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At least 19 recordsLinked to original sources

PubMed1997

Helicobacter salomonis sp. nov., a canine gastric Helicobacter sp. related to Helicobacter felis and Helicobacter bizzozeronii.

During a study of the prevalence and distribution of gastric helicobacters in domestic pets, a novel group of Helicobacter-like organisms were identified. These "Helicobacter group 2" strains were initially distinguished from the species Helicobacter felis and Helicobacter bizzozeronii by their cellular morphology and the type of motility exhibited. Bacterial cells were only slightly spiral, 5 to 7 microns long, and 0.8 to 1.2 microns wide and showed an unusual slow wavelike motion. Each cell had tufts of sheathed flagella at one or both ends. Phylogenetic analysis by 16S ribosomal DNA sequence comparison revealed that H. felis, H. bizzozeronii, "Gastrospirillum hominis" 2, and the new group of helicobacters formed a distinct cluster with intraspecies similarity values of more than 98%. These taxa were clearly separated from all other known Helicobacter species. Dot blot DNA-DNA hybridization studies indicated that the Helicobacter group 2 strains are genetically homogeneous and distinct from other canine and feline gastric helicobacters. Quantitative DNA-DNA hybridization experiments showed that Helicobacter group 2 strains exhibit > 90% DNA homology to each other, but < 39% homology to the phylogenetically related taxa H. felis and H. bizzozeronii. We propose the name Helicobacter salomonis for the novel Helicobacter group 2 strains. The type strain is H. salomonis Inkinen (= CCUG 37845).

Animals↗

PubMed1995

Comparative ultrastructural and functional studies of Helicobacter pylori and Helicobacter mustelae flagellin mutants: both flagellin subunits, FlaA and FlaB, are necessary for full motility in Helicobacter species.

Helicobacter mustelae causes chronic gastritis and ulcer disease in ferrets. It is therefore considered an important animal model of human Helicobacter pylori infection. High motility even in a viscous environment is one of the common virulence determinants of Helicobacter species. Their sheathed flagella contain a complex filament that is composed of two distinctly different flagellin subunits, FlaA and FlaB, that are coexpressed in different amounts. Here, we report the cloning and sequence determination of the flaA gene of H. mustelae NCTC12032 from a PCR amplification product. The FlaA protein has a calculated molecular mass of 53 kDa and is 73% homologous to the H. pylori FlaA subunit. Isogenic flaA and flaB mutants of H. mustelae F1 were constructed by means of reverse genetics. A method was established to generate double mutants (flaA flaB) of H. mustelae F1 as well as H. pylori N6. Genotypes, motility properties, and morphologies of the H. mustelae flagellin mutants were determined and compared with those of the H. pylori flaA and flaB mutants described previously. The flagellar organizations of the two Helicobacter species proved to be highly similar. When the flaB genes were disrupted, motility decreased by 30 to 40%. flaA mutants retained weak motility by comparison with strains that were devoid of both flagellin subunits. Weakly positive motility tests of the flaA mutants correlated with the existence of short truncated flagella. In H. mustelae, lateral as well as polar flagella were present in the truncated form. flaA flaB double mutants were completely nonmotile and lacked any form of flagella. These results show that the presence of both flagellin subunits is necessary for complete motility of Helicobacter species. The importance of this flagellar organization for the ability of the bacteria to colonize the gastric mucosa and to persist in the gastric mucus remains to be proven.

Amino Acid Sequence↗

PubMed1994

Phylogeny of Helicobacter isolates from bird and swine feces and description of Helicobacter pametensis sp. nov.

Previously, nine fecal isolates from wild birds and a domestic swine were identified as helicobacters by phenotypic characterization and reaction with a helicobacter genus-specific DNA probe. These isolates fell into three biotypes by analysis of phenotypic traits. To further characterize these isolates, full 16S rRNA sequences were determined for strains representing each biotype, and sequence comparison indicated that the strains represented three novel, phylogenetically defined Helicobacter species. Three 16S rRNA-based DNA probes were designed and used to identify the remaining strains. Probe reactivity divided the strains into the same three groups identified phenotypically. Six of the isolates represented a new species of the genus Helicobacter for which we propose the name Helicobacter pametensis sp. nov. The following phenotypic features distinguished H. pametensis from other Helicobacter and Campylobacter species: positive tests for oxidase, catalase, alkaline phosphatase, nitrate reduction, growth at 42 degrees C, and growth in the presence of 1% glycine; negative tests for urease, gamma glutamyl transpeptidase, indoxyl acetate hydrolysis, and hippurate hydrolysis; and susceptibility to nalidixic acid and cephalothin. H. pametensis cells were motile and possessed one subterminal sheathed flagellum at each end. The two additional Helicobacter species were similar to H. pametensis except that they were urease positive, hydrolyzed indoxyl acetate, and were resistant to cephalothin. Because these two additional species are phenotypically similar and are represented by only two isolates for one species and one isolate for the other, they are not formally named but are referred to as Helicobacter sp. "Bird-B" and Helicobacter sp. "Bird-C."(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

Conservation and diversity of the Helicobacter pylori copper-transporting ATPase gene (copA) sequence among Helicobacter species and Campylobacter species detected by PCR and RFLP.

BACKGROUND: Helicobacter pylori is a causative pathogen of such human stomach diseases as chronic type B gastritis, ulcer, and possibly gastric carcinoma. As a cofactor in various redox enzymes and an essential trace metal required for the synthesis of metalloproteins, copper might play a role in the pathogenesis of H. pylori. A gene, copA, associated with copper transport, has been isolated from H. pylori UA802. In this study, conservation and diversity of this gene were analyzed among some Helicobacter and Campylobacter species. MATERIALS AND METHODS: Twenty-one clinical isolates and strains of helicobacters and campylobacters were used in this study. Methods including polymerase chain reaction (PCR) amplification, restriction fragment-length polymorphisms (RFLPs), and hybridization were employed to carry out this work. RESULTS: The copA gene was highly conserved in all the H. pylori isolates tested (Helicobacter nemestrinae and Helicobacter felis but not in Helicobacter mustelae and the Campylobacter species), whereas the sequence downstream of the copA appears to diverge among H. pylori isolates. In addition, two restriction patterns of the PCR-amplified copA fragments from seven H. pylori isolates and H. nemestrinae were identified, and the RFLP of H. nemestrinae was identical to that of one of the H. pylori isolate group. CONCLUSIONS: The adenosine triposphatase-derived copper-transporting mechanism is employed by various H. pylori strains, H. nemestrinae, H. felis, and perhaps by other Helicobacter species. The nucleotide mutations have risen in the copA gene. It appears that there is a genetic relatedness of the copA gene to H. pylori and H. nemestrinae.

Adenosine Triphosphatases↗

PubMed1998

Gastrin release and gastric acid secretion in the rat infected with either Helicobacter felis or Helicobacter heilmannii.

Helicobacter pylori infection in humans has been shown to be associated with changes in gastric physiology, including exaggerated basal and meal-stimulated gastrin levels. This has been suggested to be due to the direct effects of the bacterium through inflammation and its urease enzyme. The gastric bacteria Helicobacter felis and Helicobacter heilmannii colonize the antrum of rats in large numbers and induce no significant inflammatory response. Thus, the direct effect of Helicobacter infection on gastric physiology, independent of gastritis, could be studied. Basal, freely fed and stimulated acid and gastrin levels were recorded from animals infected with H. felis, H. heilmannii or uninfected controls over a 30 week period. No significant difference was found between freely fed gastrin over 7 weeks or fasting gastrin over 24 weeks or basal and stimulated acid over 30 weeks between all three groups. Triple therapy did not alter gastrin or acid output. The antrum of all Helicobacter-infected rats was well colonized; triple therapy cleared H. felis but not H. heilmannii. Very little inflammation was seen in control or Helicobacter-infected animals. In conclusion, Helicobacter-induced effects on gastric physiology are unlikely to be due to direct bacterial effects, but are best explained by other factors (i.e. inflammatory damage).

Animals↗

PubMed1995

Comparison of Helicobacter mustelae and Helicobacter pylori adhesion to eukaryotic cells in vitro.

BACKGROUND & AIMS: Bacterial adhesion to mucosal surfaces is an important pathogenic mechanism for Helicobacter-induced gastritis. The aims of this study were to compare binding of selected Helicobacter mustelae and Helicobacter pylori strains to lipids extracted from HEp-2, Chinese hamster ovary, human embryonic lung cells, and ferret gastrointestinal tissues as well as to intact tissue culture cells and to analyze the fatty acids of the receptor. METHODS: Thin-layer chromatography overlay binding and a receptor-based immunoassay detected adhesion of bacteria to commercial lipids and to individual species within the lipid extracts. H. mustelae binding to tissue culture cells was performed by whole cell bacterial adhesion assay. RESULTS: H. mustelae and H. pylori both bound to phosphatidylethanolamine and lysophosphatidylethanolamine. Adhesion of H. mustelae to intact eukaryotic cells correlated with the amount of phosphatidylethanolamine. Binding of helicobacters was greater to lipids derived from ferret antrum compared with colon (P < 0.05). Biochemical analysis suggested that heterogeneity in fatty acid composition of phosphatidylethanolamine could influence the degree of Helicobacter binding. CONCLUSIONS: Adhesion of Helicobacter strains correlates with the quantity of phosphatidylethanolamine present in the epithelial cell and with the differences in the fatty acid profile of the lipid.

Animals↗

PubMed1996

Culture and characteristics of Helicobacter bizzozeronii, a new canine gastric Helicobacter sp.

Organisms whose cells were large, tight spirals were isolated from gastric biopsies of dogs. Touch cytology samples from all of the dogs contained large spiral organisms. Characteristics of 10 strains are described. These organisms were 5 to 10 microns long by 0.3 microns wide, and each cell had 10 to 20 sheathed flagella at both ends of the cell. The cells did not have periplasmic fibrils. These organisms were microaerophilic and grew at 37 and 42 degrees C but not at 25 degrees C on brain heart infusion agar containing blood. They did not grow on brucella blood agar. They were catalase and oxidase positive, hydrolyzed urea but not hippurate, reduced nitrate, and were resistant to nalidixic acid but susceptible to cephalothin and metronidazole. In contrast to Helicobacter felis, they hydrolyzed indoxyl acetate. The sodium dodecyl sulfate-polyacrylamide gel electrophoresis protein profiles of all of the strains were similar, and the protein patterns of these organisms differed from those of other Helicobacter spp. Dot blot DNA-DNA hybridization experiments revealed that the new strains were closely related to each other but clearly different from H. felis, Helicobacter pylori, Helicobacter mustelae, and Campylobacter jejuni. The name Helicobacter bizzozeronii sp. nov. is proposed for these organisms. Our results suggest that other "uncultured" gastric helicobacters may be cultured if optimal culture conditions are found.

Animals↗

PubMed1997

Helicobacter rodentium sp. nov., a urease-negative Helicobacter species isolated from laboratory mice.

A spiral-shaped bacterium with bipolar, single, nonsheathed flagella was isolated from the intestines of laboratory mice. The organism grew at 37 and 42 degrees C under microaerobic and anaerobic conditions, did not hydrolyze urea, was weakly positive for catalase and oxidase, reduced nitrate to nitrite, did not hydrolyze indoxyl acetate or hippurate, and was resistant to cephalothin and nalidixic acid. This is the first urease-negative, murine Helicobacter spp. isolated from intestines. Also, Helicobacter pullorum and this bacterium are unique among the genus Helicobacter in having nonsheathed flagella. The new bacterium appears to be part of the normal intestinal flora; although its pathogenic potential is unknown, this organism was also isolated from scid mice with diarrhea that were co-infected with Helicobacter bilis. On the basis of 16S rRNA gene sequence analysis data and biochemical and phenotypic criteria, the new organism is classified as a novel helicobacter, for which we propose the name Helicobacter rodentium. The type strain is MIT 95-1707 (= ATCC 700285).

Animals↗

PubMed1992

Results of a multicentre European survey in 1991 of metronidazole resistance in Helicobacter pylori. European Study Group on Antibiotic Susceptibility of Helicobacter pylori.

In 1991 a multicentre survey on the prevalence of metronidazole resistance in Helicobacter pylori in vitro was carried out in 12 hospitals in 11 different European countries. The susceptibility of Helicobacter pylori to metronidazole was determined in each centre by measuring the MIC on agar with the PDM E-test (AB Biodisk) according to a standard procedure. Overall, 122 of 443 (27.5%) strains tested were resistant to metronidazole (MIC > 8 micrograms/ml). The level of resistance to metronidazole varied markedly between centres (from 7% to 49%) and was found to be substantially higher in Africans and other non-Caucasian subjects than in natives from European countries. The overall rate of resistance to metronidazole was higher in females (34.7%) than in males (23.9%), and varied according to the age group, being highest among women aged 20 to 39 (50%). Previous use of metronidazole was reported in only 16 patients, 11 of whom (68.8%) harboured resistant Helicobacter pylori strains. Although differences in the rate of metronidazole resistance in Helicobacter pylori most probably relate to variations in use of this drug in different populations, such use may frequently go unrecognized. This study emphasises the importance of monitoring the drug resistance of Helicobacter pylori on a local basis. Standardisation of the methods for testing the susceptibility of Helicobacter pylori in vitro is clearly needed for this purpose.

Adult↗

PubMed1995

Oral immunization with Helicobacter pylori urease B subunit as a treatment against Helicobacter infection in mice.

BACKGROUND & AIMS: Eradication of Helicobacter pylori infections in humans results in the healing of gastritis and gastric ulcers. This study used a mouse model to test whether oral vaccination can cure Helicobacter infection and gastritis. METHODS: Mice were infected with Helicobacter felis. Three weeks after infection, the mice were orally immunized with H. pylori urease B subunit. Control mice were simultaneously infected but sham immunized. RESULTS: Three to 8 weeks after oral immunization of H. felis-infected mice with recombinant H. pylori urease B subunit, the infection cleared and there was no evidence of gastritis. Vaccinated mice remained protected against two consecutive H. felis challenges. CONCLUSIONS: These results show that the lack of natural immunity against Helicobacter can be overcome by oral immunization and that vaccination offers a novel therapeutic approach to Helicobacter-induced gastritis.

Administration, Oral↗

PubMed1993

[Helicobacter detected in children of Helicobacter pylori-positive parents].

The authors examined 48 children of Helicobacter pylori positive parents: 52% were serologically positive for Helicobacter pylori using the Orion Diagnostics Pyloriset Latex agglutination test. Of these children 10 had upper abdominal pain, heartburn and acid eructation and osesophagogastroscopy was performed; seven were found to be Helicobacter pylori positive histologically. These results draw attention to the transmission of Helicobacter pylori infection within families. They suggest that these children should be reviewed regularly, and the diagnostical examinations need to perform if the clinical picture is suspicious of Helicobacter pylori infection.

Adult↗

PubMed1996

Helicobacter pylori infection in families of Helicobacter pylori-positive children.

Relatives of Helicobacter pylori positive patients show a higher incidence of Helicobacter pylori infection than the general population, probably due to relapses and/or reinfections between members of the family. Aim of this study was to evaluate the prevalence of the infection in 121 relatives of 41 children with Helicobacter pylori positive gastritis. Specific IgG antibodies (ELISA) were evaluated, and bacteria on gastric biopsy specimens were investigated by urease-rapid test, culture test and GIEMSA or acridine orange staining. Of the eighty-two relatives, 68% were antibody positive. Thirty-five agreed to undergo endoscopy. With the exception of one brother, all subjects (97%) were found to be infected by Helicobacter pylori. Two symptomatic relatives, with normal antibody titres, were submitted to endoscopy and found to be colonized by Helicobacter pylori. The present data confirm the high prevalence of infection within families and appear to demonstrate the usefulness of endoscopy for all subjects showing positive antibody titres as well as for symptomatic relatives, even if serologically negative, to confirm the presence of any pathological conditions and reduce the risk of relapses within families.

Antibodies, Anti-Idiotypic↗

PubMed1996

Atrophic gastric changes in both Helicobacter felis and Helicobacter pylori infected mice are host dependent and separate from antral gastritis.

BACKGROUND/AIMS: The role of host factors has been neglected in studies of the pathogenesis of Helicobacter associated disease. The aim of this study was to assess the response of different mouse strains to infection with a single strain of Helicobacter felis. METHOD: Six strains of inbred mice were infected with the identical H felis culture and were killed at one month, two months, and six months after infection to assess histopathological changes. In addition, two strains of mice were infected with a mouse adapted strain of H pylori and examined at six months after infection. RESULTS: In SJL, C3H/He, DBA/2, and C57BL/6 infected mice, severe to moderate chronic active gastritis was observed only in the body of the stomach, which increased in severity over time with specialised cells in the body glands being replaced. As the severity of this damage in the body increased and atrophic changes were seen, the level of bacterial colonisation of the antrum decreased. In contrast, in BALB/c and CBA mice, there was only mild gastritis in the antrum, no remarkable changes were detected in their body mucosa, and no atrophy was seen over time. In both these strains of mice, heavy bacterial colonisation was seen, which tended to increase over the period of the experiment. Of particular importance in this experiment was that bacterial colonisation was mainly restricted to the antrum yet the atrophy, when present, was only observed in the body of the stomach. H pylori infected C3H/He mice showed moderate colonisation of the antrum, which persisted up to six months with little development of atrophy. In contrast, H pylori in C57BL/6 mice showed excellent colonisation of the antrum at two months but six months after infection there was moderate to severe body atrophy, which was associated with a loss of bacteria from the antrum. CONCLUSIONS: These findings challenge current concepts of the development of Helicobacter induced atrophy in that active chronic gastritis of antrum or the body mucosa, or both, is not a prerequisite. They also suggest an autoimmune basis for the pathology although no autoantibody or antibody to the H+/K+ ATPase was detected. Loss of infecting helicobacters from the stomach together with development of an atrophic gastritis in the body of the stomach is similar to the pattern found in certain H pylori infected human subjects.

Animals↗

PubMed1993

Long term infection of the gastric mucosa with Helicobacter species does induce atrophic gastritis in an animal model of Helicobacter pylori infection.

Gastric atrophy is a precursor lesion in the development of gastric cancer. It has been proposed that atrophy is part of a natural progression of inflammatory changes that result from long term infection with the bacterium Helicobacter pylori. The aim of this study was to test this hypothesis using an animal model of human Helicobacter infection. Conventional mice were infected with either a cat isolate of Helicobacter felis or a human isolate of "Gastrospirillum hominis". All infected mice showed a slowly progressive chronic gastritis with increasing numbers of infiltrating mononuclear cells and polymorphonuclear leucocytes. After a year and a half, the inflammatory reaction was so severe that atrophic changes were seen in both the antral and fundic mucosa. Control animals initially showed no inflammatory changes however as the animals aged, the gastric mucosa of some animals became infected with a bacterium Helicobacter muridarum that normally inhabits the small and large bowel of the rodent. The presence of this bacterium was also associated with gastritis and atrophic changes. This is the first report of experimentally induced atrophic changes induced by a gastric bacterium and opens the way for important experiments that will help better understand the induction of gastric cancer.

Animals↗

PubMed1993

Diagnosis of Helicobacter pylori infection in adults and children by using the Malakit Helicobacter pylori, a commercially available enzyme-linked immunosorbent assay.

Malakit Helicobacter pylori (Biolab, Limal, Belgium) is a second-generation enzyme-linked immunosorbent assay (ELISA) for the detection of Helicobacter pylori infection. We evaluated its ability to diagnose H. pylori infection in 489 asymptomatic pregnant women, 427 asymptomatic children, and 95 symptomatic children. 87 asymptomatic adults (17.8%), 31 asymptomatic children (7.3%), and 27 symptomatic children (28.4%) were seropositive. We observed an increase in H. pylori infection with age. 13C-urea breath tests were performed for all seropositive and 100 randomly selected seronegative asymptomatic adults. They were also performed for all seropositive and 65 randomly chosen seronegative asymptomatic children. Breath tests were positive for 86 of 87 (98.9%) seropositive adults, 30 of 31 seropositive children (96.8%), and no seronegative individual. Compared with those of culture, the sensitivity and specificity of the Malakit Helicobacter pylori were both 96%. We conclude that the Malakit Helicobacter pylori is equally suitable for adults and children. Therefore, this ELISA can be proposed as an important alternative to other more time-consuming and/or more expensive diagnostic tests for the detection of H. pylori.

Adolescent↗

PubMed1997

Are Helicobacter pylori differences important in the development of Helicobacter pylori-related diseases?

Helicobacter pylori colonises the stomach of man and induces a strong mucosal inflammation and a local and systemic immune response. Differences in virulence characteristics of Helicobacter pylori isolates can account for different clinical outcomes of infection. Most determinants of Helicobacter pylori pathogenicity factors are present in all isolates examined; some are present only in or expressed more intensively by certain strains. Many enzymes, i.e., urease, mucinase, phospholipases, alcohol dehydrogenase, neuraminidase, etc. could promote tissue erosion and ulceration by destroying the integrity of mucous, by inducing lipid peroxidation, etc. Strains which express the vacuolating toxin VacA and the associated protein CagA are called Type I and are considered endowed with increased ulcerogenic and inflammatory potential. Type I Helicobacter pylori strains carry a 40 kb genomic fragment called cag which is absent in Type II strains (VacA and CagA negative), and which contains numerous genes encoding for protein homologues to virulence factors expressed by other bacterial pathogens. CagA positive strains are more likely to be isolated from patients with duodenal ulcer and other severe digestive diseases. A simple serological test can help to detect patients at increased risk of developing severe gastroduodenal diseases, which can, therefore, possibly be prevented.

Antibodies, Bacterial↗

PubMed1995

Helicobacter bilis sp. nov., a novel Helicobacter species isolated from bile, livers, and intestines of aged, inbred mice.

A fusiform bacterium with 3 to 14 multiple bipolar sheathed flagella and periplasmic fibers wrapped around the cell was isolated from the liver, bile, and lower intestine of aged, inbred mice. The bacteria grew at 37 and 42 degrees C under microaerophilic conditions, rapidly hydrolyzed urea, were catalase and oxidase positive, reduced nitrate to nitrite, did not hydrolyze indoxyl acetate or hippurate, and were resistant to both cephalothin and nalidixic acid but sensitive to metronidazole. On the basis of 16S rRNA gene sequence analysis, the organism was classified as a novel helicobacter, Helicobacter bilis. This new helicobacter, like Helicobacter hepaticus, colonizes the bile, liver, and intestine of mice. Although the organism is associated with multifocal chronic hepatitis, further studies are required to ascertain whether H. bilis is responsible for causing chronic hepatitis and/or hepatocellular tumors in mice.

Aging↗

PubMed1995

Oral immunization with recombinant Helicobacter pylori urease induces secretory IgA antibodies and protects mice from challenge with Helicobacter felis.

Helicobacter pylori, a gram-negative spiral bacterium, is the cause of chronic superficial (type B) gastritis and peptic ulcer disease. The urease enzyme of H. pylori was expressed as an inactive recombinant protein in Escherichia coli, purified as particulate structures of 550-600 kDa molecular mass with a diameter of approximately 12 nm. Given orally, 5 micrograms of urease with an appropriate mucosal adjuvant, such as the labile toxin of E. coli, protected 60%-100% of mice against challenge with virulent Helicobacter felis. Protection correlated with the level of secretory IgA antibodies against urease. Oral administration of antigen was as effective or better than intragastric administration. Parenteral injection of antigen or intragastric administration of high-dose antigen without adjuvant elicited serum IgG but no IgA antibodies and did not confer protection. Recombinant urease as an oral vaccine candidate deserves further investigation as an approach to the prevention of Helicobacter-induced chronic gastroduodenal diseases in humans.

Adjuvants, Immunologic↗