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Epidemiology and Pathophysiology of Campylobacter pylori Infections
Martin J. Blaser
Reviews of Infectious Diseases
Vol. 12, Supplement 1. Pathophysiology of Gastrointestinal Infections: The Role of Bismuth Subsalicylate (Jan. - Feb., 1990), pp. S99-S106
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/4455463
Page Count: 8
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Since the first isolation of Campylobacter pylori in Australia in 1982, this bacterium has been isolated from persons in all parts of the world. Although initially recognized in patients with gastrointestinal symptoms, C. pylori can also be isolated from apparently asymptomatic persons. C. pylori infection is infrequent in young children in developed countries; during adulthood C. pylori infection becomes progressively more frequent, a phenomenon that parallels the age distribution of type B gastritis. In developing countries infection is more common and begins earlier. Infection, once acquired, appears to persist, possibly for life, but the mode of transmission to humans is unknown. C. pylori is well adapted for survival in the gastric milieu, but whether C. pylori plays a causative role in gastritis is of critical importance. Favoring this hypothesis are the results of inoculation studies in volunteers and animals in which challenge with C. pylori resulted in persistent infection and histologic lesions. Treatment studies with antimicrobial agents indicate that removal of C. pylori is associated with improvement in histologic appearance of affected tissues and that when infection recurs the histologic appearance worsens. The mechanisms by which C. pylori infection may cause gastritis are unknown but possibilities include production of cytotoxin, degradation of physiologic defenses against acid-pepsin damage, and adherence to epithelial cells.
Reviews of Infectious Diseases © 1990 Oxford University Press