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尽管喹诺酮类真正杀菌作用机制涉及一种级联细胞活动,但其主要作用靶是DNA旋转酶A亚基。在实验室里能容易地筛选到高度耐萘啶酸大肠杆菌突变体,其发生频率约为10~(-7),这些突变体具有改变了的DNA旋转酶。1981年Cellert报道到目前为止所试验的全部细菌种类中都存在DNA旋转酶,在数个种包括绿脓杆菌、流感嗜血菌和弗氏柠檬酸细菌中发生DNA旋转酶A亚基密码的突变,结果对萘啶酸示低敏感性。在近几年中已发表了数篇关于喹诺酮类耐药机制的报道(表一),发现了多种突变体如nalA、norA、nfxA、cfxA和ofxA,它们十分相
Although the true mechanism of quinolone bactericidal activity involves a cascade of cellular activities, its primary target is DNA gyrase A subunit. Highly resistant nalidixinate-producing E. coli mutants were easily screened in the laboratory at frequencies of about 10 -7, and these mutants had altered DNA gyrase. In 1981 Cellert reported that DNA gyrase was present in all bacterial species tested so far, and that mutations in the DNA gyrase A subunit code occurred in several species, including Pseudomonas aeruginosa, Haemophilus influenzae and Freund citrullobacteria , The result showed low sensitivity to nalidixic acid. Several reports of quinolone resistance mechanisms have been published in recent years (Table 1) and various mutants such as nalA, norA, nfxA, cfxA and ofxA have been found that are quite