Helicobacter pylori and Other Gastric Microbiota in Gastroduodenal Pathologies

2016 ◽  
Vol 34 (3) ◽  
pp. 210-216 ◽  
Author(s):  
Christian Schulz ◽  
Kerstin Schütte ◽  
Peter Malfertheiner

The discovery of Helicobacter pylori changed the traditional view of the stomach as a hostile organ to bacterial survival. H. pylori induces chronic gastritis, which has the potential to progress to severe complications such as peptic ulcer disease and gastric neoplasia. The development of modern nucleotide sequencing techniques and new biocomputational tools allow the possibility of studying the diversity and complexity of the microbiome in the whole gastrointestinal (GI) tract and overcome the limitations of culturing techniques. However, the differentiation of alive resident and transient microbes in the upper GI tract and their role in the pathogenesis of gastroduodenal diseases requires an analysis beyond the detection of bacterial genomic material alone. Metabolomic and transcriptomic analyses of the bacteria may add important insights into their interaction with the host. Currently, the interaction of H. pylori with other microbes in the stomach and duodenum and their role for health and disease is poorly understood. This review provides a concise overview on the current knowledge of H. pylori and other gastric microbiota in the relationship with gastroduodenal pathologies.

2017 ◽  
Vol 90 (4) ◽  
pp. 369-376 ◽  
Author(s):  
Cristian Vasile Petra ◽  
Aronel Rus ◽  
Dan Lucian Dumitrașcu

The gastric environment has been long time considered bacteria-free, but the discovery of Helicobacter pylori (H. pylori) in 1982 superseded this conception. Over the last decades new diagnostic methods have been developed, starting with culture-dependent and advancing to culture-independent ones. These modern techniques provide new insight into the composition and influence of this ecosystem on the entire gastrointestinal tract. H. pylori is no longer considered the only microorganism in the stomach, other non-H. pylori microbial species may populate the same environment and exercise their role. Current knowledge suggests possible links of these bacteria with gastroduodenal diseases, such as peptic ulcer and gastric cancer but most of them need further scientific evidence. This review summarizes current information on these complex interrelations between gastric microbial communities and host in health and disease.


2006 ◽  
Vol 74 (7) ◽  
pp. 4064-4074 ◽  
Author(s):  
Mónica Oleastro ◽  
Lurdes Monteiro ◽  
Philippe Lehours ◽  
Francis Mégraud ◽  
Armelle Ménard

ABSTRACT Peptic ulcer disease (PUD) occurs after a long-term Helicobacter pylori infection. However, the disease can develop earlier, and rare cases have been observed in children, suggesting that these H. pylori strains may be more virulent. We used suppressive subtractive hybridization for comparative genomics between H. pylori strains isolated from a 5-year-old child with duodenal ulcer and from a sex- and age-matched child with gastritis only. The prevalence of the 30 tester-specific subtracted sequences was determined on a collection of H. pylori strains from children (15 ulcers and 30 gastritis) and from adults (46 ulcers and 44 gastritis). Two of these sequences, jhp0562 (80.0% versus 33.3%, P = 0.008) and jhp0870 (80.0% versus 36.7%, P = 0.015), were highly associated with PUD in children and a third sequence, jhp0828, was less associated (40.0% versus 10.0%, P = 0.048). Among adult strains, none of the 30 sequences was associated with PUD. However, both jhp0562 and jhp0870 were less prevalent in adenocarcinoma strains than in PUD strains from children and adults, the difference being statistically significant for jhp0870. In conclusion, two H. pylori genes were identified as being strongly associated with PUD in children, and their putative roles as an outer membrane protein for jhp0870 and in lipopolysaccharide biosynthesis for jhp0562, suggest that they may be novel virulence factors of H. pylori.


2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Vudumula Vijaya Lakshmi

Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication of H. pylori infection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. This study was under taken at the Department of surgery, Narayana medical college, Nellore from January 2007 to July 2008. A total of 150 patients with duodenal ulcers, gastric ulcers, antral gastritis, gastric carcinoma and dyspepsia of any kind were studied. Maximum number of cases were in the age group of 31 years to 50 years among both sexes and number of cases gradually decreased after 50 years of age in males and females. Males were more in number and male to female ratio is (2.75:1) approximately 3:1.


2020 ◽  
Vol 10 (3) ◽  
pp. 543-550
Author(s):  
Sh. T. Turdieva ◽  
E. A. Shamansurova

The aim of the study was to examine the features of the endoscopic picture in the upper digestive tract mucosa in paediatric chronic gastroduodenal pathology (CGDP) associated with Helicobacter pylori. Materials and methods. There were examined 286 patients, aged 6–15 years. Diagnostic criteria for chronic gastroduodenal pathology were anamnestic as well as instrumental and functional studies data: gastric fractional intubation, esophagogastroduodenoscopy (EPGDS) with endoscopic pH-metry without biopsy, and ultrasound examination of abdominal organs. H. pylori testing was carried out by two unrelated methods such as respiratory test and a immunochromatographic fecal test. Results. Detection of H. pylori in children with CGDP peaked in patients with peptic gastric and duodenal ulcer (up to 87.5%, p < 0.05). The main endoscopic signs were edema, hyperaemia and contact bleeding, as well as local haemorrhage were the major endoscopic signs of inflammation in the stomach and duodenum mucosa. Atrophic mucosal lesions were characterized by thinning, pale colour together with transilluminated submucosal vessels. Non-atrophic antral gastritis was featured with delayed gastric emptying, antral stasis and pyloric spasm. In contrast, hypotension of the gastric wall, duodenogastric reflux and decreased motility were more typical to chronic atrophic gastritis. Major endoscopic feature in patients with H. pylori infection was presented by dominant atrophic changes combined with gastroduodenal reflux (77.6%, p < 0.05) compared to patients without H. pylori infection. Conclusion. Detection of HP infection was peaked in children with CGDP coupled to peptic ulcer disease compared to patients with inflammatory diseases (p < 0.05). Endoscopic examination in HP-positive patients showed that atrophic changes were found by 4-fold more frequently together with gastroduodenal reflux compared to patients without HP infection (p < 0.05).


2021 ◽  
Vol 14 (7) ◽  
pp. e243912
Author(s):  
Kiyokuni Nakamura ◽  
Ryo Tamura ◽  
Yoshitomi Yasui ◽  
Hideaki Okajima

Helicobacter pylori infection could cause chronic inflammation in the stomach and induce peptic ulcer disease or even malignant tumour. The initial infection of the organism happens in childhood but most of cases are latent. We had a case of 10-year-old girl who presented with acute epigastric pain and significant thickening of the stomach wall on CT. The finding seemed atypical for acute gastritis so oesophagogastroduodenoscopy and serology examination were added and the primary infection of H. pylori was confirmed with the exclusion of other possible diagnoses like eosinophilic gastritis and IgA vasculitis. Acute gastritis is one of the most common sickness in children, however, it would be worthwhile considering further investigation including H. pylori infection in a case of atypical presentation to prevent negative consequences derived from chronic H. pylori infection.


2003 ◽  
Vol 89 (04) ◽  
pp. 741-746 ◽  
Author(s):  
Ann-Sofie Rehnberg ◽  
Marju Hein ◽  
Olga Hegedus ◽  
Per Lindmarker ◽  
Per Hellström ◽  
...  

Summary Helicobacter pylori (H. pylori) infection is associated with peptic ulcer disease and gastric cancer. The eradication of H. pylori is of special interest in patients with congenital bleeding disorders, for whom treatment of gastrointestinal hemorrhage with factor concentrates is costly. The prevalence of H. pylori varies between different populations and identification of high-risk subgroups may allow for more targeted screening and eradication of the infection. We performed a 5-year retrospective study of gastrointestinal bleeding, combined with screening and treatment for H. pylori and a long-term prospective follow-up in 168 Swedish and 23 Estonian patients with hemophilia or von Willebrand disease. The prevalence of seropositivity was lower in Sweden than in Estonia (28 versus 48%, p = 0.03), lower in native Swedes than in non-Nordic immigrants to Sweden (20 versus 76%, p = 0.0001) and lower in patients less than 40 years of age than older patients (16 versus 38%, p = 0.002). The incidence of gastrointestinal hemorrhages among the 35 Swedish patients with active H. pylori infection, confirmed by a urea breath test, was 6.0 per 100 patient-years before eradication therapy versus 1.7 during the prospective followup. A negative urea breath test one month after therapy always remained negative after one year. Screening, followed by treatment of all infected patients, yielded a reduction of direct costs over a 5-year period of 130 US-$ per screened patient. We conclude that screening and eradication therapy for infection with H. pylori in patients with congenital bleeding disorders is an effective and economic strategy.


2019 ◽  
Vol 12 ◽  
pp. 175628481989406 ◽  
Author(s):  
Christian Schulz ◽  
Kerstin Schütte ◽  
Julia Mayerle ◽  
Peter Malfertheiner

A link between chronic inflammation and carcinogenesis has been depicted in many organ systems. Helicobacter pylori is the most prevalent bacterial pathogen, induces chronic gastritis and is associated with more than 90% of cases of gastric cancer (GC). However, the introduction of nucleotide sequencing techniques and the development of biocomputional tools have surpassed traditional culturing techniques and opened a wide field for studying the mucosal and luminal composition of the bacterial gastric microbiota beyond H. pylori. In studies applying animal models, a potential role in gastric carcinogenesis for additional bacteria besides H. pylori has been demonstrated. At different steps of gastric carcinogenesis, changes in bacterial communities occur. Whether these microbial changes are a driver of malignant disease or a consequence of the histologic progression along the precancerous cascade, is not clear at present. It is hypothesized that atrophy, as a consequence of chronic gastric inflammation, alters the gastric niche for commensals that might further urge the development of H. pylori-induced GC. Here, we review the current state of knowledge on gastric bacteria other than H. pylori and on their synergism with H. pylori in gastric carcinogenesis.


Diagnostics ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 759
Author(s):  
Monika Maria Biernat ◽  
Aldona Bińkowska ◽  
Łukasz Łaczmański ◽  
Paweł Biernat ◽  
Paweł Krzyżek ◽  
...  

Antibiotic resistance of Helicobacter pylori is currently a global issue. The aim of this study was to analyze actual antibiotic resistance rates of H. pylori strains isolated from children with primary infections and to compare the incidence of mutations that determine resistance to clarithromycin (CH) and metronidazole (MET) in children with different clinical diagnoses. A total of 91 H. pylori strains were isolated from 108 children with primary infections. Drug susceptibility testing of the strains was performed using E-test method. Classical sequencing of DNA fragments was used to detect point mutations for CH and MET resistance. Resistance to CH was detected in 31% of isolated strains (28/91), while resistance to MET and CH was detected in 35% (32/91) of strains. A2143G was the most frequently detected mutation and was dominant among strains isolated from children with peptic ulcer disease (80%). Mutations in the rdxA gene were found significantly more frequently among MET-resistant strains than MET-sensitive strains (p = 0.03, Chi2 = 4.3909). In children, a higher frequency of H. pylori multiresistant strains was observed compared with the previous study in the same area. Differences were found in the occurrence of point mutations among H. pylori strains resistant to CH isolated from children with different clinical diagnoses.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 1747 ◽  
Author(s):  
David R. Scott ◽  
George Sachs ◽  
Elizabeth A. Marcus

Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments of H. pylori infection rely on acid suppression in combination with at least two antibiotics. The role of acid suppression in eradication therapy has been variously attributed to antibacterial activity of proton pump inhibitors directly or through inhibition of urease activity or increased stability and activity of antibiotics. Here we discuss the effect of acid suppression on enhanced replicative capacity of H. pylori to permit the bactericidal activity of growth-dependent antibiotics. The future of eradication therapy will rely on improvement of acid inhibition along with current antibiotics or the development of novel compounds targeting the organism’s ability to survive in acid.


2019 ◽  
Vol 2 (1) ◽  
pp. 4-10
Author(s):  
Sunit Agrawal ◽  
D Thakur ◽  
P Kafle ◽  
A Koirala ◽  
R K Sanjana ◽  
...  

Background: Helicobacter pylori is found in more than 90% cases of peptic ulcer. This study examines the possibility of association of Helicobacter pylori in perforated peptic ulcer disease and its relation to persisting ulcer as well as the influence of other risk factors; namely: smoking, alcohol, current non-steroidal anti inflammatory drugs (NSAIDs) and steroid use. Materials and Methods: In this prospective study, total of 50 cases of peptic ulcer perforation admitted in College of Medical Sciences and Teaching Hospital, Bharatpur, Nepal were selected on the basis of the non-probability (purposive) sampling method. All patients who presented with suspected peptic ulcer perforation were included in the study and the perforations were repaired by Modified Graham’s Patch and were given triple therapy postoperatively. The age, sex, incidence, mode of presentation, precipitating factors, association with the risk factors and postoperative complications were all evaluated and compared. Results: Of 50 patients studied, the age ranged from 17 to 75 years, mean age being 40.1 years with the peak incidence in the 3rd and 5th decades of life showing a male dominance (92%). H. pylori was seen in ulcer edge biopsy in 29 patients (58%). Most common clinical presentation was pain abdomen, the most common signs of perforation were tenderness, rebound tenderness and absent bowel sounds. The mean duration of stay in hospital in H. pylori positive patients was 12.07±8.15 days as compared with 11.1±5.12 days in H. pylori negative patients. The incidence of peptic ulcer perforation was higher in the patients consuming alcohol (64%) than smokers (48%), followed by NSAIDs user(22%). 20% of the patients with delayed presentation developed complications postoperatively. Perforated peptic ulcer was repaired by Modified Graham’s Patch Repair, followed by anti H. pylori therapy in all of them. Conclusion: Peptic ulcer perforation is quite common among the patients with peptic ulcer disease with history of chronic smoking, alcoholism and analgesic intake, more commonly in males. There is association of H. pylori in 58% of patients with peptic ulcer perforation.


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