Background: Guidelines on the management of Helicobacter pylori , which cover indications for management and treatment strategies, were produced in 2000. Aims: To update the guidelines at the European Helicobacter Study Group (EHSG) Third Maastricht Consensus Conference, with emphasis on the potential of H pylori eradication for the prevention of gastric cancer. Results: Eradication of H pylori infection is recommended in ( a ) patients with gastroduodenal diseases such as peptic ulcer disease and low grade gastric, mucosa associated lymphoid tissue (MALT) lymphoma; ( b ) patients with atrophic gastritis; ( c ) first degree relatives of patients with gastric cancer; ( d ) patients with unexplained iron deficiency anaemia; and ( e ) patients with chronic idiopathic thrombocytopenic purpura. Recurrent abdominal pain in children is not an indication for a “test and treat” strategy if other causes are excluded. Eradication of H pylori infection ( a ) does not cause gastro-oesophageal reflux disease (GORD) or exacerbate GORD, and ( b ) may prevent peptic ulcer in patients who are naive users of non-steroidal anti-inflammatory drugs (NSAIDs). H pylori eradication is less effective than proton pump inhibitor (PPI) treatment in preventing ulcer recurrence in long term NSAID users. In primary care a test and treat strategy using a non-invasive test is recommended in adult patients with persistent dyspepsia under the age of 45. The urea breath test, stool antigen tests, and serological kits with a high accuracy are non-invasive tests which should be used for the diagnosis of H pylori infection. Triple therapy using a PPI with clarithromycin and amoxicillin or metronidazole given twice daily remains the recommended first choice treatment. Bismuth-containing quadruple therapy, if available, is also a first choice treatment option. Rescue treatment should be based on antimicrobial susceptibility. Conclusion: The global burden of gastric cancer is considerable but varies geographically. Eradication of H pylori infection has the potential to reduce the risk of gastric cancer development.

https://gut.bmj.com/content/gutjnl/56/6/772.full.pdf

Current concepts in the management of Helicobacter pylori infection - The Maastricht III Consensus Report

The discovery of Helicobacter pylori in 1982 was the starting point of a revolution concerning the concepts and management of gastroduodenal diseases. It is now well accepted that the most common stomach disease, peptic ulcer disease, is an infectious disease, and all consensus conferences agree that the causative agent, H. pylori, must be treated with antibiotics. Furthermore, the concept emerged that this bacterium could be the trigger of various malignant diseases of the stomach, and it is now a model for chronic bacterial infections causing cancer. Most of the many different techniques involved in diagnosis of H. pylori infection are performed in clinical microbiology laboratories. The aim of this article is to review the current status of these methods and their application, highlighting the important progress which has been made in the past decade. Both invasive and noninvasive techniques will be reviewed.

Helicobacter pylori Detection and Antimicrobial Susceptibility Testing

Many classes of pathogens excreted in feces are able to initiate waterborne infections. There are bacterial pathogens, including enteric and aquatic bacteria, enteric viruses, and enteric protozoa, which are strongly resistant in the water environment and to most disinfectants. The infection dose of viral and protozoan agents is lower than bacteria, in the range of one to ten infectious units or oocysts. Waterborne outbreaks of bacterial origin (particularly typhoid fever) in the developing countries have declined dramatically from 1900s. Therefore, some early bacterial agents such as Shigella sonnei remains prevalent and new pathogens of fecal origin such as zoonotic C. jejuni and E. coli O157:H7 may contaminate pristine waters through wildlife or domestic animal feces. The common feature of these bacteria is the low inoculum (a few hundred cells) that may trigger disease. The emergence in early 1992 of serotype O139 of V. cholerae with epidemic potential in Southeast Asia suggests that other serotypes than V. cholerae O1 could also getting on epidemic. Some new pathogens include environmental bacteria that are capable of surviving and proliferating in water distribution systems. Other than specific hosts at risk, the general population is refractory to infection with ingested P. aeruginosa. The significance of Aeromonas spp. in drinking water to the occurrence of acute gastroenteritis remains a debatable point and has to be evaluated in further epidemiological studies. Legionella and Mycobacterium avium complex (MAC) are environmental pathogens that have found an ecologic niche in drinking and hot water supplies. Numerous studies have reported Legionnaires' disease caused by L. pneumophila occurring in residential and hospital water supplies. M. avium complex frequently causes disseminated infections in AIDS patients and drinking water has been suggested as a source of infection; in some cases the relationship has been proven. More and more numerous reports show that Helicobacter pylori DNA can be amplified from feces samples of infected patients, which strongly suggests fecal-to-oral transmission. Therefore, it is possible that H. pylori infection is waterbome, but these assumptions need to be substantiated. Giardiasis has become the most common cause of human waterborne disease in the U.S. over the last 30 years. However, as a result of the massive outbreak of waterborne cryptosporidiosis in Milwaukee, Wisconsin, affecting an estimated 403,000 persons, there is increasing interest in the epidemiology and prevention of new infection disease caused by Cryptosporidium spp. as well as monitoring water quality. The transmission of Cryptosporidium and Giardia through treated water supplies that meet water quality standards demonstrates that water treatment technologies have become inadequate, and that a negative coliform no longer guarantees that water is free from all pathogens, especially from protozoan agents. Substantial concern persists that low levels of pathogen occurrence may be responsible for the endemic transmission of enteric disease. In addition to Giardia and Cryptosporidium, some species of genera Cyclospora, Isospora, and of family Microsporidia are emerging as opportunistic pathogens and may have waterborne routes of transmission. More than 15 different groups of viruses, encompassing more than 140 distinct types can be found in the human gut. Some cause illness unrelated with the gut epithelium, such as Hepatitis A virus (HAV) and Hepatitis E virus (HEV). Numerous large outbreaks have been documented in the U.S. between 1950 and 1970, and the incidence rate has strongly declined in developing countries since the 1970s. Hepatitis E is mostly confined to tropical and subtropical areas, but recent reports indicate that it can occur at a low level in Europe. A relatively small group of viruses have been incriminated as causes of acute gastroenteritis in humans and fewer have proven to be true etiologic agents, including rotavirus, calicivirus, astrovirus, and some enteric adenovirus. These enteric viruses have infrequently been identified as the etiologic agents of waterborne disease outbreaks, because of inadequate diagnostic technology, but many outbreaks of unknown etiology currently reported are likely due to viral agents. Actually, Norwalk virus and Norwalk-like viruses are recognized as the major causes of waterborne illnesses world-wide. The global burden of infectious waterborne disease is considerable. Reported numbers highly underestimate the real incidence of waterborne diseases. The most striking concern is that enteric viruses such as caliciviruses and some protozoan agents, such as Cryptosporidium, are the best candidates to reach the highest levels of endemic transmission, because they are ubiquitous in water intended for drinking, being highly resistant to relevant environmental factors, including chemical disinfecting procedures. Other concluding concerns are the enhanced risks for the classic group of debilitated subjects (very young, old, pregnant, and immunocompromised individuals) and the basic requirement of to take specific measures aimed at reducing the risk of waterborne infection diseases in this growing, weaker population.

https://aquaticpath.phhp.ufl.edu/waterbiology/handouts/CRM2002-Microbial%20Agents.pdf

Microbial Agents Associated with Waterborne Diseases

Summary


Background Information regarding the effects of drug resistance on therapies for Helicobacter pylori is limited.



Aims  To determine the effect of drug resistance on the efficacy of first-line treatment regimens for H. pylori and identify the most efficacious treatments in the presence of drug resistance.



Methods  We searched for studies using the keywords: ‘Helicobacter pylori’,‘resistance’ and ‘treatment’ or ‘therapy’. Multilevel meta-regression models were used to determine the effect of drug resistance on treatment efficacy.



Results  We analysed data from 93 studies with 10 178 participants. For triple therapies, clarithromycin resistance had a greater effect on treatment efficacy than nitroimidazole resistance. Metronidazole resistance reduced efficacy by 26% in triple therapies containing a nitroimidazole, tetracycline and bismuth, while efficacy was reduced by only 14% when a gastric acid inhibitor was added to the regimen. Quadruple therapies containing both clarithromycin and metronidazole were the most efficacious; >80% of H. pylori infections were consistently eradicated with these regimens.



Conclusions  Drug resistance was a strong predictor of efficacy across triple therapies for the eradication of H. pylori in adults. Resistance to either clarithromycin or metronidazole, but not both simultaneously, may be overcome by using quadruple therapies, especially those containing both clarithromycin and metronidazole.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2036.2007.03386.x

Meta-analysis: the effect of antibiotic resistance status on the efficacy of triple and quadruple first-line therapies for Helicobacter pylori.

Diagnosis of Helicobacter pylori infection with a new non-in vasive antigen-based assay

A highly sensitive seminested PCR assay to detect Helicobacter pylori DNA in feces was developed. PCR with stool specimens and a novel antigen enzyme immunoassay (EIA) for H. pylori detection in feces were evaluated as diagnostic tools and in follow-up with samples from 63 infected and 37 noninfected persons. Infected individuals received eradication therapy followed by endoscopic follow-up 35 days after the start of treatment. At that time, a second stool specimen was obtained from 55 of these patients. Before eradication, the sensitivity of PCR was 93.7% and that of EIA 88.9%. Specificities were 100 and 94.6%, respectively. Of the 55 follow-up specimens, 41 originated from patients from whom H. pylori had been eradicated. Of these, 21 were still positive by PCR and 13 were positive by EIA, indicating that 1 month may be too short a period for follow-up evaluation of stool specimens by these tests.

Detection of Helicobacter pylori in Stool Specimens by PCR and Antigen Enzyme Immunoassay

Background

: One-week low-dose triple therapy is currently considered the gold standard regimen for treatment of Helicobacter pylori infection. However, the mechanisms involved in the synergy between antibiotics and proton pump inhibitors are controversial.



Aims

: To test the hypothesis that acid suppression represents the crucial mechanism by which the antibacterial activity of antibiotics can be enhanced, and to assess the impact of primary resistance on treatment outcome.



Methods

: One hundred and twenty patients with H. pylori infection and duodenal ulcer, gastric ulcer or non-ulcer dyspepsia were randomly assigned to a 1 week course of either famotidine 80 mg b.d., clarithromycin 250 mg b.d. and metronidazole 500 mg b.d. (FCM group; n = 60) or omeprazole 20 mg o.d., clarithromycin 250 mg b.d. and metronidazole 500 mg b.d. (OCM group; n=60). Gastroscopy was performed at baseline and 5 weeks after completion of treatment. H. pylori status was assessed by biopsy urease test, histology and culture.



Results

: In the intention-to-treat analysis, eradication of H. pylori was achieved in 47 of 60 patients (78%; 95% CI: 66–88%) in the FCM group, compared to 44 of 60 patients (73%; 95% CI: 60–84%) in the OCM group (N.S.). Using per protocol analysis, eradication therapy was successful in 47 of 52 patients (90%; 95% CI: 79–97%) treated with FCM and 44 of 57 patients (77%; 95% CI: 64–87%) treated with OCM (N.S.). Primary metronidazole resistance was present in 27% and primary clarithromycin resistance in 8% of strains. Overall per protocol eradication rates in strains susceptible to both antibiotics and strains with isolated metronidazole resistance were 93% and 84%, respectively. No patient with clarithromycin resistance responded to treatment.



Conclusions

: High-dose famotidine and omeprazole, combined with clarithromycin and metronidazole, are equally effective for eradication of H. pylori. In 1-week low-dose triple therapy, metronidazole resistance has no major impact on eradication rates whereas clarithromycin resistance is associated with a poor treatment outcome.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2036.1999.00563.x

Famotidine versus omeprazole in combination with clarithromycin and metronidazole for eradication of Helicobacter pylori--a randomized, controlled trial.

Detection of Helicobacter pylori in stool specimens by PCR and antigen EIA

The role of urease in Helicobacter pylori adherence to and internalization by Kato III cells was investigated. Kato III cells were incubated with wild-type strains (N6 or P1), with isogenic mutants lacking urease (N6ureB::TnKm or P1ureA::TnMax5) or producing the inactive apoprotein (N6ureG::TnKm), and with urease-positive clones recovered after complementation of N6ureB::TnKm with ureAB. Bacteria were stained with the green fluorescent dye PKH2, and the bacteria load of cells was analyzed by flow cytometry. With mutants lacking urease, the bacteria load was considerably increased, in comparison with the corresponding parental strains (P <.001). With clone K2(3), producing larger amounts of urease than N6, a significant reduction of bacteria load was observed, in comparison with the wild type (P <.001). N6ureG ::TnKm showed adherence characteristics similar to those of N6. The role of urease in internalization was not clear. Thus, urease significantly inhibits H. pylori adherence to Kato III cells by a mechanism largely independent of enzymatic activity.

/pdf/urease-prevents-adherence-of-helicobacter-pylori-to-kato-iii-55kg3yrgzi.pdf

Urease Prevents Adherence of Helicobacter pylori to Kato III Gastric Epithelial Cells

The role of urease in Helicobacter pylori adherence to and internalization by Kato III cells was investigated. Kato III cells were incubated with wild-type strains (N6 or P1), with isogenic mutants lacking urease (N6ureB::TnKm or P1ureA::TnMax5) or producing the inactive apoprotein (N6ureG::TnKm), and with urease-positive clones recovered after complementation of N6ureB::TnKm with ureAB. Bacteria were stained with the green fluorescent dye PKH2, and the bacteria load of cells was analyzed by flow cytometry. With mutants lacking urease, the bacteria load was considerably increased, in comparison with the corresponding parental strains ( ). With clone K2(3), producing larger amounts of urease than N6, a significant P ! .001 reduction of bacteria load was observed, in comparison with the wild type ( ). N6ureG P ! .001

Urease Prevents Adherence of Helicobacter pylori to Kato III Gastric

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Eva Pasching

Author Tools

Chat about Author