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PubMed2002

Are goats naturally resistant to gastric Helicobacter infection?

Gastric Helicobacter species are widespread and have been reported in wild and domestic mammals of different dietary habits such as humans, dogs, cats, macaques, mice, cheetahs, ferrets, swine and cattle. All have been associated with gastric pathologies. Recently, gastric Helicobacter species were shown to be widespread in cattle and swine in Europe, and there is a report of Helicobacter pylori in sheep in Italy. However, there are no reports of Helicobacter infection in the goat, another important domestic animal of human consumption. The aim of our study was to assess whether Helicobacter abomasal infection was common in goats slaughtered for human consumption. Infection was detected through PCR analysis of DNA extracted from gastric biopsies, using genus- and species-specific primers. Bovine and porcine gastric samples were also analyzed as positive controls. None of the 70 goats were positive for Helicobacter spp.; however, Candidatus Helicobacter bovis and Candidatus Helicobacter suis were detected in 85% of the bovine and 45% of the porcine samples, respectively. We discuss the possibility that goats may exhibit natural resistance to abomasal infection by Helicobacter spp.

Abomasum↗
PubMedDate not supplied

Helicobacter pylori cag pathogenicity island is associated with enhanced interleukin-8 expression in human gastric mucosa.

BACKGROUND: In vitro studies showed that Helicobacter pylori strains carrying the cag pathogenicity island are able to induce epithelial secretion of Interleukin-8. AIMS: To evaluate the assessment of cag pathogenicity island and the expression of Interleukin-8 in the gastric mucosa of Helicobacter pylori-infected patients and correlate these data with the activity of gastritis and Helicobacter pylori density. METHODS: cag status was determined by polymerase chain reaction directly on gastric biopsies from 13 Helicobacter pylori+ patients with non-ulcer dyspepsia and 13 Helicobacter pylori+ with duodenal ulcer. Interleukin-8 gene transcription and protein expression were analysed by in situ hybridization and immunofluorescence, respectively. Gastritis activity and Helicobacter pylori density were also investigated. RESULTS: cag was present in 20/26 of Helicobacter pylori+ patients: in 7/13 non-ulcer dyspepsia (53.8%] and in 13/13 duodenal ulcer patients (100%), (p<0.05). Interleukin-8 mRNA and protein expression in epithelial and inflammatory cells was higher in cag+ than in cag- patients (p<0.005). Gastritis activity significantly correlated with cag (p<0.05) and Interleukin-8 expression (p<0.005]. Helicobacter pylori density was enhanced in cag+ [p<0.005] and correlated with Interleukin-8 expression (p<0.0051. CONCLUSIONS: The present study demonstrates that in Helicobacter pylori-infected human gastric mucosa, cag+ infection is associated with enhanced Interleukin-8 expression, higher levels of active gastritis and bacterial density, and presence of duodenal ulcer.

Antigens, Bacterial↗
PubMed2000

Prevalence of Helicobacter pylori resistance to antibiotics in Northeast Italy: a multicentre study. GISU. Interdisciplinary Group for the Study of Ulcer.

AIMS: To evaluate prevalence of primary Helicobacter pylori antibiotic resistances in Northeast Italy and to identify risk factors associated with this resistance. MATERIALS AND METHODS: A total of 248 patients undergoing upper gastrointestinal endoscopy were enrolled from 19 Endoscopy Units over a 6-month period. From each patient, 4 gastric biopsies were taken for histology and 2 were sent to the Central Referral Microbiological Laboratory for culture and determination of antibiotic activity against Helicobacter pylori by means of E-test. Strains were considered resistant when minimum inhibitory concentration was >8 microg/ml for metronidazole and >1 microg/ml for clarithromycin. No cut-off value was predefined for amoxycillin. RESULTS: Culture of Helicobacter pylori was successfully performed in 167 patients. Primary resistance to metronidazole, clarithromycin or amoxycillin was 14.9%, 1.8% and 0%, respectively Patients infected with Helicobacter pylori strains resistant to antibiotics were more frequently females than males (70.3% vs 41.4%), had a significantly lower coffee intake (66.6% vs 86.6%) and lower body mass index (23.7+/-2.6 vs 25.3+/-3.6) than patients with susceptible Helicobacter pylori strains. Age, smoking, alcohol use, family history of Helicobacter pylori infection, concomitant diseases and treatments, endoscopic diagnoses, Helicobacter pylori density and histological activity of chronic gastritis were not associated with antibiotic resistance. Multivariate analysis confirmed that female gender (odds ratio = 2.74, 95% confidence interval = 1.03-7.27) was the only significant risk factor associated with antibiotic resistance. CONCLUSIONS: In this population, primary Helicobacter pylori resistance to metronidazole was higher than resistance to clarithromycin, and female gender was significantly associated with this resistance. The low prevalence of resistance to metronidazole, clarithromycin and amoxycillin identified in this geographical area suggests that proton pump inhibitor-based triple regimens including these antibiotics may still be used as first line therapies against Helicobacter pylori infection.

Adult↗
PubMedDate not supplied

Increased prevalence of Helicobacter pylori in patients with diabetes mellitus.

BACKGROUND: Whilst upper gastrointestinal disturbances are frequently observed in patients with diabetes mellitus, little is known about the prevalence of Helicobacter pylori infection and peptic disease in these patients. AIM: To evaluate prevalence of Helicobacter pylori infection and peptic disease lesions in diabetics with dyspeptic symptoms. PATIENTS AND METHODS: Study population comprises 74 consecutive diabetes mellitus patients with dyspepsia and 117 consecutive non diabetic dyspeptic patients. Upon enrolment, each patient completed an interview screening questionnaire to obtain information concerning presence and severity of dyspepsia. All patients underwent upper gastrointestinal endoscopy with biopsy specimens being collected from gastric antrum and body Helicobacter pylori was evaluated in each patient by rapid urease test and histology (Giemsa). Gastritis was classified according to the Sydney System. Statistical analysis was performed by chi-square, Fisher exact or t test and logistic regression analysis. A p value <0.05 was considered significant. RESULTS: Prevalence of Helicobacter pylori infection was found to be significantly higher in diabetics than in controls. The prevalence rate of endoscopic lesions was comparable in the two groups, but the association between endoscopic lesions and Helicobacter pylori infection was significantly higher in diabetics. Overall, the presence of chronic gastritis, both non atrophic and atrophic, as well as intestinal metaplasia were comparable in the two groups of patients, whilst the association between chronic gastritis and Helicobacter pylori infection or gastritis activity were significantly higher in diabetics. In neither group, was any correlation found between severity of dyspepsia and presence of endoscopic lesions, chronic gastritis or Helicobacter pylori infection. CONCLUSIONS: These data show a higher prevalence of Helicobacter pylori infection in diabetes mellitus patients with dyspepsia. Helicobacter pylori infection was significantly associated both with the presence of endoscopic lesions and chronic gastritis in diabetic patients, but not in the controls.

Adult↗
PubMed2002

Helicobacter pylori-induced duodenal ulcer frequently coincides with gastro-oesophageal reflux disease.

BACKGROUND: The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease is complicated. Evidence does not support a causal link. There have been reports, which have implicated successful eradication of Helicobacter pylori, in patients with a duodenal ulcer, with the subsequent development of gastro-oesophageal reflux disease. However, eradication of Helicobacter pylori in these patients with improvement in their condition and a return to normal lifestyle, weight gain and discontinuation of antacids may unmask pre-existing gastro-oesophageal reflux disease. AIMS: To determine the true prevalence of gastro-oesophageal reflux disease in patients with Helicobacter pylori-related duodenal ulceration. METHOD: Dyspeptic patients undergoing endoscopy were prospectively screened for the presence of a duodenal ulcer. Concomitant oesophagitis, when present, was recorded. All subjects with a Helicobacter pylori-related duodenal ulcer without endoscopic evidence of gastro-oesophageal reflux disease were invited to undergo a 24-hr ambulatory oesophageal pH assessment prior to receiving treatment. RESULTS: A total of 97 patients with a duodenal ulcer were identified and 83.5% were Helicobacter pylori positive. Overall, 27.8% had associated endoscopic evidence of oesophagitis, 70% grade I-II and 30% grade III-IV. Of those without evidence of oesophagitis at endoscopy, 68% underwent a 24-hr pH assessment. An additional 17% were identified by this means as having gastro-oesophageal reflux disease. Overall, 44% of symptomatic subjects with Helicobacter pylori and a duodenal ulcer were found to have coexistent gastro-oesophageal reflux disease. CONCLUSION: Gastro-oesophageal reflux disease is frequently found to coexist with Helicobacter pylori-related duodenal ulcer. In addition, almost 20% of symptomatic patients without endoscopic evidence of oesophagitis will have an abnormal oesophageal pH exposure. It is plausible that the development of gastro-oesophageal reflux disease following successful eradication of Helicobacter pylori represents unmasking of existing disease rather than de novo development.

Adolescent↗
PubMed2002

Up-regulation of heparin binding epidermal growth factor-like growth factor and amphiregulin expression in Helicobacter pylori-infected human gastric mucosa.

BACKGROUND: Host response plays a major role in pathogenesis of Helicobacter pylori-induced gastroduodenal disease including adenocarcinoma of distal stomach. Epidermal growth factor-related growth factors are important modulators of gastric homeostasis in normal and damaged gastrointestinal mucosa. AIM: To evaluate expression of heparin binding epidermal growth factor and amphiregulin in antral mucosa of Helicobacter pylori-infected and non-infected dyspeptic patients and to correlate levels of heparin binding-epidermal growth factor and amphiregulin mRNA with mitogenic activity of gastric epithelial cells. METHODS: A total of 10 Helicobacter pylori-infected and 15 Helicobacter pylori non-infected (10 with and 5 without gastritis) dyspeptic patients were studied. Diagnosis of Helicobacter pylori infection was based on rapid urease test and histology. Heparin binding-epidermal growth factor and amphiregulin mRNA expression in antral mucosa were assessed by reverse transcriptase-polymerase chain reaction. Protein expression and localization of both peptides were determined by immunohistochemistry. Mitogenic activity of antral gastric mucosa was assessed by determination of proliferating cell nuclear antigen labelling index by immunohistochemistry. RESULTS: Heparin binding-epidermal growth factor and amphiregulin mRNA expression increased in Helicobacter pylori-infected vs Helicobacter pylori non-infected patients. Heparin binding-epidermal growth factor and amphiregulin immunostaining was more intense and deeper in gastric gland compartment in infected mucosa than in non-infected mucosa. Increase in heparin binding-epidermal growth factor and amphiregulin mRNA expression significantly correlated with increase in proliferating cell nuclear antigen labelling index. CONCLUSIONS: Helicobacter pylori gastritis is associated with up-regulation of heparin binding-epidermal growth factor and amphiregulin which correlates with increased mitogenic activity of gastric mucosa. Increased heparin binding-epidermal growth factor and amphiregulin expression is postulated to contribute to reparative response of gastric mucosa to Helicobacter pylori infection.

Adult↗
PubMedDate not supplied

Chronic Helicobacter pylori infection and migraine: a case-control study.

OBJECTIVE: To determine whether chronic Helicobacter pylori infection is a risk factor for migraine. BACKGROUND: Preliminary studies have shown a high prevalence of Helicobacter pylori infection in patients with primary headaches. METHODS: One hundred three consecutive patients with migraine were enrolled in the study and compared with a group of 103 matched controls. Helicobacter pylori infection was diagnosed by means of both (13)C-urea breath test and serology. RESULTS: Of patients with migraine, 30.1% were positive for Helicobacter pylori, compared with 31.1% of controls (P = NS). The odds ratio for migraine associated with chronic Helicobacter pylori infection was 0.96 (95% confidence interval, 0.51 to 1.80). Demographic, clinical, and psychological characteristics of Helicobacter pylori-positive migraineurs were compared with those of migrainous patients without infection. Helicobacter pylori-positive patients had a significantly (P<.05) lower incidence of food sensitivity than Helicobacter pylori-negative patients. No significant difference was found in any other feature examined. CONCLUSIONS: Our study suggests that chronic Helicobacter pylori infection is not more frequent in patients with migraine than in controls and that infection does not modify clinical features of the disease.

Adult↗
PubMed2002

Comparative analysis of Helicobacter DNAs and biliary pathology in patients with and without hepatobiliary cancer.

Several Helicobacter species have recently been isolated from the bile and hepatobiliary systems of murine species, and are well recognized as a pathogen of the hepatobiliary disorder. This study was planned to investigate whether Helicobacter species possess a causative potential for human hepatobiliary disease, especially for hepatobiliary carcinogenesis. Bile and hepatobiliary tissue samples from 19 patients with hepatobiliary cancer and 19 patients with benign biliary diseases were subjected to polymerase chain reaction analyses for the detection of Helicobacter DNAs. Using a proliferating cell nuclear antigen (PCNA) staining technique, we also investigated the biliary epithelial cell kinetics with special reference to the presence of Helicobacter DNAs in the hepatobiliary system. We found that Helicobacter DNAs were positive in 10 (52.6%) of the 19 patients with hepatobiliary cancer. The incidence was significantly higher than that (15.7%) in the benign cases (P = 0.03). The PCNA labeling index in the biliary epithelium in Helicobacter DNA-positive patients was statistically higher than that in Helicobacter DNA-negative ones, regardless of whether the patient was suffering from hepatobiliary cancer and/or biliary inflammation. A close correlation between the presence of Helicobacter DNAs and an elevation of the PCNA labeling index in the biliary epithelium was demonstrated by multiple regression analysis. Our findings suggest that Helicobacter species may play a role in the pathogenesis of hepatobiliary cancer through an acceleration of biliary cell kinetics.

Adenoma↗
PubMed2006

Non-steroidal anti-inflammatory drugs have bacteriostatic and bactericidal activity against Helicobacter pylori.

BACKGROUND: Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are each associated with gastrointestinal mucosal damage, but the extent and direction of their interactions remain controversial. Therefore, the purpose of the present paper was to examine whether specific NSAIDs inhibit the growth of Helicobacter pylori in vitro. METHODS: Sodium salicylate, ibuprofen, indomethacin, the selective cyclooxygenase-2 inhibitor NS-398 and two derivatives of sulindac sulfoxide were tested against two laboratory strains of H. pylori, the mouse-adapted Sydney strain, and against seven fresh clinical isolates of Helicobacter pylori. Possible effects on Campylobacter jejuni, Staphyloccoccus aureus, Escherichia coli, Salmonella typhimurium, and Shigella boydii were also examined. RESULTS: Certain NSAIDs possess antibacterial activity against Helicobacter pylori at therapeutically achievable doses; an effect that appears to be independent of cyclooxygenase enzymes inhibition. For Helicobacter pylori, >90% growth inhibition and bactericidal activity were observed consistently for sulindac sulfide at < or =70 microg/mL and sulindac sulfone at < or =175 microg/mL. The minimal inhibitory concentration against Helicobacter pylori was 125 microg/mL for ibuprofen, 100 microg/mL for indomethacin and 300 microg/mL for NS-398 but much higher concentration of sodium salicylate (4000 microg/mL) and sulindac sulfoxide (> or =1250 microg/mL) were required to inhibit the growth of Helicobacter pylori. CONCLUSIONS: The decreased prevalence of Helicobacter pylori in specimens from some NSAID users and the chemopreventive effects of NSAIDs in gastric cancer may be related to inhibition of Helicobacter pylori growth.

Animals↗
PubMed2005

Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 1: eradication of Helicobacter in the cachexia of idiopathic parkinsonism.

BACKGROUND: Neuronal damage in idiopathic parkinsonism may be in response to ubiquitous occult infection. Since peptic ulceration is prodromal, Helicobacter is a prime candidate. AIM: To consider the candidature of Helicobacter in parkinsonism with cachexia. METHODS: We explore the relationship between being underweight and inflammatory products in 124 subjects with idiopathic parkinsonism and 195 controls, and present the first case-series evidence of efficacy of Helicobacter eradication, in parkinsonism advanced to the stage of cachexia. RESULTS: Association of a low body mass index with circulating interleukin-6 was specific to parkinsonism (p = .002), unlike that with antibodies against Helicobacter vacuolating-toxin and cytotoxicity-associated gene product (p < .04). Marked reversibility in both cachexia and disability of idiopathic parkinsonism followed Helicobacter heilmannii eradication in one case, Helicobacter pylori eradication in another, follow-up being > or = 3.5 years. The latter presented with postprandial bloating, and persistent nausea: following eradication, radioisotope gastric-emptying returned towards normal, and upper abdominal symptoms regressed. Reversibility of their cachexia/disability contrasts with the outcome of anti-Helicobacter therapy where eradication repeatedly failed (one case), and in non-Helicobacter gastritis (three cases). Anti-parkinsonian medication remained constant. Intestinal absorption and barrier function were normal in all. CONCLUSION: Categorization, according to presence or absence of Helicobacter infection, was a useful therapeutic tool in late idiopathic parkinsonism.

Aged↗
PubMed2000

Effect of triple therapy on eradication of canine gastric helicobacters and gastric disease.

Nine helicobacter-positive pet dogs with upper gastrointestinal signs were studied to evaluate the effect of a triple therapy, normally applied to humans for the eradication of gastric helicobacters, on clinical signs and gastric histology, as well as the recurrence of helicobacters after eradication in an extended follow-up in four dogs. Endoscopy was performed at entry to the study and repeated after eradication therapies and additional treatments. If the triple therapy (amoxycillin, metronidazole and bismuth subcitrate) failed, tetracycline and omeprazole were prescribed. Additional therapies were instituted if clinical signs persisted after eradication therapies. Helicobacter status was verified from gastric biopsy specimens by the urease test and histological examination, and in a few dogs also by brush cytology. Triple therapy eradicated gastric helicobacters in 7/9 dogs; gastric helicobacters were also eradicated in one dog treated with tetracycline and omeprazole. Eradication of helicobacters resulted in significant improvement, but not total resolution, of clinical signs. Subsequent additional therapies resulted in further alleviation of clinical signs. Neither triple therapy nor additional therapies had a significant effect on gastric histological changes. Gastric helicobacters recurred in 4/4 dogs within three years of the eradication treatment. Because canine gastric helicobacters alone were not definitively shown to induce clinical signs, routine eradication therapy seems not to be warranted at present.

Amoxicillin↗
PubMed1998

Detection and prevalence of Helicobacter infection in pet cats.

The presence of spiral bacteria in the feline stomach has been recognized for over a century, but the identities and degrees of prevalence of such organisms in privately owned cats are still poorly documented. The aims of this study were (i) to adapt different diagnostic tools and evaluate their practicality for diagnosing feline gastric Helicobacter colonization, (ii) to determine the prevalence of gastric Helicobacter-like organisms in pet cats, (iii) to identify the feline species, and (iv) to correlate the presence of a Helicobacter infection with gastritis. Biopsy samples were taken gastroscopically from the antra and the corpora of clinically healthy pet cats. Helicobacter-like organisms were detected by Gram staining, Warthin-Starry staining, and rapid urease testing in biopsy specimens and by [13C]urea breath testing in 79, 77, 78, and 85% of cases, respectively. PCR analysis revealed that 78% of the cats (38 of 49) were infected by Helicobacter heilmannii; however, none of them was harboring Helicobacter pylori or Helicobacter felis. Culture was positive for one cat; the organism was identified as Helicobacter pametensis by dot blot DNA hybridization. By a combination of the detection methods, 91% of the pet cats were found to be Helicobacter positive. For 46 cats (79%) diagnostic tests were concordant. All cats showed mild to moderate gastritis in either the antrum or the corpus, regardless of the presence or density of gastric bacteria. In summary, pet cats are frequently colonized by H. heilmannii without a significant correlation between infection and degree of gastritis.

Animals↗
PubMed2003

Association of the presence of Helicobacter in gallbladder tissue with cholelithiasis and cholecystitis.

The presence of Helicobacter DNA species has been investigated in the biliary epithelium of patients with biliary diseases. However, conflicting results have been observed that may have been due to the small number of subjects studied, difficulty in obtaining a healthy control group, absence of controlling for confounding factors, or differences among populations. Therefore, we investigated the presence of Helicobacter species by culture and nested PCR of 16S rRNA genes in gallbladder tissue and bile from 46 Brazilian subjects with and 18 without cholelithiasis. The control group was mainly composed of liver donors and of patients who had submitted to cholecystectomy as part of the surgical treatment for morbid obesity. No Helicobacter species were grown from the bile or gallbladder tissues. Helicobacter DNA was detected in the gallbladder tissue and bile from 31.3 and 42.9% of the patients, respectively. In a logistic regression model, cholelithiasis was positively and independently associated with the female gender (P = 0.02), increasing age (P = 0.002), and the presence of Helicobacter DNA in the gallbladder tissue (P = 0.009). The presence of Helicobacter DNA in the bile was not associated with cholelithiasis (P = 0.8). A significant association between the presence of Helicobacter DNA in the gallbladder epithelium and histological cholecystitis, even after adjusting for gender and age (P = 0.002), was also observed. The sequences of the 16S rRNA genes were >99% similar to that of Helicobacter pylori. In conclusion, our results support the hypothesis that Helicobacter is associated with the pathogenesis of human cholelithiasis and cholecystitis.

Adult↗
PubMed2005

Significance of transiently positive enzyme-linked immunosorbent assay results in detection of Helicobacter pylori in stool samples from children.

In young children, the significance of stool samples transiently positive for Helicobacter pylori antigen is unknown. As part of a larger prospective study on enteric infections, stool samples were obtained from 323 children at two time points 3 months apart and tested for H. pylori antigen using a commercially available enzyme-linked immunosorbent assay (ELISA) test. Seminested PCR for a Helicobacter-specific 16S rRNA gene was performed on all 26 pairs reverting from positive to negative (transient positives), all 4 persistent antigen-positive pairs, and 10 randomly selected persistent antigen-negative pairs. Helicobacter species were amplified from the first stool samples of 15/26 (58%) of the transient positives and 1 (25%) of 4 persistent positives. No Helicobacter species were amplified from the 10 persistent negatives. Among the 15 amplicons from transient-positive stool, H. pylori was sequenced and identified from 12 (80%; 95% confidence interval, 52% to 96%) and other Helicobacter spp. were identified from three (Helicobacter canis, Helicobacter winghamensis, and MIT 99-5504). Four of the 15 remained positive by PCR for the second (antigen-negative) stool sample, including all 3 initially identified as non-H. pylori. Helicobacter bilis was amplified from the second sample of a persistent positive. Two of eight transient positives from whom serum was available had accompanying transient elevations in anti-H. pylori antibodies. Transiently positive stool ELISAs for H. pylori are common and represent H. pylori in the majority of cases where sequences can be obtained. A not-insignificant percentage of antigen-positive stools, however, may represent other Helicobacter species.

Antigens, Bacterial↗
PubMedDate not supplied

[Helicobacter heilmanni (Gastrospirillum hominis) as a new cause of gastritis--case report].

INTRODUCTION: During the course of research into Helicobacter pylori, further microorganisms colonizing the gastric mucosa have been detected. The large spiral-shaped bacteria deviating from Helicobacter pylori was originally described by Dent. The bacteria was initially named Gastrospirillum hominis, but after sequencing of 16S rRNA it was classified as Helicobacter and named Helicobacter Heilmannii in honour of the pathologist Prof. Dr. Konrad Heilmann. We report two additional cases. CASE REPORTS: In 1997 at the Department of Pathology of General Hospital in Senta 268 gastric biopsies (151 male, 117 female), average age of 50.4 were analyzed. Helicobacter pylori was identified in 176 biopsies (65.7%). Helicobacter Heilmannii was found in two cases (0.74%). The clinical details were as follows: Case 1. A 32-year-old male complained of dyspepsia. Esophagogastroduodenoscopy disclosed hyperemia and scattered erosions in the lower third of stomach. Case 2. a 55-year-old female was admitted at the hospital with lumbar pain, loss of appetite and body weight. Esophagogastroduodenoscopy findings were normal. The patient lived in rural household in contact with various domestic animals. In the biopsy specimens of both cases in the antral gastric mucosa large bacteria resembling a corkscrew were found, 6-10 microns length, consisting of 5-9 regular tight spiral. The bacteria were midly eosinophilic and Gram negative. The bacteria stained strongly with the Warthin-Starry silver stain, and with Giemsa stain. The distribution of Helicobacter Heilmannii was patchy in the central zones of the gastric pits, deep or more superficial including the foveolar opening on the mucosal surface. A mild degree of chronic gastritis characterized both cases, with, focally active inflammation and lymphoid aggregates. None of biopsies had atrophy, intestinal metaplasia or epithelial damage. There was a symptomatic improvement after a 4-week course with triple therapy (H2 antagonist & metronidazole & amoxycillin). After treatment rebiopsy specimens displayed mild chronic gastritis and no spiral organisms. CONCLUSION: Our reported cases are the first described cases of gastritis caused by Helicobacter Heilmannii in our region with successful eradication after therapy. Morphologically similar bacteria have been found in the stomachs of domestic animals. It is a general opinion that Helicobacter Heilmannii is characteristic for animals but it is occasionally transmitted to humans.

Adult↗
PubMed2000

Eradication of infection with Helicobacter spp. by use of neonatal transfer.

BACKGROUND AND PURPOSE: Efficient methods for detection and elimination of Helicobacter spp. infections are needed to facilitate the development of Helicobacter-free mouse colonies. We developed an inexpensive, high-throughput method for preparation of fecal DNA for Helicobacter polymerase chain reaction (PCR) assays. METHODS: Fecal DNA was prepared by heating fecal pellets to 95 degrees C for 10 minutes in an alkaline solution, then adjusting the pH by addition of Tris buffer. This solution is used for PCR assays without purification of DNA. We then tested fostering as a method of generating Helicobacter-free mice. Litters born to Helicobacter-positive dams were transferred to Helicobacter-negative foster dams on the first day of life. RESULTS: Fostered pups tested Helicobacter negative up to 89 days of age, whereas pups raised by Helicobacter-positive dams were all test positive by 19 days of age. CONCLUSION: These simple methods provide an efficient system for the development of Helicobacter-free mouse colonies.

Animals↗
PubMedDate not supplied

Helicobacters of possible zoonotic origin: a review.

Since the isolation of Helicobacter pylori, many new Helicobacter species have been identified from the gastrointestinal tract in humans and animals. In humans, a spiral organism different from H. pylori and provisionally named "Helicobacter heilmannii", has been associated with gastritis, gastric ulceration and to a lesser degree, gastric cancer. In addition Helicobacter cinaedi, Helicobacter fennelliae, Helicobacter pullorum and "Flexispira rappini" have been isolated from cases of enteric disease, bacteremia and pneumonic illness. In the biliary tract, the presence of Helicobacter bilis, Helicobacter pullorum and "Flexispira rappini" has been demonstrated. Morphological, epidemiological and genotypic data suggest the involvement of animal helicobacters in these infections. In this paper, a review of the literature addressing the current knowledge about epidemiology, diagnosis, pathogenesis and therapy of these infections is given.

Animals↗
PubMedDate not supplied

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia.

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.

Aged↗