Yoshida H, Bogaki M, Nakamura M, Yamanaka L M, Nakamura S
Research Laboratories, Dainippon Pharmaceutical Co., Ltd., Osaka, Japan.
Antimicrob Agents Chemother. 1991 Aug;35(8):1647-50. doi: 10.1128/AAC.35.8.1647.
Thirteen spontaneous quinolone-resistant gyrB mutants of Escherichia coli KL16, including two that were examined previously, were divided into two types according to their quinolone resistance patterns. Type 1 mutants were resistant to all the quinolones tested, while type 2 mutants were resistant to acidic quinolones and were hypersusceptible to amphoteric quinolones. Nucleotide sequence analysis disclosed that all nine type 1 mutants had a point mutation from aspartic acid to asparagine at amino acid 426 and that all four type 2 mutants had a point mutation from lysine to glutamic acid at amino acid 447.
大肠杆菌KL16的13个自发喹诺酮抗性gyrB突变体(包括之前检测的2个)根据其喹诺酮抗性模式分为两种类型。1型突变体对所有测试的喹诺酮耐药,而2型突变体对酸性喹诺酮耐药且对两性喹诺酮高度敏感。核苷酸序列分析显示,所有9个1型突变体在氨基酸426处有一个从天冬氨酸到天冬酰胺的点突变,所有4个2型突变体在氨基酸447处有一个从赖氨酸到谷氨酸的点突变。