Understanding Bacterial Resistance and Dissemination: The Impact of Biocide Priming
type: CreativeWork
description: Background: Public awareness to infection control, for example the current covid-19 pandemic, can cause a rise in the use of biocidal products. Uncontrolled use of biocides, especially at sub-inhibitory concentrations has led to growing concerns that their selective pressure may favour the prevalence of less susceptible bacterial strains and encourage the expression and dissemination of antibiotic resistance genes. Aims: To investigate the priming effects of sub-inhibitory concentrations of biocides on antibiotic resistance in bacteria and to understand the resistance mechanisms activated by these effects. Methodology: Escherichia coli, Pseudomonas aeruginosa and Staphylococcus aureus were exposed to sub-inhibitory concentrations of biocides (hydrogen peroxide, chlorhexidine, glutaraldehyde and benzalkonium chloride). Minimum inhibitory concentrations of antibiotics and biocides were determined before and after exposure to low concentrations of biocides to test for changes in biocide tolerance and cross resistance to antibiotics. Efflux pump inhibitors (thioridazine and chlorpromazine) were used to investigate efflux as a mechanism. Known antibiotic resistance genes were sequenced to look for any mutations and Quantitative Realtime PCR was used to compare their regulation and expression between parent and primed strains. Growth assays were used to investigate if there were fitness costs attached to the antibiotic cross resistance observed. Results: Stable cross-resistance to antibiotics was observed in bacterial strains, with no observed increased tolerance to biocides. Six-fold increases in MIC to cephalothin and four-fold to ceftriaxone and ampicillin were observed in hydrogen peroxide primed E. coli and thioridazine increased the susceptibility of E. coli to cephalothin and cefoxitin. The ompF porin gene was downregulated by 30.5-fold after exposure to hydrogen peroxide and a further 37.9-fold when grown in 4 mg/l cephalothin compared to parent strain. Chlorhexid…
abstract: Background: Public awareness to infection control, for example the current covid-19 pandemic, can cause a rise in the use of biocidal products. Uncontrolled use of biocides, especially at sub-inhibitory concentrations has led to growing concerns that their selective pressure may favour the prevalence of less susceptible bacterial strains and encourage the expression and dissemination of antibiotic resistance genes. Aims: To investigate the priming effects of sub-inhibitory concentrations of biocides on antibiotic resistance in bacteria and to understand the resistance mechanisms activated by these effects. Methodology: Escherichia coli, Pseudomonas aeruginosa and Staphylococcus aureus were exposed to sub-inhibitory concentrations of biocides (hydrogen peroxide, chlorhexidine, glutaraldehyde and benzalkonium chloride). Minimum inhibitory concentrations of antibiotics and biocides were determined before and after exposure to low concentrations of biocides to test for changes in biocide tolerance and cross resistance to antibiotics. Efflux pump inhibitors (thioridazine and chlorpromazine) were used to investigate efflux as a mechanism. Known antibiotic resistance genes were sequenced to look for any mutations and Quantitative Realtime PCR was used to compare their regulation and expression between parent and primed strains. Growth assays were used to investigate if there were fitness costs attached to the antibiotic cross resistance observed. Results: Stable cross-resistance to antibiotics was observed in bacterial strains, with no observed increased tolerance to biocides. Six-fold increases in MIC to cephalothin and four-fold to ceftriaxone and ampicillin were observed in hydrogen peroxide primed E. coli and thioridazine increased the susceptibility of E. coli to cephalothin and cefoxitin. The ompF porin gene was downregulated by 30.5-fold after exposure to hydrogen peroxide and a further 37.9-fold when grown in 4 mg/l cephalothin compared to parent strain. Chlorhexid…
author: Adkin, Osaretin Patience (Pat)
license: https://dora.dmu.ac.uk/bitstreams/03f908e5-579d-4c57-8f47-b76c08784de4/download
date published: 2020-09
date modified: 2026-07-24T06:18:49Z
provider: De Montfort University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: De Montfort University