Fluorescence In Situ Hybridization Confirms Clearance of Visible Helicobacter spp. Associated with Gastritis in Dogs and Cats

Background: The results of studies examining the role of Helicobacter spp. in the pathogenesis of canine and feline gastritis are inconclusive. Furthermore, data evaluating the effectiveness of medical therapy for eradication of Helicobacter infection are limited.
Aim: To detect Helicobacter spp. in mucosal biopsies of dogs and cats diagnosed with gastritis, with fluorescence in situ hybridization (FISH).
Animals: Three dogs and 2 cats with signs of chronic gastrointestinal disease.
Methods: Dogs and cats infected with Helicobacter spp. were treated with triple antimicrobial therapy and fed an elimination diet for 21 days. Helicobacter spp. status in endoscopic (3 dogs, 1 cat) or surgical biopsies (1 cat) of gastric mucosa was compared pre- and posttreatment in each animal by histology, FISH analysis, and polymerase chain reaction (PCR).
Results: Gastritis of varying severity with intraglandular spiral bacteria was observed in all animals. Pretreatment diagnostic tests confirmed the presence of mucosal Helicobacter spp. in all animals by FISH and histopathology and in 4/5 animals by PCR. Rapid resolution of vomiting episodes was observed in all animals. Gastric biopsies performed after triple therapy revealed clearance of visible Helicobacter spp. by histopathology and negative FISH analysis, as well as PCR in all animals.
Conclusions and Clinical Importance: Application of FISH to routine biopsy specimens enabled rapid and specific identification of Helicobacter spp. within the gastric mucosa of dogs and cats. Although medical therapy was useful in resolution of clinical signs and clearance of visible Helicobacter spp. in gastric biopsies, gastric inflammation persisted.     

Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection

The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.     

Efficacy and long-term outcome of gastritis therapy in cheetahs (Acinonyx jubatus).

A prospective clinical trial evaluating efficacy and long-term outcome of treatments for lymphoplasmacytic gastritis in cheetahs (Acinonyx jubatus) was conducted. The study evaluated efficacy of 11 different antibiotic and antiinflammatory treatment protocols in 32 cheetahs (19 male, 13 female) for reducing gastric inflammation and Helicobacter colonization and monitored the course of disease through histologic grading of gastric biopsies. All cheetahs were biopsied up to I wk before treatment and then rebiopsied within 1 mo after treatment. Most animals were reassigned to a second treatment regimen within 6 mo. Each animal received from one to three treatments during the study period. After the trial, gastric biopsies were obtained from each cheetah annually until death or transfer from the facility to assess disease progression. The trial and follow-up period spanned 10 yr. At onset of the trial, all 32 cheetahs had some degree of gastritis, and 26 cheetahs (81%) were colonized with Helicobacter. Inflammatory lesions worsened regardless of treatment or the presence of Helicobacter. No treatment had a significant effect on inflammatory changes except the lansoprazole/clarithromycin/amoxicillin treatment group, which produced a short-term decrease in inflammation when compared to controls. Prednisone had no effect on gastric inflammation. Overall, 65% of colonized cheetahs were initially cleared of histologic evidence of Helicobacter by treatment, with short-term eradication occurring in 100% of the animals treated with omeprazole/clarithromycin/amoxicillin or tetracycline/metronidazole/Pepto-Bismol for 28 days. Long-term follow-up of treated animals in this study clearly demonstrated that these treatments had little effect on life-long progression of gastritis or on Helicobacter burden in individual cheetahs, although some treatments provided short-term reduction in gastritis and Helicobacter. These results provide evidence that Helicobacter alone is not the cause of gastritis in cheetahs and do not support the use of antibacterial treatments in cheetahs unless significant clinical signs (e.g., frequent vomiting/regurgitation, weight loss) are apparent.     

Detection of Helicobacter spp. DNA in the oral cavity of dogs

The mode of acquisition of gastric Helicobacter spp. infection in dogs has not been determined. It is suspected that oral-oral and faecal-oral transmission may be involved. The present study sought to determine if Helicobacter spp. DNA is present in the oral cavity of healthy and vomiting dogs. Thirty-eight pet dogs (27 vomiting and 11 clinically healthy) were studied. The presence of Helicobacter spp. was determined by single and nested PCR evaluation of DNA extracted from saliva, dental plaque and gastric biopsy samples. Helicobacter spp. DNA was detected by nested PCR in 36 (94.7%) gastric biopsies, 17 (44.7%) dental plaque and 19 (50%) saliva samples out of the 38 dogs examined. Overall 27 (71.1%) dogs screened by nested PCR were found to harbour Helicobacter spp. DNA in the oral cavity (dental plaque and/or saliva). There was no significant difference in the prevalence of Helicobacter spp. DNA in the oral cavity of vomiting and healthy dogs, and the time from vomiting to oral sampling did not have significant impact. This study confirms the high prevalence of gastric Helicobacter spp. infection in dogs, and reveals that Helicobacter spp. DNA is detectable in the oral cavity of over 70% of dogs. These findings support the possibility of oral-oral transmission between dogs and that the canine oral cavity may act as source of non-pylori Helicobacter spp. infection for humans.     

Localization of Helicobacter spp. in the fundic mucosa of laboratory Beagle dogs: an ultrastructural study

ABSTRACT: In dogs Helicobacter spp. are found in all gastric regions usually localized in the surface mucus, gastric glands and parietal cells. The aim of this study was to detail the distribution of Helicobacter spp. in the fundic mucosa of asymptomatic Beagle dogs and their intracellular localization within parietal cells, in order to evaluate species-specific pathogenetic effects on gastric cells. The presence of Helicobacter spp. was investigated by immunohistochemistry, TEM, and PCR in the fundic mucosa of six Beagle dogs. Helicobacter spp. were found in all dogs examined, and H. bizzozeronii and H. felis were identified by PCR and confirmed by TEM. In the lumen of the fundic glands, co-localization was common. H. bizzozeronii was present in larger numbers than H. felis in both intraluminal and intraparietal localization. The amounts of H. bizzozeronii were similar in superficial and basal portions of the glands. H. felis was predominantly localized in the superficial portions of gastric glands but almost absent from the base. Within parietal cells, most Helicobacter organisms were intracanalicular, but intact and degenerate Helicobacter organisms were also visualized free in the cytoplasm or in secondary lysosomes. No specific degenerative lesions were found in infected parietal cells. Helicobacter organisms were also observed within macrophages in the lamina propria. In conclusion, there is a differential distribution of H. bizzozeronii and H. felis in the fundic mucosa of Beagle dogs, and their intracellular localization in parietal cells and macrophages suggests novel pathogenic scenarios for the development of immune response and maintenance of chronic gastritis in dogs.     

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.     

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.     

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.     

The histological appearance of peroral gastric biopsies in clinically healthy and vomiting dogs.

A survey of the histology of gastric biopsies in 501 dogs, consisting of 19 clinically healthy dogs and 482 vomiting dogs is presented. Whole stomachs of four young clinically healthy laboratory dogs were used as controls. Eleven percent of forceps biopsies were unsuitable for examination; all suction biopsies were of good quality. Slight to severe gastritis was found in 168 vomiting dogs (35%), whereas five dogs (26%) of the clinically healthy group showed a mainly slight gastritis. Superficial and diffuse gastritis were the most prominent findings in the 168 dogs with gastritis. A single type of gastritis was found in 114 dogs, a combination of different types in 54 dogs. Gastric atrophy was seen in 23 (5%) vomiting dogs and in three (15%) clinically healthy dogs, atrophy with a slight to severe fibrosis in 21 (4%) vomiting dogs, and in 84 (17%) vomiting dogs and two (11%) healthy dogs, gastric fibrosis was present. Carcinomas were seen in 26 vomiting dogs, of which 17 also had gastritis. A differential diagnosis of granulomatous gastritis/carcinoma had to be made in one case. Seven dogs showed a lymphosarcoma, and in six other dogs a differential diagnosis of lymphosarcoma and/or gastritis was made. One adenomatous polyp was seen. In one clinically healthy dog an adenomyoma was diagnosed. Ulceration was found in 24 dogs, but only five of these lacked other lesions. Other biopsy findings were pseudopyloric metaplasia, hyperplasia, cysts, calcification and edema. Some dogs showed "antralization".     

The diagnosis of gastritis and helicobacter-like organisms infection in endoscopic biopsies of the canine gastric mucosa

The aim of this study was to evaluate the prevalence of gastric Helicobacter-like organisms (GHLO) and gastritis in the gastric mucosa of dogs with gastric disorders. Tissue samples of the gastric mucosa were obtained from 30 dogs with gastrointestinal symptoms (vomiting, abdominal pain or discomfort, loss of appetite) during endoscopy. Histopathological examinations were performed and occurrence of GHLO infection, gastritis and other mucosal changes were estimated. The GHLO infection and gastritis were identified in 63.3 and 36.6% of dogs respectively; other mucosal changes included fibrosis in the lamina propria, degenerative changes of the gastric glands and hyperplasia of the parietal cells. The present study has revealed that microscopically found gastritis is not frequent in dogs examined by endoscopy. GHLO infection can be responsible for some cases of gastritis and hyperplasia of parietal cells in dogs.     

Evaluation of clinical, macroscopic, and histopathologic response to treatment in nonhypoproteinemic dogs with lymphocytic-plasmacytic enteritis

BACKGROUND: Lymphocytic-plasmacytic enteritis (LPE) is a common cause of chronic vomiting and diarrhea in dogs. However, little information is available about endoscopic or histopathologic improvement after therapy in dogs with LPE. HYPOTHESIS: The objective was to study the clinical, endoscopic, and histopathologic evolution of LPE during and after immunosuppressive treatment with prednisone and metronidazole. Most dogs also were treated symptomatically with metoclopramide and cimetidine. ANIMALS: Sixteen dogs with LPE and normal serum protein concentrations diagnosed at the Veterinary Medical Teaching Hospital of the Complutense University of Madrid were monitored during and after drug treatment. The control group consisted of 9 dogs that had no gastrointestinal signs for the preceding 12 months. METHODS: In this prospective clinical treatment trial, clinical, endoscopic, and histopathologic scores were evaluated to describe disease evolution during conventional therapy. Dogs with LPE were monitored for 120 days from the start of treatment. Re-evaluation was performed on post-treatment days 30, 60, 90 (end of treatment), and 120. RESULTS: The average disease activity index observed in our study fell progressively from its initial value, and the decrease between consecutive re-evaluations was statistically significant until day 60 (P = .04). Our results indicate that 75% of the animals revealed improvement of endoscopic gastric lesions (defined as a reduction of the endoscopic score) after treatment, and 75% exhibited improvement of endoscopic duodenal lesions. Statistical analysis of the data revealed significant differences between pre- and post-treatment gastric and duodenal macroscopic endoscopic lesions (P < .05). On the other hand, treatment did not lead to any significant changes in the severity of the gastric and duodenal histopathologic lesions of the affected dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: Treatment of nonhypoproteinemic dogs with LPE led to clinical and endoscopic improvement, but histopathologic lesions were unchanged during therapy.     

Follow-up studies by peroral gastric biopsies and necropsy in vomiting dogs.

The results of follow-up studies in 139 vomiting dogs are presented. Follow-up studies were performed by biopsies in 34 dogs, by biopsies and necropsy in six dogs and by necropsy only in 99 dogs. The times between the first and the last series of biopsies varied from three to 1042 days and from one to 656 days between the first series of biopsies and necropsy. From the 55 dogs with gastritis in the first series of biopsies, 35 also showed gastritis in the following biopsies or at necropsy. These were mainly severe types of gastritis such as diffuse, hypertrophic or atrophic. Ten dogs with superficial gastritis showed no gastric changes at necropsy, two dogs had edema only and three dogs had gastric changes other than gastritis, such as multiple polyps. In general, carcinoma and lymphosarcoma were found in the biopsies as well as at necropsy, but in three cases of terminal carcinoma only gastritis had been diagnosed initially. In 35 dogs the first series of gastric biopsies showed no pathological changes, but in 22 of these dogs gastritis, ulceration, fibrosis, atrophy, gastric dilation with local necrosis, and perforation or lymphosarcoma of the submucosa were found in the second series of biopsies or at necropsy. Several dogs which did not have gastric changes at necropsy had enteritis or intestinal lymphosarcoma.     

Gastric Ollulanus tricuspis infection identified in captive cheetahs (Acinonyx jubatus) with chronic vomiting

Gastritis, vomition and weight loss are common in captive cheetahs (Acinonyx jubatus). Gastric spiral bacteria (Helicobacter spp.) and the very small, viviparous nematode Ollulanus tricuspis, a stomach worm of cats, are believed to be important causes. Three sibling cheetahs at Wellington Zoo, New Zealand, developed chronic vomiting, diarrhoea and debility. Their parents were both South African-born. Response to antibacterial treatment was poor. Endoscopic examinations revealed chronic lymphoplasmacytic gastritis and Ollulanus infection. Treatment with oxfendazole and pyrantel embonate resulted in clinical improvement; however, 1 cheetah, which died 7 months later as a result of a ruptured liver due to hepatic amyloidosis, still had Ollulanus worms present in her stomach. Ollulanus tricuspis is a significant cause of gastritis and vomiting in captive cheetahs, lions and tigers, as well as wild cougars and tigers. The parasite has not yet been found in sub-Saharan Africa. Because of the unusual characteristics of this parasite, the literature on its life history and techniques for diagnosis is reviewed.     

Spontaneaous linear gastric tears in a cat

An 11‐year‐old female cat presented for chronic vomiting. Endoscopy revealed an altered gastric mucosa and spontaneous formation of linear gastric tears during normal organ insufflations. The histopathological diagnosis was atrophic gastritis with Helicobacter pylori infection. Medical treatment permitted a complete resolution of clinical signs. The linear tears observed resembled gastric lesions rarely reported in humans, called “Mallory‐Weiss syndrome”. To the authors’ knowledge this is the first report of spontaneous linear gastric tears in animals.     

Quantitative analysis of inflammatory and immune responses in dogs with gastritis and their relationship to Helicobacter spp. infection

The present study sought to quantitatively examine mucosal inflammatory and immune responses in dogs with gastritis and the relationship of these responses to infection with Helicobacter. Gastric biopsies from 30 dogs were evaluated for B- and T-lymphocytes, neutrophils, eosinophils, macrophages, and mast cells. Mucosal atrophy, fibrosis, cellularity, and severity of gastritis were graded qualitatively. Messenger-RNA (mRNA) for actin, interleukin-1beta (IL-1beta), IL-4, IL-8, and IL-10, transforming growth factor beta (TGF-beta), and interferon gamma (IFN-gamma) was quantified by polymerase chain reaction (PCR). The presence of Helicobacter spp. was determined by urease activity, histology, PCR, and enzyme-linked immunosorbent assay. mRNA for IL-1beta, IL-8, IL-10, TGF-beta, and IFN-gamma was detected in most dogs. IL-4 mRNA was detected in only 1 dog. Correlations were observed for IL-1beta versus IL-8 and IL-10; IL-8 versus IL-10, IFN-gamma, and TGF-beta; and IL-10 versus IFN-y. Mucosal pathology was related to cytokine mRNA expression (neutrophils to IL-8 and IFN-gamma, macrophages and lymphocytes to IFN-gamma, and fibrosis to IL-1beta). Gastritis was categorized as lymphoplasmacytic in all dogs, and its histologic severity correlated with atrophy, infiltration with lymphocytes and macrophages, and expression of IL-10 and IFN-gamma. Of the dogs examined, 76.7% were infected with Helicobacter spp. Infection was associated with increased expression of TGF-beta and fibrosis. Circulating anti-Helicobacter immunoglobulin G titers were higher in uninfected than infected dogs. We conclude that lymphoplasmacytic gastritis in dogs is characterized by concurrent activation of proinflammatory and immunomodulatory cytokines, with increased mRNA expression related to mucosal pathology. No significant associations between Helicobacter infection and proinflammatory cytokine expression, severity of gastritis, or differences in the pathogenicity of different Helicobacter spp. were found.     

The first report of the ante-mortem diagnosis of Ollulanus tricuspis infection in two dogs

Ollulanus tricuspis is a small nematode parasite of the stomach, and its infection has been reported worldwide in cats but only one report in dogs as post-mortem diagnosis. Two dogs, kept in the Tokyo area, were presented for chronic vomiting. Chronic gastritis was diagnosed histologically, and many nematodes were detected in endoscopically-biopsied gastric samples and in the mucus of vomitus in both dogs. The parasites were small (<1 mm), and their morphological characteristics were consistent with those previously reported for O. tricuspis. The symptoms in one dog completely disappeared after anthelmintic therapy. To our knowledge, this is the first report describing ante-mortem diagnosis of spontaneous gastric O. tricuspis infection in dogs in which infectivity and pathogenicity of the nematode are suggested.     

Gastric adenocarcinoma and chronic gastritis in two related Persian cats

Two 12.5-year-old castrated male Persian cats from the same household, whose dams were littermates, presented simultaneously with gastric adenocarcinoma associated with proliferative and fibrosing gastritis. Intralesional adult Ollulanus tricuspis nematodes and rare surface-associated spiral-shaped bacteria were identified in one cat. No etiologic agents were identified in tissues from the second cat; however, gastric mucosa was examined following anthelmintic treatment. Clinical signs in each cat had commenced 2 months apart and included vomiting, hematemesis, intermittent melena, and weight loss. This is the first report of gastric adenocarcinoma occurring in housemate cats or cats of common descent. Carcinogenesis may have been influenced by shared undetermined genetic and environmental factors, possibly including Ollulanus tricuspis, spiral-shaped bacteria, or other etiologies for chronic gastritis that remain unidentified.     

Enterohepatic Helicobacter spp. in colonic biopsies of dogs: molecular, histopathological and immunohistochemical investigations

Enterohepatic Helicobacter spp. have been described colonizing the large intestine and liver of healthy and symptomatic subjects and are thought to have a role in the development of inflammatory bowel disease (IBD). The prevalence of enterohepatic Helicobacter spp. infection in dogs is largely unknown and to our knowledge there are no data about their potential pathogenic role. In light of these considerations, the aims of this study were (i) to assess the prevalence of enterohepatic Helicobacter spp. in colonic biopsies of symptomatic pet dogs and (ii) to evaluate a possible association between Helicobacter spp. colonization status (heavily colonized, poorly colonized and uncolonized biopsies) and histological lesions. Colonic biopsies from 27 pet dogs of different ages were evaluated by family Helicobacteraceae and enterohepatic Helicobacter spp. PCR, histology, and immunohistochemistry for the in situ detection of Helicobacter spp. organisms. 85% and 52% of colonic biopsies were positive by Helicobacteraceae and enterohepatic Helicobacter spp. PCR, respectively. Immunohistochemistry revealed Helicobacter spp. were localized both in the superficial mucus (55%) and within intestinal crypts (33%). Dogs with heavy enterohepatic Helicobacter spp. colonization were significantly younger and had a higher level of mucosal fibrosis/atrophy than dogs with uncolonized or poorly colonized biopsies (p<0.05). These findings contribute to widen current knowledge regarding canine enterohepatic Helicobacter spp., suggesting the infection is rather common in dogs and acquired at an early age. Furthermore, heavy colonization of colonic crypts is associated with chronic inflammatory lesions (fibrosis/atrophy), supporting the role of enterohepatic Helicobacter spp. in the development of canine IBD.     

Gastritis-associated adenocarcinoma and intestinal metaplasia in a Syrian hamster naturally infected with Helicobacter species

The objective of this study was to evaluate stomachs of 2-year-old Syrian hamsters that were naturally colonized by multiple Helicobacter species including Helicobacter aurati. A previous report on 7- to 12-month-old Syrian hamsters described chronic gastritis and intestinal metaplasia, a putative preneoplastic lesion in the stomach, without cancer. This report describes an invasive adenocarcinoma at the pyloric-duodenal junction in one of nine hamsters at a site of helicobacter-associated inflammation and marked intestinal metaplasia. Ceca of nine of nine animals were culture positive and polymerase chain reaction positive for Helicobacter spp. Furthermore, immunohistochemical analysis of the stomach using a H. pylori polyclonal antibody detected positive-staining bacteria within the pyloric region of three of nine hamsters including the neoplastic glands. However, argyrophilic bacteria were demonstrated only within the stomach of the hamster with gastric adenocarcinoma. This is a first report of gastric adenocarcinoma in helicobacter-infected hamsters. Syrian hamsters appear suitable as potential model for studying development of helicobacter-associated gastric adenocarcinomas.     

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.