scholarly journals Determination of Antibiotic Resistance and Relevance of 23S Rrna Gene in Helicobacter Pylori with Clarithromycin Resistance in Chronic Gastritis

2020 ◽  
Vol 5 (8) ◽  
pp. 1-7
Author(s):  
S.A. Abdelsami ◽  
A.A. Fari ◽  
S.I. Abbas ◽  
A.A. Elgazzar
Keyword(s):  
Helicobacter Pylori ◽  
Antibiotic Resistance ◽  
Chronic Gastritis ◽  
23S Rrna ◽  
Rrna Gene ◽  
Clarithromycin Resistance ◽  
23S Rrna Gene

STUDY ON POINT MUTATIONS AT POSITIONS 2132 AND 2143 IN 23S RRNA GENE OF HELICOBACTER PYLORI AMONG PATIENTS WITH CHRONIC GASTRITIS

2016 ◽  
pp. 12-20
Author(s):  
Thi Minh Thi Ha ◽  
Van Huy Tran ◽  
Viet Nhan Nguyen ◽  
Thanh Hoa Nguyen ◽  
Phan Tuong Quynh Le
Keyword(s):  
Helicobacter Pylori ◽  
Chronic Gastritis ◽  
Point Mutations ◽  
23S Rrna ◽  
Rrna Gene ◽  
Clarithromycin Resistance ◽  
Pcr Rflp ◽  
23S Rrna Gene ◽  
History Of ◽  
H Pylori

Background: Clarithromycin resistance in Helicobacter pylori has been found to be associated with point mutations at positions 2142 and 2143 in 23SrRNA gene. The aims of this study were: (1) to determine the rates of point mutations A2143G, A2142G and A2142C in 23SrRNA gene of H. pylori among patients with chronic gastritis by PCR-RFLP technique; and (2) to assessthe association between these mutations and some clinical, endoscopic and histopathological characteristics of chronic gastritis. Patients and methods: two hundreds and twenty six patients with H. pylori-positive chronic gastritis were determined A2143G, A2142G and A2142C mutations by PCR-RFLP technique with DNA extracted from endoscopic biopsy specimens of gastric mucosa. Results: The rate of point mutations at positions 2142 and 2143 in 23S rRNA gene of H. pylori was 35.4% in total, the A2143G and A2142G mutationsaccounted for 92.5% and 7.5% of all point mutations, respectively. No A2142C mutation was found. These mutations were not associated with age, gender,distribution of gastritis, and the presence of atrophic gastritis. The rate of A2143G mutation in groups with and without a history of clarithromycin treatment were 44.9% and 24.8%, respectively (p = 0,0065). The A2142G mutation was associated with intestinal metaplasia and/or dysplasia. Conclusion: The point mutations at positions 2142 and 2143 in 23S rRNA gene were found at a high rate in H. pylori strains amongpatients with chronic gastritis, with the absolute predominance of A2143G mutation. The A2143G mutation was associated with a history of clarithromycin treatment. Key words: 23S rRNA gene, Helicobacter pylori, A2143G, A2142G, A2142C mutation, clarithromycin resistance, chronic gastritis.

DETERMINATION OF MUTATIONS IN 23S RRNA GENE OF HELICOBACTER PYLORI AND THE ASSOCIATION OF THESE GENE MUTATIONS WITH CLARITHROMYCIN-RESISTANCE IN CHRONIC GASTRITIS

2015 ◽  
pp. 36-46
Author(s):  
Thi Minh Thi Ha ◽  
Van Huy Tran ◽  
Viet Nhan Nguyen ◽  
Phan Tuong Quynh Le ◽  
Trung Nam Phan ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Chronic Gastritis ◽  
Point Mutations ◽  
23S Rrna ◽  
Rrna Gene ◽  
Biopsy Specimens ◽  
Clarithromycin Resistance ◽  
Resistant Phenotype ◽  
23S Rrna Gene ◽  
Domain V

Background: Resistance of Helicobacter pylori to clarithromycin is mostly due to the point mutations in the 23S rRNA. The aims of the present study were to determine mutations in domain V of 23S rRNA gene of Helicobacter pylori in chronic gastritis patients by sequencing; and to assess the association of these mutations with clarithromycin-resistant phenotype determined by E-test. Patients and methods: Gastric mucosal biopsy specimens from 170 patients with chronic gastritis were entered in the study. DNA was extracted from biopsy specimens obtained by endoscopy and prepared for sequencing domain V of gene 23S rRNA. 80 biopsy specimens were determined MIC by E-test. Results: Eight point mutations were detected. At 2142 and 2143 sites of gene, A2143G and A2142G mutations were detected in 35.3% and 3.5%, respectively. Six remaining mutations were G2172T (0.6%), T2182C (86.5%), C2195T (5.3%), A2223G (42.9%), T2244C (98.2%) và A2302G (8.8%). A2143G mutation was associated with clarithromycin-resistant phenotype, OR = 368.58 (95%CI: 34.53 – 3934.12). The rate of clarithromycin-resistance in the group with A2143G mutation was 96.7%, while in the group without A2143G mutation was 10%. Predicted probabilities for clarithromycin-resistance were calculated by logistic regression model with the accuracy rate of 96.1%. Conclusions: There was the association between A2143G mutation and clarithromycin-resistant phenotype. Genotypes determined by sequencing domain V of 23S rRNA gene could be used to predict the probabilities of clarithromycin-resistance. Key words: 23S rRNA gene, clarithromycin-resistance, Helicobacter pylori

scholarly journals Genotypic Characterization of Clarithromycin-Resistant and -Susceptible Helicobacter pylori Strains from the Same Patient Demonstrates Existence of Two Unrelated Isolates

1998 ◽  
Vol 36 (9) ◽  
pp. 2730-2731 ◽  
Author(s):  
Ge Wang ◽  
Qin Jiang ◽  
Diane E. Taylor
Keyword(s):  
Helicobacter Pylori ◽  
Gel Electrophoresis ◽  
Genomic Dna ◽  
Pulsed Field Gel Electrophoresis ◽  
23S Rrna ◽  
Rrna Gene ◽  
Clarithromycin Resistance ◽  
23S Rrna Gene ◽  
Mode Of Development

Clarithromycin-susceptible and clarithromycin-resistantHelicobacter pylori isolates from the same patient were investigated for the mode of development and mechanism of clarithromycin resistance. The clarithromycin-resistant strain UA1182 harbors homozygous A-to-G mutations at position 2143 in both copies of the 23S rRNA gene and has a phenotype of resistance to clarithromycin and clindamycin but no significant resistance to streptogramin B. Pulsed-field gel electrophoresis patterns of NruI- andNotI-digested genomic DNA from the Clas and Clar isolates demonstrated that they are genetically distinct, suggesting that the development of clarithromycin resistance is not from the mutation of the existing Clas strain but from a completely new strain.

scholarly journals Mutations in the 23S rRNA gene are associated with clarithromycin resistance in Helicobacter pylori isolates in Brazil

2003 ◽  
Vol 2 (1) ◽  
Author(s):  
Marcelo L Ribeiro ◽  
Lea Vitiello ◽  
Maira CB Miranda ◽  
Yune HB Benvengo ◽  
Anita PO Godoy ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
23S Rrna ◽  
Rrna Gene ◽  
Clarithromycin Resistance ◽  
23S Rrna Gene

scholarly journals New Site of Modification of 23S rRNA Associated with Clarithromycin Resistance of Helicobacter pylori Clinical Isolates

2002 ◽  
Vol 46 (12) ◽  
pp. 3765-3769 ◽  
Author(s):  
Carla Fontana ◽  
Marco Favaro ◽  
Silvia Minelli ◽  
Anna Angela Criscuolo ◽  
Antonio Pietroiusti ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
23S Rrna ◽  
Dilution Method ◽  
Rrna Gene ◽  
Functional Sites ◽  
Biopsy Specimens ◽  
Clarithromycin Resistance ◽  
Pcr Product ◽  
23S Rrna Gene ◽  
H Pylori

ABSTRACT Resistance of Helicobacter pylori to clarithromycin occurs with a prevalence ranging from 0 to 15%. This has an important clinical impact on dual and triple therapies, in which clarithromycin seems to be the better choice to achieve H. pylori eradication. In order to evaluate the possibility of new mechanisms of clarithromycin resistance, a PCR assay that amplified a portion of 23S rRNA from H. pylori isolates was used. Gastric tissue biopsy specimens from 230 consecutive patients were cultured for H. pylori isolation. Eighty-six gastric biopsy specimens yielded H. pylori-positive results, and among these 12 isolates were clarithromycin resistant. The latter were studied to detect mutations in the 23S rRNA gene. Sequence analysis of the 1,143-bp PCR product (portion of the 23S rRNA gene) did not reveal mutation such as that described at position 2142 to 2143. On the contrary, our findings show, for seven isolates, a T-to-C transition at position 2717. This mutation conferred a low level of resistance, equivalent to the MIC for the isolates, selected using the E-test as well as using the agar dilution method: 1 μg/ml. Moreover, T2717C transition is located in a highly conserved region of the 23S RNA associated with functional sites: domain VI. This fact has a strong effect on the secondary structure of the 23S RNA and on its interaction with macrolide. Mutation at position 2717 also generated an HhaI restriction site; therefore, restriction analysis of the PCR product also permits a rapid detection of resistant isolates.

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