Molecular Patterns of Resistance Among Helicobacter pylori Strains in South-Western Poland

Abstract

Treatment failure of Helicobacter pylori infection is caused mainly by progressive antibiotic resistance among H. pylori strains. In Poland, the prevalence of H. pylori strains resistant to metronidazole is higher than in other developed countries, reaching almost 50%, and resistance to clarithromycin is as high as 30% and is still increasing, contributing to the failure of first-line therapy in approximately 70% of patients. Moreover, the introduction of levofloxacin to eradication therapy of H. pylori infection quickly led to the emergence of resistant strains. Therefore, a necessary approach in microbiological diagnostics of H. pylori infection should be determination of susceptibility of H. pylori strains before the eradication treatment.Aim: In this study was to evaluate the molecular mechanisms of resistance among 170 H. pylori strains to clarithromycin, involving mutations in the 23S rRNA gene (A2143G, A2142G, A2143G) and to levofloxacin, involving mutations of gyrA and gyrB. Analysis was performed by using polymerase chain reaction and classical sequencing of DNA fragments.Results: Among examined strains, 26% were fully sensitive and 74% were resistant to at least one of the tested antibiotics. The overall resistance rate to metronidazole was as high as 56%, whereas to clarithromycin 46%, respectively. Resistance to LEV occurred among 6% of strains. All tested strains were susceptible to AMC and TET. The A2143G point mutation was found in 72% of clarithromycin-resistant strains. The most common mutation, present in 40% of H. pylori strains resistant to levofloxacin, was a change at position 91 of gyrA.Conclusion: The increasing number of point mutations in the 23S rRNA gene leads to an increase in the rates of antimicrobial resistance. Presence of the GCG allele at position 122 of the gyrA gene may cause an eightfold increase in risk of development of resistance to levofloxacin.

Molecular Assessment of Resistance to Clarithromycin in Helicobacter pylori Strains Isolated from Patients with Dyspepsia by Fluorescent In Situ Hybridization in the Center of Iran

“…In our study, A2143G was the most common type of mutation in strains. This finding verified previous studies by other researchers [7,26]. Furthermore, 9.5% of clarithromycin-resistant H. pylori strains lacked the studied mutations.…”

<p>Mutations in the Antibiotic Target Genes Related to Clarithromycin, Metronidazole and Levofloxacin Resistance in <em>Helicobacter pylori</em> Strains from Children in China</p>

“…23 H. pylori strains were found to carry A2143G, A2142G, A2147G and A2146G mutations that can lead to clarithromycin-resistance in Africa, Asia, South America, Europe and North America. [24][25][26][27][28][29][30] The T2183C and A2223G transformations have been frequently found to be the cause of observed clarithromycin resistance in Asian countries than those in Europe and North America, 31 but not be observed in our study. In addition to these mutations, other mutations in different positions have been found in other parts of the world to confer clarithromycin resistance in H. pylori strains (T2182C, T2190C, C2195T, A2223G, G2141A, C2694A, G2224A, C2245T, T2289C).…”

“…Binkowska et al reported that the most common mutation presented in 40% of H. pylori strains resistant to levofloxacin was a change at position 91 of gyrA in children. 25 De Palma et al reported that resistance of levofloxacin was due to substitution at position 87 (K,I) and 91 (G,N,A) of gyrA QRDR in the 92.8% of the resistant isolates. 40 Miftahussurur et al reported that mutations at Asn-87 and/or Asp-91 were predominantly in levofloxacinresistant strains, and the gyrB mutation had a steady relationship with gyrA 87-91 mutations.…”

Rapid, field-deployable nucleobase detection and identification using FnCas9

“…We then isolated bacteria DNA from patient gut biopsy samples and successfully distinguished the antibiotic resistance genotype from another closely matched synthetic wild type sequence ( Figure 3C). Importantly, this procedure takes a few hours from obtaining sample to diagnosing the variant, a significant improvement over existing regimens which rely on antimicrobial susceptibility tests that can take several days to complete 27 .…”