Godfrey-Faussett P, Stoker N G, Scott J A, Pasvol G, Kelly P, Clancy L
Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, UK.
Tuber Lung Dis. 1993 Aug;74(4):240-3. doi: 10.1016/0962-8479(93)90049-4.
Drug-resistant tuberculosis has become a major public health problem. Resistance to rifampicin probably arises through mutations in the mycobacterial RNA polymerase. Patients may acquire rifampicin resistant tuberculosis by three mechanisms: (1) infection with a resistant organism, (2) selection of a sub-population of resistant organisms that remain contained whilst the more virulent wild type is present, (3) mutations within the population of bacilli causing the original infection. Sequential isolates of Mycobacterium tuberculosis were collected from 2 patients who developed rifampicin resistance whilst on treatment. One patient was immunosuppressed with HIV-infection; in the other patient the original isolate was also resistant to isoniazid. DNA fingerprinting techniques were used to type the isolates. No differences were found between the fingerprints of isolates from before and after the development of resistance. These data suggest that the third of the mechanisms listed above was responsible for the acquisition of rifampicin resistance in these 2 patients.
耐多药结核病已成为一个主要的公共卫生问题。对利福平的耐药性可能是由于分枝杆菌RNA聚合酶发生突变而产生的。患者可能通过三种机制感染耐利福平结核病：（1）感染耐药菌；（2）在存在毒性更强的野生型菌的情况下，选择出一群仍存在的耐药菌亚群；（3）引起初始感染的杆菌群体内发生突变。从2例在治疗期间出现利福平耐药的患者中收集了结核分枝杆菌的连续分离株。1例患者因感染HIV而免疫抑制；另1例患者的初始分离株也对异烟肼耐药。采用DNA指纹技术对分离株进行分型。耐药发生前后分离株的指纹图谱未发现差异。这些数据表明，上述三种机制中的第三种机制导致了这2例患者获得利福平耐药。
