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PubMed2005

Comparison of Helicobacter spp. genetic sequences in wild and captive seals, and gulls.

Helicobacter species are widely distributed in the gastrointestinal system of humans and many animal taxa. Investigations of natural infections are essential to elucidating their role within the host. The feces of fur seals Arctocephalus pusillus doriferus and sea lions Neophoca cinerea from 3 separate captive populations, as well as a wild colony from Kangaroo Island, Australia, were examined for the occurrence of Helicobacter spp. The feces from several wild silver gulls Larus novahollandiae were also investigated. As detected by PCR, 18 of 21 samples from captive and 12 of 16 samples from wild seals were positive for Helicobacter spp. Three species were identified in these animals. Whilst one possibly novel type was identified from wild fur seals, the majority of wild and captive individuals had the same species. This species also occurred in more than 1 seal type and in silver gulls, and shared a 98.1 to 100% identity to other Helicobacter spp. from harp seals and sea otters. A similar sequence type to species identified from cetaceans was also detected in several captive seals. This study reports for the first time the presence of Helicobacter spp. in wild and captive seals and demonstrates the diversity and broad-host range of these organisms in the marine host.

Animals↗
PubMed2005

Gastroinvasive Helicobacter infection in an Ocelot (Leopardus pardalis).

Highly invasive Helicobacter-like organisms were found in a 19-year-old female ocelot (Leopardus pardalis) with multiple ulcers in the fundic region of the stomach. The bacteria, resembling Helicobacter heilmannii, were located largely within canaliculi or in the cytosol of parietal cells. Except in the ulcerative lesions, parietal cells were hyperplastic, while chief cells and neck mucous cells were reduced in number. The term "gastroinvasive Helicobacter-like organism" was applied. It seems probable that this organism differs from other Helicobacter organisms in pathogenicity, and possible that its behaviour in vitro would help it to evade antibacterial treatment.

Animals↗
PubMed1997

Local immunoglobulin G antibodies in the stomach may contribute to immunity against Helicobacter infection in mice.

BACKGROUND & AIMS: Orogastric immunization of mice with Helicobacter antigens, together with a mucosal adjuvant (cholera toxin), has been shown to confer immunity in the Helicobacter felis infection model. The aim of the study was to investigate the humoral immune responses associated with immunity and to compare these with responses in H. felis-infected mice. METHODS: Enzyme-linked immunoassays were used to characterize the antibody-secreting cells and antibodies present at mucosal and systemic sites in mice. Animals were immunized orally with either whole-cell H. felis sonicates or Helicobacter pylon urease or heat-shock proteins. RESULTS: Infection of mice with H. felis preferentially induced the recruitment of plasma cells committed to immunoglobulin (Ig) A synthesis in salivary gland and gastric tissues. Antigen-specific IgA was the major antibody class detected in mucosal secretions recovered from these tissues. In contrast, immunization of mice against H. felis infection induced the proliferation of large numbers of IgG-secreting cells, as well as the synthesis of local IgG antibodies, in the gastric mucosa of the animals. Protection against H. felis infection occurred in the absence of gastric IgA responses in sonicate-immunized mice. CONCLUSIONS: It is proposed that locally synthesized specific IgG antibodies contribute to immunity against gastric Helicobacter infection.

Animals↗
PubMed2002

Gastric Helicobacter species infection in murine and gerbil models: comparative analysis of effects of H. pylori and H. felis on gastric epithelial cell proliferation.

C57BL/6 mice and Mongolian gerbils were infected with Helicobacter felis and Helicobacter pylori SS1 strain to investigate the effects of different Helicobacter species on gastric inflammation and epithelial cell proliferation in different animal models. At 4 weeks, gerbils infected with H. pylori or H. felis developed antral gastritis. Onset of gastritis varied between the models, with mice infected with H. pylori having minimal inflammation at 8 weeks. In mice, H. felis, but not H. pylori, induced significantly increased epithelial cell proliferation in the cardia and corpus at 8 weeks, but no changes were observed at 4 weeks. In gerbils, both H. pylori and H. felis significantly increased antral epithelial cell proliferation at 4 weeks. Epithelial cell proliferation induced by H. felis in gerbils was twice that stimulated by H. pylori. These studies demonstrate host differences in the development of Helicobacter species-induced gastric inflammation and a marked difference in epithelial cell proliferation induced by H. pylori and H. felis in 2 animal models.

Animals↗
PubMed2006

Relationship between the severity of hepatitis C virus-related liver disease and the presence of Helicobacter species in the liver: a prospective study.

AIM: To determine the presence of Helicobacter species DNA in the liver of chronic hepatitis C (CHC) patients with and without cirrhosis as compared to controls, and to identify the bacterial species involved. METHODS: Seventy-nine consecutive patients (HBV and HIV negative) with a liver sample obtained after liver biopsy or hepatic resection were studied: 41 with CHC without cirrhosis, 12 with CHC and cirrhosis, and 26 controls (HCV negative). Polymerase chain reactions (PCRs) targeting Helicobacter 16S rDNA and species-specific were performed on DNA extracted from the liver. A gastric infection with H pylori was determined by serology and confirmed by 13C-urea breath test. RESULTS: Overall, Helicobacter 16S rDNA was found in 16 patients (20.2%). Although positive cases tended to be higher in CHC patients with cirrhosis (41.6%) than in those without cirrhosis (17.0%) or in controls (15.4%), the difference was not statistically significant (P = 0.08). H pylori-like DNA was identified in 12 cases and H. pullorum DNA in 2, while 2 cases remained unidentified. Gastric infection with H pylori was found in only 2 of these patients. CONCLUSION: Our results do not confirm the association of Helicobacter species DNA in the liver of CHC patients with advanced liver disease. The lack of correlation between positive H pylori serology and the presence of H pylori-like DNA in the liver may indicate the presence of a variant of this species.

Biopsy↗
PubMed2000

[Helicobacter heilmannii ulceronecrotic acute gastritis: apropos of 5 cases ].

We report 5 cases of Helicobacter heilmannii associated ulceronecrotic gastritis in patients presenting with acute epigastric pain. These bacteria were known to be associated with chronic active gastritis, less severe than those associated with Helicobacter pylori. Helicobacter heilmannii appears as spiral shaped organisms larger and longer but less numerous than Helicobacter pylori. Our five patients were cured by 4 weeks treatment with proton-pomp inhibitors without antibiotics. Endoscopic control, done in 4 patients, showed a complete cure and eradication of the germ. No ulcer relapse had occurred.

Acute Disease↗
PubMed2002

Impact of the recommendations made by Spanish Club for the Study of Helicobacter pylori on eradication indications.

AIM: A Spanish Consensus Conference had been arranged by the Spanish Club for the Study of Helicobacter pylori to encourage the use of eradication regimens in appropriate indications. The aim of our study was to assess whether the publication of these recommendations in November 1999 induced a change on the indications of eradication in the referring primary care district. METHOD: Patients who had undergone Helicobacter pylori eradication therapy indicated by a gastroenterologist and referred to perform the 13C-labelled marked urea breath test were evaluated. Indications of eradication therapy were analysed and divided in: a) use of Conference recommended procedures (duodenal or gastric ulcer, erosive duodenitis, gastric MALT lymphoma and after resection of gastric adenocarcinoma); and b) other procedures not included in the recommendations (the rest). Indications established during former and latter years of publication of the Club's recommendations were compared. RESULTS: A total of 659 established eradications in 1999 against 537 in 2000, were studied. Regarding established eradications in 1999, 418 out of 659 (63%) followed the recommendations made by the Spanish Club, while 241 (37%) did not. In 2000, the proportion of eradication therapy administered using the recommendations made by the Spanish Club was similar to previous year: 338 (63%) followed the recommendations, against 199 (37%) that did not (p = not significant). In both years, considering those indications not recommended, patients either with superficial chronic gastritis with or without dyspepsia or with gastrooesophageal reflux disease were the main disorders to indicate eradication therapy. CONCLUSIONS: The recommendations of the Spanish Helicobacter pylori Study Club have not triggered a significant change after their publication on the indications for Helicobacter pylori eradication therapy in the setting studied.

Adolescent↗
PubMed2003

[Helicobacter pylori and the others].

Since the discovery of H. pylori, several new Helicobacter species have been isolated from man and mainly from animals. Helicobacter species can be broadly grouped according to whether they colonize the gastric or enterohepatic niche. H. pylori is a bacterium of great clinical importance, essentially in the domain of gastroenterology. H. pylori infection is the first chronic infection known to give rise to cancer in man (gastric carcinoma and MALT lymphoma). The pathogenesis of H. pylori is now well studied. Two H. pylori strains have been sequenced: the first one isolated from a patient with gastric ulcer, the second one associated with gastritis. Global analysis of the gene content of H. pylori strains gives insight into the extent of its genetic diversity. Substantial evidence attests to certain extragastric Helicobacter species playing a role in the pathogenesis of enteric, hepatic and biliary disorders, especially for H. hepaticus which have just been sequenced. But isolation of non-pylori Helicobacter species continues to be a major problem, substantially limiting a better understanding of their prevalence and role. Therefore, animal models are of interest because of their value for modeling human disease and testing therapeutic strategies such as vaccines.

DNA, Bacterial↗
PubMed2003

Detection and isolation of Helicobacter mustelae from stoats in New Zealand.

AIM: To determine the incidence of Helicobacter mustelae in stoats (Mustela erminea) in New Zealand. METHODS: Helicobacter-like organisms and total genomic DNA were isolated from gastric tissue of stoats and identified using a combination of bacterial culture, phenotypic testing and molecular techniques. RESULTS: A Helicobacter-specific 16S rRNA polymerase chain reaction product was detected in 16/32 gastric tissue biopsies tested. Nine of 13 partially sequenced 16S rRNA DNA identified H. mustelae 16S DNA. Bacteria, subsequently identified as H. mustelae, were successfully cultured from the stomachs of 4/32 stoats. Other Helicobacter species were also identified by DNA sequence analysis, but were not cultured. CONCLUSIONS: Helicobacter mustelae is present in stoats from both the North and South Islands of New Zealand.

Journal Article↗
PubMed1991

Helicobacter nemestrinae sp. nov., a spiral bacterium found in the stomach of a pigtailed macaque (Macaca nemestrina)

A new microaerophilic, spirally curved, rod-shaped bacterium was isolated from the gastric mucosa of a pigtailed macaque (Macaca nemestrina). The gram-negative cells of this bacterium are oxidase, catalase, and urease positive and strongly resemble Helicobacter pylori (Campylobacter pylori) cells. Like H. pylori, this organism does not metabolize glucose, does not reduce nitrate or produce indole, does not produce H2S from triple sugar iron agar, does not hydrolyze hippurate or esculin, and does not grow in the presence of 1% glycine, 1.5% salt, or 1% bile. Also like H. pylori, it is resistant to nalidixic acid and susceptible to cephalothin. However, unlike H. pylori, the colorless colonies are flat and have irregular edges. This organism has a unique cellular fatty acid composition, forming a new gas-liquid chromatography group, group K, and a distinctive DNA content (24 mol% guanine plus cytosine). It exhibits less than 10% DNA-DNA homology (as determined by the nylon filter blot method at 65 degrees C) with other members of the genus Helicobacter. Although the levels of DNA relatedness between previously described Helicobacter species and the new organism are low (less than 10%) and the difference in guanine-plus-cytosine content is large (24 versus 36 to 41 mol%), the genus Helicobacter is the only genus in which it is logical to include the organism at this time. We propose that our single strain represents a new species, Helicobacter nemestrinae, and we designate strain T81213-NTB (= ATCC 49396) as the type strain.

Animals↗
PubMed1991

Inhibition of acid secretion from parietal cells by non-human-infecting Helicobacter species: a factor in colonization of gastric mucosa?

Helicobacter pylori has been shown to produce a protein that inhibits acid secretion from parietal cells. We have examined other non-human-infecting Helicobacter species for this property by measuring the uptake of [14C]aminopyrine into rabbit parietal cells as an indirect assessment of acid secretion. Helicobacter felis and an isolate from a rhesus monkey were shown to inhibit acid secretion. Isolates of Helicobacter mustelae gave variable responses. Whole bacteria and cell-free sonicates impaired the uptake of [14C]aminopyrine. We also tested other bacteria, including Escherichia coli, Proteus vulgaris, Klebsiella oxytoca, and Campylobacter jejuni. As whole organisms, these control bacteria had little effect on acid secretion, but sonicates caused pronounced inhibition that was partially heat labile. Pronase treatment of H. pylori destroyed its inhibitory effect. These results suggest that most Helicobacter species, but not all isolates, are able to inhibit acid secretion from rabbit parietal cells. This property may be a factor in the establishment of long-term infection by these species.

Aminopyrine↗
PubMed1999

Treatment of Helicobacter pylori infection.

The availability of clinic-based diagnostic tests means that screening for and the eradication of Helicobacter pylori can be done by primary care physicians. However, confusion still exists regarding indication and treatment regimens. It is universally accepted that patients with Helicobacter pylori infection and peptic ulcer disease require eradication therapy. But the benefits of Helicobacter pylori eradication in gastro-oesophageal reflux disease, non-steroidal anti-inflammatory drug-related peptic ulceration, and non-ulcer dyspepsia remain unclear. There is no evidence that the elimination of Helicobacter pylori is beneficial for asymptomatic patients or in preventing gastric cancer. One-week triple therapy with a proton pump inhibitor or ranitidine bismuth citrate in combination with clarithromycin/metronidazole and amoxycillin is the recommended first-line treatment for Helicobacter pylori infection. Problems with patient compliance and the development of antibiotic resistance are the two most important factors to consider when choosing the treatment regimen. The optimal retreatment therapy for treatment failure is still unknown, and quadruple therapy is best reserved for these cases.

Journal Article↗
PubMed1999

Helicobacter pylori infection and gastric cancer.

Gastric cancer is the second most common fatal malignant neoplasm in the world. In mainland China, gastric cancer is now the second most common malignant neoplasm, while in Hong Kong the mortality rate ranked fourth of all cancers in 1995. Dietary factors seem to be involved in gastric carcinogenesis, and beta carotene, selenium, and vitamin E (tocopherols) have been shown to help reduce gastric cancer mortality. Prospective case-control studies have shown an increased risk for the development of gastric cancer of between 2.8 and 6.0 among carriers of Helicobacter pylori. In addition, cagA-positive strains of Helicobacter pylori have been found to be associated with gastric cancer and duodenal ulceration. The exact role of Helicobacter pylori in gastric carcinogenesis is still being investigated. Helicobacter pylori eradication programmes to help prevent gastric cancer are being conducted in China and other parts of the world. In high-risk areas such as China, a combination approach that includes Helicobacter pylori eradication and dietary supplementation may be necessary.

Journal Article↗
PubMed1998

The combination of omeprazole, amoxycillin, and clarithromycin eradicates Helicobacter pylori in 95% of patients---7 days of therapy is as good as 10 days.

More than half of the known Helicobacter pylori strains are resistant to metronidazole, according to previous Hong Kong studies. The response rates to treatment regimens that comprise metronidazole as one of the antimicrobial agents have usually been disappointing in cases involving metronidazole-resistant strains. The objective of this open cohort evaluation was to assess the efficacy of an alternative regimen that combines omeprazole with amoxycillin and clarithromycin in Helicobacter pylor-positive ulcer and non-ulcer patients in Hong Kong. Furthermore, we aimed to investigate if 7 days were as good as 10 days of therapy. We studied 186 Helicobacter pylor-positive subjects; 149 subjects received 7 days of combination therapy and 37 subjects received 10 days. Our results showed that the overall Helicobacter pylori eradication efficiency was identical (94.6%) for both treatments. The incidences of adverse effects were also very similar (16.8% versus 16.2%) and both treatments were well tolerated. Thus, we propose that omeprazole in combination with amoxycillin and clarithromycin should be considered as one of the first-line therapies for patients with Helicobacter pylor infection in Hong Kong.

Journal Article↗
PubMed2000

[Antigen detection in stools as a first choice for laboratory diagnosis of Helicobacter pylori disease].

BACKGROUND: Several techniques have been suggested for Helicobacter pylori infection diagnosis, invasive (histology) and not invasive (Urea Breath Test C13, or serological assays). An enzyme immunoassay able to detect Helicobacter pylori antigen directly in stool specimens was recently developed. A study was carried out in order to evaluate the sensibility and the specificity of this test comparing it with the Urea Breath Test C13 and histology. The patients studied are all in pediatric age, and great are the advantages of a non-invasive method to detect infection. METHODS: In this study 60 patients were enrolled. In 34 of them Helicobacter pylori infection was diagnosed by Urea Breath Test C13, all confirmed by histology. In all the 60 patients studied the fecal antigen was researched by an immunoenzymatic method (Premier Platinum HpSA, Meridian Diag.). RESULTS: The detection of Helicobacter pylori in stool shows a sensibility of 100% and a specificity of 97%. CONCLUSIONS: Sensibility and specificity, considering also the low cost of the examination, the short time to perform it and the very easy technique, allows us to propose the test as the first choice in the diagnosis of Helicobacter pylori disease.

English Abstract↗
PubMed1990

[Effect of alcohol and cirrhosis on the presence of Helicobacter pylori in the gastric mucosa].

The aim of this study was to determine whether there was any relationship between alcohol consumption, cirrhosis and Helicobacter pylori associated antral gastritis. One hundred and forty-four patients undergoing upper gastrointestinal endoscopy were prospectively included and classified in four groups. The first group of 23 patients had cirrhosis and an alcohol consumption below 80 g per day. The second group of 31 patients had cirrhosis and an alcohol consumption over 80 g per day. The third group of 34 patients had an alcohol consumption over 80 g per day without cirrhosis. The fourth group of 56 patients had an alcohol consumption below 80 g per day without any preexisting liver disease and underwent upper gastrointestinal endoscopy for non specific digestive symptoms. The diagnosis of Helicobacter pylori was made at histological examination using the hematoxylin and eosin stain and the Whartin-Starry stain in each case. Histopathological results were confirmed by a bacteriological study in 15 cases. One hundred and twelve of 144 patients (78 percent) had gastritis. Gastritis was more frequent (p less than 0.01) when Helicobacter pylori was present than when it was not (90 percent vs 68 percent). Gastritis was more frequent when alcohol consumption was high (86 percent vs 72 percent). Helicobacter pylori was found in 26 percent of the first group, 48 percent of the second group, 65 percent of the third group and 45 percent of the fourth group. These differences were significantly different (p less than 0.05). A statistically significant relationship between high alcohol consumption and the presence of Helicobacter pylori was noted, even in the presence of cirrhosis (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Helicobacter pylori is not associated with the manifestations of gastroesophageal reflux disease.

HYPOTHESIS: Helicobacter pylori is not associated with gastroesophageal reflux disease and its complications, including adenocarcinoma of the esophagus and the gastroesophageal junction (GEJ). DESIGN: Retrospective analysis. SETTING: University tertiary referral center. PATIENTS: Two hundred twenty-nine patients with symptoms suggestive of foregut disease underwent esophageal manometry, 24-hour pH monitoring, and upper gastrointestinal tract endoscopy, with biopsy specimens obtained from the gastric antrum, the GEJ, and the distal esophagus. In these and in an additional 114 patients with adenocarcinoma of the esophagus and the GEJ, the presence of H. pylori was determined by Giemsa stain. The presence of gastroesophageal reflux disease, defined by abnormal esophageal acid exposure, and its manifestations (carditis, erosive esophagitis, intestinal metaplasia limited to the GEJ, Barrett esophagus, and adenocarcinoma of the esophagus and GEJ) were correlated with the presence of H. pylori. RESULTS: Helicobacter pylori was found on the biopsy specimens of the gastric antrum in 14.0% (32/229) of the patients with benign disease. It was not related to the features of gastroesophageal reflux disease, including abnormal esophageal acid exposure, erosive esophagitis, or Barrett esophagus. The presence of inflamed cardiac mucosa at the GEJ or carditis was inversely related to H. pylori infection and strongly associated with increased esophageal acid exposure. There was no association between the presence of intestinal metaplasia and H. pylori infection. Helicobacter pylori was found in 22 (19.3%) of the 114 patients with esophageal adenocarcinoma, which was not different from the prevalence of H. pylori in patients with benign disease. CONCLUSION: Helicobacter pylori plays no role in the pathogenesis of gastroesophageal reflux disease or its complications.

Adolescent↗
PubMed1997

Helicobacter pylori lipopolysaccharide inhibits acid secretion in pylorus-ligated conscious rats.

To examine the effect of Helicobacter pylori lipopolysaccharide on gastric secretion, the present study was carried out using pylorus ligated conscious rats. Intraperitoneal administration of Helicobacter pylori lipopolysaccharide significantly inhibited gastric acid secretion (4 hr) in a dose-dependent manner (0.033-1.0 mg/rat). The Helicobacter pylori lipopolysaccharide (1 mg/rat)-induced acid inhibition was still observed 8 hr after injection. Gastric acid secretion (4 hr) was compared in the rats that had received intraperitoneal administration of 1 mg/rat dose of Helicobacter pylori lipopolysaccharide or saline alone 24 hr before. There was no significant difference in gastric acid secretion between the saline- and H. pylori lipopolysaccharide-treated rats. These results suggest for the first time that H. pylori lipopolysaccharide may inhibit acid production, and this acid inhibition may be long-lasting. It is also demonstrated that this anti-secretory action of H. pylori lipopolysaccharide has a reversible effect on gastric secretion. All these results suggest that H. pylori lipopolysaccharide might be involved in the low acid secretory function seen in patients with acute H. pylori infection.

Animals↗