Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Infectious Diseases, Microbiology, Pharmacology & Pharmacy, GYRASE GYRA GENE, DNA GYRASE, TOPOISOMERASE-IV, QUINOLONE RESISTANCE, STAPHYLOCOCCUS-AUREUS, IN-VITRO, STREPTOCOCCUS-PNEUMONIAE, ESCHERICHIA-COLI, ANTIMICROBIAL SUSCEPTIBILITY, PRIMARY TARGET, Amino Acid Substitution, Animals, Anti-Infective Agents, DNA Topoisomerase IV, DNA, Bacterial, Dose-Response Relationship, Drug, Drug Resistance, Bacterial, Enrofloxacin, Fluoroquinolones, Genes, Bacterial, Microbial Sensitivity Tests, Mycoplasma hyopneumoniae, Point Mutation, Polymerase Chain Reaction, Sequence Analysis, DNA, Swine, 06 Biological Sciences, 07 Agricultural and Veterinary Sciences, 11 Medical and Health Sciences, 30 Agricultural, veterinary and food sciences, 31 Biological sciences, 32 Biomedical and clinical sciences

Abstract:

The quinolone resistance-determining regions (QRDR) of gyrA, gyrB, parC, and parE of ten Mycoplasma hyopneumoniae field isolates that were either sensitive (5) or resistant (5) to the fluoroquinolones flumequine and enrofloxacin were characterized. In all five resistant isolates, one point mutation (C A) in parC was found, resulting in an amino acid change from serine to tyrosine at position 80 (Escherichia coli numbering). For four of these isolates, this was the only mutation found. These isolates had a minimum inhibitory concentration (MIC) of enrofloxacin of 0.5 g/ml, whereas for sensitive isolates the MIC of enrofloxacin was 0.06 g/ml. One resistant isolate (Mh 20) had an extra mutation (C T) in gyrA resulting in an amino acid change from alanine to valine at position 83 (E. coli numbering), leading to a further increase in the MIC of enrofloxacin (1 g/ml). No mutations resulting in an amino acid change were detected in the QRDR of the gyrB and parE genes of the selected isolates. This is the first description of the mechanism of stepwise resistance against fluoroquinolones in M. hyopneumoniae.