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. 33 – 39 Stress is a critical factor in the development of peptic ulcers and chronic gastritis in humans, and herpesviruses are known to be reactivated by stress. 40 , 41 Stress appears to be a contributing factor to EGGD in horses. Additionally, the

Open access
in American Journal of Veterinary Research

treatment is available, resulting in a short overall survival time for affected dogs. 2,4,5 Clinical signs associated with gastric carcinoma are indistinguishable from those of chronic gastritis and commonly include vomiting, weight loss, and anorexia and

Full access
in Journal of the American Veterinary Medical Association

Chronic gastritis is a commonly diagnosed condition in dogs evaluated for signs of chronic gastrointestinal disease. 1 After proper anamnestic, clinical, biological, and ultrasonographic evaluations have been conducted, diagnosis of CG is

Full access
in Journal of the American Veterinary Medical Association

Objectives

To determine prevalence, colonization density, and distribution of helicobacters and gastric histologic findings in healthy dogs and dogs with signs of gastritis; to evaluate association of colonization density and gastric inflammation; and to compare the number of Helicobacter spp with degree of inflammation.

Design

Cross-sectional prevalence survey.

Animals

25 healthy dogs and 21 dogs with signs of gastritis.

Procedure

During endoscopy, gastric mucosal biopsy specimens were obtained from healthy and affected client-owned dogs. Histologic and cytologic evaluation and results of a urease test were used for detecting helicobacters, which were identified definitively by use of transmission electron microscopy and bacterial culture.

Results

Helicobacters were detected in all 25 healthy and 20 of 21 affected dogs. Cytologic examination was a more sensitive method than histologic examination or the urease test. Helicobacters were found least frequently and in fewest number in the antrum in both groups of dogs. Gastric inflammation was evident in both groups of dogs and did not differ significantly between groups. A significant association was not detected between colonization density or the number of Helicobacter spp and degree of gastric inflammation. In both groups, H bizzozeronii, H felis, and H salomonis were cultured.

Clinical Implications

Histologically verified chronic gastritis is common in dogs with signs of gastritis as well as in healthy dogs. Colonization density of helicobacters was not associated with degree of gastric inflammation in the dogs of our study. It remains to be determined whether certain strains of Helicobacter spp can induce gastritis in dogs. (J Am Vet Med Assoc 1998;213:1767–1774)

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

A double-blind study was conducted to compare gastri ulcer healing time in nontreated dogs with that in dogs treated with either cimetidine or omeprazole. Single ulcers were created in the gastric antrum by use of a suction biopsy capsule. Each dog was given 25 mg of aspirin/kg of body weight orally for 20 days after ulcer induction. Five control dogs were given aspirin only (no anti-ulcer medication) during the 20-day study. Six dogs were given cimetidine at dosage of 10 mg/kg orally every 8 hours, and 6 dogs were given omeprazole orally at dosage of 2 μmol/kg (0.7 mg/kg) once daily. All dogs were examined endoscopically on days 5, 10, 15, and 20 and were given a score for the size of the mechanically created ulcer and a score for the degree of aspirin-induced gastritis. All dogs were euthanatized on day 21, and gastric lesions were examined histologically. Significant differences were not evident in ulcer healing scores or degree of aspirin-induced gastritis among treated and nontreated dogs on days 5, 10, 15, and 20. However, aspirin-induced gastritis was less severe in dogs of the omeprazole group than in dogs of the cimetidine or control group on each day observations were made. The effect of omeprazole given once daily was comparable with that of cimetidine given every 8 hours in lessening aspirin-induced gastritis.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether 2 isolates of recently isolated swine-origin Helicobacter pylori-like bacteria are pathogenic in pigs and compare the signs of gastric disease induced by these isolates with those detected in H pylori- and Helicobacter heilmannii-in fected pigs.

Animals—36 neonatal gnotobiotic pigs.

Procedure—Groups of separately housed pigs were inoculated orally with swine-origin Helicobacter-like isolates 2662 or 1268, H pylori (human gastric pathogen), or a gastric homogenate from gnotobiotic swine containing H heilmannii. Noninoculated pigs were used as control animals. Clinical signs and development of homologous and heterologous antibodies against Helicobacter organisms were assessed. After euthanasia, gastric tissues were examined grossly and microscopically; Helicobacter organisms were detected by use of Warthin-Starry and immunohistochemical stains.

Results—Both porcine Helicobacter-like isolates colonized the stomachs of swine. Isolate 2662 was highly pathogenic; in 13 isolate 2662-inoculated pigs, gastroesophageal ulcerations developed in 9 and ulceration of the gastric glandular mucosa was detected in 5. Histologically, inflammatory gastritis consisting of multifocal to diffuse lymphocytic and plasmacytic cellular infiltrates and lymphoid follicle formation in the gastric lamina propria accompanied bacterial colonization of the gastric compartment. In contrast, H heilmannii was minimally pathogenic in that only modest inflammatory cell infiltrates were seen. Gastroesophageal or mucosal ulcers were not evident in pigs inoculated with H heilmannii.

Conclusions and Clinical Relevance—These data indicate that swine-origin H pylori-like bacteria can be pathogenic in pigs and suggest that porcine gastric disease may be mediated, in part, by colonization of the stomach by swine-origin H pylori-like bacteria. (Am J Vet Res 2005;66:945–952)

Full access
in American Journal of Veterinary Research
in Journal of the American Veterinary Medical Association

Gastritis in dogs can be caused by several factors. The main triggers are systemic disease, diet, environmental influences, stress, and behavioral factors. 1,2 Similar to the situation for humans, it has been proposed that Helicobacter spp

Full access
in American Journal of Veterinary Research

fat, and absorbs some vitamins and minerals. 1,2 Gastric disease in dogs is poorly characterized. Gastritis is defined as inflammation of the stomach. 1 Acute-onset vomiting occurs frequently in dogs 3 and is often attributed to acute gastritis

Full access
in Journal of the American Veterinary Medical Association

seasons. Metallic gastric foreign bodies have also been identified in other avian species. 10–15 Metallic objects can cause traumatic gastritis and perforation of the proventriculus or, more commonly, the ventriculus. Indeed, during gastric cycles

Full access
in Journal of the American Veterinary Medical Association