Campylobacter pyloridis, gastritis, and peptic ulceration

Abstract

Campylobacter pyloridis is a spiral bacterium which was seen by histopathologists several years before it was cultured in 1982 in Perth, Western Australia. It has unique cellular fatty acids, predominantly tetradecanoic acid and cis-11, 12 methylene octadecanoic acid. It also has a unique ultrastructure which is different from that of other campylobacters. C pyloridis possesses a powerful urease enzyme and produces large amounts of extracellular catalase. Both these features may be important virulence factors, allowing it to occupy a protected niche in the stomach below the mucus layer but above the gastric mucosa. Specific lesions are found in the gastric mucosa, and ultrastructural studies show the presence of adherence pedestals identical with those found with enteropathogenic Escherichia coli of the intestine. Histological examination of gastric biopsy tissue has shown that C pyloridis is strongly associated with active chronic gastritis, when polymorphonuclear leucocytes are present, and is not found on normal mucosa except when a biopsy specimen from elsewhere in the stomach shows active chronic gastritis. When patients with symptoms caused by gastritis are identified dual antibacterial treatment, combining the action of bismuth in the stomach with a systemic antibiotic, can eradicate C pyloridis, with remission of symptoms and restoration of normal epithelial morphology. Most peptic ulcers relapse after modern acid reducing treatment, and antibacterial treatment may be beneficial in preventing relapse.