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 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.
Godfrey-Faussett
P
P
Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, UK.
Stoker
N G
NG
Scott
J A
JA
Pasvol
G
G
Kelly
P
P
Clancy
L
L
D000328:Adult; D016172:DNA Fingerprinting; D004269:DNA, Bacterial / Q000235:genetics; D004352:Drug Resistance, Microbial / Q000235:genetics; D006801:Humans; D008297:Male; D009169:Mycobacterium tuberculosis / Q000187:drug effects* / Q000235:genetics*; D012293:Rifampin / Q000494:pharmacology*; D014397:Tuberculosis, Pulmonary / Q000188:drug therapy / Q000235:genetics*
D004269:DNA, Bacterial; D012293:Rifampin