Abstract
The frequent presence of Helicobacter pylori in healthy individuals without peptic ulcer disease suggests that as yet unidentified specific microbe-host interactions are important in determining whether an infected individual does or does not develop ulcer disease. Development of a peptic ulcer following H. pylori infection may require the genetic predisposition of the infected individual, infection with an “ulcer-virulent” H. pylori strain, or both.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsReferences
Goodwin CS, Armstrong JA, Chilvers T, Peters M, Collins MD, Sly L, McConnell W, Harper WES (1989) Transfer of Campylobacter pylori and Campylobacter mustelae to Helicobacter gen. nov. as Helicobacter pylori comb. nov. and Helicobacter mustalae comb. nov., respectively. Int J Syst Bacteriol 39 : 397–405
Graham DY, Yoshimura HH, Estes MK (1983) DNA hybridization studies of the association of Pseudomonas maltophilia with inflammatory bowel diseases. J Lab Clin Med 101 : 940–945
Wetmur JG, Davidson N (1968) Kinetics of renaturation of DNA. J Mol Biol 31 : 349–370
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1993 Springer-Verlag Berlin Heidelberg
About this paper
Cite this paper
Yoshimura, H.H., Graham, D.Y. (1993). Helicobacter pylori strains from Duodenal Ulcer Patients Differ at the Genomic Level from Those Patients with simple Gastritis. In: Pajares, J.M., Peña, A.S., Malfertheiner, P. (eds) Helicobacter pylori and Gastroduodenal Pathology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77486-7_3
Download citation
DOI: https://doi.org/10.1007/978-3-642-77486-7_3
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-77488-1
Online ISBN: 978-3-642-77486-7
eBook Packages: Springer Book Archive