International journal of microbiology · 2026
Phenotypic and Genotypic Characterization of Antimicrobial Resistance in Helicobacter pylori: Association of 23S rRNA, gyrA, and rdxA Gene Mutations With Resistance Patterns.
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Makled Amal F, Abdelaziz Hany A, Allam Dina M, Salama Mona F, Khamis Nashwa N, Sleem Asmaa S
Аннотация
BACKGROUND: Antibiotic-resistant Helicobacter pylori pose a significant global health challenge. This Egyptian study is aimed at characterizing resistant H. pylori isolates and investigate the association between 23S rRNA, gyrA, and rdxA mutations and phenotypic profiles.
PATIENTS AND METHODS: Gastric biopsies collected in the internal medicine endoscopy unit were H. pylori tested by rapid urease, histopathology, and culture confirmed by ureC PCR. Antimicrobial susceptibility to clarithromycin, levofloxacin, and metronidazole was evaluated by disk diffusion and agar dilution methods. Sanger sequencing was employed to detect 23S rRNA, gyrA, and rdxA mutations.
RESULTS: Among 81 cultivable H. pylori isolates, bacillary 37/81 (45.7%), coccobacillary 30/81 (37.1%), and coccoid 14/81 (17.2%) forms were seen. Agar dilution confirmed resistance to metronidazole, clarithromycin, and levofloxacin by 72.8%, 23.5%, and 9.9%, respectively. Dual resistance was confirmed by 22.3% versus 2.5% triple resistance. Sequencing results of eight resistant isolates revealed 23S rRNA mutations (A2143G, A2142G; 5/8), whereas gyrA mutations included D91N (2/8), D91G, and N87K (1/8 each). A 200-bp rdx deletion was detected (3/8) along with D59N (2/8), R131K, A68N, and truncation mutations (each 1/8). Coccoid (4/8) and coccobacillary (2/8) H. pylori forms mixed with gastric microbiota (6/8), which also demonstrated dual (4/8) or triple (2/8) antibiotic resistance, and showed an association with the A2143G and A2142G mutations plus 200-bp deletion in the rdxA gene.
CONCLUSION: Integrating molecular genotyping with phenotypic diagnostics may improve H. pylori resistance characterization. Findings from this limited number of sequenced resistant isolates suggest a possible association between 23S rRNA, gyrA, and rdxA mutations and virulent, resistant, coccoid-microbiota mixed strains.
PATIENTS AND METHODS: Gastric biopsies collected in the internal medicine endoscopy unit were H. pylori tested by rapid urease, histopathology, and culture confirmed by ureC PCR. Antimicrobial susceptibility to clarithromycin, levofloxacin, and metronidazole was evaluated by disk diffusion and agar dilution methods. Sanger sequencing was employed to detect 23S rRNA, gyrA, and rdxA mutations.
RESULTS: Among 81 cultivable H. pylori isolates, bacillary 37/81 (45.7%), coccobacillary 30/81 (37.1%), and coccoid 14/81 (17.2%) forms were seen. Agar dilution confirmed resistance to metronidazole, clarithromycin, and levofloxacin by 72.8%, 23.5%, and 9.9%, respectively. Dual resistance was confirmed by 22.3% versus 2.5% triple resistance. Sequencing results of eight resistant isolates revealed 23S rRNA mutations (A2143G, A2142G; 5/8), whereas gyrA mutations included D91N (2/8), D91G, and N87K (1/8 each). A 200-bp rdx deletion was detected (3/8) along with D59N (2/8), R131K, A68N, and truncation mutations (each 1/8). Coccoid (4/8) and coccobacillary (2/8) H. pylori forms mixed with gastric microbiota (6/8), which also demonstrated dual (4/8) or triple (2/8) antibiotic resistance, and showed an association with the A2143G and A2142G mutations plus 200-bp deletion in the rdxA gene.
CONCLUSION: Integrating molecular genotyping with phenotypic diagnostics may improve H. pylori resistance characterization. Findings from this limited number of sequenced resistant isolates suggest a possible association between 23S rRNA, gyrA, and rdxA mutations and virulent, resistant, coccoid-microbiota mixed strains.