Analysis of topoisomerase mutations in fluoroquinolone-resistant and -susceptible Campylobacter jejuni strains isolated in Senegal

Antimicrobial susceptibility and mechanism of quinolone resistance in Campylobacter jejuni strains isolated from diarrheal patients in a hospital in Tokyo

“…This suggests that this amino-acid substitution at codon 86 is not involved in the acquisition of resistance to CPFX, but that it may be involved in the acquisition of intermediate resistance to NA. 14,24 In regard to the gyrB gene, there were point mutations in base sequences of the QRDR, although none of them caused amino-acid substitution, irrespective of the resistance or susceptibility of strains to quinolones; this suggests that mutations in the gyrB gene are not involved in the development of quinolone resistance in the isolated strains tested in the present study. 14,25 Although the parC gene is registered in the gene bank, we could not successfully obtain any amplifi ed fragments from this gene.…”

“…14,24 In regard to the gyrB gene, there were point mutations in base sequences of the QRDR, although none of them caused amino-acid substitution, irrespective of the resistance or susceptibility of strains to quinolones; this suggests that mutations in the gyrB gene are not involved in the development of quinolone resistance in the isolated strains tested in the present study. 14,25 Although the parC gene is registered in the gene bank, we could not successfully obtain any amplifi ed fragments from this gene. Failure to detect the parC gene by PCR or in the whole genome database has been mentioned in many other reports, in which it has been suggested that campylobacters lack genes for topoisomerase IV.…”

“…5,7,[12][13][14] Thus, in the present study, to elucidate the mechanism of quinolone resistance, we investigated the presence of mutations in the QRDR of the gyrA gene. We found amino-acid substitution at codon 86 (Thr → IIe) in all the 37 strains showing resistance to CPFX; in contrast, such amino-acid substitution was not observed at codon 86 in any of the 18 strains susceptible to CPFX.…”

“…Failure to detect the parC gene by PCR or in the whole genome database has been mentioned in many other reports, in which it has been suggested that campylobacters lack genes for topoisomerase IV. 12,14,[25][26][27] Lou et al 10 have demonstrated the involvement of an effl ux pump in the acquisition of resistance to CPFX. Accordingly, we examined the inhibitory effect of the effl ux pump inhibitor L-phenylalanine-arginine-N-naphthylamide (PAβN; Sigma-Aldrich, St. Louis, MI, USA), on the resistance of C. jejuni strains to CPFX by determining the MIC of CPFX in the presence of PAβN.…”

“…10,11 Recently, many reports have suggested that mutations in quinolone-resistance determining regions (QRDRs) of DNA gyrase genes are substantially involved in the bacterial acquisition of resistance to quinolone agents. [12][13][14][15][16] In the present study, we carried out drug susceptibility tests of various drugs in C. jejuni strains isolated from patients with recent diarrheal diseases. In addition, in strains resistant to quinolones, we investigated the presence of mutations in their gyrA and gyrB genes.…”