Pathogenesis and clinical pictures: H. pylori occurs only in humans and is transmitted by the fecal-oral pathway. The pathogen colonizes and infects the stomach mucosa. The pathogenicity factors include pronounced motility for efficient target cell searching, adhesion to the surface epithelial cells of the stomach, urease that releases ammonia from urea to facilitate survival of the cells in a highly acidic environment and a vacuolizing cytotoxin that destroys epithelial cells. Once the pathogen has infected the stomach tissues an acute gastritis results, the course of which may or may not involve overt symptoms. Potential sequelae include:
1. Mild chronic gastritis that may persist for years or even decades and is often asymptomatic.
2. Duodenal ulceration, sometimes gastric ulceration as well.
3. Chronic atrophic gastritis from which a gastric adenocarcinoma sometimes develops.
4. Rarely B cell lymphomas of the gastric mucosa.
Diagnosis: Histopathological, cultural and, molecular identification of the bacteria in stomach lining biopsies. A noninvasive breath test involving ingestion of 13C-labeled urea and measurement of 13CO2 in the expelled air. Antigen detection in stool. Antibodies can be identified with an ELISA or Western blotting.
Therapy: In patients with ulcers and/or gastritis symptoms, a triple combination therapy with omeprazole (proton pump blocker), metronidazole, and clarithromycin lasting seven days is successful in 90% of cases.
Epidemiology: Based on sero epidemiological studies we know that H. pylori occur worldwide. Generalized contamination of the population begins in childhood and may reach 100% in adults in areas with poor hygiene. The contamination level is about 50% among older adults in industrialized countries. Transmission is by the fecal-oral route.
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