Yokoi Shigeaki, Yasuda Mitsuru, Ito Shin-ichi, Takahashi Yoshihito, Ishihara Satoshi, Deguchi Takashi, Maeda Shin-ichi, Kubota Yasuaki, Tamaki Masayoshi, Fukushi Hideto
Department of Urology, Graduate School of Medicine, Gifu University, 1-1 Yanagaido, Gifu, 501-1194, Japan.
J Infect Chemother. 2004 Oct;10(5):262-7. doi: 10.1007/s10156-004-0332-4.
Twenty-three clinical strains of Chlamydia trachomatis were isolated from men with chlamydial nongonococcal urethritis and examined for the presence of fluoroquinolone resistance-associated alterations in GyrA and ParC. The minimum inhibitory concentrations (MICs) of fluoroquinolones, erythromycin, and tetracycline were determined for 6 of the 23 isolates. In 12 of the 23 isolates, a single amino-acid change was found in GyrA, and in 1 isolate, two amino acids were changed. In all 23 isolates, an Arg-83-to-Gly substitution was observed in ParC, and in 3 isolates, an additional amino-acid change was found. Some changes occurred within the quinolone resistance-determining regions (QRDRs) of GyrA and ParC, but not at positions critical for fluoroquinolone resistance. Of the 6 isolates for which MICs of the agents were determined, 1 isolate had a Cys-66 --> Arg substitution in GyrA, and all had the Arg-83 --> Gly substitution in ParC. However, all 6 isolates were susceptible to fluoroquinolones. First-pass urine specimens were obtained from two men who were positive for C. trachomatis after levofloxacin treatment, and the gyrA and parC genes of C. trachomatis were amplified by polymerase chain reaction (PCR) and examined for fluoroquinolone resistance-associated mutations. Pre- and post-treatment C. trachomatis persisting in each of them had identical amino-acid sequences in the QRDR of GyrA and ParC. Further, the substitutions found in GyrA and ParC were not located at positions critical for fluoroquinolone resistance. The present study suggests that fluoroquinolone resistance-associated alterations in GyrA and ParC may be uncommon in clinical strains of C. trachomatis.
从患有衣原体非淋菌性尿道炎的男性中分离出23株沙眼衣原体临床菌株,并检测其GyrA和ParC中与氟喹诺酮耐药相关的改变。测定了23株分离株中6株对氟喹诺酮、红霉素和四环素的最低抑菌浓度(MIC)。在23株分离株中的12株中,GyrA中发现了单个氨基酸变化,在1株中发现了两个氨基酸变化。在所有23株分离株中,ParC中均观察到Arg-83到Gly的取代,在3株分离株中还发现了另外的氨基酸变化。一些变化发生在GyrA和ParC的喹诺酮耐药决定区(QRDR)内,但并非在对氟喹诺酮耐药至关重要的位置。在测定了药物MIC的6株分离株中,1株在GyrA中有Cys-66→Arg取代,所有分离株在ParC中均有Arg-83→Gly取代。然而,所有6株分离株对氟喹诺酮均敏感。从两名左氧氟沙星治疗后沙眼衣原体呈阳性的男性中获取首段尿标本,通过聚合酶链反应(PCR)扩增沙眼衣原体的gyrA和parC基因,并检测与氟喹诺酮耐药相关的突变。他们各自体内治疗前和治疗后持续存在的沙眼衣原体在GyrA和ParC的QRDR中具有相同的氨基酸序列。此外,在GyrA和ParC中发现的取代并非位于对氟喹诺酮耐药至关重要的位置。本研究表明,GyrA和ParC中与氟喹诺酮耐药相关的改变在沙眼衣原体临床菌株中可能并不常见。