scholarly journals Where to Biopsy to Detect Helicobacter pylori and How Many Biopsies Are Needed to Detect Antibiotic Resistance in a Human Stomach

2020 ◽  
Vol 9 (9) ◽  
pp. 2812 ◽  
Author(s):  
Maxime Pichon ◽  
Cong Tri Tran ◽  
Gaëtan Motillon ◽  
Charlotte Debiais ◽  
Sylvain Gautier ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Dna Typing ◽  
Resistant Isolate ◽  
Subtotal Resection ◽  
Routine Practice ◽  
Gene Detection ◽  
Antibiotic Resistant ◽  
The Third ◽  
H Pylori ◽  
Different Strains

This study aims to determine the gastric distribution, density, and diversity of Helicobacter pylori infection. Subtotal resection of the stomachs of three H. pylori-infected and asymptomatic obese patients were collected after a sleeve gastrectomy. Distribution and density of H. pylori were determined using culture and RT-PCR on multiple gastric sites (88, 176, and 101 biopsies per patient). Diversity of H. pylori strains was studied using antibiotic susceptibility testing, random amplified polymorphism DNA (RAPD) typing and cagA gene detection on single-colony isolates (44, 96, and 49 isolates per patient). H. pylori was detected in nearly all analyzed sites (354/365 biopsies, 97%). Antral density was higher in one patient only. The three stomachs were almost exclusively infected by an antibiotic-susceptible strain. One clarithromycin-resistant isolate in one biopsy was detected in two stomachs (1/44 and 1/49 isolates), while in the third one, eight (8/96 isolates) metronidazole-resistant isolates were detected. DNA typing showed infection with cagA-negative strains for one patient, cagA-positive strains for a second patient and the third patient was infected with two different strains of distinct cagA genotypes. Infection with H. pylori is shown to spread to the whole surface of the stomach, but a possibility of minor sub-population of antibiotic-resistant clones, undetectable in routine practice.

scholarly journals Epidemiology of the Antibiotic Resistance ofHelicobacter pyloriin Canada

2000 ◽  
Vol 14 (10) ◽  
pp. 879-882 ◽  
Author(s):  
Carlo A Fallone
Keyword(s):  
Helicobacter Pylori ◽  
Antibiotic Resistance ◽  
Digestive Disease ◽  
Study Group ◽  
Cure Rate ◽  
Antibiotic Resistant ◽  
Treatment Regimens ◽  
Metronidazole Resistance ◽  
American Gastroenterology Association ◽  
H Pylori

BACKGROUND: The rate ofHelicobacter pyloriresistance to antibiotics determines the cure rate of treatment regimens containing such antibiotics. AIMS: To review the literature to determine the rates ofH pyloriresistance to metronidazole and clarithromycin in Canada, and whether these rates vary in different regions of Canada.METHODS: The literature was reviewed extensively for the prevalence of antibiotic-resistantH pyloriin Canada by searching MEDLINE from January 1980 to May 1999, as well as abstracts of the American Gastroenterology Association Digestive Disease Week, Canadian Digestive Disease Week and The EuropeanH pyloriStudy Group Meetings from January 1995 to May 1999.RESULTS: Eleven studies that estimatedH pyloriresistance to metronidazole resistance and nine that estimated resistance to clarithromycin in Canada were identified. Rates of resistance for metronidazole and clarithromycin varied from 11% to 48% and 0% to 12%, respectively. Studies that obtained their estimates using the E-test and those that did not clearly exclude patients who had undergone previous attempts atH pylorieradication had higher estimates of resistance, accounting for this variability in results.CONCLUSIONS: The prevalence of primaryH pyloriresistance in Canada appears to be 18% to 22% for metronidazole and less than 4% for clarithromycin. These rates appear to be consistent across the different regions studied in Canada, but many regions have not been studied.

scholarly journals Serum Antibody Responses to Helicobacter pylori and the cagA Marker in Patients with Mucosa-Associated Lymphoid Tissue Lymphoma

1999 ◽  
Vol 6 (4) ◽  
pp. 633-638 ◽  
Author(s):  
Anne Taupin ◽  
Alessandra Occhialini ◽  
Agnès Ruskone-Fourmestraux ◽  
Jean-Charles Delchier ◽  
Jean-Claude Rambaud ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Antibody Response ◽  
Malt Lymphoma ◽  
Lymphoid Tissue ◽  
Serum Antibody ◽  
Dot Blot ◽  
Homologous Strain ◽  
H Pylori ◽  
Different Strains ◽  
Dot Blot Analysis

ABSTRACT The lymphoma of the mucosa-associated lymphoid tissue (MALT) of the stomach has been linked to Helicobacter pylori infection, but the mechanisms involved in B-cell proliferation remain elusive. In a search for putative H. pylori-specific monoclonal immunoglobulin production, an H. pylori strain was isolated from 10 patients with MALT lymphoma and used to detect the specific serum antibody response to the homologous strain by immunoblotting. Moreover, the antigenicity of the different strains was compared by using each of the 10 sera. We found that the different strains induced highly variable patterns of systemic immunoglobulin G antibody response, although several bacterial antigens, such as the 60-kDa urease B, were often recognized by the different sera. ThecagA marker was detected in the strains by PCR with specific primers and by dot blot analysis, and the CagA protein was found in the sera of 4 of the 10 patients by immunoblotting. In conclusion, MALT lymphoma patients, like other patients with H. pylori gastritis, exhibit a polymorphic systemic antibody response, despite an apparently similar antigenic profile. The CagA marker of pathogenicity is not associated with this disease.

scholarly journals Detection and variability analyses of CRISPR-like loci in the H. pylori genome

2018 ◽  
Author(s):  
Jerson Alexander Garcia-Zea ◽  
Roberto de la Herrán ◽  
Francisca Robles Rodríguez ◽  
Rafael Navajas-Pérez ◽  
Carmelo Ruiz Rejón
Keyword(s):  
Helicobacter Pylori ◽  
Geographical Area ◽  
Pathogenic Bacterium ◽  
Gene Location ◽  
Phylogenetic Marker ◽  
Genomic Plasticity ◽  
Human Pathogenic Bacterium ◽  
H Pylori ◽  
Different Strains ◽  
Genomic Locations

Helicobacter pylori is a human pathogenic bacterium with a high genomic plasticity. Although the functional CRISPR-Cas system has not been found in its genome, CRISPR like loci have been recently identified. In this work, 53 genomes from different geographical areas are analyzed for the search and analysis of variability of this type of structure. We confirm the presence of a locus that was previously described in the VlpC gene in al lgenomes, and we characterize new CRISPR-like loci in other genomic locations. By studying the variability and gene location of these loci, the evolution and the possible roles of these sequences are discussed. Additionally, the usefulness of this type of sequences as a phylogenetic marker has been demonstrated, associating the different strains by geographical area.

scholarly journals Synergistic Therapies as a Promising Option for the Treatment of Antibiotic-Resistant Helicobacter pylori

Antibiotics ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 658 ◽  
Author(s):  
Paweł Krzyżek ◽  
Emil Paluch ◽  
Grażyna Gościniak
Keyword(s):  
Helicobacter Pylori ◽  
Antimicrobial Properties ◽  
Multidrug Resistant ◽  
Future Application ◽  
Gastric Diseases ◽  
Antibiotic Resistant ◽  
Minimal Inhibitory Concentrations ◽  
Current Review ◽  
H Pylori

Helicobacter pylori is a Gram-negative bacterium responsible for the development of gastric diseases. The issue of spreading antibiotic resistance of H. pylori and its limited therapeutic options is an important topic in modern gastroenterology. This phenomenon is greatly associated with a very narrow range of antibiotics used in standard therapies and, as a consequence, an alarmingly high detection of multidrug-resistant H. pylori strains. For this reason, scientists are increasingly focused on the search for new substances that will not only exhibit antibacterial effect against H. pylori, but also potentiate the activity of antibiotics. The aim of the current review is to present scientific reports showing newly discovered or repurposed compounds with an ability to enhance the antimicrobial activity of classically used antibiotics against H. pylori. To gain a broader context in their future application in therapies of H. pylori infections, their antimicrobial properties, such as minimal inhibitory concentrations and minimal bactericidal concentrations, dose- and time-dependent mode of action, and, if characterized, anti-biofilm and/or in vivo activity are further described. The authors of this review hope that this article will encourage the scientific community to expand research on the important issue of synergistic therapies in the context of combating H. pylori infections.

EFFICACY OF RACM REGIMEN ON HELICOBACTER PYLORI ERADICATION IN PATIENTS OF CHRONIC GASTRITIS

2016 ◽  
pp. 88-93
Author(s):  
Thi Hoai Thai ◽  
Van Huy Tran
Keyword(s):  
Helicobacter Pylori ◽  
Side Effects ◽  
Chronic Gastritis ◽  
Eradication Rate ◽  
Statistical Significance ◽  
Rapid Urease Test ◽  
Antibiotic Resistant ◽  
Helicobacter Pylori Eradication ◽  
Urease Test ◽  
H Pylori

Background: H. pylori eradication still remains a challenge to clinicians, especially with the increasing antibiotic-resistant H. pylori. Concomitant therapy showed effective, even in some multiresistant population, but data in Vietnam is still very limited. The study ''Study of Helicobacter pylori eradication with RACM regimen in chronic gastritis patients at Da Nang Hospital from 1/4/2014 to 30/6/2015, is aimed at: (1) Evaluating the results of Helicobacter pylori eradication of Amoxicillin-Clarithromycin-Rabeprazole-Metronidazole therapy for 14 days.(2) Assessing some side effects of this regimen.Method: prospective, consisting of 83 patients examined and treated in Danang hospital from1/ 4/2014 to 30/6/2015, H.pylori was tested by rapid Urease test; H.pylori positive patients received RACM for 14 days. Results: H.pylori eradication rate was 83.1%. H. pylori eradication rates in different locations: antrum 63.8%, higher than corpus (17.4%), antrum and corpus (18.8%), with statistical significance at p<0.05. Common side effects was nausea (27.7%), diarrhea (19.3%). Abdominal pain, lightheadedness, dizziness, insomnia, headache account for low percentage: 8%; 6%; 3,6% and 2.4% respectively. Conclusion: The effect of 14 day RACM regimen for H. pylori eradication was 83.1%, common side effects are nausea (27.7%), diarrhea (19.3%). Key words: chronic gastritis;H. pylori; eradication of H. pylori(ITT); RACM regimen.

scholarly journals High-Level β-Lactam Resistance Associated with Acquired Multidrug Resistance in Helicobacter pylori

2003 ◽  
Vol 47 (7) ◽  
pp. 2169-2178 ◽  
Author(s):  
Dong H. Kwon ◽  
M. P. Dore ◽  
J. J. Kim ◽  
M. Kato ◽  
M. Lee ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Multidrug Resistance ◽  
Natural Transformation ◽  
Multidrug Resistant ◽  
Resistant Isolate ◽  
Terminal Portion ◽  
Nucleotide Substitutions ◽  
H Pylori ◽  
High Level ◽  
Level Resistance

ABSTRACT Four clinical Helicobacter pylori isolates with high-level resistance to β-lactams exhibited low- to moderate-level resistance to the structurally and functionally unrelated antibiotics ciprofloxacin, chloramphenicol, metronidazole, rifampin, and tetracycline. This pattern of multidrug resistance was transferable to susceptible H. pylori by natural transformation using naked genomic DNA from a clinical multidrug-resistant isolate. Acquisition of the multidrug resistance was also associated with a change in the genotype of the transformed multidrug-resistant H. pylori. DNA sequence analyses of the gene encoding penicillin binding protein 1A (PBP 1A) showed 36 nucleotide substitutions resulting in 10 amino acid changes in the C-terminal portion (the putative penicillin binding domain). Acquisition of β-lactam resistance was consistently associated with transfer of a mosaic block containing the C-terminal portion of PBP 1A. No changes of genes gyrA, rpoB, rrn16S, rdxA, and frxA, and nine other genes (ftsI, hcpA, llm, lytB, mreB, mreC, pbp2, pbp4, and rodA1) encoding putative PBPs or involved in cell wall synthesis were found among the transformed resistant H. pylori. Antibiotic accumulations of chloramphenicol, penicillin, and tetracycline were all significantly decreased in the natural and transformed resistant H. pylori compared to what was seen with susceptible H. pylori. Natural transformation also resulted in the outer membrane protein profiles of the transformed resistant H. pylori becoming similar to that of the clinical resistant H. pylori isolates. Overall, these results demonstrate that high-level β-lactam resistance associated with acquired multidrug resistance in clinical H. pylori is mediated by combination strategies including alterations of PBP 1A and decreased membrane permeability.

scholarly journals Impact of Helicobacter pylori resistance in unsuccessfully pluritreated patients in a Department of Infectious Diseases in Rome

2010 ◽  
Vol 1 (1) ◽  
pp. 3
Author(s):  
Maria Teresa Mascellino ◽  
Barbara Porowska ◽  
Rosa Nicosia ◽  
Alessandra Oliva ◽  
Priscilla Boccia ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Resistance Rate ◽  
Test Method ◽  
Resistance Testing ◽  
Antibiotic Resistant ◽  
Diffusion Technique ◽  
Resistant Strains ◽  
Unrelated Strain ◽  
H Pylori ◽  
Rapid Emergence

Twenty-five pluritreated patients were examined. Fifty-six percent yielded Helicobacter pylori (H. Pilory); of these, 9 patients showed a concomitant colonization of the three gastric regions. The highest resistance rate was found for metronidazole (71.8%) followed by chlaritromycin (53.1%). Amoxycillin showed the best susceptibility (only 6% of resistance), tetracycline showed 12% of resistant strains and levofloxacin appeared to be a promising antibacterial agent (18% of resistance). The E-test method was shown to be more suitable than disk diffusion technique for resistance testing. Combined resistance to both chlaritromycin and metronidazole appeared in 50% of the strains. The isolates showing this dual resistance are known to be difficult to eradicate. Resistotypes were shown to be genotypically different even if the strains with the resistance to both chlaritromycin and metronidazole are more likely to belong to genotype cagA+ and vacA s1m1. Heteroresistance (different susceptibility of the isolated strains in a single stomach) resulted in 36% of patients with pangastritis. Indeed, the concomitant presence of H. pylori strains in the same subject, either susceptible or resistant or vice versa, may interfere with the eradication outcomes. In our study, antibiotic resistant H. pylori typically develops from pre-existing susceptible strains rather than from co-infection with a different and unrelated strain. In fact, each pair of isolates detected in our 4 patients with heteroresistance belonged to the same genotype (cagA+ s1m2 in patient 1 and cagA+ s1m1 in patients 2, 3 and 4). In conclusion, H. pylori antibiotic resistance does present several issues in pluritreated patients owing to the rapid emergence of multi-resistant strains.

scholarly journals Molecular Characterization of Benzimidazole Resistance in Helicobacter pylori

2004 ◽  
Vol 48 (7) ◽  
pp. 2524-2530 ◽  
Author(s):  
Scott D. Mills ◽  
Wei Yang ◽  
Kathleen MacCormack
Keyword(s):  
Helicobacter Pylori ◽  
Amino Acid ◽  
Amino Acid Change ◽  
Genomic Library ◽  
Single Point ◽  
Resistant Isolate ◽  
Benzimidazole Derivatives ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Single Point Mutation ◽  
H Pylori

ABSTRACT A family of benzimidazole derivatives (BI) was shown to possess potent and selective activity against Helicobacter pylori, although the precise cellular target of the BIs is unknown. Spontaneous H. pylori mutants were isolated as resistant to a representative BI (compound A). Genomic DNA was isolated from a BI-resistant mutant, transformed into a BI-sensitive strain, and found to be sufficient to confer BI resistance. The resistance determinant was localized to a 17-kb clone after screening a lambda-based genomic library constructed from the BI-resistant strain. Upon sequencing and mapping onto the H. pylori strain J99 genome, the 17-kb clone was shown to contain the entire nuo operon (NADH:ubiquinone oxidoreductase). Further subcloning and DNA sequencing revealed that a single point mutation in nuoD was responsible for BI resistance. The mutation resulted in a G398S amino acid change at the C terminus of NuoD. Thirty-three additional spontaneous BI-resistant mutants were characterized. Sequencing of nuoD from 32 isolated mutants revealed three classes of missense mutation resulting in amino acid changes in NuoD: G398S, F404S, and V407M. One BI-resistant isolate did not have a mutation in nuoD. Instead, a T27A amino acid change was identified in NuoB. MIC testing of the wild-type H. pylori strain and four classes of nuo mutants revealed that all NuoD mutant classes were hypersensitive to rotenone, a known inhibitor of complex I (NADH:ubiquinone oxidoreductase) suggested to bind to NuoD. Further, a nuoD knockout verified that it is essential in H. pylori and may be the target of the BI compounds.

scholarly journals Heterogeneity among Helicobacter pylori Strains in Expression of the Outer Membrane Protein BabA

2004 ◽  
Vol 72 (6) ◽  
pp. 3429-3435 ◽  
Author(s):  
Ewa E. Hennig ◽  
Ray Mernaugh ◽  
Jennifer Edl ◽  
Ping Cao ◽  
Timothy L. Cover
Keyword(s):  
Helicobacter Pylori ◽  
Membrane Protein ◽  
Outer Membrane ◽  
Outer Membrane Protein ◽  
Recombinant Antibody ◽  
Wild Type ◽  
Single Chain ◽  
H Pylori ◽  
Different Strains

ABSTRACT The BabA adhesin of Helicobacter pylori is an outer membrane protein that binds to the fucosylated Lewis b histo-blood group antigen on the surface of gastric epithelial cells. We screened a phage-displayed ScFv (single-chain fragment variable) recombinant antibody library for antibodies reactive with a recombinant BabA fragment and identified two such antibodies. Each antibody recognized an ∼75-kDa protein present in wild-type H. pylori strain J99 but absent from an isogenic babA mutant strain. An immunoreactive BabA protein was detected by at least one of the antibodies in 18 (46%) of 39 different wild-type H. pylori strains and was detected more commonly in cagA-positive strains than in cagA-negative strains. Numerous amino acid polymorphisms were detected among BabA proteins expressed by different strains, with the greatest diversity occurring in the middle region of the proteins. Among the 18 strains that expressed a detectable BabA protein, there was considerable variation in the level of binding to Lewis b in vitro. Heterogeneity among H. pylori strains in expression of the BabA protein may be a factor that contributes to differing clinical outcomes among H. pylori-infected humans.

scholarly journals Analysis of Helicobacter pylori vacA andcagA genotypes and serum antibody profile in benign and malignant gastroduodenal diseases

Gut ◽  
1998 ◽  
Vol 43 (2) ◽  
pp. 182-186 ◽  
Author(s):  
D Basso ◽  
F Navaglia ◽  
L Brigato ◽  
M G Piva ◽  
A Toma ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Adenocarcinoma ◽  
Western Blotting ◽  
Serum Antibody ◽  
Serological Response ◽  
Benign Diseases ◽  
Antral Gastritis ◽  
Antibody Profile ◽  
H Pylori ◽  
Different Strains

Background—Helicobacter pylori species comprise different strains, cytotoxic and non-cytotoxic, which can be identified on the basis of their genomic pattern.Aims—(1) To evaluate the polymorphism of the vacA gene and to ascertain whether thecagA gene is present in patients with gastric adenocarcinoma. (2) To study the anti-H pylori antibody profile using western blotting.Patients—Twenty one patients with gastric adenocarcinoma and 71 with H pyloriassociated benign disease (nine gastric ulcer, 29 duodenal ulcer, 25 antral gastritis, and eight duodenitis).Methods—The polymerase chain reaction was used to verify the presence or absence ofcagA and to study the polymorphism of vacA in gastric mucosal samples obtained during endoscopy for patients with benign diseases and at surgery for patients with gastric adenocarcinoma. Fasting sera were used to assess anti-H pylori antibodies against different H pyloriantigens by western blotting.Results—cagAgene and the allele s1 of vacAwere significantly less frequent in patients with antral gastritis (60% and 60%) compared with patients with gastric adenocarcinoma (94% and 100%) and with other non-malignant gastroduodenal diseases (93% and 87%) (χ2=16.01, p<0.001; and χ2=13.97, p<0.01). In patients with gastric adenocarcinoma, antibodies against a 74 kDa H pylori antigen were less frequently found than in patients with benign diseases.Conclusions—H pylori infection caused bycagApositive/vacA s1 strains is a frequent finding in patients with gastric adenocarcinoma. Prospective studies are needed to confirm whether the low incidence of positive serological response to the 74 kDa H pyloriantigen in patients with gastric adenocarcinoma is important.

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