Quinolone-resistant gyrase mutants demonstrate decreased susceptibility to triclosan

Webber, Mark A.; Buckner, Michelle M. C.; Redgrave, Liam Stephen; Ifill, Gyles; Mitchenall, Lesley A.; Webb, Carly; Iddles, Robyn; Maxwell, Anthony; Piddock, Laura J. V.

doi:10.1093/jac/dkx201

Cited by 29 publications

(17 citation statements)

References 31 publications

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“…46–48 In the collected experimental data, this mutation confers a median fold increase in MIC of 24 (range: 4-133x fold increase). 11, 49–55 This mutation is most often followed by Ser80Ile in parC 11,46,48 and finally by Asp87Asn or Asp87Gly in gyrA . 46–48 As mutations in gyrA and parC accumulate, ciprofloxacin MIC increases steeply.…”

Section: Resultsmentioning

confidence: 99%

Quantifying the contribution of four resistance mechanisms to ciprofloxacin minimum inhibitory concentration inEscherichia coli: a systematic review

Remondini

Pasquini

et al. 2018

Preprint

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SynopsisIntroductionCiprofloxacin resistance in Escherichia coli is widespread and adds to the burden of E. coli infections. Reviews assessing the genetic basis of ciprofloxacin resistance have mostly been qualitative. However, to allow for the prediction of a resistance phenotype of clinical relevance based on genotypic characteristics, it is essential to quantify the contribution of prevalent genotypic determinants to resistance. We carried out a systematic review to assess the relative contribution of currently known genomic resistance determinants to the minimum inhibitory concentration (MIC) of ciprofloxacin in E. coli.MethodsPubMed and Web of Science were searched for English language studies that assessed both ciprofloxacin MIC and the presence or introduction of genetic determinants of ciprofloxacin resistance in E. coli. We included experimental and observational studies without time restrictions. Medians and ranges of MIC fold changes were calculated for each resistance determinant and for combinations of determinants.ResultsWe included 66 studies, describing 604 E. coli isolates that carried at least one genetic resistance determinant. Genes coding for targets of ciprofloxacin (gyrA and parC) are strongest contributors to ciprofloxacin resistance, with median MIC fold increases ranging from 24 (range 4-133) for single Ser83Leu (gyrA) mutants to 1533 (range 256-8533) for triple Ser83Leu, Asp87Asn/Gly (gyrA) and Ser80Ile/Arg (parC) mutants. Other resistance mechanisms, including efflux, physical blocking or enzymatic modification, conferred smaller increases in ciprofloxacin MIC (median MIC fold increases typically around 15, range 1-125). However, the (combined) presence of these other resistance mechanisms further increases resistance with median MIC fold increases of up to 4000, and even in the absence of gyrA and parC mutations up to 250.ConclusionThis report provides a comprehensive and quantitative overview of the contribution of different genomic determinants to ciprofloxacin resistance in E. coli. Additionally, the data demonstrate the complexity of resistance phenotype prediction from genomic data and could serve as a reference point for studies aiming to address ciprofloxacin resistance prediction using genomics, in E. coli.

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Section: Resultsmentioning

confidence: 99%

Quantifying the contribution of four resistance mechanisms to ciprofloxacin minimum inhibitory concentration inEscherichia coli: a systematic review

Remondini

Pasquini

et al. 2018

Preprint

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“…But VRE strains (Beier et al, 2008) and Pseudomonas aeruginosa strains (Beier et al, 2014) were resistant to triclosan, as were all the C. coli strains evaluated here. Triclosan has long been described as a biocide since it is a synthetic product, but triclosan functions like an antibiotic as it has a specific cellular target (Webber et al, 2017). In E. coli, triclosan inhibits the highly conserved enzyme enoyl-acyl carrier protein reductase (ENP), which is the last enzyme in the bacterial fatty-acid biosynthesis elongation cycle (Heath & Rock, 2000).…”

Section: Food Microbiology and Safetymentioning

confidence: 99%

Disinfectant and Antimicrobial Susceptibility Profiles of Campylobacter coli Isolated in 1998 to 1999 and 2015 from Swine and Commercial Pork Chops

Beier

Harvey

Hernandez

et al. 2019

Journal of Food Science

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Susceptibility profiles were determined for 111 Campylobacter coli strains obtained in 1998 to 1999 and 2015 from market age pigs and pork chops against 22 disinfectants and 9 antimicrobials. Resistance to tetracycline (TET) was observed in 44.4% of 1998 to 1999 strains, and the antibiotic resistance profile was TET. But strains obtained in 2015 from swine and retail pork chops had 75% TET resistance and the antibiotic resistance profile was TET, followed by azithromycin‐erythromycin‐TET‐telithromycin‐clindamycin. Antimicrobial resistance increased in 2015 strains. All strains were resistant to triclosan, and 84.1% and 95.8% of strains in 1998 to 1999 and 2015, respectively, were chlorhexidine resistant. All strains were susceptible to benzalkonium chloride. There was a shift toward higher susceptibility to chlorhexidine, triclosan, P‐128, OdoBan, CPB, and CPC in 2015 swine and pork chop strains compared with 1998 to 1999 strains. The disinfectants Tek‐Trol and providone‐iodine, tris(hydroxylmethyl)nitromethane (THN) and formaldehyde demonstrated the highest susceptibilities. Didecyldimethylammonium chloride (C10AC) appeared to be about equally effective as benzyldimethyltetradecylammonium chloride (C14BAC) for inhibiting C. coli, and both were more effective than C8AC and C12BAC, but C16BAC was not efficient at inhibiting C. coli. The BACs, C12BAC and C14BAC, were the most effective ingredients in DC&R. Also, C12BAC and C14BAC, or these two in synergy with C10AC were responsible for inhibition of C. coli at high P‐128 MICs. No cross‐resistance was observed between antibiotics and disinfectants. The continued use of THN and formaldehyde in DC&R should be evaluated since these components are not effective, and their inclusion adds unwanted chemicals in the environment. Practical Application Campylobacter species cause diarrheal disease throughout the world. Disinfectants are often used on the farm, in veterinary medicine, by the food processing industry, in restaurants, and in consumer's homes. Limited information is available in the literature showing how disinfectants or disinfectant components may affect the many different foodborne pathogens, and, specifically, Campylobacter coli studied here. The knowledge generated in this study concerning the interactions of a broad array of disinfectants against C. coli may well affect the types of disinfectants and disinfectant formulations allowable for use by medical personnel, producers, food processors, restaurants, and consumers.

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“… 2017 ). In addition to human and animal use, many cleaning and personal hygiene products contain biocides, such as triclosan, which can select for mutants resistant to biocides, and in some cases to antibiotics used in medicine (Meek, Vyas and Piddock 2015 ; Webber et al 2015 , 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Strategies to combat antimicrobial resistance: anti-plasmid and plasmid curing

Buckner

Ciusa

Piddock

2018

FEMS Microbiology Reviews

Self Cite

143

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Antimicrobial resistance (AMR) is a global problem hindering treatment of bacterial infections, rendering many aspects of modern medicine less effective. AMR genes (ARGs) are frequently located on plasmids, which are self-replicating elements of DNA. They are often transmissible between bacteria, and some have spread globally. Novel strategies to combat AMR are needed, and plasmid curing and anti-plasmid approaches could reduce ARG prevalence, and sensitise bacteria to antibiotics. We discuss the use of curing agents as laboratory tools including chemicals (e.g. detergents and intercalating agents), drugs used in medicine including ascorbic acid, psychotropic drugs (e.g. chlorpromazine), antibiotics (e.g. aminocoumarins, quinolones and rifampicin) and plant-derived compounds. Novel strategies are examined; these include conjugation inhibitors (e.g. TraE inhibitors, linoleic, oleic, 2-hexadecynoic and tanzawaic acids), systems designed around plasmid incompatibility, phages and CRISPR/Cas-based approaches. Currently, there is a general lack of in vivo curing options. This review highlights this important shortfall, which if filled could provide a promising mechanism to reduce ARG prevalence in humans and animals. Plasmid curing mechanisms which are not suitable for in vivo use could still prove important for reducing the global burden of AMR, as high levels of ARGs exist in the environment.

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Quinolone-resistant gyrase mutants demonstrate decreased susceptibility to triclosan

Cited by 29 publications

References 31 publications

Quantifying the contribution of four resistance mechanisms to ciprofloxacin minimum inhibitory concentration inEscherichia coli: a systematic review

Quantifying the contribution of four resistance mechanisms to ciprofloxacin minimum inhibitory concentration inEscherichia coli: a systematic review

Disinfectant and Antimicrobial Susceptibility Profiles of Campylobacter coli Isolated in 1998 to 1999 and 2015 from Swine and Commercial Pork Chops

Strategies to combat antimicrobial resistance: anti-plasmid and plasmid curing

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