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PubMed1994

[High incidence of Helicobacter pylori infections in an endoscopic pediatric patient series].

We evaluated in children with abdominal complaints the prevalence of Helicobacter pylori gastric and duodenal colonization and the histological features of gastric and duodenal mucosae. Fifty patients, aged 1-17 years, underwent upper endoscopy for recurrent abdominal pain, vomiting and/or gastrointestinal bleeding. With serological, bacteriological and/or histological methods twenty-eight children were demonstrated to be Helicobacter pylori-positive. No statistically significant differences were observed with regard to age, sex and indication to perform endoscopy. Eighty-two percent of Helicobacter pylori-positive patients had gastritis and/or duodenitis. The Helicobacter pylori-positive children had higher Helicobacter pylori specific IgG levels than the Helicobacter pylori-negative ones (p < 0.001). No statistically significant differences were found between Helicobacter pylori-positive and Helicobacter pylori-negative subjects, for gastrin and pepsinogen I. Since the frequency of Helicobacter pylori infection in children with gastrointestinal complaints is high, in patients undergoing upper endoscopy, the sistematical examination of bioptic samples for bacteriological and histologic procedures is of great importance.

Abdominal Pain↗
PubMed1996

Helicobacter pylori, gastritis and non-ulcer dyspepsia in Ethiopian patients.

The aim of this study is to find out the prevalence of Helicobacter pylori infection in patients with nonulcer dyspepsia (NUD) and asymptomatic controls and to see if there is an etiological association between gastritis, NUD and Helicobacter pylori. One hundred thirty six patients with NUD and 71 controls had six endoscopic biopsies from different sites of the gastric mucosa for histological diagnosis. Helicobacter pylori was looked for in all biopsy specimens utilizing half Gram, Giemsa and Gimenez staining techniques. Type B chronic gastritis was detected in 96% of the NUD cases and in 100% of the asymptomatic controls (P > 0.05). Helicobacter pylori was found in 82 (65%) patients with NUD and in 38 (56%) asymptomatic controls (P > 0.05). Type B chronic gastritis is almost universal in both NUD cases and asymptomatic controls. There is no difference in the prevalence of Helicobacter pylori infection between the two groups. The absence of Helicobacter pylori in a significant number of patients (36%) and controls (45%) with gastritis contradicts the etiological association between Helicobacter pylori and gastritis reported by others, suggesting that in Ethiopia there may be a chronic environmental gastritis which may not be helicobacter-related. There is no correlation between NUD and Type B gastritis, and between symptoms and Helicobacter pylori infection in this population.

Adolescent↗
PubMedDate not supplied

Cirrhosis negatively affects the efficiency of serologic diagnosis of Helicobacter pylori infection.

In cirrhosis, Helicobacter pylori infection may be implicated, together with portal hypertension, bile reflux and alcohol abuse, in damage to gastric mucosa. Aim of this study was to define the influence of non-alcoholic liver disease on the incidence of Helicobacter pylori infection and on the diagnostic accuracy of specific serology. Enrolled in the study were 232 individuals, 105 also had cirrhosis. Infection by Helicobacter pylori, diagnosed by a positive concordance of quick urease test and histology, was detected in 97 (48 with cirrhosis) out of 184 patients. Severe gastritis was more frequent in patients with Helicobacter pylori infection than in patients without. Cirrhosis did not significantly affect the prevalence of Helicobacter pylori infection or the histological features of gastritis. Specific anti-Helicobacter pylori IgG and IgA assay (Bio-Rad GAP test) was used for serological diagnosis. Anti-Helicobacter pylori IgG showed a high sensitivity (85% in cirrhotics, 89% in non-cirrhotics) and low specificity being more evident in cirrhotics (38% vs 56% non-cirrhotics). Serum specific IgA showed low sensitivity (approximately 25% in both groups) and specificity of 79% in cirrhotics vs 84% in non-cirrhotics. In conclusion, non-alcoholic cirrhosis does not affect the incidence of Helicobacter pylori infection and the histological features of chronic gastritis but does decrease diagnostic efficiency of serological tests for Helicobacter pylori.

Antibodies, Bacterial↗
PubMedDate not supplied

Current treatment of Helicobacter pylori infection and peptic ulcer disease.

Since the initial report by Warren and Marshall in 1984, Helicobacter pylori has assumed an increasingly important role in the pathogenesis of peptic ulcer disease and gastric carcinoma in all ages. A recent National Institutes of Health Consensus Development conference acknowledges the relationship between H. pylori infection and peptic ulcer disease and recommends that the medical community treat H. pylori infection in all patients with Helicobacter pylori and peptic ulcer. Although the same organism, the response to Helicobacter pylori infection in childhood differs somewhat from that seen in adults. The paediatric patient mounts a different inflammatory response, has different macroscopic appearances and has a markedly diminished peptic ulcer disease frequency compared with their adult counterparts. The appearances of antral nodularity appear to be characteristic of Helicobacter pylori infections. The appearances, however, are unrelated to symptoms and the underlying cause for this nodularity remains obscure. Younger children with peptic ulcer diseases are more likely to be Helicobacter pylori negative. This may suggest an increased susceptibility to gastric acid or possibly a very transient Helicobacter pylori infection rather than the well described lifelong infection without treatment. It is well known that the epidemiology of Helicobacter pylori would suggest that the incidence of infection increases with age. There is also geographical variations with the incidence being higher in countries of a third world background. These epidemiological observations fly in the face of all other infections where the major period of acquisition is in childhood. There has been recent evidence to suggest that in fact the incidence in childhood is decreasing in developed countries which could support the observation that there is a decreasing positive serology with successive decades in some countries. It is felt that the most likely mode of transmission to Helicobacter pylori is faecal to oral or oral to oral route. These are similar modes of transmission to Hepatitis A infections. It is obvious that most infections in childhood remain asymptomatic. It is also clear that there is no relationship between chronic recurrent abdominal pain of childhood syndrome and the presence of Helicobacter pylori infections. It remains to be seen as to who should be treated, what with and when. All of these issues will be discussed in the paper.

Child↗
PubMed1997

The role of Helicobacter species in newly recognized gastrointestinal tract diseases of animals.

Because Helicobacter pylori is now known to be a significant human pathogen, experimental animal models are increasingly being used to study the pathogenesis of this organism. Unfortunately, early studies failed to establish H. pylori in animal models, and surprisingly, Koch's postulates were initially fulfilled in two human volunteers. Germfree experiments performed in pigs and pups however established that H. pylori would colonize in these animals, and gastritis was induced. Certain macaque species and cats are now known to be naturally infected with H. pylori, and these animals are susceptible to experimentally induced infection with the organism as well. Interestingly, as the ability to manipulate and grow H. pylori in vitro increased, so did the ability to colonize it in animal models. Helicobacter pylori has now experimentally induced gastritis in germfree euthymic and nude mice and in conventionally housed mice. Six additional Helicobacter species have been isolated and identified from the stomachs of various mammals, including dogs, cats, ferrets, pigs, monkeys, and cheetahs; these organisms, similar to H. pylori, are associated with variable degrees of gastritis in their hosts. In addition to the discovery of gastric helicobacters, an increasing number of Helicobacter spp. have been isolated from the distal part of the gastrointestinal tracts of mammals and birds. Importantly, in one inbred strain of mice, A/JCr, persistent infection with H. hepaticus is linked to development of hepatic adenomas and adenocarcinomas. To date, the genus Helicobacter includes 17 named species as well as other formally unnamed closely related organisms. An overview of gastric helicobacters and naturally acquired Helicobacter spp.-induced disease in laboratory animals and, where appropriate, use of animal models to study H. pylori-associated gastric disease is presented. Similarities between Helicobacter infections and the epidemiology of the diseases induced by these bacteria in humans and animals also are highlighted.

Animals↗
PubMed1997

Helicobacter pylori eradication in the healing and recurrence of benign gastric ulcer: a two-year, double-blind, placebo controlled study.

BACKGROUND: Helicobacter pylori infection is associated with idiopathic gastric ulcer in about 90% of the cases, but only a few controlled studies aimed at evaluating gastric ulcer healing and the natural history after Helicobacter pylori-eradication have been carried out. OBJECTIVE: The aim of the present study was to evaluate the efficacy of omeprazole coupled with amoxicillin in the eradication of Helicobacter pylori and healing and prevention of gastric ulcer recurrence. PATIENTS: Fifty-nine patients with active gastric ulcer were randomized under double-blind conditions to receive either omeprazole 20 mg twice daily for four weeks plus amoxicillin 3 g daily during the first and second week (29 patients, Group A) or omeprazole .20 mg twice daily for 4 weeks plus placebo for two weeks (30 patients, Group B). METHODS: Endoscopic studies were carried out at the end of the 4 weeks treatment (or after 8 weeks in non-healed patients) as well as 2, 6 and 12 months later. A total of 3 biopsies in the antrum, 3 in the gastric body and at least seven at the edge of the crater were taken at each endoscopic control for exclusion, of malignancy, histological detection of Helicobacter pylori and for evaluation of gastric histology according to the Sydney system. RESULTS: With intention to treat analysis, the percentage of healing after 4 and 8 weeks was 86% and 100% in Group A patients and 86% and 93% in Group B, respectively. Two patients dropped out in Group B for non medical reasons. The percentage of eradication was 63% in Group A and 7% in Group B. During a 12-month follow-up gastric ulcer relapsed in 20/32 (63%) of the persistently Helicobacter pylori positive patients. Only two out 20 (10%) Helicobacter pylori cured patients showed a gastric ulcer relapse and Helicobacter pylori reinfection. Twenty out of 30 patients, still healed after 12 months, underwent endoscopic control after two years. A gastric ulcer relapse was observed in three out of nine (33%) patients with persisting infection after treatment. No gastric lesions, but one case of erosive oesophagitis were observed in the 11 Helicobacter pylori-eradicated patients. CONCLUSIONS: In our experience, Helicobacter pylori eradication does not favour gastric ulcer healing but does positively influence the subsequent natural history.

Amoxicillin↗
PubMed1998

Differential pathogenic effect of two Helicobacter-like organisms in dog gastric mucosa.

Two forms of Helicobacter were detected in the gastric mucosa of twelve healthy beagle dogs. According to ultrastructural criteria they could be classified as Helicobacter bizzozeronii-like and Helicobacter felis-like species. In five animals, the light fundic load of Helicobacter bizzozeronii-like did not affect the integrity of the glandular epithelium. In three animals, the heavy bacterial load extended in the lumens of antral glands and coincided with increased intraepithelial lymphoid infiltrate. The heavy bacterial load observed in 4 animals was mixed (Helicobacter bizzozeronii-like and Helicobacter felis-like), fundic and antral, luminal and intracellular. Adherence of Helicobacter felis-like to epithelial cells and intracellular penetration were responsible for focal necrosis, and glandular atrophy might be observed. Helicobacter bizzozeronii-like thus appeared non pathogenic in beagle dogs, even when the heavy bacterial load extended to the antrum. By contrast, Helicobacter felis-like showed a constant pathogenic effect linked to its properties of adhesion and penetration into epithelial cells. A wider comparative study in humans and domestic carnivorous will determine if the latter may play a role of reservoir-host for pathogenic bacteria.

Animals↗
PubMed1998

Autoantibodies reacting with gastric antigens in Helicobacter pylori associated body gastritis of dyspeptic children.

BACKGROUND: Helicobacter pylori induced antibodies reacting with fundal mucosa have been shown to be involved in the pathogenesis of chronic atrophic gastritis in adults. Furthermore, previous reports have indicated that Helicobacter pylori increases the risk of gastric carcinoma, suggesting that the bacterium plays a role in mucosal changes representing especially in adulthood important steps in the progression from gastritis to cancer. PATIENTS AND METHODS: We investigated 16 Helicobacter pylori+ children from a series of 53 dyspeptic patients. Diagnosis of Helicobacter pylori infection was based on the positivity of at least 3 of the following tests: serology, 13C-urea breath test, rapid urease test and histology. Autoreaction was detected by incubation of gastric body sections with autologous sera and revealed by immunohistochemistry. Positive sera were tested with samples of unaffected gastric body to exclude a link with residual bacterial antigens. Proliferating cell nuclear antigen immunohistostain was also performed to evaluate the epithelial proliferative state. RESULTS: Histologically 6 out of 16 Helicobacter pylori+ patients showed chronic pangastritis. In the remaining 10 Helicobacter pylori-related mucosal inflammation was confined to the antrum. All 6 subjects with pangastritis and 3 out of 10 with antral gastritis were anti-CagA+. The autoreaction was found in a 10-year old male child with Helicobacter pylori+ pangastritis and a clinical history of ulcer-like dyspepsia. Parietal cells, in particular, were involved and showed diffuse cytoplasm staining. Proliferating cell nuclear antigen expression demonstrated, only in this case, a zone of regeneration extending from the normal site in the neck towards the base of the glands. CONCLUSIONS: Our finding demonstrates that an autoreaction of gastric mucosa may be found in Helicobacter pylori gastritis of childhood. Its association with some known risk factors (i.e., cytotoxic strains and increased proliferation of gastric epithelium with a changed pattern) may play a role in the progression from gastritis to atrophy and account for the increased risk of late gastric cancer when Helicobacter pylori infection occurs in paediatric age.

Adolescent↗
PubMed1998

Hepatic Helicobacter species identified in bile and gallbladder tissue from Chileans with chronic cholecystitis.

BACKGROUND & AIMS: Cancer of the gallbladder is the number one cause of cancer mortality in Chilean women. Incidence rates for this tumor vary widely on a worldwide basis, being approximately 30 times higher in high-risk than in low-risk populations, suggesting that environmental factors such as infectious microorganisms, carcinogens, and nutrition play a role in its pathogenesis. Because several Helicobacter sp. colonize the livers of animals and induce hepatitis, the aim of this study was to determine whether Helicobacter infection was associated with cholecystitis in humans. METHODS: Bile or resected gallbladder tissue from 46 Chileans with chronic cholecystitis undergoing cholecystectomy were cultured for Helicobacter sp. and subjected to polymerase chain reaction (PCR) analysis using Helicobacter-specific 16S ribosomal RNA primers. RESULTS: Recovery of Helicobacter sp. from frozen specimens was unsuccessful. However, by PCR analysis, 13 of 23 bile samples and 9 of 23 gallbladder tissues were positive for Helicobacter. Eight of the Helicobacter-specific PCR amplicons were sequenced and subjected to phylogenetic analysis. Five sequences represented strains of H. bilis, two strains of "Flexispira rappini" (ATCC 49317), and one strain of H. pullorum. CONCLUSIONS: These data support an association of bile-resistant Helicobacter sp. with gallbladder disease. Further studies are needed to ascertain whether similar Helicobacter sp. play a causative role in the development of gallbladder cancer.

Adult↗
PubMed2003

Cytolethal distending toxin B gene (cdtB) homologues in taxa 2, 3 and 8 and in six canine isolates of Helicobacter sp. flexispira.

The presence of the cytolethal distending toxin B gene (cdtB) was examined in eight Helicobacter sp. flexispira reference strains, Helicobacter trogontum ATCC 700114(T) and 12 Finnish porcine H. trogontum strains and canine flexispira isolates. Part of the cdtB gene was amplified by PCR with degenerate primers VAT2 and DHF1, cloned and sequenced. The presence/absence of the cdtB gene as determined by PCR was confirmed by Southern hybridization and toxin production by HeLa cell-line experiments. PCR amplification resulted in approximately 700 bp fragments from Helicobacter sp. flexispira taxa 2 (ATCC 49314), 3 (ATCC 49320) and 8 (ATCC 43880, ATCC 49308, ATCC 43879), from six canine isolates as well as from the control strains Helicobacter bilis and Helicobacter hepaticus. The hybridization patterns of HaeIII-, HindIII- and AseI-digested chromosomal DNA confirmed the results of the PCR experiments. The cdtB-positive strains had effects ranging from weak to strong on HeLa cell cultures. PCR amplification from the reference strains Helicobacter sp. flexispira taxa 1 (ATCC 43968), 4 (ATCC 49310) and 5 (ATCC 43966) and H. trogontum (ATCC 700114(T)), and also six of the Finnish strains, was unsuccessful. No toxic effect on HeLa cells was evident when bacterial suspensions of PCR-negative strains were used for toxicity assay. Our results are in accordance with previous observations that the cdtB gene is not present in all Helicobacter species. Further, the presence/absence of the cdtB gene in Helicobacter sp. flexispira strains was in accordance with recent taxonomic analysis of the same strains, which suggests that it could serve as a useful marker in Helicobacter taxonomy.

Amino Acid Sequence↗
PubMed2006

CD4+ CD25+ regulatory T cells modulate the T-cell and antibody responses in helicobacter-infected BALB/c mice.

Gastric Helicobacter spp. induce chronic gastritis that may lead to ulceration and dysplasia. The host elicits a T helper 1 (Th1) response that is fundamental to the pathogenesis of these bacteria. We analyzed immune responses in Helicobacter-infected, normal mice depleted of CD4+ CD25+ T cells to investigate the in vivo role of regulatory T cells (Tregs) in the modulation of Helicobacter immunopathology. BALB/c and transgenic mice were depleted of CD4+ CD25+ T cells by administration of an anti-CD25 antibody either at the time of infection with Helicobacter or during chronic infection and gastritis. Depletion of CD25+ Tregs prior to and during infection of mice with Helicobacter spp. did not affect either bacterial colonization or severity of gastritis. Depletion of CD25+ Tregs was associated with increased Helicobacter-specific antibody levels and an altered isotype distribution. Paragastric lymph node cells from CD25+ Treg-depleted and control infected mice showed similar proliferation to Helicobacter antigens, but only cells from anti-CD25-treated animals secreted Th2 cytokines. CD25+ Tregs do not control the level of gastritis induced by gastric Helicobacter spp. in normal, thymus-intact BALB/c mice. However, CD25+ Tregs influence the cytokine and antibody responses induced by infection. Autoimmune gastritis is not induced in Helicobacter-infected mice depleted of CD25+ Tregs but is induced in CD25+ Treg-depleted mice, which have a higher frequency of autoreactive T cells.

Animals↗
PubMed1999

Healthy cats are commonly colonized with "Helicobacter heilmannii" that is associated with minimal gastritis.

Gastric Helicobacter infection in healthy pet cats is not well characterized. We performed endoscopy with gastric biopsy on 15 healthy pet cats that were rigorously screened to exclude underlying or concurrent diseases that might affect Helicobacter colonization. Gastric mucosa biopsy specimens were examined by histology, culture, and PCR for the presence of Helicobacter infection and by histology for the presence of gastritis. Of 15 cats, all but 1 had gastric Helicobacter-like organisms (GHLOs) on examination by light microscopy, and in the one histologically negative cat, GHLOs were detected by PCR. Gastric inflammation was mild or was absent for all cats. No Helicobacter species were identified by culture. Analysis of the 16S rRNA sequence from Helicobacter strains from 10 cats showed that all bacteria were closely related to Helicobacter felis, although there was heterogeneity among the sequences. These results suggest that the gastric mucosa of healthy pet cats is commonly colonized with an uncultivated Helicobacter that is closely related to H. felis, is associated with little or no gastritis, and shows heterogeneity in its 16S rRNA sequence. The epithet "Helicobacter heilmannii" continues to be an appropriate working designation for these bacteria.

Animals↗
PubMed1994

[Non ulcerative dyspepsia: relationship of symptomatology, gastritis and Helicobacter pylori].

BACKGROUND: histological alterations of gastric mucosa and its colonization by Helicobacter pylori are postuled to be implicated in the pathogenesis of non ulcer dyspepsia. AIM: to study the possible relationships between histological gastritis and Helicobacter pylori in non ulcer dyspepsia symptomatology. PATIENTS AND METHODS: fifty four patients (39 females) with non ulcer dyspepsia whose ages ranged from 17 to 68 years were subjected to an upper GI endoscopy with gastric mucosa biopsy samples for histological study and microbiological identification of Helicobacter pylori. Gastrointestinal complains were blindly quantified using a scored questionnaire. RESULTS: thirty one subjects (57.4%) had Helicobacter pylori in their gastric mucosa. There was acute inflammatory activity in 26 of the 31 patients with Helicobacter pylori (81%) and 15 of 23 without Helicobacter (65%). The median score of symptoms was 7 (range 2-13) in patients with Helicobacter and 6 (range 2-10) in patients without Helicobacter. CONCLUSIONS: there were no significant differences in gastric mucosa acute inflammatory activity and non ulcer dyspepsia symptomatology between patients with or without Helicobacter pylori colonization of gastric mucosa.

Adolescent↗
PubMed2003

Helicobacter DNA in bile: correlation with hepato-biliary diseases.

BACKGROUND: Helicobacter has been identified in isolated cases of hepato-biliary diseases, but its role in the pathogenesis of these conditions remains unclear. AIM: To determine whether Helicobacter could be detected in bile obtained at endoscopic retrograde cholangiopancreatography, and to evaluate the prevalence of this infection in patients with hepato-biliary diseases. METHODS: Bile was collected from 125 patients with various hepato-biliary diseases undergoing endoscopic retrograde cholangiopancreatography. Among them, 75 were diagnosed with biliary stones, 15 with pancreatico-biliary malignancies and four with primary sclerosing cholangitis. The detection of Helicobacter in DNA extracted from these bile samples was performed using Helicobacter genus-specific primers (capable of detecting 100-1000 organisms/mL). RESULTS: Helicobacter was detected in all positive controls. Only three samples had polymerase chain reaction inhibitors. All remaining bile samples (122 patients with hepato-biliary diseases) were negative for Helicobacter DNA. CONCLUSIONS: Helicobacter can be detected in bile samples using polymerase chain reaction. This infection, however, was not present in any of our patients diagnosed with gallstones or hepato-biliary malignancies, raising doubt as to the possible association between Helicobacter and these entities. Given the low sample size of patients with primary sclerosing cholangitis, more studies are required to determine whether an association exists with this condition.

Adolescent↗
PubMed2005

Molecular identification of Helicobacter DNA present in human colorectal adenocarcinomas by 16S rDNA PCR amplification and pyrosequencing analysis.

Seroepidemiological studies have indicated that Helicobacter pylori infection might be a possible risk factor for colorectal adenocarcinoma (CRC) development. However, limited information is available as to whether or not Helicobacter species are present in CRC tissues. In this study the presence of Helicobacter DNA in 77 CRC biopsies was investigated by means of a Helicobacter species-specific 16S rDNA PCR assay and real-time DNA pyrosequencing of the 16S rDNA variable V3 region. Pyrosequencing revealed the presence of Helicobacter DNA sequences in 21 of 77 biopsy specimens (27%). 16S rDNA sequences corresponding to H. pylori 26695 and H. pylori J99 were most commonly found. Intriguingly, one sequence belonged to Helicobacter mustelae, previously identified in ferrets. No significant correlations were found in the prevalence of Helicobacter DNA between colon and rectum tumour biopsies (P = 0.815), nor between Dukes' classes A/B and C/D (P = 0.262). 16S rDNA PCR amplification combined with pyrosequencing analysis of 16S rDNA variable V3 regions provides a powerful molecular tool to identify Helicobacter species in human biopsy specimens.

Aged↗
PubMed2005

Association of Helicobacter species with hepatitis C cirrhosis with or without hepatocellular carcinoma.

BACKGROUND AND AIMS: Recent studies have suggested that bacterial coinfection with Helicobacter species in patients already infected with hepatitis C virus (HCV) could be involved in the development of cirrhosis and hepatocellular carcinoma (HCC). A retrospective cross sectional study was performed in order to explore the association between Helicobacter species and HCV associated liver diseases. METHODS: The presence of Helicobacter species was tested by polymerase chain reaction on liver samples from four groups of patients. RESULTS: Helicobacter 16S rDNA was found in only 4.2% of liver samples from control patients (n=24) and in 3.5% of liver samples from patients with non-cirrhotic chronic hepatitis C (n=29) while it was found in 68.0% of liver samples from patients with HCV positive cirrhosis without HCC (n=25) as well as in 61.3% of cirrhotic liver samples from patients with HCV positive cirrhosis and HCC (n=31). In addition, when the HCC tumour tissue was tested (n=21), 90.5% of samples were positive. DNA from Helicobacter pylori- and Helicobacter pullorum-like organisms was found. CONCLUSIONS: There is an association between the presence of Helicobacter species DNA in the liver and hepatitis C cirrhosis, with or without HCC. Indeed, the presence of these bacteria could be the result of structural changes in the liver. Alternatively, Helicobacter species could be a co-risk factor in HCV chronic liver diseases. This result warrants prospective studies to determine the possible causal role of these bacteria in the progression of chronic hepatitis C.

Adult↗
PubMed1997

The expanding genus of Helicobacter: pathogenic and zoonotic potential.

The microbial flora of stomachs of humans and animals have been the focus of considerable research since the discovery that Helicobacter pylori in humans caused a variety of gastric diseases. Other Helicobacter species have now been isolated from the stomachs of various mammals, including dogs, cats, ferrets, pigs, monkeys, and cheetahs, all of which are associated with various degrees of gastritis in their hosts. Helicobacter species have also been isolated from the intestinal tracts of humans, animals, and birds. Helicobacter species have not only been isolated from intestines of mice but have, in addition, been isolated from diseased livers of inbred and outbred mice, and one of these, H hepaticus is linked to liver tumors. H canis and H pullorum isolated from dogs and chickens, respectively, have also been cultured from feces of diarrheic humans. H fennelliae and H cinaedi are two additional helicobacters primarily associated with lower bowel disease in immunocompromised humans. To date, there are at least 13 formally named species of the new genus, Helicobacter, the majority being proven or suspected gastrointestinal or hepatic pathogens. Several of these helicobacters have zoonotic potential as well. It is predicted that additional Helicobacter species will be identified, and they, too, may be important pathogens in humans and animals.

Acinonyx↗
PubMed1991

Helicobacter pylori and gastric acid output in peptic ulcer disease.

Helicobacter pylori is associated with peptic ulcer, and a causal relationship has been postulated. We investigated the association between Helicobacter pylori and gastric acid output. Two hundred forty-one patients were studied: 173 with duodenal ulcer, 51 with gastric ulcer (41 corpus, 10 prepyloric), and 17 with combined gastric and duodenal ulcer. In 194 patients (80%), Helicobacter pylori could be demonstrated histologically from gastric antral biopsies. The presence or absence of Helicobacter pylori was not influenced by age, sex, or use of tobacco or analgesics. Patients with duodenal ulcer or combined gastric and duodenal ulcer had similar gastric acid outputs irrespective of the presence or absence of Helicobacter pylori. However, gastric ulcer patients with Helicobacter had higher basal and maximal acid outputs when compared to patients without Helicobacter (mean basal output: 4.1 mmol/hr vs 2.4, P less than 0.05; mean maximal output 19.5 mmol/hr vs. 14.4, P less than 0.05). Although Helicobacter pylori is associated with both gastric ulcer and duodenal ulcer, its significance may be different in the two diseases.

Duodenal Ulcer↗