In Vitro Susceptibility of Helicobacter pylori to Antibiotics and Bismuth Salts and the Importance of Acquired Resistance to Antibiotics in Treatment Failures of H. pylori Infection

Abstract

There is now overwhelming evidence that Helicobacter pylori(formerly Campylobacter pylori) is the major etiological agent of chronic active (type B) gastritis and that it may further predispose to peptic ulceration. Challenge studies in gnotobiotic piglets [1,2] and in two human volunteers [3,4] have reproduced the typical features of gastritis. Clearance of the organism with amoxicillin, furazolidone, or bismuth salts leads to improvement or even total resolution of gastritis [5–8]. Moreover, well-designed controlled studies have shown that patients with healed peptic ulcer who remain persistently infected with H. pylori relapse much more frequently than patients cleared of the organism [9,10]. In vitro, H. pylori is sensitive to most antibiotics (penicillin, ampicillin, cephalosporins, macrolides, quinolones, aminoglycosides, tetracyclines, and nitraimidazoles) except vancomycin, trimethoprim, and sulfonamides [11–15]. Among the various antiulcer drugs, bismuth salts are the only compounds that possess an antibacterial activity, though only a moderate one (minimal whibitory, concentration MIC₉₀, 8–32 mg/l), against H. pylori [12,13]. There does not seems to be any difference in the levels of antimicrobial activity of the numerous existing forms of bismuth salts (subsalicylate, colloidal bismuth subcitrate, subcarbonate, nitrate, subnitrate, or oxychloride) (Glupczynski and Thibaumont 1989, unpublished data).