M Lutfey, P Della-Latta, V Kapur, LA Palumbo, D Gurner, G Stotzky, K Brudney, J Dobkin, A Moss, JM Musser and BN Kreiswirth
Tuberculosis Center, Public Health Research Institute, Columbia Presbyterian Medical Center, New York, New York 10016, USA.

Historically, infections caused by Mycobacterium tuberculosis have been treated simultaneously with isoniazid and rifampin. As a consequence of this combined therapy, strains resistant only to rifampin were rarely recovered. However, recently there has been an increasing number of reports describing HIV-positive patients infected with mono-rifampin- resistant M. tuberculosis strains. Organisms cultured from seven patients (including six with AIDS) with infections caused by mono- rifampin-resistant M. tuberculosis, and seen at one New York City hospital, were analyzed by molecular techniques to test the hypothesis that dissemination of a single clone had occurred. IS6110 DNA fingerprinting and automated DNA sequencing of a region of the RNA polymerase beta subunit structural gene (rpoB) containing mutations that confer rifampin resistance showed that all organisms independently acquired the mono-rifampin-resistant phenotype. Molecular analysis of mono-rifampin-resistant organisms cultured from 13 additional patients in New York City confirmed independent strain origin. The data rule out the possibility of person-to-person strain transmission among these patients, and they suggest that host factors such as poor compliance with antituberculosis medications or decreased absorption of rifampin have been a driving force in the origin of these strains.

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