Abstract
Whether or not a microbe is virulent is at its root a biological question. Clinical and pathological consequences of the host-microbial interaction may be important determinants of the relationship, but ultimately the question turns on the role of the microbe in enhancing or diminishing the evolutionary fitness of its host. It is from this context that we must consider the relationship of Helicobacter pylori to humans.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Mackowiak P. The normal microbial flora. N Engl J Med. 1982;307:83–93.
Rosebury T. Microorganisms Indigenous to Man. New York: McGraw Hill; 1962:1–8.
Bocchi V. The neglected organ: bacterial flora has a crucial immunostimulatory role. Persp Biol Med. 1992;35:251–60.
Savage DC. Microbial ecology of the gastrointestinal tract. Annu Rev Microbiol. 1977; 31:107–33.
Wilson KH. Biota of the human gastrointestinal tract. In: Mackie RI, White BA, Isaacson RE, editors. Gastrointestinal Microbiology. New York: Chapman & Hall; 1996:2:39–58.
Polk BF, Kasper DL. Bacteroides fragilis subspecies in clinical isolates. Ann Intern Med. 1977;86:569–71.
Woese C, Olsen GJ. Ribosomal RNA: a key to phylogeny. FASEB. 1993;7:113–23.
Ochman H, Wilson AC. Evolution in bacteria: evidence for a universal substitution rate in cellular genomes. J Mol Evol. 1987;26:74–86.
Blaser MJ. Helicobacter pylori eradication and its implications for the future. Aliment Pharmacol Ther. 1997;11(Suppl. 1):103–7.
Courillon-Mallet A, Launay JM, Roucayrol AM et al. Helicobacter pylori infection: physiopathologic implication of N-a-methyl histamine. Gastroenterology. 1995;108:959–66.
El-Omar E, Penman I, Dorrian CA, Ardill JES, McColl KEL. Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcers. Gut. 1993;34:1060–5.
El-Omar EM, Penman ID, Ardill JE, Chittajallu RS, Howie C, McColl KEL. Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer. Gastroenterology. 1995;109:681–91.
Allison AC. Polymorphism and natural selection in human populations. Cold Spring Harbor Symp Quant Biol. 1964;29:137–49.
Dixon MJ Helicobacter pylori and peptic ulceration: histopathological aspects. J Gastroenterol Hepatol. 1991;6:125–30.
NIH Consensus Conference, 1994. Helicobacter pylori in peptic ulcer disease. J Am Med Assoc. 1994;272:65–9.
International Agency for Research of Cancer. Monographs on the Evaluation of Carcinogenic Risks to Humans. Infection with Helicobacter pylori. 1994;60:177–240.
Axon A, Forman D. Helicobacter pylori gastroduodenitis: a serious infectious disease. Br Med J. 1997;314:1430–1.
Blaser MJ. Not all Helicobacter pylori strains are created equal: should all be eliminated? Lancet. 1997;349:1020–2.
Pavia AT, Shipman LD, Wells JG et al. Epidemiologic evidence that prior antimicrobial exposure decreases resistance to infection by antimicrobial-sensitive Salmonella. J Infect Dis. 1990;161:255–60.
Prach AT, MacDonald TA, Hopwood DA, Johnston DA. Increasing incidence of Barrett’s oesophagus: education, enthusiasm, or epidemiology. Lancet. 1997;350:933.
Blot WJ, Devesa SS, Kneller RW, Fraumeni JF Jr. Rising incidence of adenocarcinoma of the esophagus and gastric cardia. J Am Med Assoc. 1991;265:1287–9.
Powell J, McConkey CC. The rising trend in esophageal adenocarcinoma and gastric cardia. Eur J Cancer Prey. 1992;1:265–9.
Hansen S, Wiig JN, Giercksky KE, Tretli S. Esophageal and gastric carcinoma in Norway 1958–1992: incidence time trend variability according to morphological subtypes and organ subsites. Int J Cancer. 1997;71:340–4.
Labenz J, Blum AL, Bayerdörffer E, Meining A, Stolte M, Börsch G. Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology. 1997;112:1442–7.
Werdmuller BFM, Loffeld RJLF. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci. 1997;42:103–5.
Vicari JJ, Peek RM, Falk GW et al. The seroprevalence of cagA positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology. 1998 (in press).
Chow W-H, Blaser MJ, Blot WJ et al. An inverse relation between cagA strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma. Cancer Res. 1998;58:588–90.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1998 Springer Science+Business Media Dordrecht
About this chapter
Cite this chapter
Blaser, M.J. (1998). Considerations of virulence by Helicobacter pylori . In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4882-5_6
Download citation
DOI: https://doi.org/10.1007/978-94-011-4882-5_6
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-010-6046-2
Online ISBN: 978-94-011-4882-5
eBook Packages: Springer Book Archive