scholarly journals Presence of Helicobacter pylori and H. suis DNA in Free-Range Wild Boars

Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1269
Author(s):  
Francisco Cortez Nunes ◽  
Teresa Letra Mateus ◽  
Sílvia Teixeira ◽  
Patrícia Barradas ◽  
Chloë de Witte ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Transmission Risk ◽  
Duodenal Ulcers ◽  
Wild Boars ◽  
Ulcer Disease ◽  
Transmission Cycle ◽  
Free Range ◽  
Bacterial Transmission ◽  
Gastric Or Duodenal Ulcers ◽  
H Pylori

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that infects half of the human population worldwide, causing gastric disorders, such as chronic gastritis, gastric or duodenal ulcers, and gastric malignancies. Helicobacter suis (H. suis) is mainly associated with pigs, but can also colonize the stomach of humans, resulting in gastric pathologies. In pigs, H. suis can induce gastritis and seems to play a role in gastric ulcer disease, seriously affecting animal production and welfare. Since close interactions between domestic animals, wildlife, and humans can increase bacterial transmission risk between species, samples of gastric tissue of 14 free range wild boars (Sus scrofa) were evaluated for the presence of H. pylori and H. suis using PCR. Samples from the antral gastric mucosa from two animals were PCR-positive for H. pylori and another one for H. suis. These findings indicate that these microorganisms were able to colonize the stomach of wild boars and raise awareness for their putative intervention in Helicobacter spp. transmission cycle.

scholarly journals Prevalence of Helicobacter pylori infection among patients undergoing upper gastrointestinal endoscopy

2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Vudumula Vijaya Lakshmi
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Normal Population ◽  
Gastric Ulcers ◽  
Upper Gastrointestinal Endoscopy ◽  
Contributing Factors ◽  
Duodenal Ulcers ◽  
Female Ratio ◽  
Ulcer Disease ◽  
H Pylori

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.

scholarly journals ABO blood group, secretor status and detection ofHelicobacter pyloriamong patients with gastric or duodenal ulcers

1991 ◽  
Vol 106 (2) ◽  
pp. 221-229 ◽  
Author(s):  
A. Mentis ◽  
C. C. Blackwell ◽  
D. M. Weir ◽  
C. Spiliadis ◽  
A. Dailianas ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Blood Group ◽  
Local Population ◽  
Abo Blood Group ◽  
Duodenal Ulcers ◽  
Secretor Status ◽  
Gastric Or Duodenal Ulcers ◽  
H Pylori

SUMMARYPatients (454) referred for gastroscopy to the General Hospital of Athens were examined to determine (1) if non-secretors were over-represented among patients with ulcers and (2) is there was an association with ABO blood group or secretor status and carriage ofHelicobacter pylori.Compared with the local population, among patients with either gastric ulcer (51) or duodenal ulcer (96) there was a significant increase in the proportion of those who were blood group O (P< 0·025); however, there were no significant differences in the proportions of non-secretors.H. pyloriwas identified in 62 % of the 454 patients: 59·5 % of those without evidence of ulcers; 62·5 % of those with gastric ulcer; 88% of those with duodenal ulcer (P< 0·0005). These bacteria were cultured more often and in higher numbers from patients with duodenal ulcer (P< 0·025). There was no association between ABO blood group and prevalence ofH. pylori. The prevalence ofH. pyloriamong non-secretors with gastric ulcer (12·5%) was significantly lower than that for non-secretors with duodenal ulcer (100%) (P< 0·0005). This was not observed for secretors.

scholarly journals Prevalence of Helicobacter pylori in patients with peptic ulcer disease

2018 ◽  
Vol 5 (4) ◽  
pp. 1315
Author(s):  
Mrutyunjay I. Uppin ◽  
Kapildev K. Hannurkar
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Histopathological Examination ◽  
Rapid Urease Test ◽  
Duodenal Ulcers ◽  
Ulcer Disease ◽  
Urease Test ◽  
H Pylori ◽  
Upper Gastrointestinal

Background: Prevalence of Helicobacter pylori (H. pylori) emerges throughout the world and instigates peptic ulcer disease (PUD). The study was conducted with the aim to determine the prevalence of H. pylori in patients with PUD undergoing upper gastrointestinal endoscopy.Methods: This prospective study was conducted on 150 cases of PUD from August 2009 to February 2011. Endoscopy was done in all cases. Biopsy was done and sent for histopathological examination and rapid urease test for confirmation of presence of H. pylori.Results: Out of 150 patients with mean age of 45.76 years, 109 patients were diagnosed to have been infected with Helicobacter pylori (72.66%). Out of 89 patients with gastric ulcer, 61 patients were infected with Helicobacter pylori (68.53%). Forty two out of 51 patients (82.35%) with duodenal ulcers and 06 of 10 patients (60%) with carcinoma of stomach were positive for H. pylori. The remaining patients were found to be negative for the H. pylori infection.Conclusions: The findings of the study conclude that H. pylori was consistently associated with PUD.

scholarly journals Motion – Helicobacter pylori Causes or Worsens GERD: Arguments for the Motion

2002 ◽  
Vol 16 (9) ◽  
pp. 611-614 ◽  
Author(s):  
Colm A O’Morain ◽  
Asghar Qasim
Keyword(s):  
Helicobacter Pylori ◽  
Epidemiological Data ◽  
Acid Suppression ◽  
Duodenal Ulcers ◽  
Ulcer Disease ◽  
Acid Suppression Therapy ◽  
Premalignant Condition ◽  
H Pylori ◽  
Gerd Symptoms

There are several reasons for eradicating Helicobacter pylori in patients with chronic gastroesophageal reflux disease (GERD). Perhaps the most compelling is the evidence that chronic acid suppression therapy can lead to the development of atrophic gastritis, a premalignant condition, in patients with H pylori infection. Epidemiological data that suggest that H pylori is less prevalent in GERD patients than in control subjects may be susceptible to publication bias, and confounding social and environmental factors may also be involved. Although it has been thought that eradication of the organism might lead to increased esophageal acid exposure, this has not been demonstrated in practice. Studies that appeared to show that GERD could be provoked by antimicrobial therapy of duodenal ulcers also have methodological weaknesses. Underlying GERD symptoms might be unmasked after withdrawal of acid-suppression therapy, for reasons that are unrelated to H pylori. In fact, eradication of the organism has been shown to decrease heartburn in patients with peptic ulcer disease. When H pylori is successfully eradicated in patients with GERD, relapse rates are not increased, and the disease- free interval seems to be prolonged. Eradication of the organism is a wise policy in patients who face long term acid-suppression therapy for GERD.

scholarly journals Helicobacter pylori cag pathogenicity island genes: clinical relevance for peptic ulcer disease development in Brazil

2007 ◽  
Vol 56 (1) ◽  
pp. 9-14 ◽  
Author(s):  
Rejane Mattar ◽  
Sergio Barbosa Marques ◽  
Maria do Socorro Monteiro ◽  
Anibal Ferreira dos Santos ◽  
Kiyoshi Iriya ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Gastric Ulcers ◽  
Disease Development ◽  
Duodenal Ulcers ◽  
Ulcer Disease ◽  
Significant Difference ◽  
H Pylori ◽  
The Right

The purpose of this study was to verify whether the presence of any of the Helicobacter pylori cagPAI genes or segments – cagA, cagA promoter, cagE, cagM, tnpB, tnpA, cagT and the left end of the cag II (LEC) region – would be a useful marker for the risk of peptic ulcer disease development. H. pylori DNA extracted from positive urease tests of 150 peptic ulcer patients and 65 dyspeptic controls was analysed by PCR. Duodenal ulcers were present in 110, gastric ulcers in 23 and both gastric and duodenal ulcers in 17 patients. A significant association (P <0.001) was found between a conserved cagPAI and peptic ulcer disease (34 %). The positivity of the cagA gene varied according to the region of the gene that was amplified. The region near to the promoter was present in almost all of the H. pylori isolates (97.2 %). The segment from nt 1764 to 2083 and the extreme right end were frequently deleted in the isolates from the controls (P <0.01). The positivity of the promoter region of cagA and cagT, cagE, cagM and LEC showed a significant difference between the isolates from peptic ulcer patients and from the controls (P <0.01). Patients usually had moderate gastritis; however, the intensity of the active inflammation was higher in the peptic ulcer group (P <0.001). cagT, cagM, LEC and the right end terminus of the cagA-positive H. pylori isolates were associated with a 27-fold, 8-fold, 4-fold and 4-fold risk of peptic ulcer disease, respectively, and may be useful markers to identify individuals at higher risk of peptic ulcer disease development in Brazil.

scholarly journals Incidence of Duodenal Ulcers and Gastric Ulcers in a Western Population: Back to Where It Started

2009 ◽  
Vol 23 (9) ◽  
pp. 604-608 ◽  
Author(s):  
Marcel JM Groenen ◽  
Ernst J Kuipers ◽  
Bettina E Hansen ◽  
Rob J Th Ouwendijk
Keyword(s):  
Gastric Ulcers ◽  
Bleeding Complications ◽  
Upper Gastrointestinal Endoscopy ◽  
Peptic Ulcers ◽  
Duodenal Ulcers ◽  
Ulcer Disease ◽  
Treatment Regimens ◽  
H Pylori ◽  
Upper Gastrointestinal ◽  
Over Time

BACKGROUND/OBJECTIVES: As recently as 40 years ago, a decline in the incidence of peptic ulcers was observed. The discovery of Helicobacter pylori had a further major impact on the incidence of ulcer disease. Our aim was to evaluate the trends in the incidence and bleeding complications of ulcer disease in the Netherlands.METHODS: From a computerized endoscopy database of a district hospital, the data of all patients who underwent upper gastrointestinal endoscopy from 1996 to 2005 were analyzed. The incidence of duodenal and gastric ulcers, with and without complications, were compared over time.RESULTS: Overall, 20,006 upper gastrointestinal endoscopies were performed. Duodenal ulcers were diagnosed in 696 (3.5%) cases, with signs of bleeding in 158 (22.7%). Forty-five (6.5%) of these ulcers were classified as Forrest I and 113 (16.2%) as Forrest II. Gastric ulcers were diagnosed in 487 cases (2.4%), with signs of bleeding in 60 (12.3%). A Forrest 1 designation was diagnosed in 19 patients (3.9%) and Forrest 2 in 41 patients (8.4%). The incidence of gastric ulcers was stable over time, while the incidence of duodenal ulcers declined.CONCLUSIONS: The incidence of duodenal ulcer disease in the Dutch population is steadily decreasing over time. Test and treatment regimens for H pylori have possibly contributed to this decline. With a further decline in the prevalence of H pylori, the incidence of gastric ulcers is likely to exceed the incidence of duodenal ulcers in the very near future, revisiting a similar situation that was present at the beginning of the previous century.

scholarly journals Identification of Markers for Helicobacter pylori Strains Isolated from Children with Peptic Ulcer Disease by Suppressive Subtractive Hybridization

2006 ◽  
Vol 74 (7) ◽  
pp. 4064-4074 ◽  
Author(s):  
Mónica Oleastro ◽  
Lurdes Monteiro ◽  
Philippe Lehours ◽  
Francis Mégraud ◽  
Armelle Ménard
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Subtractive Hybridization ◽  
Suppressive Subtractive Hybridization ◽  
Ulcer Disease ◽  
Lipopolysaccharide Biosynthesis ◽  
The Difference ◽  
H Pylori

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.

scholarly journals Incidence of Gastric Metaplasia and Helicobacter pylori Infection in Duodenal Bulb – With Specific Reference to Patients With Duodenal Ulcers

1999 ◽  
Vol 6 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Minoru Kawaguchi ◽  
Toshihiko Saito
Keyword(s):  
Helicobacter Pylori ◽  
Duodenal Bulb ◽  
Mucosal Injury ◽  
Transitional Zone ◽  
Specific Reference ◽  
Rapid Urease Test ◽  
Duodenal Ulcers ◽  
Gastric Metaplasia ◽  
Urease Test ◽  
H Pylori

We determined the incidence of gastric metaplasia in the duodenal bulb of duodenal ulcer patients and the Helicobacter pylori (H. pylori) infection rate at sites with gastric metaplasia. Biopsy of the duodenal bulb showed the presence of gastric metaplasia in 61 of 86 patients (71%) overall and in 18 of 47 patients (38.3%) who had gastrectomy at an early gastric cancer. The histological diagnosis of H. pylori infection showed good agreement (83.3%) with the result of the rapid urease test, indicating that H. pylori occurs in regions with gastric metaplasia. This finding suggests that H. pylori infects gastric metaplasia in the duodenal bulb, causing mucosal injury, which is then transformed into duodenal ulcers. The exact mechanism by which gastric metaplasia is caused is unknown, but it is believed to occur in the transitional zone in the duodenal mucosa.

scholarly journals Causes and Management of Gastric and Duodenal Ulcer in Adolescents

2021 ◽  
pp. 289-297
Author(s):  
Bader Maiedh Mohsen Aladainan ◽  
Mahdi Turki Bin Ali Alfataih ◽  
Alhassan Ahmed Mohammed Aldundur ◽  
Rashed Saleh Mohammed Balhareth ◽  
Eisa Yazeed Ghazwani
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Review Literature ◽  
Peptic Ulcers ◽  
Significant Progress ◽  
Duodenal Ulcers ◽  
Ulcer Disease ◽  
Last 300 Years ◽  
Made In

Many etiological hypotheses have been suggested to explain the development of peptic ulcers during the last 300 years (including gastric ulcer and duodenal ulcer). In the last two decades, significant progress has been made in understanding the pathophysiology of peptic ulcer disease, particularly with regard to the involvement of Helicobacter pylori and nonsteroidal anti-inflammatory medications (NSAIDs). This study will attempt to review literature on etiology and management of gastric and duodenal ulcers among adolescents.

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