Helicobacter pylori infection in an urban African population

We have studied 221 adults drawn from an impoverished urban population with high human immunodeficiency virus (HIV) seroprevalence (35%) to determine the prevalence of gastroduodenal pathology and its relationship to serological markers of Helicobacter pylori virulence proteins and other potential environmental and immunological determinants of disease including HIV infection. Eighty-one percent were H. pylori seropositive, and 35% were HIV seropositive. Urban upbringing and low CD4 count were associated with a reduced likelihood of H. pylori seropositivity, as was current Ascaris infection, in keeping with recent evidence from an animal model. One hundred ninety-one adults underwent gastroduodenoscopy, and 14 had gastroduodenal pathology. Mucosal lesions were a major cause of abdominal pain in this population. While the majority of patients with gastroduodenal pathology (12 of 14) were seropositive for H. pylori, none were seropositive for HIV. Smoking was associated with increased risk of macroscopic pathology, and a history of Mycobacterium bovis BCG immunization was associated with reduced risk. Antibodies to H. pylori lipopolysaccharide were associated with pathology. HIV infection was associated with protection against mucosal lesions, suggesting that fully functional CD4 lymphocytes may be required for the genesis of gastroduodenal pathology.     

Seroprevalence of Helicobacter pylori infection in Malagasy population

Helicobacter pylori is a worldwide infection. However very few data are actually available on H. pylori seroprevalence in the Malagasy population. We carried out a transversal study in a sample of persons who met the following criteria: older than 15 years old, presence in the medicine internal unit 2 (University Hospital Center of Antananarivo) during the period of the study whatever the reason. H. pylori infection was identified serologically by using ELISA (G.A.P IgG H. pylori ELISA, Bio-Rad, France). Several factors were evaluated including serological status, demographic information, the reason of the presence in the unit, factors influencing H. pylori infection: socio-economic status, siblings, promiscuity consumption of alcohol, use of tobacco, water source and history of gastroscopy. The presence of clinical symptoms, such as dyspepsia and abdominal pain, was determined. Forty-five men and 45 women were included (mean age: 41.8 +/- 3.4 years). The seroprevalence of H. pylori infection was 82%. H. pylori infection was higher in men than in women (p < 0.02). Promiscuity constituted the principal factor influencing H. pylori infection. The seroprevalence of the H. pylori infection appears to be comparable to the rate encountered in developing countries. Considering this high rate of the H. pylori infection, eradication of H. pylori should be commonly recommended when facing gastrointestinal pathologies potentially induced by H. pylori.     

Comparison of biopsy-based methods for the detection of Helicobacter pylori infection

Various biopsy-based methods for the detection of Helicobacter pylori are evaluated to determine their sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV), followed by polymerase chain reaction (PCR) for the 16S ribosomal RNA (rRNA) gene of H. pylori (16S PCR) to confirm the results. Seventyfive patients (65% [49] males, age range: 17-77 years, mean 42+/-14.6 years) with dyspeptic symptoms are included in the study. Gastric antrum biopsy specimens collected during endoscopy are tested using a urea agar base enriched with 40% urea solution (eUAB, Oxoid)), a commercial rapid urease test (Pronto Dry, Medical Instrument Corp, Switzerland), histopathology and 16S PCR. The eUAB test showed 97% sensitivity, 86% specificity, 84% PPV, 97% NPV and 91% accuracy when the diagnosis of H. pylori infection was made with positive Pronto Dry and histopathology. Pronto Dry showed 100% sensitivity, 82% specificity, 80% PPV, 100% NPV and 89% accuracy when the diagnosis of H. pylori infection was made on positive histopathology and eUAB. Thus, the eUAB can be used as a rapid urease test. It is economical and has a sensitivity and specificity comparable to a commercially available rapid urease test to detect urease activity of H. pylori in gastric biopsy.     

Helicobacter pylori stains and association between H. pylori and inflammation in gastric specimens

Gastric cancer has been strongly associated with presence of the bacterium Helicobacter pylori. To improve techniques in identifying H. pylori so that gastric cancer may be predicted early, this project was formulated to determine whether one particular stain is more effective in displaying H. pylori microscopically. In addition, this study attempted to determine whether the degree of inflammatory elements present in tissue could be used to predict the likelihood of H. pylori presence. Protocols for the staining techniques, Steiner and alcian yellow/toluidine blue (AY/TB), were employed on specimens to semi-quantitate H. pylori presence. Serial sections from the same specimens were stained with hematoxylin and eosin to determine the amount of inflammation. Spearman rho correlation was used to evaluate the association between amount of H. pylori and inflammation in each case. It was determined that AY/TB was more easily performed, more effective in demonstrating H. pylori, and more cost effective than the Steiner stain. Additionally, it was determined that a moderate positive association was indicated between high levels of inflammation and marked presence of H. pylori.     

Helicobacter pylori infection in Korea

Helicobacter pylori is a gram-negative bacterium that was first isolated in 1982. Since then, H. pylori infection in humans has been shown to be associated with gastritis, peptic ulcer disease, gastric carcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma as well. The epidemiology, transmission, and pathogenicity of H. pylori has been a subject of intensive study. Successful treatment improves the cure rate of peptic ulcerations and treatment with antimicrobials also decreases the recurrence rate of these diseases. Better regimens having less toxicity and a good eradication rate have also been developed. A better understanding of the pathophysiologic mechanisms relating to H. pylori induced mucosal damages would result in more options for the prevention of peptic ulcers and carcinogenesis. Korea has a relatively high incidence of H. pylori infection and gastric cancer. Growing interest has developed in view of its importance in being associated with various gastroduodenal diseases. Furthermore, along with a high incidence of H. pylori-related disease in Korea, because the interaction between H. pylori, host factors and environmental factors is important in disease pathogenesis, we need to have precise data on the characteristics of H. pylori-related diseases that occur in Korea. In the present report we review the epidemiology, transmission route, diagnosis, pathogenesis, treatment methods and relationship with gastroduodenal diseases with in special references to basic and clinical data that have been published.     

细胞自噬与幽门螺杆菌感染

幽门螺杆菌是一种广泛定植于人胃黏膜的革兰阴性菌,它通过逃逸机体局部免疫杀灭而持续感染,最终导致胃上皮损伤,与多种胃部疾病相关.自噬是进化过程中保留的细胞机制,既能清除胞质内容物,又不影响细胞的生存.幽门螺杆菌能够入侵胃上皮细胞和某些免疫细胞,诱导自噬的发生,并在自噬体中自我复制后被清除,推测自噬可能在幽门螺杆菌感染中扮...     

Dynamics of Helicobacter pylori-specific immunoglobulin G for 2 years after successful eradication of Helicobacter pylori infection in an American Indian and Alaska Native population

Helicobacter pylori antibodies were measured over 24 months in American Indian and Alaska Native persons who cleared their infections. Two months after treatment, 82% of H. pylori-negative persons remained seropositive. While there were declines in H. pylori antibodies for 12 months, after 24 months 71% of persons remained seropositive.     

Helicobacter pylori infection in patients with Barrett's oesophagus: a prospective immunohistochemical study.

The prevalence of Helicobacter pylori infection in patients with Barrett's oesophagus was studied prospectively. A sensitive immunohistochemical staining of H pylori was performed in oesophageal and gastric biopsies of 73 patients from a surveillance group with this condition. H pylori was detected in 11 cases of Barrett's mucosa (15%) and in 26 gastric mucosa specimens (35.6%). All cases positive in Barrett's mucosa were also positive in the stomach. In Barrett's oesophagus, H pylori was never found on specialised epithelium. The percentage of Barrett's mucosa showing inflammatory changes was similar in specimens with and without H pylori, both for chronic (81% v 79%) and acute (9% v 10%) infiltrates. These results indicate that H pylori infection does not play an aetiological role in Barrett's oesophagus and that colonisation of the metaplastic mucosa by this bacteria is related with the presence of gastric type mucosa in the oesophagus and of H pylori infection in the stomach.     

Pathogenesis of Helicobacter pylori infection

Helicobacter pylori induces chronic gastritis, the strongest known risk factor for peptic ulcer disease and distal gastric cancer, yet only a fraction of colonized individuals ever develop clinical disease. H. pylori isolates possess substantial genotypic diversity, which engenders differential host inflammatory responses that influence pathologic outcome. However, clinical sequelae are not completely dependent upon bacterial virulence factors, and disease is also influenced by host genetic diversity, particularly within immune response genes. The focus of this article will be to provide an understanding of mechanisms that underlie H. pylori persistence and pathogenesis as a framework for understanding disease processes that develop from chronic inflammation. Identification of mechanisms that regulate ongoing H. pylori–host interactions will not only improve targeted diagnostic and therapeutic modalities, but may also provide insights into other diseases that arise within the context of pathogen-initiated inflammatory states.     

Pathogenicity of Helicobacter pylori infection

Numerous Helicobacter pylori virulence factors, including various enzymes (urease, catalase, lipase, phospholipase and proteases), vacuolating cytotoxin (a product of expression of the vacA gene), and the immunogenic protein CagA, encoded by the cagA gene localised in the H. pylori pathogenicity island, are involved in the pathomechanism of infection caused by these organisms. This review presents the current state of knowledge concerning the molecular mechanisms and epidemiology of H. pylori infection, based on the published literature and recent unpublished observations.     

Pathogenesis of Helicobacter pylori infection

Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonize a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonization of the gastric mucosa and subsequently seem to modulate the host's immune system. This review focuses on the microbiological, clinical, immunological, and biochemical aspects of the pathogenesis of H. pylori.     

Incidence of Helicobacter felis and the effect of coinfection with Helicobacter pylori on the gastric mucosa in the African population

Helicobacter pylori and Helicobacter felis are two of the Helicobacter spp. that infect humans. H. pylori has been linked to significant gastric pathology. Coinfection with Helicobacter spp. may influence infectious burden, pathogenesis, and antibiotic resistance; however, this has not been studied. The aims of this study were to identify the incidence of H. felis and to analyze the effects of coinfection with both organisms on gastric pathology in a well-characterized South African population. Biopsy samples from the gastric corpora and antra of volunteers (n = 90) were subjected to histological examination and PCR for the identification of H. pylori and H. felis. We further investigated the effect of global strain type on the occurrence of precursor lesions by assigning nucleotide sequences derived from PCR amplification of three genes to global groupings (ancestral Africa1, ancestral Africa2, ancestral Europe, ancestral Asia, and mixed). H. pylori was detected in 75 (83.3%), H. felis in 23 (25.6%), and coinfection in 21 (23.3%) of the volunteers by PCR. H. felis was randomly distributed among adults and children but clustered within families, suggesting intrafamilial transmission. Analysis of histopathology scores revealed no differences in atrophy, activity, and helicobacter density between H. felis-positive and H. felis-negative volunteers. H. pylori substrains common to southern Africa showed no differences in inflammation or atrophy scores. The incidences of H. felis and coinfection with H. pylori in the African population are high. H. felis infection, however, does not influence specific gastric pathology in this population.     

Comparison of Giemsa and acridine orange stains for the diagnosis of Leishmania donovani in biopsies of infected hamsters

Identical impression smears of spleen, liver and bone marrow biopsy materials from Leishmania donovani-infected hamsters were stained using either acridine orange or Giemsa. Spleen parasite-loads calculated from the two stains for identical biopsy material were significantly different from each other. However, liver and bone marrow parasite- loads calculated from either Giemsa-stained or acridine orange-stained biopsies were not significantly different from each other. This study has shown that acridine orange, which is a quick and simple technique, has great potential in the diagnosis of kala-azar when liver and bone marrow biopsies are used.     

Evidence for an oral-faecal transmission of Helicobacter pylori infection in an experimental murine model.

An experimental murine model was used to evaluate the possible animal-to-animal transmission of Helicobacter pylori and the mechanism involved. Twenty-four Balb/C mice were infected with H. pylori type I strain culture and kept with 24 noninoculated mice to evaluate the possible transmission of the microorganism. Twelve inoculated mice were housed with 12 noninoculated mice in a grated cage (supporting an oral-oral transmission); the remaining inoculated and noninoculated mice were housed in another cage without grating on the floor (supporting a faecal-oral transmission). The bacterial colonization was assessed by culture and immunohistochemistry. The systemic antibody response to H. pylori and the histopathological changes were evaluated; controls were examined at 2, 4, 8, 12 weeks after the start of the experiment. Faecal samples were also collected from each mouse on the day before sacrifice, to assess the presence of H. pylori by culture and by immunohistochemistry. In the gastric mucosa of inoculated mice, histopathological changes were recorded at each control time and H. pylori was detected both by immunohistochemistry and by a systemic antibody response; the microorganism was also cultured at 2, 4, 8 weeks postinoculation. H. pylori was detected in noninoculated mice, housed in the cage without grating, using an immunoperoxidase technique at 2, 4, 8 weeks after starting the experiment, and these positive values were supported by histopathological changes, and, in one case, at 8 weeks, also by the serum immune response. No colonies of H. pylori were detected by culturing faecal samples from either noninoculated or inoculated mice. The results obtained in this study seem to support an oral-faecal route as the mode of transmission of H. pylori infection in this animal model.     

Helicobacter pylori infection and erosive gastritis

One hundred and eleven patients were included in the study. Thirty seven had erosive gastritis, thirty four chronic gastritis and forty were controls without any gastrointestinal diseases confirmed by symptoms and upper gastrointestinal endoscopy. Patients with erosive gastritis were divided into non-steroidal anti-inflammatory drug (NSAID) users and non-users. H pylori status was determined by urease test, serology and/or histology. The prevalence of H pylori was compared between the various groups. The prevalence of H pylori infection in erosive gastritis, chronic gastritis and controls was 68%, 76% and 65%, respectively, the difference was not significant (P > 0.05), 8 out of 11 patients with erosive gastritis and NSAID use (73%) were positive for H pylori. Likewise 17/26 patients with erosive gastritis without NSAID use (65%) were positive for H pylori (P > 0.05). Body of the stomach (65%) was the commonest site for erosions compared to antrum (43%) or fundus (27%) (P < 0.02). H pylori infection does not predispose to erosive gastritis. NSAID use does not affect H pylori prevalence. Routine H pylori eradication is, therefore, not indicated in patients with erosive gastritis infection. Body of the stomach is the most predominant site for erosions.     

Diagnosis and treatment of Helicobacter pylori infection

National Danish guidelines for the diagnosis and treatment of Helicobacter pylori (Hp) infection have been approved by the Danish Society for Gastroenterology. All patients with peptic ulcer disease, gastric cancer, and MALT lymphoma should be tested for Hp. We also recommend testing in first degree relatives to patients with gastric cancer, in NSAID-naive patients, who need long-term NSAID therapy, and in patients presenting with dyspepsia and no alarm symptoms. Non-endoscoped patients can be tested with a urea-breath test or a faecal antigen test. Endoscoped patients can be tested with a rapid urease test. Proton pump inhibitor therapy should be stopped at least 1 week prior to Hp testing. All infected patients should be offered Hp eradication therapy. First-line treatment is 7-day triple therapy with a proton pump inhibitor and clarithromycine in combination with metronidazole or amoxicilline. Quadruple therapy for 2 weeks with bismuthsubsalicylate, tetracycline, metronidazole and a proton pump inhibitor is recommended in case of treatment failure. Hp testing should be offered to all patients after eradication therapy but is mandatory in patients with ulcer disease, noninvasive gastric cancer or MALT lymphoma. Testing after eradication should not be done before 4 weeks after treatment has ended.