Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Helicobacter heilmannii”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Acute symptomatic gastritis due to Helicobacter heilmannii.

Helicobacter heilmannii is a Gram-negative spiral-shaped organism predominantly associated with zoonotic infection. Human pathology has also been described, but acute symptoms with complete resolution have been infrequently reported. We present a 50-year-old man in whom H. heilmannii gastritis presented as an acute febrile illness and was successfully treated with antibiotics and proton pump inhibitor. Epidemiology, diagnosis, and treatment of similar cases are reviewed.

Gastritis↗

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↗

Gastric B-cell mucosa-associated lymphoid tissue (MALT) lymphoma in an animal model of 'Helicobacter heilmannii' infection.

While Helicobacter pylori is accepted as the dominant human gastric bacterial pathogen, a small percentage of human infections have been associated with another organism, commonly referred to as 'Helicobacter heilmannii', which is more prevalent in a range of animal species. This latter bacterium has been seen in association with the full spectrum of human gastric diseases including gastritis, peptic ulceration, and gastric carcinomas, including gastric B-cell mucosa-associated lymphoid tissue (MALT) lymphoma. This study describes an analysis of the pathogenic potential of a number of 'H heilmannii' isolates in an animal model of gastric MALT lymphoma. BALB/c mice were infected with ten different 'H heilmannii' isolates originating from both human and animal hosts. The animals were examined at various time points for up to 28 months after infection. The infected animals initially developed a chronic inflammatory response within 6 months. This histological response increased in severity with the length of infection, with the development of overt lymphoma in some animals 18 months after infection. MALT lymphomas were detected in up to 25% of the infected animals. The prevalence of lymphoma was dependent on the length of infection and the origin of the infecting isolates. A range of other histological features accompanied the lymphocytic infiltration, including invaginations of the gastric epithelium and associated hyperplastic tissue, mucus metaplasia, and a small number of diffuse large B-cell lymphomas. The ability to manipulate experientially the presence of the bacterium in the animal model will allow further studies examining the role of antigen drive in the development of Helicobacter-associated MALT lymphoma.

Animals↗

Helicobacter pylori can be induced to assume the morphology of Helicobacter heilmannii.

Cultures of Helicobacter pylori obtained from the American Type Culture Collection (strain 43504) were grown as isolated colonies or lawns on blood agar plates and in broth culture with constant shaking. Examination of bacterial growth with Gram-stained fixed preparation and differential interference contrast microscopy on wet preparations revealed that bacteria grown on blood agar plates had a morphology consistent with that normally reported for H. pylori whereas bacteria from broth cultures had the morphologic appearance of Helicobacter heilmannii. Bacteria harvested from blood agar plates assumed an H. heilmannii-like morphology when transferred to broth cultures, and bacteria from broth cultures grew with morphology typical of H. pylori when grown on blood agar plates. Analysis by PCR of bacteria isolated from blood agar plates and broth cultures indicated that a single strain of bacteria (H. pylori) was responsible for both morphologies.

Bacteriological Techniques↗

[Chronic gastritis in Helicobacter heilmannii infection].

BACKGROUND: The presence of Helicobacter pylori in the gastric mucosa used to be associated with gastritis and peptic ulcer. Helicobacter heilmannii is a similar but much less frequent and less known gastric pathogen. METHODS AND RESULTS: We evaluated 1250 gastric biopsies. Helicobacteria were detected after silver impregnation. Helicobacter pylori was found in 62%. In 3 cases (0.24%), we found Helicobacter heilmannii. In one of the cases, also Helicobacter pylori was present. All patients had gastrointestinal symptoms and histological chronic active gastritis. CONCLUSIONS: Helicobacter heilmannii is an uncommon pathogen which appears to be a cause of gastric inflammation. It can be differentiated from Helicobacter pylori by routine histology examination.

Chronic Disease↗

[Using polymerase chain reaction to detect Helicobacter heilmannii in gastric biopsy materials].

Helicobacter heilmannii is one of the species of Helicobacter other than Helicobacter pylori noticed in human gastric mucosa. In our study, a polymerase chain reaction (PCR) was designed for the detection of Helicobacter heilmannii in gastric biopsy specimens. Two broad-range bacterial 16S rDNA primers and one Helicobacter genus-specific 16S rDNA primer were matched for detecting Helicobacter genus bacteria. A Hp-specific primer pair was used simultaneously to exclude the presence of Hp. The PCR assay detected 11 out of 12 Hh strains which were confirmed by smears, but did not amplify DNA extracts from some other enteric bacteria such as E. coli, C. jejuni, bifidobacteria. Serial dilution experiments revealed the detection of as little as 0.1 pg DNA by PCR and 0.01 pg by nested PCR. Our data showed that PCR is a rapid, accurate and sensitive method for the detection of Hh and is thought valuable in the epidemiological investigation of Helicobacter and follow-up studies after treatment.

Biopsy↗

"Candidatus Helicobacter heilmannii" from a cynomolgus monkey induces gastric mucosa-associated lymphoid tissue lymphomas in C57BL/6 mice.

Both Helicobacter pylori and "Candidatus Helicobacter heilmannii" infections are associated with peptic ulcers, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphomas. However, good animal models of H. pylori clinical diseases are rare. In this study, we aimed to establish an animal model of "Candidatus Helicobacter heilmannii" gastric MALT lymphoma. We used a urease-positive gastric mucosal and mucus homogenate from a cynomolgus monkey maintained in C57BL/6 mouse stomachs. The bacterium in the homogenate was identified as "Candidatus Helicobacter heilmannii" based on a DNA sequence analysis of the 16S rRNA and urease genes. Mucosal and mucus homogenates were used to inoculate C57BL/6 mice, which were then examined for 24 months. We observed a gradual increase in the surface area of protrusive lesions in almost all infected C57BL/6 mouse fundic stomachs 6 months after infection. Light microscopic observations revealed an accumulation of B lymphocytes along with destruction of glandular elements and the presence of lymphoepithelial lesions consistent with low-grade MALT lymphomas. Electron microscopic observation revealed numerous "Candidatus Helicobacter heilmannii" bacilli in the fundic glandular lumen, the intracellular canaliculi, and the cytoplasm of intact cells, as well as damaged parietal cells. In conclusion, "Candidatus Helicobacter heilmannii" induced gastric MALT lymphomas in almost 100% of infected C57BL/6 mice after a 6-month period associated with the destruction of parietal cells.

Animals↗

The role of IFN-gamma and IL-4 in gastric mucosa inflammation associated with Helicobacter heilmannii type 1 infection.

Although Helicobacter heilmannii infection is less common than H. pylori infection in humans, it is considered to be of medical importance because of its association with gastritis, gastric ulcer, carcinoma, and mucosa-associated lymphoid tissue lymphoma of the stomach. However, there have been no studies evaluating the role of the Th cell response in H. heilmannii gastric infection. We evaluated the participation of pro-inflammatory and anti-inflammatory cytokines, IFN-gamma and IL-4, in H. heilmannii gastric infection in genetically IFN-gamma- or IL-4-deficient mice. The serum IFN-gamma and IL-4 concentrations were determined by ELISA. The gastric polymorphonuclear infiltrate was higher (P = 0.007) in H. heilmannii-positive than in H. heilmannii-negative wild-type (WT) C57BL/6 mice, whereas no significant inflammation was demonstrable in the stomach of H. heilmannii-positive IFN-gamma(-/-) C57BL/6 mice. The degree of gastric inflammatory cells, especially in oxyntic mucosa, was also higher (P = 0.007) in infected IL-4(-/-) than in WT BALB/c mice. Serum IFN-gamma levels were significantly higher in IL-4(-/-) than in WT BALB/c mice, independently of H. heilmannii-positive or -negative status. Although no difference in serum IFN-gamma levels was seen between H. heilmannii-positive (11.3 +/- 3.07 pg/mL, mean +/- SD) and -negative (11.07 +/- 3.5 pg/mL) WT BALB/c mice, in the group of IL-4(-/-) animals, the serum concentration of IFN-gamma was significantly higher in the infected ones (38.16 +/- 10.5 pg/mL, P = 0.04). In contrast, serum IL-4 levels were significantly decreased in H. heilmannii-positive (N = 10) WT BALB/c animals compared to the negative (N = 10) animals. In conclusion, H. heilmannii infection induces a predominantly Th1 immune response, with IFN-gamma playing a central role in gastric inflammation.

Animals↗

[Low-grade gastric MALT lymphoma and helicobacter heilmannii (Gastrospirillum hominis].

We report the fourth case of low-grade gastric MALT lymphoma associated to Helicobacter heilmannii. This spiral organism may be present in the gastric mucosa of animals where it is non pathogenic while, in humans, its presence is always associated with chronic gastritis. In this case, Helicobacter heilmannii was observed in the absence of Helicobacter pylori. Regression of endoscopic and histological lesions after Helicobacter heilmannii eradication suggests its role in gastric lymphoma. This observation underlines the need for searching for Helicobacter heilmannii by careful histological examination, in the absence of Helicobacter pylori, and the importance of its eradication in the treatment of gastric lymphoma.

Helicobacter Infections↗

[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↗

Helicobacter heilmannii associated erosive gastritis.

The spiral bacteria, Helicobacter heilmannii (H. heilmannii), distinct from Helicobacter pylori (H. pylori), was found in the gastric mucosa of a 71-year-old man without clinical symptoms. The endoscopic examination revealed erosive gastritis. Rapid urease test from the antral specimen was positive, but both culture and immunohistological staining for H. pylori were negative. Touch smear cytology showed tightly spiral bacteria, which were consistent with H. heilmannii. At the second endoscopy after medication regimen for eradication of H. pylori, inflammation was decreased and the rapid urease test was negative. The second cytology showed no evidence of H. heilmannii. Anti-H. pylori therapy may be a useful medication for H. heilmannii.

Abietanes↗

A cultured strain of "Helicobacter heilmannii," a human gastric pathogen, identified as H. bizzozeronii: evidence for zoonotic potential of Helicobacter.

We compared the characteristics of a cultured human "Helicobacter heilmannii" isolate with those of other helicobacters found in animals. Phenotypic, protein profile, 16S rDNA sequence, and DNA-DNA hybridization analyses identified the human strain as H. bizzozeronii, a species frequently found in dogs. Thus, H. bizzozeronii may have zoonotic potential.

Animals↗

Helicobacter heilmannii infection: clinical, endoscopic and histopathological features in Japanese patients.

Gastric biopsy materials of 4074 consecutive Japanese patients undergoing esophagogastroduodenoscopy were reviewed, along with those of 15 patients with Helicobacter heilmannii infection (11, chronic gastritis; four, mucosa-associated lymphoid tissue (MALT) lymphoma). In four patients with H. heilmannii infection, the materials were examined by transmission electronmicroscopy. Urea breath test (three patients) and antibody test (five patients) were performed in patients with H. heilmannii infection. In two patients with MALT lymphoma, H. heilmannii was eradicated. The prevalence of H. heilmannii was 0.1% in the consecutive series. In chronic gastritis, the gastric mucosa was endoscopically normal (13.3%), had erythema (33.3%), or had erosions (53.3%); histologically, it showed no epithelial change, mild mononuclear cell infiltration, and slight and focal neutrophil infiltration; Helicobacter heilmannii was positive with anti-H. pylori antibody, and was detected in the mucous gel layer and in foveolae. In MALT lymphoma, the gastric mucosa was coarsely granular with enlarged mucosal folds without ulcers (two cases), with small ulcers (one case), or with multiple erosions (one case). Urea breath test and antibody test were both negative. Eradication of H. heilmannii resulted in remission of MALT lymphoma. Helicobacter heilmannii infection is therefore uncommon in Japanese adults, but is associated with chronic gastritis and gastric MALT lymphoma.

2-Pyridinylmethylsulfinylbenzimidazoles↗

Description of 'Candidatus Helicobacter heilmannii' based on DNA sequence analysis of 16S rRNA and urease genes.

While Helicobacter pylori is accepted as the major bacterial agent of gastric disease in humans, some patients and many animals are infected with a larger, tightly helical-shaped bacterium previously referred to as 'Helicobacter heilmannii' or 'Gastrospirillum hominis'. Taxonomic classification of these bacteria has been hampered by the inability to cultivate them in vitro and by the inadequate discriminatory power of 16S rRNA gene sequence analysis. This study describes the detection and phylogenetic analysis of 26 different gastrospirillum isolates from humans and animals, which incorporates sequence data based on the 16S rRNA and urease genes. Fifteen gastrospirilla detected in humans, primates and pigs clustered with 'Candidatus Helicobacter suis', thus expanding the host range for this organism. By comparison, based on 16S rRNA data, the remaining 11 gastrospirilla could not be differentiated from Helicobacter felis, Helicobacter bizzozeronii and Helicobacter salomonis. However, urease gene sequence analysis allowed for the discrimination of this latter group into four discrete clusters, three of which contained the above recognized species. The fourth cluster contained isolates from human and feline hosts, and should provisionally be considered a unique bacterial species, for which the name 'Candidatus Helicobacter heilmannii' is proposed.

Adult↗

[Gastritis caused by Helicobacter heilmannii (Gastrospirillum hominis). Report of 3 cases].

Helicobacter heilmannii infection is rare. Its clinical picture is rather different from that caused by Helicobacter pylori: alterations in the gastric mucosa are milder and mainly located in the gastric antrum, and the frequency of erosions and ulcers is lower. It has been described in association with conditions similar to those related to H. pylori: peptic ulcer, chronic gastritis, gastric adenocarcinoma, intestinal metaplasia and MALT (mucose associated lymphoid tissue) lymphoma, although the incidence is lower. We describe three cases of gastritis caused by H. heilmannii, which we consider to be of interest because of the absence of cases published in Spain. One of the cases is especially unusual because of its association with a duodenal ulcer. We also describe the main features of H.r heilmannii. Its clinical treatment is similar to that used in H. pylori, with demonstrated morphological improvement of the lesions after eradication of the infectious agent.

Adult↗

Helicobacter heilmannii gastritis: association with acid peptic diseases and comparison with Helicobacter pylori gastritis.

We analyzed 2 antral and 1 corpus full-thickness random endoscopic gastric mucosal samples obtained from 946 patients with duodenal ulcers (6077 biopsies) and from 281 patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (1794 biopsies). We stained tissue sections with hematoxylin and eosin and Warthin-Starry silver stain and immunostained them with polyclonal antibodies against Helicobacter pylori. Hematoxylin- and eosin-stained sections from 6 patients with Helicobacter heilmannii (18 biopsies) and 23 randomly selected patients with H. pylori (68 biopsies) were evaluated and semiquantitated for the presence of acute inflammation, chronic inflammation, glandular atrophy, intestinal metaplasia, H. pylori, H. heilmannii, lymphoid follicles, or vasodilatation. Additional specimens were obtained for H. pylori culture, a CLO test, and serologic examination. H. heilmannii was detected in 6 (0.49%) of 1227 patients (14 [0.18%] of 7871 biopsies). Of these, 4 (0.42%) of 946 were patients with duodenal ulcers (9 [0.15%] of 6077 biopsies), and 2 (0.71%) of 281 were patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (5 [0.28%] of 1794 biopsies). We found H. heilmannii with hematoxylin and eosin stain, Warthin-Starry stain, and immunoperoxidase stain for H. pylori. Culture for H. pylori was negative in the four patients with duodenal ulcers. The CLO and serologic tests were positive in three of five and five of five patients, respectively. Our results indicate that H. heilmannii, like H. pylori, is associated with peptic ulcer disease (both active and inactive gastritis) and that it preferentially colonizes the gastric antrum. The severity of the H. heilmannii-associated gastritis is less intense and lymphoid aggregates are less common than in H. pylori-associated gastritis. Morphologic detection seems to be the method of choice for detecting H. heilmanni. Immunoperoxidase stain specific for H. pylori also stains H. heilmannii, indicating cross-reacting antigenic epitopes between H. heilmannii and H. pylori.

Adult↗

[Endoscopic aspect of ulcerated tumor-like gastritis associated with Helicobacter heilmannii].

We report on 5 cases with an endoscopic aspect exceptionally described of ulcerated tumor-like gastritis associated with Helicobacter heilmannii. This rare but ubiquitary bacteria, belonging to the same family as Helicobacter pylori, is epidemiologically and structuraly different. When these endoscopic lesions are detected, Helicobacter heilmannii has to be looked for carefully. The treatment, which is the same than for Helicobacter pylori, must lead to complete repair of endoscopic and histologic lesions.

Aged↗

Helicobacter heilmannii (formerly Gastrospirillum hominis) gastritis: an infection transmitted by animals?

BACKGROUND: The source of infection with Helicobacter heilmannii (formerly Gastrospirillum hominis), a relatively rare causative agent of gastritis in humans, is not clear. It has long been known that this organism occurs in the stomach of domestic animals and pets. METHODS: By performing an epidemiologic investigation on possible contact of patients with Helicobacter heilmannii gastritis with such animals, we made an attempt to gain further information about the source of infection. RESULTS: Of 125 patients with confirmed H. heilmannii infection, 111 provided us with information about contact with animals. Some 70.3% of the patients had contact with one or more animals (as compared with 37% in the 'normal' population); 73% were males, and 1.6% had concomitant infection with H. pylori. CONCLUSIONS: Our analysis indicates that H. heilmannii gastritis is due to its transmission to humans by domestic animals or pets. Concomitant infections by H. heilmannii and H. pylori are very rare, and it is possible that H. heilmannii might protect from infection with H. pylori. However, the results of our retrospective analysis will have to be tested against those of a prospective study investigating the day-to-day situation of the individual patients in greater detail and also be compared with patients not infected with H. heilmannii.

Adolescent↗