Yuan, Qian Tao, Tianming Xu, Jing Liu, Zhenhua Huang, Qian Wu, Yingjie Pan, Yong Zhao and Zhaohuan Zhang
Antibiotics 2023, 12(4), 638; https://doi.org/10.3390/antibiotics12040638 - 24 Mar 2023
Cited by 4 | Viewed by 1714
Abstract
Inappropriate use of antibiotics eventually leads to the emergence of antibiotic-resistant strains and invalidates the treatment of infectious diseases. Aminoglycoside antibiotics (AGAs) are a class of broad-spectrum cationic antibiotics widely used for the treatment of Gram-negative bacterial infections. Understanding the AGA resistance mechanism [...] Read more.
Inappropriate use of antibiotics eventually leads to the emergence of antibiotic-resistant strains and invalidates the treatment of infectious diseases. Aminoglycoside antibiotics (AGAs) are a class of broad-spectrum cationic antibiotics widely used for the treatment of Gram-negative bacterial infections. Understanding the AGA resistance mechanism of bacteria would increase the efficacy of treating these infections. This study demonstrates a significant correlation between AGA resistance and the adaptation of biofilms by Vibrio parahaemolyticus (VP). These adaptations were the result of challenges against the aminoglycosides (amikacin and gentamicin). Confocal laser scanning microscope (CLSM) analysis revealed an enclosure type mechanism where the biological volume (BV) and average thickness (AT) of V. parahaemolyticus biofilm were significantly positively correlated with amikacin resistance (BIC) (p < 0.01). A neutralization type mechanism was mediated by anionic extracellular polymeric substances (EPSs). The biofilm minimum inhibitory concentrations of amikacin and gentamicin were reduced from 32 µg/mL to 16 µg/mL and from 16 µg/mL to 4 µg/mL, respectively, after anionic EPS treatment with DNase I and proteinase K. Here, anionic EPSs bind cationic AGAs to develop antibiotic resistance. Transcriptomic sequencing revealed a regulatory type mechanism, where antibiotic resistance associated genes were significantly upregulated in biofilm producing V. parahaemolyticus when compared with planktonic cells. The three mechanistic strategies of developing resistance demonstrate that selective and judicious use of new antibiotics are needed to win the battle against infectious disease. Full article
(This article belongs to the Special Issue Mechanisms of Bacterial Antibiotic Resistance and Interventions to Prevent Their Spread)
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12 pages, 1421 KiB  
Article
Genome-Wide Analysis of Innate Susceptibility Mechanisms of Escherichia coli to Colistin
by Muhammad Yasir, A. Keith Turner, Sarah Bastkowski, Martin Lott, Emma R. Holden, Andrea Telatin, Andrew J. Page, Mark A. Webber and Ian G. Charles
Antibiotics 2022, 11(11), 1668; https://doi.org/10.3390/antibiotics11111668 - 21 Nov 2022
Viewed by 1571
Abstract
Colistin is an antibiotic that has seen increasing clinical use for the treatment of human infections caused by Gram-negative pathogens, particularly due to the emergence of multidrug-resistant pathogens. Colistin resistance is also a growing problem and typically results from alterations to lipopolysaccharides mediated [...] Read more.
Colistin is an antibiotic that has seen increasing clinical use for the treatment of human infections caused by Gram-negative pathogens, particularly due to the emergence of multidrug-resistant pathogens. Colistin resistance is also a growing problem and typically results from alterations to lipopolysaccharides mediated by phosphoethanolamine (pETn) transferase enzymes which can be encoded on the chromosome, or plasmids. In this study, we used ‘TraDIS-Xpress’ (Transposon Directed Insertion site Sequencing with expression), where a high-density transposon mutant library including outward facing promoters in Escherichia coli BW25113 identified genes involved in colistin susceptibility. We examined the genome-wide response of E. coli following exposure to a range of concentrations of colistin. Our TraDIS-Xpress screen confirmed the importance of overexpression of the two-component system basSR (which regulates pETn transferases) but also identified a wider range of genes important for survival in the presence of colistin, including genes encoding membrane associated proteins, DNA repair machinery, various transporters, RNA helicases, general stress response genes, fimbriae and phosphonate metabolism. Validation experiments supported a role in colistin susceptibility for novel candidate genes tested. TraDIS-Xpress is a powerful tool that expands our understanding of the wider landscape of genes involved in response to colistin susceptibility mechanisms. Full article
(This article belongs to the Special Issue Mechanisms of Bacterial Antibiotic Resistance and Interventions to Prevent Their Spread)
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13 pages, 1419 KiB  
Article
Iron Effects on Clostridioides difficile Toxin Production and Antimicrobial Susceptibilities
by Jason Yamaki, Swati Chawla, Shirley Tong, Kate Alison Lozada and Sun Yang
Antibiotics 2022, 11(5), 537; https://doi.org/10.3390/antibiotics11050537 - 19 Apr 2022
Cited by 6 | Viewed by 2532
Abstract
Despite the benefits of red blood cell (RBC) transfusion therapy, it can render patients vulnerable to iron overload. The excess iron deposits in various body tissues cause severe complications and organ damage such as cardiotoxicity and mold infections. Clostridioides difficile infection (CDI) is [...] Read more.
Despite the benefits of red blood cell (RBC) transfusion therapy, it can render patients vulnerable to iron overload. The excess iron deposits in various body tissues cause severe complications and organ damage such as cardiotoxicity and mold infections. Clostridioides difficile infection (CDI) is the most common cause of nosocomial diarrhea among cancer patients and is associated with significant morbidity and mortality. Our study aims to determine the role of iron overload and the effects of iron chelators on CDI. Our results demonstrated that iron (Fe3+) stimulated the growth of C. difficile with increased colony formation units (CFU) in a dose-dependent manner. Exposure to excess iron also increased the gene expression levels of tcdA and tcdB. The production of C. difficile toxin A, necessary for the pathogenesis of C. difficile, was also elevated after iron treatment. In the presence of excess iron, C. difficile becomes less susceptible to metronidazole with significantly elevated minimum inhibitory concentration (MIC) but remains susceptible to vancomycin. Iron-stimulated colony formation and production of C. difficile toxins were effectively diminished by iron chelator deferoxamine co-treatment. Incorporating iron overload status as a potential factor in developing a risk prediction model of CDI and antibiotic treatment response may aid clinical practitioners in optimizing CDI management in oncology patients. Full article
(This article belongs to the Special Issue Mechanisms of Bacterial Antibiotic Resistance and Interventions to Prevent Their Spread)
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6 pages, 452 KiB  
Communication
Imipenem Resistance Mediated by blaOXA-913 Gene in Pseudomonas aeruginosa
by Dong-Chan Moon, Abraham Fikru Mechesso, Hee-Young Kang, Su-Jeong Kim, Ji-Hyun Choi, Hyun-Ju Song, Soon-Seek Yoon and Suk-Kyung Lim
Antibiotics 2021, 10(10), 1188; https://doi.org/10.3390/antibiotics10101188 - 29 Sep 2021
Cited by 2 | Viewed by 1912
Abstract
Treatment of infectious diseases caused by carbapenem-resistant Pseudomonas aeruginosa is becoming a greater challenge. This study aimed to identify the imipenem resistance mechanism in P. aeruginosa isolated from a dog. Minimum Inhibitory Concentration (MIC) was determined by the broth microdilution method according to [...] Read more.
Treatment of infectious diseases caused by carbapenem-resistant Pseudomonas aeruginosa is becoming a greater challenge. This study aimed to identify the imipenem resistance mechanism in P. aeruginosa isolated from a dog. Minimum Inhibitory Concentration (MIC) was determined by the broth microdilution method according to the Clinical and Laboratory Standards Institute recommendations. We performed polymerase chain reaction and whole-genome sequencing to detect carbapenem resistance genes. Genomic DNA of P. aeruginosa K19PSE24 was sequenced via the combined analysis of 20-kb PacBio SMRTbell and PacBio RS II. Peptide-Peptide Nucleic Acid conjugates (P-PNAs) targeting the translation initiation region of blaOXA-913 were synthesized. The isolate (K19PSE24) was resistant to imipenem and piperacillin/tazobactam yet was susceptible to most of the tested antimicrobials. Whole-genome sequencing revealed that the K19PSE24 genome comprised a single contig amounting to 6,815,777 base pairs, with 65 tRNA and 12 rRNA genes. K19PSE24 belonged to sequence type 313 and carried the genes aph(3)-IIb, fosA, catB7, crpP, and blaOXA-913 (an allele deposited in GenBank but not described in the literature). K19PSE24 also carried genes encoding for virulence factors (exoenzyme T, exotoxin A, and elastase B) that are associated with adhesion, invasion, and tissue lysis. Nevertheless, we did not detect any of the previously reported carbapenem resistance genes. This is the first report of the blaOXA-913 gene in imipenem-resistant P. aeruginosa in the literature. Notably, no viable colonies were found after co-treatment with imipenem (2 µg/mL) and either of the P-PNAs (12.5 µM or 25 µM). The imipenem resistance in K19PSE24 was primarily due to blaOXA-913 gene carriage. Full article
(This article belongs to the Special Issue Mechanisms of Bacterial Antibiotic Resistance and Interventions to Prevent Their Spread)
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