Veterinary Pathology, Vol 36, Issue 3 237-248, Copyright © 1999 by American College of Veterinary Pathologists

ARTICLES

Helicobacter felis infection in dogs: effect on gastric structure and function

K. W. Simpson, P. L. McDonough, D. Strauss-Ayali, Y. F. Chang, P. Harpending and B. A. Valentine
Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA. KWS5@cornell.edu

The relationship of Helicobacter felis, an organism that is observed in the stomachs of dogs, to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter felis infection alters gastric morphology and gastric secretory function in dogs. Five specific-pathogen-free (SPF), Helicobacter-free Beagle dogs were examined before and for 26 weeks after inoculation with H. felis (ATCC 49179). Three SPF uninfected dogs served as controls. All five dogs became colonized by H. felis as determined by urease activity, histopathology, polymerase chain reaction, and transmission electron microscopic examination of serial gastric biopsies. The degree of colonization ranged from < 1 organism/400 x field to > 10 organisms/400 x field. The fundus, body, and cardia were most heavily colonized. Evaluation of gastric biopsies showed mild gastric inflammation and lymphoid follicles in both infected and uninfected dogs. There was no correlation between the number of organisms observed and the degree of gastric inflammation or number of lymphoid follicles. The gastric secretory axis, assessed by fasting and meal-stimulated plasma gastrin, mucosal gastrin and somatostatin immunoreactivity, fasting gastric pH, and pentagastrin-stimulated gastric acid secretion, was similar in both infected and uninfected dogs. Fasting gastric pH was not a reliable indicator of gastric secretory function. These findings suggest that H. felis may not be a gastric pathogen in dogs. However, the density of colonization and limited duration of infection should be considered when interpreting these findings.

This article has been cited by other articles:

				J. G. Kusters, A. H. M. van Vliet, and E. J. Kuipers Pathogenesis of Helicobacter pylori Infection Clin. Microbiol. Rev., July 1, 2006; 19(3): 449 - 490. [Abstract] [Full Text] [PDF]

				T. KOGA, K. TAKAHASHI, K. SATO, I. KIKUCHI, Y. OKAZAKI, T. MIURA, M. KATSUTA, and T. NARITA The effect of colonisation by Helicobacter pylori in Praomys (Mastomys) natalensis on the incidence of carcinoids J. Med. Microbiol., September 1, 2002; 51(9): 777 - 785. [Abstract] [Full Text] [PDF]

				J. V. Solnick and D. B. Schauer Emergence of Diverse Helicobacter Species in the Pathogenesis of Gastric and Enterohepatic Diseases Clin. Microbiol. Rev., January 1, 2001; 14(1): 59 - 97. [Abstract] [Full Text] [PDF]

				K. W. Simpson, D. Strauss-Ayali, E. Scanziani, R. K. Straubinger, P. L. McDonough, A. F. Straubinger, Y.-F. Chang, C. Domeneghini, N. Arebi, and J. Calam Helicobacter felis Infection Is Associated with Lymphoid Follicular Hyperplasia and Mild Gastritis but Normal Gastric Secretory Function in Cats Infect. Immun., February 1, 2000; 68(2): 779 - 790. [Abstract] [Full Text] [PDF]