Analysis of antimicrobial susceptibility and virulence factors in Helicobacter pylori clinical isolates in the United Arab Emirates

Abstract number: 1733_15

Alfaresi M., Elkouch A., Abdulsalam A.

Objectives: The gastric pathogen Helicobacter (H.) pylori produces virulence factors such as CagA and VacA that are associated with symptom severity in infected individuals. In this study, we asked whether there is a correlation between the clarithromycin resistance status of H. pylori clinical isolates and vacA and cagA status, as well as whether these characteristics correlated with the clinical symptoms of gastric disease.

Methods: DNA was extracted from antral gastric biopsy samples from 91 dyspeptic patients in the United Arab Emirates (UAE). Real-time PCR and melting curve analysis was 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. Clinical examination and patient histories were used to classify the clinical symptoms of H. pylori-infected patients.

Results: Real-time PCR analysis detected the presence of H. pylori in 55 samples (60%); further PCR analysis found that 36 of the pathogen-positive samples (65.5%) contained at least one of three point mutations associated with clarithromycin resistance. Patients from the UAE had the same mutation incidence as non-UAE patients. The vacA gene was present in 72.7% and cagA was present in 75.5% of the positive samples. The 55 H. pylori-positive patients were clinically categorised as having non-ulcer dyspepsia (19 patients), peptic ulcers (20 patients) or gastroesophageal reflux disease (16 patients).

Conclusions: The presence of each clarithromycin-resistance inducing mutation was largely independent of the others. The A(2142/43)G mutations were strongly associated with the presence of both the vacA gene and the cagA gene, and there was a strong association of the presence of both the vacA and the cagA genes. Both genes were more likely to be present than absent in samples from all patients, regardless of the symptoms exhibited, but there was no correlation in the incidence of any of the point mutations with any of the categories of clinical symptoms.

Taken together, these results may help physicians identify patients likely to be responsive to standard clarithromycin-based therapy, and also underscore the value of using real-time PCR methods for rapid identification of clarithromycin-resistant H. pylori strains.