Antimicrobial Resistance Mechanisms: Occurrence, Dissemination, Detection and Treatment

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 (30 June 2023) | Viewed by 6697

Special Issue Editors

Department of Microbiology, Immunology, and Parasitology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil
Interests: antimicrobial resistance; bacterial genomics
Programa de Pós-Graduação Em Ciências Farmacêuticas, Faculdade de Farmácia, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
Interests: mechanisms of antimicrobial resistance; methods for detection of antimicrobial resistance; epidemiology of resistant bacteria
Departamento de Física e Ciência Interdiciplinar, Instituto de Física de São Carlos, Universidade de São Paulo, São Carlos, Brazil
Interests: mechanisms of antimicrobial resistance; epidemiology of resistant bacteria; search for new antimicrobial compounds

Special Issue Information

Dear Colleagues,

Antimicrobial resistance (AMR) has been a subject of major concern worldwide in recent years, as a threat to human health. Indeed, the infection rates caused by multidrug-resistant bacteria are worryingly high in some regions, and increase patient morbidity and mortality. Although mutations in genes could be involved in AMR, the major concern is related to those located on mobile genetic elements, such as transposons and plasmids, which are easily transferred horizontally among bacteria. The acknowledgment of this dynamic of dissemination is crucial in order to interrupt it efficiently. It is known that the majority of AMR cases are healthcare-associated infections, but the dissemination of resistance genes runs throughout the whole environment, demanding a holistic approach when considering this issue (One Health), including water environments, veterinary medicine, and livestock.

Considering that it is well-recognized that the prompt establishment of proper antimicrobial therapy increases the chances of survival, the accurate detection of AMR in vitro is crucial to improve patient outcomes. Hence, the implementation of methodologies (phenotypic or genotypic) able to detect resistance faster than the current reference methods is urgently required.

In a context of reduced therapeutic options, where the need for the approval of a new antibiotic is significantly lower than the occurrence and dissemination of AMR, the rapid determination of susceptibility/resistance to antimicrobials enables the implementation of optimal therapy, represented mainly by a combination of two or more antibiotics, corroborating antimicrobial stewardship policies.

Therefore, this Special Issue welcomes submissions from different research fields focusing on the occurrence, dissemination, detection, and treatment of antimicrobial resistance, aiming to contribute to the state-of-the-art treatment of this issue. We look forward to receiving your contributions.

Dr. Andreza Franciso Martins
Dr. Juliana Caierão
Dr. Ilana Lopes Baratella da Cunha Camargo
Guest Editors

Manuscript Submission Information

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Keywords

  • antimicrobial resistance
  • dissemination of resistance genes
  • detection of antimicrobial resistance
  • multidrug-resistant bacteria
  • antimicrobial stewardship
  • new antimicrobials

Published Papers (3 papers)

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Research

15 pages, 1120 KiB  
Article
Characterization of blaKPC-2 and blaNDM-1 Plasmids of a K. pneumoniae ST11 Outbreak Clone
by Camila Maria dos Santos Boralli, Julian Andres Paganini, Rodrigo Silva Meneses, Camila Pacheco Silveira Martins da Mata, Edna Marilea Meireles Leite, Anita C. Schürch, Fernanda L. Paganelli, Rob J. L. Willems and Ilana Lopes Baratella Cunha Camargo
Antibiotics 2023, 12(5), 926; https://doi.org/10.3390/antibiotics12050926 - 18 May 2023
Cited by 3 | Viewed by 1796
Abstract
The most common resistance mechanism to carbapenems is the production of carbapenemases. In 2021, the Pan American Health Organization warned of the emergence and increase in new carbapenemase combinations in Enterobacterales in Latin America. In this study, we characterized four Klebsiella pneumoniae isolates [...] Read more.
The most common resistance mechanism to carbapenems is the production of carbapenemases. In 2021, the Pan American Health Organization warned of the emergence and increase in new carbapenemase combinations in Enterobacterales in Latin America. In this study, we characterized four Klebsiella pneumoniae isolates harboring blaKPC and blaNDM from an outbreak during the COVID-19 pandemic in a Brazilian hospital. We assessed their plasmids’ transference ability, fitness effects, and relative copy number in different hosts. The K. pneumoniae BHKPC93 and BHKPC104 strains were selected for whole genome sequencing (WGS) based on their pulsed-field gel electrophoresis profile. The WGS revealed that both isolates belong to ST11, and 20 resistance genes were identified in each isolate, including blaKPC-2 and blaNDM-1. The blaKPC gene was present on a ~56 Kbp IncN plasmid and the blaNDM-1 gene on a ~102 Kbp IncC plasmid, along with five other resistance genes. Although the blaNDM plasmid contained genes for conjugational transfer, only the blaKPC plasmid conjugated to E. coli J53, without apparent fitness effects. The minimum inhibitory concentrations (MICs) of meropenem/imipenem against BHKPC93 and BHKPC104 were 128/64 and 256/128 mg/L, respectively. Although the meropenem and imipenem MICs against E. coli J53 transconjugants carrying the blaKPC gene were 2 mg/L, this was a substantial increment in the MIC relative to the original J53 strain. The blaKPC plasmid copy number was higher in K. pneumoniae BHKPC93 and BHKPC104 than in E. coli and higher than that of the blaNDM plasmids. In conclusion, two ST11 K. pneumoniae isolates that were part of a hospital outbreak co-harbored blaKPC-2 and blaNDM-1. The blaKPC-harboring IncN plasmid has been circulating in this hospital since at least 2015, and its high copy number might have contributed to the conjugative transfer of this particular plasmid to an E. coli host. The observation that the blaKPC-containing plasmid had a lower copy number in this E. coli strain may explain why this plasmid did not confer phenotypic resistance against meropenem and imipenem. Full article
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12 pages, 1457 KiB  
Article
Meropenem MICs at Standard and High Inocula and Mutant Prevention Concentration Inter-Relations: Comparative Study with Non-Carbapenemase-Producing and OXA-48-, KPC- and NDM-Producing Klebsiella pneumoniae
by Maria V. Golikova, Elena N. Strukova, Kamilla N. Alieva, Vladimir A. Ageevets, Alisa A. Avdeeva, Ofeliia S. Sulian and Stephen H. Zinner
Antibiotics 2023, 12(5), 872; https://doi.org/10.3390/antibiotics12050872 - 08 May 2023
Cited by 2 | Viewed by 1694
Abstract
The minimal inhibitory concentration (MIC) is conventionally used to define in vitro levels of susceptibility or resistance of a specific bacterial strain to an antibiotic and to predict its clinical efficacy. Along with MIC, other measures of bacteria resistance exist: the MIC determined [...] Read more.
The minimal inhibitory concentration (MIC) is conventionally used to define in vitro levels of susceptibility or resistance of a specific bacterial strain to an antibiotic and to predict its clinical efficacy. Along with MIC, other measures of bacteria resistance exist: the MIC determined at high bacterial inocula (MICHI) that allow the estimation of the occurrence of inoculum effect (IE) and the mutant prevention concentration, MPC. Together, MIC, MICHI and MPC represent the bacterial “resistance profile”. In this paper, we provide a comprehensive analysis of such profiles of K. pneumoniae strains that differ by meropenem susceptibility, ability to produce carbapenemases and specific carbapenemase types. In addition, we have analyzed inter-relations between the MIC, MICHI and MPC for each tested K. pneumoniae strain. Low IE probability was detected with carbapenemase-non-producing K. pneumoniae, and high IE probability was detected with those that were carbapenemase-producing. MICs did not correlate with the MPCs; significant correlation was observed between the MICHIs and the MPCs, indicating that these bacteria/antibiotic characteristics display similar resistance properties of a given bacterial strain. To determine the possible resistance-related risk due to a given K. pneumoniae strain, we propose determining the MICHI. This can more or less predict the MPC value of the particular strain. Full article
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11 pages, 889 KiB  
Article
Occurrence of cfr-Positive Linezolid-Susceptible Staphylococcus aureus and Non-aureus Staphylococcal Isolates from Pig Farms
by Gi Yong Lee and Soo-Jin Yang
Antibiotics 2023, 12(2), 359; https://doi.org/10.3390/antibiotics12020359 - 09 Feb 2023
Cited by 2 | Viewed by 1390
Abstract
The emergence and spread of cfr-mediated resistance to linezolid in staphylococci have become a serious global concern. The acquisition of cfr confers multidrug resistance to phenicols, lincosamides, oxazolidinones, pleuromutilins, and streptogramin A (PhLOPSA phenotype). However, occurrence of cfr-positive and linezolid-susceptible [...] Read more.
The emergence and spread of cfr-mediated resistance to linezolid in staphylococci have become a serious global concern. The acquisition of cfr confers multidrug resistance to phenicols, lincosamides, oxazolidinones, pleuromutilins, and streptogramin A (PhLOPSA phenotype). However, occurrence of cfr-positive and linezolid-susceptible staphylococci has been identified. To investigate the mechanism underlying linezolid susceptibility in cfr-positive Staphylococcus aureus and non-aureus staphylococci (NAS) isolates from pig farms in Korea. Eleven cfr-positive and linezolid-susceptible staphylococci were analyzed for mutations in domain V of 23S rRNA, ribosomal proteins (L3, L4, and L22), cfr open reading frames (ORFs), and cfr promoter regions. The effect of the cfr mutation (Q148K) on the PhLOPSA phenotype was determined using plasmid constructs expressing either the mutated (cfrQ148K) or nonmutated cfr genes. All 11 (six S. aureus and five NAS) cfr-positive and linezolid-susceptible isolates had a point mutation at position 442 in cfr ORFs (C to A) that resulted in the Q148K mutation. No mutations were detected in 23S rRNA, L3, L4, or L22. The Q148K mutation in Cfr is responsible for phenotypes susceptible to PhLOPSA antimicrobial agents. To our knowledge, this is the first study to report the causal role of a single nucleotide mutation (Q148K) in cfr of S. aureus and NAS isolates in PhLOPSA resistance. Continued nationwide surveillance is necessary to monitor the occurrence and dissemination of mutations in cfr that affect resistance phenotypes in staphylococci of human and animal origin. Full article
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