Journal of Antimicrobial Chemotherapy (1999) 43, 659-666
© 1999 The British Society for Antimicrobial Chemotherapy
Bismuth-mediated disruption of the glycocalyx- cell wall of Helicobacter pylori:ultrastructural evidence for a mechanism of action for bismuth salts

a Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN 37232-5310; b Miami Valley Laboratories, Procter & Gamble Co., Cincinnati, OH 45242; c Pathology and Laboratory Medicine Service, Veteran' s Administration Medical Center, Richmond, VA 23249-0001, USA
The mechanism of bismuth' s bactericidal activity against Helicobacter pyloriwas investigated using transmission electron microscopy (TEM) and analytical electron microscopy (AEM); time- kill kinetic methods evaluated the effect of excess divalent cations. TEM analysis of untreated H. pylori revealed a normal morphology. In contrast, H. pylori exposed to bismuth salts had swollen, distorted cells with membranecell wall blebbing and a cytoplasm containing electron-dense, sometimes crystalline aggregates. By AEM, swollen cells contained bismuth at the cell periphery, whereas bacillary forms contained cytoplasmic bismuth localizations. Timekill studies showed that the bactericidal activity of bismuth could be prevented by pretreatment with divalent cations. The effects of bismuth salts on the glycocalycescell walls of H. pylori with reversal of bactericidal activity by divalent cations are identical to those produced by other polycationic agents on various Gram-negative bacilli. We conclude that disruption of the glycocalycescell walls of H. pylori is one mechanism of action for bismuth salts.
* Correspondence address. Clinical Microbiology Laboratory, Room 4525-TVC, The Vanderbilt Clinic, 21st and Edgehill, Nashville, TN 37232-5310, USA. Tel: +1-615-343-9144; Fax: +1-615-343-8420.
Present address. School of Library and Information Science,
Kent State University, PO Box 5190, Kent, OH 44242, USA
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