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PubMed1999

Detection of Helicobacter DNA in bile from bile duct diseases.

Several species of Helicobacter colonize the hepatobiliary tract of animals and cause hepatobiliary diseases. The aim of this study is to investigate Helicobacter found in the biliary tract diseases of humans. Thirty-two bile samples (15 from bile duct cancer, 6 from pancreatic head cancer, and 11 from intrahepatic duct stone) were obtained by percutaneous transhepatic biliary drainage. Polymerase chain reaction analysis using Helicobacter specific urease A gene and 16S rRNA primers, bile pH measurement, and Helicobacter culture were performed. Helicobacter DNA was detected in 37.5%, and 31.3% by PCR with ureA gene, and 16S rRNA, respectively. The bile pH was not related to the presence of Helicobacter. The cultures were not successful. In conclusion, Helicobacter can be detected in the bile of patients with bile duct diseases. The possibility of pathogenesis of biliary tract diseases in humans by these organisms will be further investigated.

Adenocarcinoma↗
PubMed1999

[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↗
PubMed2003

[Elevated level of Helicobacter pylori antibodies in Henoch-Schonlein purpura].

INTRODUCTION: Henoch-Schönlein purpura is a non-thrombocytopenic haemorrhagic syndrome characterized by deposition of immunocomplexes in the wall of the arterioles, capillaries and venules, involving the skin, joints, gastrointestinal mucosa, and glomeruli. Several causal factors could be responsible for its evaluation, however the exact exciting agent have not been identified yet. The Helicobacter pylori infection is suggested as a possible cause of Henoch-Schönlein purpura by some authors too (Gasparini and al: Eur J Gastroenterol, 1997, 9, 231-233). AIM: Between 1995-2000 11 adult patients (64 +/- 10 year) suffering from Henoch-Schönlein purpura were admitted in our department taking particular care over detecting Helicobacter pylori infection. METHOD: Patients were classified as having either Henoch-Schönlein purpura in acute phase (5) or in remission phase (6). Each patient underwent panendoscopy with 2-2 biopsies being taken from the corpus, antral and duodenal mucosa. It was investigated the type of inflammation and the existence of Helicobacter pylori. The authors studied laboratory and immunological profiles of all the patients. Previously non of the patients got eradication therapy. RESULT: The serological investigations revealed Helicobacter pylori infection in ten investigated patients. Patients in the acute phase had significantly higher level of anti H. pylori IgG (86 +/- 32 versus 32.5 +/- 23 U/ml) (p < 0.05) compared to remission. Anti H. pylori IgA were elevated with significant difference in remission phase (3.09 +/- 1.78 versus 1.96 +/- 0.58 ratio) (p < 00.5). TNF-alpha level were significantly increased in acute phase (58.8 +/- 18 versus 27.3 +/- 5 pg/ml) (p < 0.001). Serum IgA level were also significantly higher in acute phase (5.44 +/- 1.04 versus 3.49 +/- 1.14) (p < 0.05). Anti Streptococcus DN-ase B were higher only in two patients. ANCA were negative in the all patients. CONCLUSION: According to authors findings the results suggest that seropositivity for Helicobacter pylori may be a risk factor for Henoch-Schönlein purpura. The causal role of Helicobacter pylori in the developing of Helicobacter pylori induced extraintestinal manifestations is equivocal however, it can not be ruled out with absolute certainty. To better understanding of this entity further clinical and experimental examinations have to be performed.

Acute Disease↗
PubMed2004

Is Helicobacter pylori infection a risk factor for migraine? A case-control study.

BACKGROUND: The relation between Helicobacter pylori and Migraine and usefulness of the eradication treatment on headache is controversial. The aim of this study was to determine whether Helicobacter pylori infection is a risk factor for migraine and whether the eradication of the bacterium can reduce frequency, duration and severity of clinical attacks of the disease. METHODS: A total 70 consecutive patients with migraine with aura and without aura who came to Gastroenterology polyclinic with various complaints were enrolled in the study and compared with a group of 60 matched controls. Helicobacter pylori infection was diagnosed by histopathological biopsies, which was taken by endoscopy (Olympus-GIFXQ240 endoscope). The diagnosis and classification of migraine was made according to the International Headache Society (IHS) criteria. We assessed the frequency, duration and severity of clinical attacks of migraine before and after eradication treatment. The eradication control of Helicobacter pylori was made by Helicobacter pylori fecal antigen test by PCR after 2 months. RESULTS: Helicobacter pylori positiveness is more relevant in the migranous patients compared with controls. 84.6% of patients with eradication treatment and 75% of classically treated patients informed to get benefit from the treatment. CONCLUSION: Helicobacter pylori should be examined in migranous patients and eradication of the infection may be helpful for the treatment of the disease.

Adult↗
PubMed1996

Helicobacter-specific cell-mediated immune responses display a predominant Th1 phenotype and promote a delayed-type hypersensitivity response in the stomachs of mice.

Studies regarding the nature of cell-mediated immunity in Helicobacter pylori infection and its role in pathogenesis have yielded controversial results. To address this issue in a controlled manner, we have employed the well-characterized Helicobacter felis-mouse model. Immunized/challenged and nonimmunized/infected mice were evaluated for cellular proliferation, gastric inflammation, and cytokine and Ab production at various times after infection. We observed two types of cell-mediated immune responses depending on the nature of the Ag preparation. The first response is a Helicobacter-independent response, present in all experimental groups, which is directed toward Ags such as urease and heat shock proteins. The second is a Helicobacter-dependent cellular response restricted to mice previously exposed to Helicobacter Ags either by immunization or infection. This response was not seen in noninfected controls. The Helicobacter-dependent cellular response had a Th1 phenotype, as either infected or immunized/challenged mice demonstrated local and systemic production of IFN-gamma and undetectable levels of IL-4 or IL-5. Cellular proliferation correlated with the severity of gastric inflammation in both immunized/challenged (protected) and nonimmunized/infected mice. Finally, in vivo neutralization of IFN-gamma resulted in a significant reduction of gastric inflammation in H. felis-infected, as well as immunized/challenged, mice. This treatment also revealed the presence of Th2 cells, restricted to immunized/challenged mice, as demonstrated by local and systemic production of IL-4 in these mice. These data demonstrate that Helicobacter infection and/or immunization stimulate a predominantly Th1-type, Ag-specific response and promote a local delayed-type hypersensitivity response in the stomach that may be inhibited by depletion of IFN-gamma.

Animals↗
PubMed2003

Evaluation of Helicobacter species in inflammatory bowel disease.

BACKGROUND: Bacteria have been implicated in the pathogenesis of inflammatory bowel disease. Helicobacter species have been shown to cause colitis in animal models and have been identified in human diarrhoeal illness and Crohn's disease. AIM: To determine whether Helicobacter species are present in human inflammatory bowel disease tissue. METHODS: Thirty patients undergoing colonoscopy for clinical reasons were studied. Nine had Crohn's disease, 11 had ulcerative colitis and 10 had histologically normal colons. Tissue was snap-frozen at -70 degrees C. DNA was extracted and examined by five different polymerase chain reaction (PCR) assays that were either genus or species specific for Helicobacter. RESULTS: Analyses of colonic biopsies by two Helicobacter genus-specific PCR assays, two H. pylori-specific assays and a PCR assay designed to amplify fragments of 'H. heilmannii'-like organisms demonstrated that product was not generated by any test. Internal control PCR demonstrated that PCR results for the five assays were not negative due to the presence of residual substances inhibitory to PCR. CONCLUSIONS: Helicobacter species were not identified in this study, using multiple PCRs to eliminate the problems of non-specific cross-reaction. This suggests that Helicobacter species do not play a role in the pathogenesis of inflammatory bowel disease.

Adult↗
PubMed1996

Therapeutic immunization against Helicobacter mustelae in naturally infected ferrets.

BACKGROUND & AIMS: Helicobacter infection of the gastric antrum is responsible for a number of gastric disorders. Antibiotic therapy is lengthy and is not always effective. It has been shown previously that oral immunization against Helicobacter felis in mice can prevent colonization after challenge. The aim of this study was to investigate the efficacy of therapeutic immunization in eradicating an established Helicobacter infection and in reducing gastritis. METHODS: Domestic ferrets, confirmed to be infected with Helicobacter mustelae by gastric endoscopy, were orally immunized with varying doses of purified Helicobacter pylori urease in combination with the mucosal adjuvant cholera toxin. Ferrets were assessed 1 week and 6 weeks after treatment for infection and pathology. RESULTS: Therapeutic immunization eradicated Helicobacter colonization in 30% of all immunized ferrets, although there was no difference in efficacy between the varying doses of antigen tested. The difference was statistically significant when compared with animals administered cholera toxin alone or buffer (P = 0.04). The intensity of inflammation was also significantly reduced in immunized animals (P = 0.0003). CONCLUSIONS: Oral immunization with purified H. pylori urease and cholera toxin can eradicate H. mustelae in a natural host pathogen model. Oral immunization of chronically infected animals markedly reduced gastric inflammation.

Administration, Oral↗
PubMed2000

Gastric helicobacters in cats.

The types of helicobacter which are found in the stomachs of carnivorous pets, especially cats, have been traditionally referred to as 'gastric helicobacter-like organisms' (GHLOs). These are microaerophilic, Gram-negative, spiral bacteria with multiple terminal flagellae and are endowed with high-level urease activity which allows them to survive in an acidic environment. Certain species have one or more periplasmic fibrils. The two GHLOs most commonly found in cats are Helicobacter felis and a species related to H heilmannii which was recently cultured from dogs. All phenotypic and genotypic (16S RNA gene sequences) evidence suggests that both of these bacteria belong in the genus Helicobacter. Whether or not helicobacters can be transmitted to humans from carnivorous pets is controversial but the recent discovery of H pylori -infected cats may be evidence of an animal reservoir for this pathogen. Although the role of H pylori in inducing antral gastritis and perpetuating pyloric ulcers in humans is well established, whether or not Helicobacter spp are causally involved in any feline gastric inflammatory conditions is unknown.

Animals↗
PubMed2000

Helicobacter infection and cirrhosis in hepatitis C virus carriage: is it an innocent bystander or a troublemaker?

Since it has been shown that Helicobacter hepaticus causes both chronic hepatitis and hepatocellular carcinoma (HCC) in mice, it is suggested that differences in the progression of chronic hepatitis C may be due to a cofactor stemming from co-infection by bacteria, especially Helicobacter pylori, and/or other Helicobacter species. An assessment was made of the prevalence of H. pylori infection in HCV-positive cirrhotic patients. The presence of Helicobacter species (spp). was evaluated in resected liver tissue from HCC patients. Serum anti-H. pylori IgG antibodies were determined in 70 males with a clinical and/or histological diagnosis of cirrhosis and HCV infection and in 310 age-matched male blood donors. The prevalences of H. pylori antibody were 77% (54/70) and 59% (183/310) (P 0.004). Primers identifying 26 Helicobacter species were used to determine the presence of the genomic 16S rRNA of this genus in liver tissue resected from 25 cirrhotic HCC patients. Genomic sequences corresponding to H. pylori and H. pullorum were identified in 23 of these 25 livers. Together, these findings support the proposal that H. pylori is implicated in the pathogenesis and progression of cirrhosis, particularly in HCV-infected individuals. Involvement of Helicobacter spp. in HCC also seems highly possible.

Animals↗
PubMed2006

Urea, fluorofamide, and omeprazole treatments alter helicobacter colonization in the mouse gastric mucosa.

BACKGROUND: Helicobacter pylori is a causative agent of gastric and duodenal ulcers and gastric cancer. Its urease enzyme allows survival in acid conditions and drives bacterial intracellular metabolism. We aimed to investigate the role of urease in determining the intragastric distribution of Helicobacter species in vivo. MATERIALS AND METHODS: The C57BL/6 mouse model of gastritis was used for infection with Helicobacter felis (CS1) or H. pylori (SS1). Urease-modulating compounds urea and/or fluorofamide (urease inhibitor) were administered to mice over 7 days. Concurrent gastric acid inhibition by omeprazole was also examined. Bacterial distribution in the antrum, body, antrum/body, and body/cardia transitional zones was graded "blindly" by histologic evaluation. Bacterial colony counts on corresponding tissue were also conducted. RESULTS: Urease inhibition by fluorofamide decreased H. pylori survival in most gastric regions (p < .05); however, there were no marked changes to H. felis colonization after this treatment. There was a consistent trend for decreased antral colonization, and an increase in antrum/body transitional zone and body colonization with excess 5% or 6% (w/v) urea treatment. Significant reductions of both Helicobacter species were observed with the co-treatment of urea and fluorofamide (p < .05). Collateral treatment with omeprazole did not alter H. pylori colonization patterns caused by urea/fluorofamide. CONCLUSIONS: Urease perturbations affect colonization patterns of Helicobacter species. Combined urea and fluorofamide treatment reduced the density of both Helicobacter species in our infection model.

Animals↗
PubMed2002

Molecular evidence of Helicobacter cinaedi organisms in human gastric biopsy specimens.

One hundred twenty-six urease-negative gastric biopsy specimens were evaluated for the presence of Helicobacter genus-specific 16S ribosomal DNA (rDNA) and H. pylori-specific glmM DNA sequences by PCR. The species specificity of the glmM PCR assay was demonstrated, as H. pylori was the only Helicobacter species that yielded the expected glmM amplicon. Most urease-negative specimens (118 of 126 specimens) lacked Helicobacter DNA. However, 8 of 126 urease-negative specimens contained Helicobacter 16S rDNA. In order to identify the Helicobacter species present in urease-negative gastric biopsy specimens, 16S rDNA amplicons were cloned and sequenced. Sequence comparisons were performed by analyses of the sequences in public sequence databases. Two samples contained 16S rDNA that was identified as H. cinaedi with 100% identity and that spanned approximately 400 bp (398 and 398 bp, respectively). In contrast, multiple differences (97% identity; 390 of 398 bp) were observed with H. pylori 16S rDNA in this region. This finding was verified by sequencing an overlapping 537-bp fragment within the 5' portion of 16S rDNA. Although the clinical findings were consistent with H. pylori infection (e.g., duodenal ulcer disease), rapid urease testing and DNA sequence analyses suggested the presence of H. cinaedi organisms and the absence of H. pylori in two human antral biopsy specimens. This study represents the first report of an enteric urease-negative helicobacter in the human stomach. Although these organisms were previously associated with extragastric infections, the roles of these organisms in the pathogenesis of chronic gastritis or peptic ulcer disease remain unclear.

Base Sequence↗
PubMedDate not supplied

Fecal polymerase chain reaction with 16S ribosomal RNA primers can detect the presence of gastrointestinal Helicobacter in dogs.

Questions about pathogenesis and therapy for Helicobacter infections in dogs could be answered with a simple, noninvasive, sensitive, and specific diagnostic test. We hypothesized that a fecal polymerase chain reaction (PCR) assay would detect Helicobacter and could be useful for assessing therapeutic responses. Paired gastric biopsies and fecal samples were obtained from 39 random source dogs (group 1). Gastric biopsies from each of these dogs had histologic evidence of gastric spiral bacteria, and paired gastric tissue and fecal samples produced a 375-base pair (bp) product when amplified by PCR with Helicobacter-specific primers. Specificity of the PCR product was confirmed by detection of expected 60-, 119-, and 196-bp products following Hinfl digestion. Direct sequencing of amplicons from paired PCR products from gastric biopsy and fecal samples from 8 group I dogs showed that gastric products had the highest homologies with known gastric Helicobacter species, whereas fecal products had the highest homologies with intestinal species. Healthy mixed-breed dogs (group II; n = 8) with histologically confirmed spiral bacteria infection were treated with a 21-day course of metronidazole, amoxicillin, and famotidine. Fecal samples were collected from group II dogs twice before and within 3 days of completion of treatment. The PCR results correctly identified 15/16 pretreatment samples as positive: 1 pretreatment sample was negative. PCR results identified 8/8 posttreatment samples as Helicobacter negative. Fecal PCR is a useful test for detecting Helicobacter infection in dogs. This assay may be useful as a screening test for infection and could be used to address questions relevant to pathogenesis and therapy.

Animals↗
PubMed1998

Severe atrophic gastritis with Helicobacter pylori infection and gastric cancer.

BACKGROUND: We conducted a case-control study to evaluate whether patients with severe gastric atrophy (indicated by serum pepsinogen concentration) have a high risk of gastric cancer.METHODS: At the time of diagnosis of gastric cancer, sera from 301 patients (cases) and 602 sex- and age-matched cancer-free individuals (controls) were tested for the presence of anti- Helicobacter pylori IgG antibody (HM-CAP enzyme-linked immunoassay [ELISA] kit; Kyowa Medix, Tokyo, Japan) and serum pepsinogen (PG) levels (PG I and II Riabead Kits; Dainabot, Tokyo, Japan). We defined positivity for pepsinogen a pepsinogen I concentration of less than 70 ng/mL and a PG I/II ratio of less than 3.0. We categorized the subjects according to serum pepsinogen levels and anti- Helicobacter pylori IgG antibody, creating four categories.RESULTS: Of the 301 cancer cases, 177 had positive serum pepsinogen levels, and 172 were positive for anti- Helicobacter pylori IgG antibody. The category in which subjects had positive serum pepsinogen levels and were negative for anti- Helicobacter pylori IgG antibody had the highest proportion (76.9%) of individuals with gastric cancer and the highest odds ratio (4.20) of the four categories. The odds ratios were 2.55 (95% confidence interval; 1.92-3.88) for positive serum pepsinogen levels and 0.93 (95% confidence interval; 0.63-1.27) for positive anti- Helicobacter pylori IgG antibody.CONCLUSION: These results suggest that patients with positive serum pepsinogen levels who are negative for IgG antibody to Helicobacter pylori, constitute a high-risk group for gastric cancer. Helicobacter pylori infection is associated with the development of gastric cancer by providing a suitable environment i.e., severe gastric atrophy, for carcinogenesis of the gastric mucosa.

Journal Article↗
PubMed2002

What effect does Helicobacter pylori infection have on the risk of peptic ulceration in patients receiving NSAIDs for rheumatoid arthritis?

BACKGROUND: Patients with rheumatoid arthritis (RA) frequently develop dyspepsia which may be due to peptic ulceration. There have been conflicting published data on the possible interactive roles of nonsteroidal anti-inflammatory drugs (NSAIDs) and colonisation of the gastric antrum with Helicobacter pylori in the development of peptic ulceration. METHODS: We have prospectively assessed the prevalence of peptic ulcers in dyspeptic RA patients and investigated the factors responsible. We endoscoped 100 RA patients comparing the endoscopic findings to those in 100 age- and sex-matched dyspeptic control subjects. Data on NSAID consumption and Helicobacter colonisation were collected for each patient. RESULTS: Endoscopic evidence of peptic ulceration was found in 29 RA patients and in 16 of the control subjects (P=0.03). Multiple ulcers (>2) were found in significantly more RA patients than in controls (10 vs. 2). NSAIDs were being used by 60 RA patients and 22 controls (P<0.001). Helicobacter was found in 41 RA patients and in 33 controls (P=NS). The consumption of NSAIDs conferred a relative risk (RR) of ulceration of 8.67 (1.19-62.87), while the presence of Helicobacter gave a RR for ulcers of 3.71 (0.37-37.35) in RA patients. The RR for the combination of NSAID consumption and Helicobacter colonisation was 14.44 (2.05-101). The corresponding RRs for the dyspeptic controls were 2.13, 1.57 and 1.42 (all P=NS). CONCLUSIONS: Rheumatoid patients have more major and more multiple pathology than age-, sex- and symptom-matched controls. This is due mainly to their increased consumption of NSAIDs. The prevalence of Helicobacter was no greater in RA patients than in controls, but Helicobacter infection increased the risk of NSAID-induced ulceration.

Journal Article↗
PubMed2000

Helicobacter pylori infection and risk of gastric cancer in Changle County,Fujian Province,China.

AIM:To evaluate the effects of Helicobacter pylor infection and other environmental factors on the development of gastric cancer.METHODS:A population-based case control study was conducted in Changle County, Fujian Province. The primary gastric cancer cases were histologically confirmed or diagnosed by surgery between January 1996 and March 1998. Healthy controls were randomly selected and matched by age, sex, and neighborhood of residence.A total of 101 pairs were included in the study. Specially trained interviewers conducted face-to-face interviews with the subjects according to a standardized questionnaire. Helicobacter pylori infections were measured by serum IgG antibody to Helicobacter pylori. Conditional Logistic Regression analysis was used.RESULTS:The presence of IgG antibody to Helicobacter pylori was 63.7% in study subjects, 56.0% in patients with cardiac cancer, and 60.5% in patients with non-cardiac gastric cancer. The risk factors of gastric cancer in Changle County were identified such as low educational level (OR = 3.864; 95% confidence interval (95%CI) 1.604-9.311), low consumption of fresh vegetables (OR = 4.925; 95%CI 1.356-17.885), high intake of fish sauce (OR = 10.587; 95%CI 2.821-39.738), unscheduled meals (OR = 4.254; 95%CI 1.445-12.552), and Helicobacter pylori infection (OR = 3.453; 95%CI 0.901-13.224).CONCLUSION:Helicobacter pylori infection may be important in the etiology of gastric cancer, but major risk factors other than Helicobacter pylori are responsible for the high gastric morbidity in Changle County.

Journal Article↗
PubMed1999

Helicobacter pylori infection: the reduced need for ulcer surgery.

The success of the eradication treatment for Helicobacter pylori in managing ulcer disease has further refined the indications for ulcer surgery. More patients are spared unnecessary surgery and its untoward sequelae. It is intriguing that surgery has been effective, given that Helicobacter pylori infection is the underlying culprit. Recent studies show that the prevalence of Helicobacter pylori infection remains high after a vagotomy but is more markedly reduced following a partial gastrectomy. Such a reduction may be due to the removal of distal stomach, which is the usual site of infection. In addition, bile appears to be bactericidal to Helicobacter pylori. The association between Helicobacter pylori infection and perforated duodenal ulcer has not been completely settled. A recent study demonstrates that male gender and positive Helicobacter pylori status are independent factors that are associated with recurrent duodenal ulcer after surgery for perforation. Hence, eradication therapy should be given to any patient who has a Helicobacter pylori infection, after surgery has been performed for perforated duodenal ulceration.

Journal Article↗
PubMed2002

The effect of Helicobacter pylori eradication on symptoms and gastric emptying in patients with nonulcer dyspepsia.

BACKGROUND/AIMS: This study was undertaken to evaluate the effect of eradication therapy on the symptoms of Helicobacter pylori positive non-ulcer dyspepsia patients. METHODS: Twenty-four patients participated in the study and the symptoms of daytime epigastric pain, night or hunger pain, nausea, vomiting, regurgitation, bloating, belching, early satiety and anorexia were scored at the beginning, the 15th day after starting eradication therapy (amoxicillin 2 gr bid, clarithromycin 2 gr bid and omeprazole 40 mg daily for two weeks) and during the third and sixth months. Gastric emptying of radiolabelled solid meal was determined at baseline and during the third month. RESULTS: The Helicobacter pylori eradication rate was 79% and symptom scores significantly decreased during the follow-up period in both of the groups, irrespective of Helicobacter pylori status. The mean symptom scores of the 24 patients at baseline, day 15 and and months three and six were as follows: 1.275, 0.274, 0.496 and 0.238 respectively. Symptom scores for the 19 patients with Helicobacter pylori eradication were 1.084, 0.263, 0.347 and 0.215 respectively while in the five patients in whom Helicobacter pylori eradication therapy failed it was 2.0, 0.314, 1.06 and 0.32 respectively. Of the 16.6% Helicobacter pylori positive non-ulcer dyspepsia patients who had delayed gastric emptying of solids, there was no change after eradication therapy. Nine patients, including all of those in whom eradication therapy failed, required further medication (antacids/prokinetics) for continuing symptoms one month after completion of treatment. CONCLUSIONS: The results of this study suggest that Helicobacter pylori is a causal factor in symptoms of non-ulcer dyspepsia and that eradication therapy improves symptoms and endoscopic findings but has no effect on gastric emptying.

Journal Article↗
PubMed2005

Identification of Helicobacter sp. in gastric mucosa from captive marmosets (Callithrix sp.; callitrichidae, primates).

The aim of this study was to identify the presence of Helicobacter sp. in the gastric mucosa of captive marmosets (Callithrix sp.). Histologic specimens from the fundic, corpus, and antral gastric regions of six Callithrix jacchus, 12 C. kuhli, and 12 C. geoffroyi specimens were evaluated. The sections were stained with hematoxylin-eosin (H&E) and the Warthin-Starry silver impregnation method, and immunostained with rabbit anti-H. pylori polyclonal antibody. Helicobacter-like organisms (HLOs) and coccoid forms were present in silver-stained sections from 29 stomachs, whereas immunohistochemistry (IHC) tests revealed bacterial aggregates in 15 stomachs. No statistical difference relative to the presence of Helicobacter sp. was found among the gastric regions or marmoset species. Gastric lesions were found in the groups of marmosets that had positive and negative IHC results, but no correlation between inflammation and Helicobacter sp. infection was established. These findings demonstrate that marmosets are susceptible to naturally-occurring Helicobacter sp. infection, and open the way to the development of comparative studies on Helicobacter sp. infection in humans.

Animals↗