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Escherichia coli from Human Wounds: Analysis of Resistance to β-Lactams and Expression of RND Efflux Pumps

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62156489%3A43210%2F23%3A43924355" target="_blank" >RIV/62156489:43210/23:43924355 - isvavai.cz</a>

  • Nalezeny alternativní kódy

    RIV/00216224:14110/23:00133383

  • Výsledek na webu

    <a href="https://doi.org/10.2147/IDR.S435622" target="_blank" >https://doi.org/10.2147/IDR.S435622</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.2147/IDR.S435622" target="_blank" >10.2147/IDR.S435622</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Escherichia coli from Human Wounds: Analysis of Resistance to β-Lactams and Expression of RND Efflux Pumps

  • Popis výsledku v původním jazyce

    Purpose: Resistance of pathogenic strains of Escherichia coli to β-lactams, particularly to ampicillin, is on the rise and it is attributed to intrinsic and acquired mechanisms. One important factor contributing to resistance, together with primarily resistance mechanisms, is a mutation and/or an over-expression of the intrinsic efflux pumps in the resistance-nodulation-division (RND) superfamily. Among these efflux pumps, AcrA, AcrB, TolC, and AcrD play an important role in antimicrobial co-resistance, including resistance to β-lactams.Materials and Methods: Twelve E. coli isolates obtained from patients&apos; wounds and the control strain of E. coli ATCC 25922 were analyzed. The phenotypic resistance of these isolates to selected β-lactams was assessed by determination of the minimal inhibitory concentration. Additionally, the prevalence of β-lactamase genes (blaTEM, blaCTX-M, blaSHV, and blaAmpC) was screened by PCR. Real- time qPCR was used to determine the expression of the selected efflux pumps acrA, acrB, tolC, and acrD and the repressor acrR after the exposure of E. coli to ampicillin.Results: Phenotypic resistance to β-lactams was detected in seven isolates, mainly to ampicillin and piperacillin. This was corroborated by the presence of at least one acquired bla gene in each of these isolates. Although E. coli strains varied in the expression of RND-family efflux pumps after the ampicillin exposure, their gene expression indicated that these pumps did not play a major role in the phenotypic resistance to ampicillin.Conclusion: Each E. coli isolate displayed unique characteristics, differing in minimum inhibitory concentration (MIC) values, prevalence of acquired blaTEM and blaCTX-M genes, and expression of the RND-family pumps. This together demonstrates that these clinical isolates employed distinct intrinsic or acquired resistance pathways for their defense against ampicillin. The prevalence and spread of ampicillin resistant E. coli has to be monitored and the search for ampicillin alternatives is needed.

  • Název v anglickém jazyce

    Escherichia coli from Human Wounds: Analysis of Resistance to β-Lactams and Expression of RND Efflux Pumps

  • Popis výsledku anglicky

    Purpose: Resistance of pathogenic strains of Escherichia coli to β-lactams, particularly to ampicillin, is on the rise and it is attributed to intrinsic and acquired mechanisms. One important factor contributing to resistance, together with primarily resistance mechanisms, is a mutation and/or an over-expression of the intrinsic efflux pumps in the resistance-nodulation-division (RND) superfamily. Among these efflux pumps, AcrA, AcrB, TolC, and AcrD play an important role in antimicrobial co-resistance, including resistance to β-lactams.Materials and Methods: Twelve E. coli isolates obtained from patients&apos; wounds and the control strain of E. coli ATCC 25922 were analyzed. The phenotypic resistance of these isolates to selected β-lactams was assessed by determination of the minimal inhibitory concentration. Additionally, the prevalence of β-lactamase genes (blaTEM, blaCTX-M, blaSHV, and blaAmpC) was screened by PCR. Real- time qPCR was used to determine the expression of the selected efflux pumps acrA, acrB, tolC, and acrD and the repressor acrR after the exposure of E. coli to ampicillin.Results: Phenotypic resistance to β-lactams was detected in seven isolates, mainly to ampicillin and piperacillin. This was corroborated by the presence of at least one acquired bla gene in each of these isolates. Although E. coli strains varied in the expression of RND-family efflux pumps after the ampicillin exposure, their gene expression indicated that these pumps did not play a major role in the phenotypic resistance to ampicillin.Conclusion: Each E. coli isolate displayed unique characteristics, differing in minimum inhibitory concentration (MIC) values, prevalence of acquired blaTEM and blaCTX-M genes, and expression of the RND-family pumps. This together demonstrates that these clinical isolates employed distinct intrinsic or acquired resistance pathways for their defense against ampicillin. The prevalence and spread of ampicillin resistant E. coli has to be monitored and the search for ampicillin alternatives is needed.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    10606 - Microbiology

Návaznosti výsledku

  • Projekt

    <a href="/cs/project/EF16_025%2F0007314" target="_blank" >EF16_025/0007314: Multioborový výzkum pro zvýšení aplikačního potenciálu nanomateriálů v zemědělské praxi</a><br>

  • Návaznosti

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Ostatní

  • Rok uplatnění

    2023

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    Infection and Drug Resistance

  • ISSN

    1178-6973

  • e-ISSN

    1178-6973

  • Svazek periodika

    16

  • Číslo periodika v rámci svazku

    29 November

  • Stát vydavatele periodika

    NZ - Nový Zéland

  • Počet stran výsledku

    11

  • Strana od-do

    7365-7375

  • Kód UT WoS článku

    001113170700001

  • EID výsledku v databázi Scopus

    2-s2.0-85183934699