Age-dependent seroprevalence of antibodies against a Helicobacter pylori-like organism and Helicobacter pylori in commercially reared swine

OBJECTIVE: To determine the prevalence of antibodies against a swine-origin Helicobacter pylori-like organism (HPLO) and H pylori in conventionally reared swine. ANIMALS: 640 conventionally reared swine of various ages from 16 high-health farms in Canada, 20 sows from Ohio, and 35 gnotobiotic swine. PROCEDURES: Blood was collected from the cranial vena cava. Sera were collected and tested via ELISA for antibodies against antigen prepared from a swine-origin HPLO and human H pylori strain 26695. RESULTS: Antibodies reactive with a swine HPLO, H pylori, or both were detected in 483 of 640 swine from all 16 farms in western Canada. Seroprevalence varied with age and was low (5.6%) in suckling ( 4 weeks old to adulthood. CONCLUSIONS AND CLINICAL RELEVANCE: Findings suggested that colonization by a swine-origin HPLO, H pylori, or both and resultant seroconversion, like that of H pylori infection in humans, were common in commercial swine operations. Furthermore, data indicated that gastric infection was acquired at an early age. The relationships to gastric colonization by HPLOs and clinical manifestations of disease such as gastritis and gastroesophageal ulceration remain to be determined.     

Isolation and preliminary characterization of a novel Helicobacter species from swine

OBJECTIVE: To determine whether a Helicobacter sp similar to Helicobacter pylori in the stomachs of humans could be isolated from the stomachs of pigs. ANIMALS: 4 young conventionally reared and 21 gnotobiotic pigs. PROCEDURE: Gastric mucosal homogenates (10% wt/vol) from 4 young conventionally reared pigs were cultured on Skirrow medium under microaerophilic conditions to assess the presence of Helicobacter spp. Colonies with morphologic features compatible with Helicobacter organisms were selected, tested for urease activity, and subpassaged on Skirrow medium. Isolates were examined via SDS-PAGE electrophoresis and reciprocal western blot analyses involving convalescent sera from monoinfected gnotobiotic pigs. RESULTS: Urease- and catalase-positive, gram-negative, microaerophilic, small, curved rod bacteria were isolated from the gastric mucosa of young healthy pigs. The first isolate (2662) was structurally and immunologically closely related to H pylori isolated from humans. The second isolate (1268) displayed an SDS-PAGE profile dissimilar to that of H pylori and isolate 2662, yet it shared limited immunologic cross-reactivity with these microbes. CONCLUSIONS AND CLINICAL RELEVANCE: Findings of this study indicate that development of gastric mucosal ulcers and ulceration of the nonglandular pars esophagea in pigs may be associated with gastric colonization by swine-origin Helicobacter spp, which are similar to H pylori isolated from humans.     

Reproduction of severe gastroesophageal ulcers (GEU) in gnotobiotic swine infected with porcine Helicobacter pylori-like bacteria

Groups of gnotobiotic piglets were orally inoculated at 3 days of age with either Helicobacter heilmannii (Hh) or a newly described porcine-origin gastric Helicobacter pylori (Hp)-like bacterium. Three Hh-infected and 6 porcine Hp-like-infected swine were fed a milk replacement diet containing 5-10% (v/v) sterile corn syrup as a dietary source of fermentable carbohydrate. None of the piglets infected with Hh and supplemented with corn syrup developed gastric mucosal ulcers; 2 developed small erosive lesions in the pars esophagea. In contrast, all 6 dietary carbohydrate-supplemented Hp-like-infected swine developed severe gastroesophageal ulcers; 1 of these ex-sanguinated into the stomach and died before the end of the experiment. Four of these 6 piglets had grossly evident partially digested blood in the intestinal lumens, indicative of bleeding into the gastrointestinal tract from the stomach. These data suggest that a high carbohydrate diet and gastric colonization by porcine Hp-like bacteria facilitate development of clinically significant gastroesophageal ulcers.     

Detection of Helicobacter-like Bacteria in Porcine Gastric Biopsy Samples by Amplification of 16S rRNA,ureB, vacA and cagA Genes by PCR

Preliminary evidence for the presence of Helicobacter-like bacteria was sought in 395 porcine gastric samples by a urease test. Of the samples, 37% (146/395) were urease-positive and 82% (82/100) of the Gram-stained urease-positive samples showed large, tightly spiralled organisms. Several methods were applied to culture the organisms but isolation was unsuccessful, contaminant organisms being considered to be one of the major problems. PCR with Helicobacter genus-specific primers for 16S rRNA and ureB genes, and primers for H. pylori vacA and cagA genes were tested with 102 urease-positive biopsy samples. The PCR results showed some evidence for the presence of the urease and the vacA genes in porcine Helicobacter-like bacteria and raises the possibility of pathogenicity by these organisms.     

Helicobacter spp. infection in cats: evaluation of the humoral immune response and prevalence of gastric Helicobacter spp

The principal aims of this study were to evaluate the humoral immune response (IgG) of cats with gastric Helicobacter spp. infection, and to determine the prevalence of different types of Helicobacter spp. in the stomachs of cats. The Helicobacter infection status of 45 cats (12 healthy spay/neuter cats, 9 sick cats, 24 colony cats) was determined by evaluating endoscopic gastric biopsies for urease activity, presence of Helicobacter-like organisms (HLO) on histopathology, and genus and species-specific PCR. Serum samples were evaluated with a kinetic enzyme linked immunosorbent assay (ELISA) utilizing the high molecular cell-associated protein (HM-CAP) fraction of H. felis ATCC 49179.Seventeen of 45 cats were infected with Helicobacter spp.: "H. heilmannii" 9/17, H. felis 4/17, mixed "H. heilmannii" and H. felis 3/17, unclassified-Helicobacter spp. 7/17. H. pylori was not detected in any cat. Kinetic ELISA results were significantly higher for infected cats, than for uninfected cats. Cats infected with different Helicobacter spp. showed similar distribution of OD/min values. There were no effects of age or clinical signs on the results of kinetic ELISA. No correlation between colonization density and seroconversion was observed. There were statistically significant, but weak correlations between the degree of seroconversion and the degree of inflammation, and the number of lymphoid follicles. Infected cats had more severe inflammation in the pylorus and fundus than uninfected cats. Infected sick cats had a higher degree of pyloric, but not fundic inflammation, than healthy infected cats and uninfected sick cats.The results indicate that naturally acquired infection with gastric Helicobacter spp. is associated with seroconversion (IgG) in cats. The similar ELISA values in cats infected with a variety of Helicobacter spp. suggests substantial antigenic homology between different Helicobacter spp. The higher degree of inflammation in infected than uninfected cats, supports a role for Helicobacter as a cause of gastritis in cats.     

In situ detection of urease-positive Helicobacter pylori-like organisms on swine gastric mucosa

The objective of this study was to improve the visual localization of urease activity of Helicobacter pylori-like organisms (HPLO) on swine gastric mucosa by in vitro optimization of the urea concentration and pH indicator of a urease test reagent. Five 21-day-old conventional pigs were infected orally with HPLO (3 pigs) or Brucella broth alone (2 pigs). At 17 d after infection the pigs were euthanized and their stomachs excised and tested for HPLO by a modified urease test formulation sprayed onto the gastric mucosa, as well as confirmatory culture and isolation of HPLO from urease-positive sites. This study showed improved detection of HPLO in porcine gastric mucosa with the use of a modified urease test formulation containing 5% urea and the pH indicator bromocresol purple compared with the use of a conventional formulation of 2% urea and phenol red. This test can readily be applied to achieve a presumptive diagnosis of HPLO in cases of gastritis or gastric esophageal ulceration in pigs.     

Histological and immunohistochemical detection of different Helicobacter species in the gastric mucosa of cats.

Detailed histopathological evaluation of the gastric mucosa of Helicobacter-infected cats is complicated by the difficulty of recognizing Helicobacter organisms on hematoxylin and eosin (HE)-stained sections and the ability of multiple Helicobacter species to infect cats. In this study, the presence and localization of different species of Helicobacter in the stomachs of cats was investigated using silver staining and immunohistochemistry. Five groups containing 5 cats each were established (group 1: urease negative and Helicobacter free; groups 2, 3, 4, and 5: urease positive and infected with Helicobacter heilmannii, unclassified Helicobacter spp., Helicobacter felis, and Helicobacter pylori, respectively). Gastric samples were evaluated by HE and silver staining and by immunohistochemistry with 3 different anti-Helicobacter primary antibodies. Helicobacter were detected by Steiner stain in all infected cats at the mucosal surface, in the lumen of gastric glands, and in the cytoplasm of parietal cells. In silver-stained sections, H. pylori was easily differentiated from H. felis, H. heilmannii, and unclassified Helicobacter spp., which were larger and more tightly coiled. No organisms were seen in uninfected cats. Helicobacter antigen paralleled the distribution of organisms observed in Steiner-stained sections for 2 of the 3 primary antibodies tested. The antisera were not able to discriminate between the different Helicobacter species examined. A small amount of Helicobacter antigen was present in the lamina propria of 3 H. pylori-, 3 H. felis-, and 1 H. heilmannii-infected cat. Minimal mononuclear inflammation was present in uninfected cats and in those infected with unclassified Helicobacter spp. and H. heilmannii cats. In H. felis-infected cats, lymphoid follicular hyperplasia with mild pangastric mononuclear inflammation and eosinophilic infiltrates were present. The H. pylori-infected cats had severe lymphoid follicular hyperplasia and mild to moderate mononuclear inflammation accompanied by the presence of neutrophils and eosinophils. These findings indicate that Steiner staining and immunohistochemistry are useful for detecting Helicobacter infections, particularly when different Helicobacter species can be present. Monoclonal antibodies specific for the different Helicobacter species could be important diagnostic aids. There appear to be differences in the severity of gastritis in cats infected with different Helicobacter species.     

Genome sequence of Helicobacter suis supports its role in gastric pathology

ABSTRACT: Helicobacter (H.) suis has been associated with chronic gastritis and ulcers of the pars oesophagea in pigs, and with gastritis, peptic ulcer disease and gastric mucosa-associated lymphoid tissue lymphoma in humans. In order to obtain better insight into the genes involved in pathogenicity and in the specific adaptation to the gastric environment of H. suis, a genome analysis was performed of two H. suis strains isolated from the gastric mucosa of swine. Homologs of the vast majority of genes shown to be important for gastric colonization of the human pathogen H. pylori were detected in the H. suis genome. H. suis encodes several putative outer membrane proteins, of which two similar to the H. pylori adhesins HpaA and HorB. H. suis harbours an almost complete comB type IV secretion system and members of the type IV secretion system 3, but lacks most of the genes present in the cag pathogenicity island of H. pylori. Homologs of genes encoding the H. pylori neutrophil-activating protein and γ-glutamyl transpeptidase were identified in H. suis. H. suis also possesses several other presumptive virulence-associated genes, including homologs for mviN, the H. pylori flavodoxin gene, and a homolog of the H. pylori vacuolating cytotoxin A gene. It was concluded that although genes coding for some important virulence factors in H. pylori, such as the cytotoxin-associated protein (CagA), are not detected in the H. suis genome, homologs of other genes associated with colonization and virulence of H. pylori and other bacteria are present.     

Evaluation of lansoprazole (an H+/K+-ATPase inhibitor) and azithromycin (an antibiotic) for control of gastric ulceration in swine during periods of feed deprivation.

Helicobacter-like organisms as well as fermentative bacteria have been implicated in gastric ulcer production in swine. Irregular feeding schedules are also considered a major risk factor. A research trial was conducted to determine whether medication with an acid secretion inhibitor (lansoprazole), either alone or in combination with an antibiotic (azithromycin), would protect pigs from gastric ulceration if the animals were subjected to a 48 h period of fasting. In a 2 x 3 factorial design, 48 pigs were fasted, while an equal number were fed ad libitum. Within these 2 study groups, pigs were randomly assigned to 1 of 3 treatments: control, 30 mg lansoprazole s.i.d. for 7 d, or lansoprazole (30 mg s.i.d. for 7 d) and azithromycin (500 mg s.i.d. for 3 d). Overall, fasted pigs were 1.9 times more likely to develop erosive or ulcerative lesions of the pars esophagea (chi2 = 9.89, P < 0.002). Treatment with an acid secretion inhibitor alone or in combination with an antibiotic did not protect pigs from developing gastric lesions. Helicobacter-like organisms were not detected in any of the stomachs. Possibly, the lansoprazole dose of 30 mg given once per day was insufficient to prevent pH levels from becoming low enough to cause damage to epithelial tissue. Alternatively other substances such as bile acids may have caused the ulcerative lesions, even though stomach acid production was suppressed.     

Postweaning multisystemic wasting syndrome produced in gnotobiotic pigs following exposure to various amounts of porcine circovirus type 2a or type 2b

In late 2005, a postweaning, high mortality syndrome spread rapidly through finishing barns in swine dense areas of the United States. Diagnostic investigations consistently detected porcine circovirus type 2 (PCV2) from diseased tissues. Subsequent genetic analysis revealed that the infectious agent was a PCV2 type termed "PCV2b". Prior to late 2004, only the PCV2a type, but not PCV2b, had been reported in North America. In this communication, we produce severe postweaning multisystemic wasting syndrome (PMWS) in gnotobiotic pigs using infectious PCV2a and PCV2b generated from DNA clones constructed from field isolates identified in the 2005 outbreak. Clinical signs exhibited by diseased pigs included anorexia, dyspnea and listlessness. Mortality was typically observed within 12h of onset of dyspnea. The most striking microscopic lesions in affected animals were severe hepatic necrosis and depletion of germinal centers in lymph nodes with associated abundant PCV2 viral antigen. Clinical signs and lesions observed in these studies were comparable to those reported in experiments with gnotobiotic pigs inoculated with a PCV2a isolate while concurrently receiving immune-stimulation or co-infection with porcine parvovirus or torque teno virus. The animals in these studies were confirmed to be free of detectable porcine parvovirus, porcine reproductive and respiratory syndrome virus, bovine viral diarrhea virus, swine hepatitis E virus, and aerobic and anaerobic bacteria. Seven out of 24 PCV2 inoculated pigs had a detectable congenital torque teno virus infection with no correlation to clinical disease. Thus, in these studies, both PCV2a and PCV2b isolates were singularly capable of inducing high mortality in the absence of any detectable infectious co-factor.     

Helicobacter infection in dogs and cats: facts and fiction

The discovery of the spiral bacterium Helicobacter pylori and its causative role in gastric disease in humans has brought a dramatic change to gastroenterology. Although spiral bacteria have been known for more than a century to infect the stomachs of dogs and cats, recent research has been conducted mainly in the wake of interest in H. pylori. H. pylori has not been found in dogs and only very rarely in cats and zoonotic risk is minimal. A variety of other Helicobacter spp. can infect the stomach of pets; however, their pathogenic role is far from clear, and they have a small but real zoonotic potential. The prevalence of gastric Helicobacter spp. in dogs and cats is high, irrespective of clinical signs, and as in human medicine, mode of transmission is unclear. The relationship of Helicobacter spp. to gastric inflammation in cats and dogs is unresolved, with inflammation, glandular degeneration, and lymphoid follicle hyperplasia accompanying infection in some but not all subjects. Circulating anti-Helicobacter immunoglobulin G antibodies have been detected in 80% of dogs with naturally acquired infection and most dogs and cats with experimental infection. The gastric secretory axis is similar in infected and uninfected cats and dogs and no relationship of infection to gastrointestinal ulcers has been found. Differences in the pathogenicity of Helicobacter spp. are apparent, because infection with H pylori is associated with a more severe gastritis than infection with other Helicobacter spp. in both cats and dogs. Rapid urease test, histopathology, and touch cytology are all highly accurate invasive diagnostic tests for gastric Helicobacter-like organisms in dogs and cats, whereas culture and polymerase chain reaction are the only means to identify them to the species level. Urea breath and blood tests or serology can be used to diagnose Helicobacter spp. noninvasively in dogs and cats. Most therapeutic studies in pets have not shown long-term eradication of Helicobacter spp. Whether this is due to reinfection or recrudescence has not been established.     

Detection and isolation of Helicobacter mustelae from stoats in New Zealand

AIM: To determine the incidence of Helicobacter mustelae in stoats (Mustela erminea) in New Zealand. METHODS: Helicobacter-like organisms and total genomic DNA were isolated from gastric tissue of stoats and identified using a combination of bacterial culture, phenotypic testing and molecular techniques. RESULTS: A Helicobacter-specific 16S rRNA polymerase chain reaction product was detected in 16/32 gastric tissue biopsies tested. Nine of 13 partially sequenced 16S rRNA DNA identified H. mustelae 16S DNA. Bacteria, subsequently identified as H. mustelae, were successfully cultured from the stomachs of 4/32 stoats. Other Helicobacter species were also identified by DNA sequence analysis, but were not cultured. CONCLUSIONS: Helicobacter mustelae is present in stoats from both the North and South Islands of New Zealand.     

The high prevalence of Helicobacter sp. in porcine pyloric mucosa and its histopathological and molecular characteristics

This study examined the prevalence of Helicobacter infection in the pyloric mucosa of pigs and its histopathological and molecular characteristics. Forty porcine pyloric samples were examined for Helicobacter infection by silver staining and PCR assay. The PCR product (376 bp) was digested with NdeII to differentiate between Helicobacter heilmannii and Helicobacter pylori. Another PCR assay run to produce an 1157 bp fragment was performed using a primer set designed from the 16S rRNA gene of Candidatus H. suis, and its product was cloned and sequenced. Infection rates were 62.5% (25/40) and 95.0% (38/40) as determined by silver staining and the PCR assay, respectively. On histopathological examination, lymphoid follicle aggregation in the pyloric mucosa and granulocytic migration into the lumen of pyloric glands were observed in 24 (60.0%) and 33 (82.5%) gastric samples, respectively. All PCR products, except that of H. pylori, were cut into two fragments of 147 and 229 bp by enzymatic digestion with NdeII. Sequencing of the 16S rRNA gene showed that the bacterium had 99.57% (1152 bp/1157 bp) homology to the 16S rRNA gene of Candidatus H. suis.     

The first description of gastric Helicobacter in free-ranging wild boar (Sus scrofa) from Poland

Specimens of gastric mucosa of 17 free-ranging wild boars (Sus scrofa) shot in the Central Poland during 2007/2008 hunting season were investigated for the presence of Helicobacter species. Histopathology, Helicobacter genus-specific 16S rRNA PCR, and DNA sequence analysis were employed. In PCR analysis the presence of Helicobacter's DNA was detected in one stomach. Obtained sequence analysis showed its relatedness to Helicobacter heilmannii type 2. In histopathology of the PCR-positive sample the presence of tightly coiled spiral bacteria was detected on the surface of the antral mucosa, in gastric pits and lumen of the upper parts of antral glands. Potential pathologic significance of the presence of Helicobacter in the stomach of free-ranging wild boars was obscured by the parasitic invasion-caused gastritis, and remains unknown.     

A Lawsonia intracellularis transmission study using a pure culture inoculated seeder-pig sentinel model

Transmission of Lawsonia intracellularis from experimentally inoculated pigs to naive swine was demonstrated in this study. The study was conducted using conventional pigs divided into three groups as follows: principles inoculated with L. intracellularis, sentinels, and controls. The pigs were inoculated and paired on 13 and 9 days post-inoculation with a sentinel pig for 7 days. Fecal samples and serum samples were collected throughout the study for polymerase chain reaction (PCR) and antibody testing by indirect fluorescent antibody techniques. After co-mingling, the inoculated group was necropsied; sentinel and control pigs were necropsied 7-14 days later. The intestinal tracts were evaluated grossly and microscopically for lesions. PCR was performed on intestinal mucosal scrapings and feces. Warthin-Starry and fluorescent antibody staining procedures were conducted to confirm colonization with L. intracellularis. Gross and microscopic lesions typical of porcine proliferative enteropathy (PPE) were observed in both the inoculated and sentinel groups. Transmission was demonstrated from inoculated principle pigs to sentinel pigs. PCR results detected cyclical shedding of L. intracellularis in the feces. Seroconversion occurred in pigs that were exposed to L. intracellularis. From this study, it was demonstrated that transmission of L. intracellularis can occur easily in an environment with experimentally infected pigs and that PCR can be a useful tool to monitor fecal shedding of the organism.     

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.     

Isolation and genetic characterization of avian origin H9N2 influenza viruses from pigs in China

As pigs are susceptible to infection with both avian and human influenza A viruses, they have been proposed to be an intermediate host for the adaptation of avian influenza viruses to humans. In April 2006, a disease caused by highly pathogenic porcine reproductive and respiratory syndrome virus (PRRSV) occurred in several pig farms and subsequently overwhelmed almost half of China with more than 2,000,000 cases of pig infection. Here we report a case in which four swine H9N2 influenza viruses were isolated from pigs infected by highly pathogenic PRRSVs in Guangxi province in China. All the eight gene segments of the four swine H9N2 viruses are highly homologous to A/Pigeon/Nanchang/2-0461/00 (H9N2) or A/Wild Duck/Nanchang/2-0480/00 (H9N2). Phylogenetic analyses of eight genes show that the swine H9N2 influenza viruses are of avian origin and may be the descendants of A/Duck/Hong Kong/Y280/97-like viruses. Molecular analysis of the HA gene indicates that our H9N2 isolates might have high-affinity binding to the alpha2,6-NeuAcGal receptor found in human cells. In conclusion, our finding provides further evidence about the interspecies transmission of avian influenza viruses to pigs and emphasizes the importance of reinforcing swine influenza virus (SIV) surveillance, especially after the emergence of highly pathogenic PRRSVs in pigs in China.     

The presence of Helicobacter-like microorganisms in the gastric mucosa in dogs

The aim of this study was the evaluation of the occurrence of Helicobacter-like organisms in the gastric mucosa of dogs. The study was performed on samples of gastric mucosa obtained during necropsies from 94 dogs euthanasized for various reasons. Histopathological examination and also urease test was performed. Helicobacter sp. was found in 85.10% of examined dogs. In 36% cases the presence of bacteria was accompanied by chronic inflammation of gastric mucosa localized mainly in pyloric region. In 97.59% samples positive results of urease test were associated with histopathological confirmation of gastric Helicobacter-like organisms.     

Pre-infection of pigs with Mycoplasma hyopneumoniae modifies outcomes of infection with European swine influenza virus of H1N1, but not H1N2, subtype

Swine influenza virus (SIV) and Mycoplasma hyopneumoniae (Mhp) are widespread in farms and are major pathogens involved in the porcine respiratory disease complex (PRDC). The aim of this experiment was to compare the pathogenicity of European avian-like swine H1N1 and European human-like reassortant swine H1N2 viruses in na?ve pigs and in pigs previously infected with Mhp. Six groups of SPF pigs were inoculated intra-tracheally with either Mhp, or H1N1, or H1N2 or Mhp+H1N1 or Mhp+H1N2, both pathogens being inoculated at 21 days intervals in these two last groups. A mock-infected group was included. Although both SIV strains induced clinical signs when singly inoculated, results indicated that the H1N2 SIV was more pathogenic than the H1N1 virus, with an earlier shedding and a greater spread in lungs. Initial infection with Mhp before SIV inoculation increased flu clinical signs and pathogenesis (hyperthermia, loss of appetite, pneumonia lesions) due to the H1N1 virus but did not modify significantly outcomes of H1N2 infection. Thus, Mhp and SIV H1N1 appeared to act synergistically, whereas Mhp and SIV H1N2 would compete, as H1N2 infection led to the elimination of Mhp in lung diaphragmatic lobes. In conclusion, SIV would be a risk factor for the severity of respiratory disorders when associated with Mhp, depending on the viral subtype involved. This experimental model of coinfection with Mhp and avian-like swine H1N1 is a relevant tool for studying the pathogenesis of SIV-associated PRDC and testing intervention strategies for the control of the disease.     

Gastritis and intestinal metaplasia in Syrian hamsters infected with Helicobacter aurati and two other microaerobes

Chronic gastritis and intestinal metaplasia associated with naturally occurring colonization by Helicobacter aurati and two other microaerobic species were observed in Syrian hamsters. Thirty-five hamsters, between 7 and 12 months of age, were evaluated from two research and three commercial facilities. Microaerobic bacteria were cultured from the hamster stomachs. These bacteria included H. aurati, a fusiform, urease-positive species; a second novel helical, urease-negative Helicobacter sp.; as well as a smaller, urease-negative Campylobacter sp. Southern blot analysis detected Helicobacter spp. DNA in the gastric tissues of all 35 hamsters; 15 hamsters also had Campylobacter sp. DNA in their gastric tissues. When examined by light microscopy, argyrophilic bacteria consistent with H. aurati or the second Helicobacter sp. were present in antral sections of 12 out of the 15 hamsters where bacteria were seen, while 9 out of the 15 hamsters had bacteria resembling the Campylobacter sp. The presence of Helicobacter spp. but not the presence of Campylobacter sp. was significantly correlated to gastritis severity (P < 0.0001 for Helicobacter spp., P = 0.6025 for Campylobacter sp.) and intestinal metaplasia, as measured by numbers of goblet cells (P = 0.0239 for Helicobacter spp., P = 0.5525 for Campylobacter sp.). Severely affected hamsters also had Giardia sp. within their metaplastic gastric pits. Hamsters with naturally occurring helicobacter-associated gastritis provide a model for studying the development of intestinal metaplasia and gastric giardiasis in H. pylori-infected humans.