Molecular detection of clarithromycin-resistant Helicobacter pylori in stool samples using real-time PCR | ||||
Microbes and Infectious Diseases | ||||
Articles in Press, Accepted Manuscript, Available Online from 27 January 2025 | ||||
Document Type: Original Article | ||||
DOI: 10.21608/mid.2025.337736.2447 | ||||
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Authors | ||||
Menna allah Samir Mohamed ![]() | ||||
1Clinical Pathology Department, Faculty of Medicine, Ain Shams University, Egypt | ||||
2Internal Medicine Department, Faculty of Medicine, Ain Shams University, Egypt | ||||
Abstract | ||||
Background: Helicobacter pylori is a spiral-shaped bacterium that thrives in the digestive system. This bacterial infection is highly prevalent, it affects more than 50% of the world's population. It is common among children in developing countries. Transmission can occur through close personal contact. Factors that increase the likelihood of infection include residing in densely populated areas with limited access to clean water sources. Gene mutations in Helicobacter pylori can lead to clarithromycin resistance by altering the bacterial ribosomal target site. These mutations, particularly in the 23S rRNA gene, prevent clarithromycin from binding, allowing the bacteria to survive in the stomach. Aim of Work: This research seeks to identify point mutations linked to Helicobacter pylori's resistance to clarithromycin in stool samples through real-time PCR analysis, aiming to assist physicians in effectively treating patients infected with H. pylori. Methods: From December 2019 to May 2020, this cross-sectional investigation involved 90 patients exhibiting symptoms indicative of Helicobacter pylori infection. These individuals were examined at the endoscopy unit of Ain Shams University Hospitals' Hepatology, Gastroenterology, and Infectious Disease Department. Results: prevalence rate of clarithromycin resistance (46%), with A2143G accounting for 28% and A2142G for 18%. Conclusion: The study found a high rate of clarithromycin-resistant H. pylori (46%), mainly linked to the A2143G point mutation, and also identified the A2142G point mutation. Neither age nor gender showed a significant association with clarithromycin resistance. Given these findings, clarithromycin-based H. pylori treatment regimen may not be advisable as an empirical treatment approach in Egypt. | ||||
Keywords | ||||
Key words: Molecular identification; Helicobacter pylori; Resistance to Clarithromycin | ||||
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