DNA FINGERPRINTS OF MYCOBACTERIUM-TUBERCULOSIS DO NOT CHANGE DURING THE DEVELOPMENT OF RIFAMPICIN RESISTANCE

Drug-resistant tuberculosis has become a major public health problem. Resistance to rifampicin probably arises through mutations in the myco bacterial RNA polymerase. Patients may acquire rifampicin resistant tu berculosis by three mechanisms: (1) infection with a resistant organis m, (2) selection of a sub-population of resistant organisms that remai n contained whilst the more virulent wild type is present, (3) mutatio ns within the population of bacilli causing the original infection. Se quential 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 fingerprinti ng techniques were used to type the isolates. No differences were foun d between the fingerprints of isolates from before and after the devel opment of resistance. These data suggest that the third of the mechani sms listed above was responsible for the acquisition of rifampicin res istance in these 2 patients.