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. 1999 Jun;43(6):1497-9.
doi: 10.1128/AAC.43.6.1497.

Rifampin and rifabutin resistance mechanism in Helicobacter pylori

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Rifampin and rifabutin resistance mechanism in Helicobacter pylori

M Heep et al. Antimicrob Agents Chemother. 1999 Jun.

Abstract

Eighty-one clinical isolates of Helicobacter pylori showed no resistance to rifampin (MIC range, 0.032 to 2 microg/ml; MIC at which 50% of isolates are inhibited [MIC50], 0.25 microg/ml). The MIC50 of rifabutin was 0.008 microg/ml (n = 16). All resistant laboratory mutants of H. pylori ATCC 43504 showed amino acid exchanges in codons 524 to 545 or codon 585 of the rpoB gene, corresponding to the gene sequences from Mycobacterium tuberculosis and Escherichia coli.

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Figures

FIG. 1
FIG. 1
Codon substitutions in resistant mutants of H. pylori type strain ATCC 43504 and correlation to the rpoB resistance-determining regions in E. coli (9) and M. tuberculosis (12). E. coli clusters I and II are resistance-determining regions (9) (GenBank accession no. U77436). For M. tuberculosis (M.tub), bold letters indicate the most frequent in vivo mutations (GenBank accession no. AF060282). HP, H. pylori. The amino acid sequence of the H. pylori 26695 rpoB gene product has been published (10) (GenBank accession no. AE000625). The corresponding sequences from 26 clinical isolates and H. pylori ATCC 43504 were identical to that of H. pylori 26695. Strain designations for laboratory mutants of H. pylori ATCC 43504 are as in Table 2.

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