RESUMEN
Background Clarithromycin therapy is effective in eradicating Helicobacter pylori. However, the resistance of H. pylori to clarithromycin is increasingly reported. The present study aimed to characterize the types of mutations present in the 23S rRNA genes of isolates of clarithromycin-resistant H. pylori from the UAE. Methods Clarithromycin susceptibility of H. pylori isolates (n=26) was determined by E tests. Analyses for point mutations in domain V of the 23S rRNA genes in clarithromycin-resistant and-sensitive strains were performed by sequence analysis of amplified PCR products. Results Out of 100 gastric antral biopsy samples, 26 were positive for H. pylori by culture, and 29 were positive by PCR. Of the 26 culture isolates, five (19.2%) were resistant to clarithromycin and 24 were sensitive. The MIC of the resistant strains ranged from 3 to 24 μg/mL (median 24). All of the clarithromycin-resistant isolates had point mutations in the 23S rRNA gene. Two isolates had an A2142G 23S rRNA mutation, and three had A2143G mutations. Conclusion Clarithromycin resistance was common in this small collection of H. pylori isolates from the UAE. The A2142G and A2143G mutations were associated with clarithromycin resistance.
RESUMEN
AIM: To determine the virulence attributes (presence of cagA and vacA genes) of Helicobacter pylori , and presence of clarithromycin resistance genes in gastric mucosal biopsy samples obtained in the United Arab Emirates. METHODS: DNA was extracted from antral gastric biopsy samples from 91 dyspeptic patients. Real-time PCR and melting curve analysis were used to identify patients infected with H. pylori and to further identify strains containing the A(2142/43)G or the A(2142)C mutations that are associated with clarithromycin resistance. PCR was also used to identify cagA - and vacA -positive strains. RESULTS: Real-time PCR analysis detected the presence of H. pylori in 55 (60%) samples. Thirty-six pathogen-positive samples contained at least one of three point mutations associated with clarithromycin resistance. The vacA gene was present in 40 (72.7%) and cagA was present in 41 (74.5%) of the positive samples. Both genes were present in 36 (65%) of the positive samples. The presence of each clarithromycin-inducing mutation was largely independent of the others. Mutation at one position, A(2142/43)G, was strongly associated with the presence of both the vacA gene and the cagA gene. CONCLUSIONS: A high proportion of gastric mucosal biopsies obtained in the UAE is positive for genes associated with clarithromycin resistance. This may have implications for treatment of the infection.