Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations in quinolone-resistant Escherichia coli isolated from humans and swine in Denmark

Lina Cavaco, Niels Frimodt-Møller, Henrik Hasman, Luca Guardabassi, Lene Nielsen, Frank Møller Aarestrup

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations (MICs) of nalidixic acid (NAL) and ciprofloxacin (CIP) were investigated in 124 Escherichia coli isolated from humans (n = 85) and swine (n = 39) in Denmark. The collection included 59 high-level CIP-resistant isolates (MIC >= 4) from human (n = 51) and pig origin (n = 8) and 65 low-level CIP-resistant isolates (MIC >= 0.125) from human (n = 34) and pig origin (n = 31). Resistance by target modification was screened by PCR amplification and sequencing, of the quinolone resistance determining regions (QRDRs) of gyrA, gyrB, parC, and parE. QRDR mutations occurred in all except two isolates (98%). All high-level CIP-resistant E. coli had one or two mutations in gyrA in combination with mutations in parC or parE. Mutations in parC and parE were only found in combination with gyrA mutations, and no mutations were observed in gyrB. Efflux pump mechanisms were detected in 10 human (11.8%) and 29 porcine (74.4%) isolates by an efflux pump inhibitor (EPI) agar dilution assay. The aac(6')-Ib-cr gene mediating resistance by enzymatic modification was found in 12 high-level CIP-resistant human isolates. The qnrA and qnrS genes conferring quinolone resistance by target protection were detected in two human low-level CIP-resistant isolates that did not display NAL resistance. As expected, target mutation in QRDRs was the most prevalent mechanism of quinolone resistance. This mechanism was complemented by efflux mechanisms in most porcine isolates. Transferable resistance by target protection or enzymatic modification was less common (10%) and restricted to human isolates.
Original languageEnglish
JournalMicrobial Drug Resistance
Volume14
Issue number2
Pages (from-to)163-169
ISSN1076-6294
DOIs
Publication statusPublished - 2008

Cite this

@article{ebfa4d9ccbaf4979b505d2ec8ef70438,
title = "Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations in quinolone-resistant Escherichia coli isolated from humans and swine in Denmark",
abstract = "Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations (MICs) of nalidixic acid (NAL) and ciprofloxacin (CIP) were investigated in 124 Escherichia coli isolated from humans (n = 85) and swine (n = 39) in Denmark. The collection included 59 high-level CIP-resistant isolates (MIC >= 4) from human (n = 51) and pig origin (n = 8) and 65 low-level CIP-resistant isolates (MIC >= 0.125) from human (n = 34) and pig origin (n = 31). Resistance by target modification was screened by PCR amplification and sequencing, of the quinolone resistance determining regions (QRDRs) of gyrA, gyrB, parC, and parE. QRDR mutations occurred in all except two isolates (98{\%}). All high-level CIP-resistant E. coli had one or two mutations in gyrA in combination with mutations in parC or parE. Mutations in parC and parE were only found in combination with gyrA mutations, and no mutations were observed in gyrB. Efflux pump mechanisms were detected in 10 human (11.8{\%}) and 29 porcine (74.4{\%}) isolates by an efflux pump inhibitor (EPI) agar dilution assay. The aac(6')-Ib-cr gene mediating resistance by enzymatic modification was found in 12 high-level CIP-resistant human isolates. The qnrA and qnrS genes conferring quinolone resistance by target protection were detected in two human low-level CIP-resistant isolates that did not display NAL resistance. As expected, target mutation in QRDRs was the most prevalent mechanism of quinolone resistance. This mechanism was complemented by efflux mechanisms in most porcine isolates. Transferable resistance by target protection or enzymatic modification was less common (10{\%}) and restricted to human isolates.",
author = "Lina Cavaco and Niels Frimodt-M{\o}ller and Henrik Hasman and Luca Guardabassi and Lene Nielsen and Aarestrup, {Frank M{\o}ller}",
year = "2008",
doi = "10.1089/mdr.2008.0821",
language = "English",
volume = "14",
pages = "163--169",
journal = "Microbial Drug Resistance",
issn = "1076-6294",
publisher = "Mary AnnLiebert, Inc. Publishers",
number = "2",

}

Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations in quinolone-resistant Escherichia coli isolated from humans and swine in Denmark. / Cavaco, Lina; Frimodt-Møller, Niels; Hasman, Henrik; Guardabassi, Luca; Nielsen, Lene; Aarestrup, Frank Møller.

In: Microbial Drug Resistance, Vol. 14, No. 2, 2008, p. 163-169.

Research output: Contribution to journalJournal articleResearchpeer-review

TY - JOUR

T1 - Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations in quinolone-resistant Escherichia coli isolated from humans and swine in Denmark

AU - Cavaco, Lina

AU - Frimodt-Møller, Niels

AU - Hasman, Henrik

AU - Guardabassi, Luca

AU - Nielsen, Lene

AU - Aarestrup, Frank Møller

PY - 2008

Y1 - 2008

N2 - Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations (MICs) of nalidixic acid (NAL) and ciprofloxacin (CIP) were investigated in 124 Escherichia coli isolated from humans (n = 85) and swine (n = 39) in Denmark. The collection included 59 high-level CIP-resistant isolates (MIC >= 4) from human (n = 51) and pig origin (n = 8) and 65 low-level CIP-resistant isolates (MIC >= 0.125) from human (n = 34) and pig origin (n = 31). Resistance by target modification was screened by PCR amplification and sequencing, of the quinolone resistance determining regions (QRDRs) of gyrA, gyrB, parC, and parE. QRDR mutations occurred in all except two isolates (98%). All high-level CIP-resistant E. coli had one or two mutations in gyrA in combination with mutations in parC or parE. Mutations in parC and parE were only found in combination with gyrA mutations, and no mutations were observed in gyrB. Efflux pump mechanisms were detected in 10 human (11.8%) and 29 porcine (74.4%) isolates by an efflux pump inhibitor (EPI) agar dilution assay. The aac(6')-Ib-cr gene mediating resistance by enzymatic modification was found in 12 high-level CIP-resistant human isolates. The qnrA and qnrS genes conferring quinolone resistance by target protection were detected in two human low-level CIP-resistant isolates that did not display NAL resistance. As expected, target mutation in QRDRs was the most prevalent mechanism of quinolone resistance. This mechanism was complemented by efflux mechanisms in most porcine isolates. Transferable resistance by target protection or enzymatic modification was less common (10%) and restricted to human isolates.

AB - Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations (MICs) of nalidixic acid (NAL) and ciprofloxacin (CIP) were investigated in 124 Escherichia coli isolated from humans (n = 85) and swine (n = 39) in Denmark. The collection included 59 high-level CIP-resistant isolates (MIC >= 4) from human (n = 51) and pig origin (n = 8) and 65 low-level CIP-resistant isolates (MIC >= 0.125) from human (n = 34) and pig origin (n = 31). Resistance by target modification was screened by PCR amplification and sequencing, of the quinolone resistance determining regions (QRDRs) of gyrA, gyrB, parC, and parE. QRDR mutations occurred in all except two isolates (98%). All high-level CIP-resistant E. coli had one or two mutations in gyrA in combination with mutations in parC or parE. Mutations in parC and parE were only found in combination with gyrA mutations, and no mutations were observed in gyrB. Efflux pump mechanisms were detected in 10 human (11.8%) and 29 porcine (74.4%) isolates by an efflux pump inhibitor (EPI) agar dilution assay. The aac(6')-Ib-cr gene mediating resistance by enzymatic modification was found in 12 high-level CIP-resistant human isolates. The qnrA and qnrS genes conferring quinolone resistance by target protection were detected in two human low-level CIP-resistant isolates that did not display NAL resistance. As expected, target mutation in QRDRs was the most prevalent mechanism of quinolone resistance. This mechanism was complemented by efflux mechanisms in most porcine isolates. Transferable resistance by target protection or enzymatic modification was less common (10%) and restricted to human isolates.

U2 - 10.1089/mdr.2008.0821

DO - 10.1089/mdr.2008.0821

M3 - Journal article

VL - 14

SP - 163

EP - 169

JO - Microbial Drug Resistance

JF - Microbial Drug Resistance

SN - 1076-6294

IS - 2

ER -