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Veterinary Pathology, Vol 32, Issue 5 489-497, Copyright © 1995 by American College of Veterinary Pathologists
ARTICLES |
K. A. Eaton, M. J. Radin and S. Krakowka
Department of Veterinary Pathobiology, Ohio State University, 1925 Coffey Road, Columbus, OH.
Conventional female BalbC mice were inoculated with Gastrospirillum-like bacteria in mouse gastric homogenate or in 5.0-microns filtrate of gastric homogenate. The bacteria were originally isolated from cheetahs with gastritis. The mice were killed 6 months, 7 months, or 1 year after inoculation. All mice became infected with Gastrospirillum-like bacteria that were confined to the gastric mucosa. Control mice, given either sterile Brucella broth, 0.22-microns filtrate of infected gastric homogenate, or uninfected gastric homogenate did not become infected with bacteria. Lesions in infected mice included severe lymphoplasmacytic gastritis (26/26 infected mice), gastric epithelial hyperplasia (25/26 infected mice), and gastric ulceration (11/26 infected mice). Neutrophilic inflammatory cell infiltrates were inconsistent. None of the uninfected control mice had Gastrospirillum-like bacteria, gastritis, gastric epithelial hyperplasia, or gastric ulceration. These results implicate Gastrospirillum-like bacteria from cheetahs in the pathogenesis of gastric ulceration. This model will be useful in investigating the mechanisms of gastric ulceration associated with bacterial gastritis.
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