Journal Article

Helicobacter pylori may be the world's commonest chronic infection. Estimates suggest that more than half the world's population is infected by this gastric bacterium. Since the discovery and successful culture of H. pylori in the 1980s, it has become clear that the infection is important in the initiation of gastritis, resulting in numerous manifestations of gastroduodenal disease. Clinical outcomes associated with H. pylori infection include duodenal ulcer, gastric ulcer, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Specific genetic or phenotypic factors in infectious agents have been implicated as single causal factors in a variety of infectious diseases and associated outbreaks. It is well recognized that Escherichia coli 0157:H7 is causally associated with hemolytic uremic syndrome in the young and elderly. [104] Strains of two related cell lineages of Streptococcus pyogenes account for nearly half of all cases of toxic shock-like syndrome, with almost all strains expressing the exotoxin A gene. [70] H. pylori infection alone appears insufficient to explain fully the spectrum of diseases that are associated with chronic infection, however. Current data suggest that the pathogenicity of H. pylori depends on bacterial and host factors. Virulence of this infectious pathogen is based on factors that allow colonization and adaptation to the gastric environment and the stimulation of mediators of inflammation that contribute to the host physiologic and histologic changes. This article discusses bacterial and host immune factors important in gastroduodenal pathogenesis.