Since Warren and Marshall rediscovered in 1983 the presence of a spiral microorganism on the gastric mucosa, and named it Campylobacter Pylori (CP), its significance and characteristics have been largely studied. CP has fulfilled Koch's postulates, which need to proven before a microorganism can be said to cause a disease. The natural source of infection is unknown, but in human volunteer studies, ingestion of a suspension of CP was followed by the development of severe dyspepsia associated with colonization of gastric antrum and histologically proven gastritis B. CP is found overying the gastric epithelium, in the gastric crypts and in the mucus gel layer that protects it from gastric acid. There it causes infiltration of the mucosa by polymorphonuclear leucocytes and mononuclear cells, and mucin depletion. It is found in 60-70% of children with chronic active antral gastritis and can cause various lesions of upper intestinal tract, like esophagitis, duodenitis and gastric or duodenal ulcers. Several tests have been proposed to detect serum antibody against CP, but they are not yet commercially available. Breath test with C 13 or C 14-urea are promising, but up to now the diagnosis can be made only by upper G.I. endoscopy and antral biopsy. A pseudopolypoid antral gastritis seems to be the peculiar lesion caused by CP, but in children it is present only in 40% of cases. CP is easily seen in antral biopsies by Giemsa or Hematoxylin-Eosin staining, or can be cultured in Skirrow's agar under microaerophilic conditions.(ABSTRACT TRUNCATED AT 250 WORDS)