Abstract
Introduction: The aim of the study was to determine the evolutionary role of the Cag A presence in the outcome of eradication treatment of H. pylori. Materials and methods: Sixty-seven pediatric dyspeptic patients (mean age 13.7 years, range 5 to 17 years, male/female 24/43) underwent endoscopy for H.pylori presence. Gastric biopsy specimens were taken for histology and/or culture and one biopsy sample was used for CagA PCR determination. H. pylori positive patients were treated for 2 weeks by amoxycilline (50 mg/kg/day), bismuth subcitrate (8 mg/kg/day), nifuratel (30 mg/kg/day) plus omeprazole (1 mg/kg, once daily). Results: Forty one of 67 children (61.2%) were H. pylori positive. Nineteen of 41 strains (46.3%) were CagA positive and 22 were CagA negative (53.7%). H. pylori was eradicated in 33 patients (80.4%). Among the patients with successful eradication 18 children were CagA positive, fourteen were CagA negative. Thus, more patients with CagA-negative status had evidence of ongoing H. pylori infection (36.4% (8/22) versus 5.3% (1/19); χ2=4.08, p=0.0021; Fisher’s exact test p= 0.0238). Conclusion: In our study the carriage of CagA-lacking strain was associated with failure of treatment. In our opinion, this phenomenon, related to extraordinary genome plasticity, not only allows the microbe to maintain balanced relationship with the host, but also to survive in antibacterial therapy conditions.
Highlights
IntroductionMany bacterial pathogens probably have affected humans for more than 15,000 years [2]
The aim of the study was to determine the evolutionary role of the CagA presence in the outcome of eradication treatment of H. pylori
The CagA gene is located at one end of the cag pathogenicity island (PAI), an approximately 40-kilobase region that is incorporated into the H. pylori genome by horizontal transfer from an unknown natural source [7]
Summary
Many bacterial pathogens probably have affected humans for more than 15,000 years [2] It is obvious, that the host-bacterial interaction can potentially be accompanied with microevolution of bacteria during long-term colonization protracting for lifelong persistence. Environmental forces (the release of large amounts of antibacterials et cetera) might change natural ecosystem to alteration of the population dynamics of the microorganisms, including selection of resistance with consequences for human health that is difficult to predict [4]. H. pylori infection is associated with chronic gastritis and peptic ulceration development and is considered to be a risk factor for development of gastric cancer [2]. The CagA gene is located at one end of the cag pathogenicity island (PAI), an approximately 40-kilobase region that is incorporated into the H. pylori genome by horizontal transfer from an unknown natural source [7].
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