Background:
Iran has a relatively high prevalence of H. pylori, which correlates with
high-risk areas for gastric cancer worldwide.
Methods:
Our study aimed to investigate the underlying genetic mechanisms associated with resistance
to metronidazole (frxA, rdxA), clarithromycin (23S rRNA), tetracycline (16S rRNA),
and fluoroquinolone (gyrA) in H. pylori-positive dyspeptic patients using PCR and sequencing.
We further examined the potential correlation between resistance profiles and various virulence
genotypes.
Results:
The rates of genetic mutations associated with resistance to metronidazole, fluoroquinolone,
clarithromycin, and tetracycline were found to be 68%, 32.1%, 28.4%, and 11.1%, respectively.
Well-documented multiple antibiotic resistance mutations were detected, such as rdxA and
frxA (with missense and frameshift alterations), gyrA (Asp91, Asn87), 23S rRNA (A2142G,
A2143G), and 16S rRNA (triple-base-pair substitutions AGA926-928→TTC). The cagA+ and
vacA s1/m1 types were the predominant genotypes in our study. With the exception of metronidazole
and tetracycline, no significant correlation was observed between the cagA+ and cagL+
genotypes and resistance-associated mutations.
Conclusion:
The prevalence of antibiotic resistance-associated mutations in H. pylori was remarkably
high in this region, particularly to metronidazole, ciprofloxacin, and clarithromycin. By
conducting a simultaneous screening of virulence and resistance genotypes, clinicians can make
informed decisions regarding the appropriate therapeutic regimen to prevent the escalation of
antibiotic resistance against H. pylori infection in this specific geographical location.