Prevalence of Quinolone Resistance Mechanisms and Associations to Minimum Inhibitory Concentrations in Quinolone-ResistantEscherichia coliIsolated from Humans and Swine in Denmark
Autor: | Henrik Hasman, Frank Møller Aarestrup, Lina Cavaco, Niels Frimodt-Møller, Lene Nørby Nielsen, Luca Guardabassi |
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Rok vydání: | 2008 |
Předmět: |
Microbiology (medical)
Nalidixic acid Swine medicine.drug_class Denmark Immunology Microbial Sensitivity Tests Quinolones Biology medicine.disease_cause Microbiology law.invention Nalidixic Acid Quinolone resistance Bacterial Proteins Ciprofloxacin law Drug Resistance Bacterial Escherichia coli Prevalence medicine Animals Humans heterocyclic compounds Escherichia coli Infections Polymerase chain reaction Swine Diseases Pharmacology biochemical phenomena metabolism and nutrition bacterial infections and mycoses Quinolone Anti-Bacterial Agents Mutation bacteria Efflux medicine.drug |
Zdroj: | Microbial Drug Resistance. 14:163-169 |
ISSN: | 1931-8448 1076-6294 |
DOI: | 10.1089/mdr.2008.0821 |
Popis: | 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 (MICor= 4) from human (n=51) and pig origin (n=8) and 65 low-level CIP-resistant isolates (MICor= 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. |
Databáze: | OpenAIRE |
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