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. 1997 Nov;41(11):2550-3.
doi: 10.1128/AAC.41.11.2550.

Macrolide resistance in Helicobacter pylori: mechanism and stability in strains from clarithromycin-treated patients

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Macrolide resistance in Helicobacter pylori: mechanism and stability in strains from clarithromycin-treated patients

K Hultén et al. Antimicrob Agents Chemother. 1997 Nov.

Abstract

Helicobacter pylori strains from seven patients treated with clarithromycin were investigated for development, mechanism, and stability of resistance. Genetic relatedness between pre- and posttreatment isolates was shown by arbitrary primed PCR. Clarithromycin resistance was associated with A-to-G transitions at either position 2143 or 2144 or at both positions 2116 and 2142. In four cases, the mutations were homozygous. The Cla(r) phenotype was stable after 50 subcultivations in vitro. No erythromycin-modifying enzymes or rRNA methylases were found by biological assays, PCR and sequencing, or cloning methods.

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