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HERDIN Record #: PCHRD17011911084764 Submitted: 19 January 2017 Modified: 21 November 2017

New site of modification of 23S rRNA associated with clarithromycin resistance of Helicobacter pylori clinical isolates.

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Resistance of Helicobacter pylori to clarithromycin occurs with a prevalence ranging from 0 to 15%. This has an important clinical impact on dual and triple therapies, in which clarithromycin seems to be the better choice to achieve H. pylori eradication. In order to evaluate the possibility of new mechanisms of clarithromycin resistance, a PCR assay that amplified a portion of 23S rRNA from H. pylori isolates was used. Gastric tissue biopsy specimens from 230 consecutive patients were cultured for H. pylori isolation. Eighty-six gastric biopsy specimens yielded H. pylori-positive results, and among these 12 isolates were clarithromycin resistant. The latter were studied to detect mutations in 23S rRNA gene. Sequence analysis of the 1,143-bp PCR product (portion of the 23S rRNA gene ) did not reveal mutation such as that described at position 2142 to 2143. On the contrary, our findings show, for even isolates, a T-to-C transition at position 2717. This mutation conferred a low level of resistance, equivalanet to the MIC for the isolates, selected using the E-test as well as using the agar dilution method: 1ug/ml. Moreover, T2717C transition is located in a highly conserved region of the 23S RNA associated with functional sites: domain VI. This fact has a strong effect on the secondary structure of the 23S RNA and on its interaction with macrolide. Mutation at position 2717 also generated an HhaI restriction site; therefore, restriction analysis of the PCR product also permits a rapid detection of resistant isolates.

Publication Type
Publication Sub Type
Journal Article, Reprint
Antimicrobial Agents and Chemotherapy
Publication Date
December 2002
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Philippine Council for Health Research and Development Library Fulltext Print Format (Request Document)
U.S. National Library of Medicine: PubMed/Medline Abstract External Link (View)
U.S. National Library of Medicine: PubMed/Medline Fulltext pdf (Request Document)

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