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Prevalence and Variability of Helicobacter pylori Clarithromycin Resistance Mutations in Pediatric Patients in
Tomasz Bogiel1, Anna Szaflarska-Popławska2, Agnieszka Krawczyk3
1Department of Propaedeutics of Medicine and Infection Prevention Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University and Clinical Microbiology Laboratory, Dr. Antoni Jurasz University Hospital No. 1 in Bydgoszcz, 9 Maria Skłodowska-Curie Street, 85-094 Bydgoszcz, Poland.
Insights
Clarithromycin resistance in Helicobacter pylori pediatric infections is significant, with the A2143G mutation being most common. Understanding these mutations is key to effective treatment strategies.
Area of Science:
- Microbiology
- Genetics
- Gastroenterology
Background:
- Helicobacter pylori causes gastrointestinal diseases like ulcers and gastric cancer.
- Clarithromycin resistance, driven by 23S rRNA gene mutations, complicates H. pylori eradication.
- Pediatric H. pylori infections present unique challenges due to evolving resistance patterns.
Purpose of the Study:
- To determine the prevalence and types of clarithromycin resistance mutations in H. pylori from pediatric patients in Bydgoszcz, Poland.
- To analyze the genetic variability associated with antibiotic resistance in pediatric H. pylori isolates.
- To provide data for optimizing H. pylori eradication therapies in children.
Main Methods:
- Analysis of 45 gastric biopsy samples from pediatric patients.
- Utilized the Bosphore® Helicobacter pylori Genotyping Kit v1 for mutation detection.
- Focused on identifying point mutations in the 23S rRNA gene linked to clarithromycin resistance.
Main Results:
- 12 out of 45 samples showed clarithromycin resistance-associated mutations.
- The A2143G mutation was most prevalent (58.3%), followed by A2142G (33.3%).
- Mixed infections with wild-type and mutant strains were observed; A2142C mutation was absent.
Conclusions:
- The A2143G mutation is the dominant cause of clarithromycin resistance in pediatric H. pylori in this region, aligning with global trends.
- The presence of mixed strains necessitates further investigation into co-infections and subpopulations.
- Tailored treatment strategies based on resistance profiling are essential for effective H. pylori eradication and combating antibiotic resistance.
Abstract:
Background: Helicobacter pylori is a Gram-negative bacterium responsible for various gastrointestinal diseases, including peptic ulcers and gastric cancer. Despite available antibiotic therapies, increasing resistance to clarithromycin-a key antibiotic in eradication regimens-poses a significant challenge. This resistance is primarily linked to point mutations in the 23S rRNA gene, particularly A2143G, A2142G, and A2142C, which hinder clarithromycin binding, reducing its bacteriostatic efficacy. This study aimed to assess the prevalence and variability of clarithromycin resistance mutations in pediatric patients from Bydgoszcz, Poland. Methods: A total of 45 gastric biopsy samples from pediatric patients were analyzed using the Bosphore®Helicobacter pylori Genotyping Kit v1 to detect clarithromycin resistance-associated mutations. Results: Among the 45 tested samples, 30 were classified as wild-type, while 12 contained resistance-associated mutations. The most frequently detected mutation was A2143G (58.3%), followed by A2142G (33.3%). One sample exhibited both A2142G and A2143G mutations, and another contained a mixture of wild-type and mutant strains. The A2142C mutation was not detected in any sample. Conclusions: Our findings confirm the predominance of A2143G among clarithromycin-resistant H. pylori strains, consistent with global trends. The detection of both mutant and wild-type strains in a single patient highlights potential co-infections or subpopulations with varying resistance profiles. Continuous surveillance and improved diagnostic tools are crucial for optimizing treatment strategies. Tailored eradication protocols based on resistance profiling are necessary to enhance treatment efficacy and mitigate the spread of resistant strains. Further research is needed to understand the clinical implications of mixed infections and double mutations in H. pylori resistance development.
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