RT Journal Article
SR Electronic
T1 Mutation in DNA gyrase of norfloxacin-resistant clinical isolates of Neisseria gonorrhoeae.
JF Genitourinary Medicine
JO Genitourin Med
FD BMJ Publishing Group Ltd
SP 295
OP 297
DO 10.1136/sti.72.4.295
VO 72
IS 4
A1 M Tanaka
A1 M Otsuki
A1 T Nishino
A1 I Kobayashi
A1 T Matsumoto
A1 J Kumazawa
YR 1996
UL http://sti.bmj.com/content/72/4/295.abstract
AB BACKGROUND AND OBJECTIVES: Recently a rapid decrease in the susceptibility of Neisseria gonorrhoeae isolates to fluoroquinolones has occurred and gonococcal fluoroquinolone resistance is now a significant problem in the treatment of gonorrhoea in Japan. Thus, in order to investigate the quinolone resistance mechanisms in clinical isolates of N gonorrhoeae we studied an alteration in the DNA gyrase subunit A (GyrA) which is well-known as a common mechanism of bacterial quinolone resistance. MATERIALS AND METHODS: Four clinical isolates of N gonorrhoeae resistant to norfloxacin and 5 strains susceptible to norfloxacin, including 2 clinical isolates and 3 WHO reference strains, were tested in this study. To identify mutations in the GyrA genes of gonococcal strains, polymerase chain reaction and direct DNA sequencing were performed. RESULTS: A single base change (serine codon TCC changed to phenylalanine codon TTC), which resulted in an amino acid change in GyrA at position 91, was identified in all 4 norfloxacin-resistant strains for which the MICs of norfloxacin ranged from 1.0 to 8.0 micrograms/ml, while no mutation within GyrA was detected in 5 norfloxacin-susceptible strains for which the MICs of norfloxacin ranged from 0.004 to 0.063 microgram/ml. CONCLUSIONS: The results from this study suggest that the serine-91 to phenylalanine substitution in GyrA is probably an essential mutation in fluoroquinolone resistance in clinical isolates of N gonorrhoeae.