Helicobacter pylori-Clarithromycin Resistance in Symptomatic Pediatric Patients in a High Prevalence Country

Area of Science:

• Medical Microbiology
• Pediatric Infectious Diseases
• Genetics of Bacterial Resistance

Background:

• Antibiotic resistance in Helicobacter pylori, particularly clarithromycin resistance due to 23S-rRNA gene mutations and metronidazole resistance from rdxA gene deletion, is a major cause of treatment failure.
• Limited data exists on these resistance mechanisms in pediatric populations, especially in developing countries with high H. pylori infection rates.

Purpose of the Study:

• To investigate the prevalence of A2142G/C and A2143G mutations in the 23S-rRNA gene and rdxA gene deletion in symptomatic H. pylori-infected children.
• To assess the impact of these mutations on the eradication success of a standard antibiotic regimen in this pediatric cohort.

Main Methods:

• A cohort of 118 children with gastrointestinal symptoms underwent upper endoscopy for H. pylori detection (urease test, histology).
• Polymerase chain reaction-restriction fragment length polymorphism was used to identify 23S-rRNA gene mutations (A2142G/C, A2143G) and rdxA gene deletion.
• Treatment efficacy was evaluated 8 weeks post-14-day omeprazole, amoxicillin, and clarithromycin therapy using stool antigen tests.

Main Results:

• Approximately 21% of infected children harbored 23S-rRNA gene mutations, with A2143G being the most prevalent. RdxA gene deletion was found in 2% of patients.
• Treatment failure occurred in 25% of patients, and a significant majority (67%) of these treatment failures were associated with the A2143G mutation.

Conclusions:

• Pediatric H. pylori infections in Chile exhibit a high prevalence of the A2143G mutation, a key driver of clarithromycin resistance.
• The presence of the A2143G mutation is strongly linked to the failure to eradicate H. pylori in children, underscoring the need for resistance-guided therapy.