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Abstract
BACKGROUND It was recently reported that A to G transition mutations at positions 2143 and 2144 in the 23S rRNA gene are associated with clarithromycin resistance in Helicobacter pylori.
AIMS To study the incidence and mechanism of development of clarithromycin resistance by analysing these mutations.
SUBJECTS Eighty twoH pylori positive patients who had an endoscopic examination and no history of treatment with macrolide antibiotics.
METHODS Clarithromycin resistance was screened for by polymerase chain reaction-restriction fragment length polymorphism of the 23S rRNA gene coupled with antibiotic susceptibility testing. In clinical isolates with mutations or resistance, mutations in individual colonies were analysed by direct sequencing.
RESULTS Of the 79 amplicons (DNA fragments amplified by polymerase chain reaction),Alw26I and MboII digestion disclosed the mutation in four (5%) and one (1%) respectively. However, the Alw26I cleavage was incomplete in two of the four amplicons, as was theMboII cleavage. Individual colony analysis of the isolates with incomplete cleavage patterns showed the presence of both wild type and mutated strains in the 23S rRNA genes.
CONCLUSIONS Both clarithromycin sensitive and resistant strains colonised in some patients with no history of exposure to macrolides. The results suggest that resistant strains may not be formed but selected by clarithromycin administration.
- Helicobacter pylori
- clarithromycin resistance
- 23S rRNA gene
- point mutation
- mixed strain colonisation
Abbreviations used in this paper
- PCR
- polymerase chain reaction
- RFLP
- restriction fragment length polymorphism
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Abbreviations used in this paper
- PCR
- polymerase chain reaction
- RFLP
- restriction fragment length polymorphism