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Typus
Verschleierung
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 3, Zeilen: 1-15, 17ff
Quelle: Wanken 2003
Seite(n): 4, 5, Zeilen: 4: 1ff; 5: 1ff
1.1.3 Disease and epidemiology

For most of the twentieth century, peptic ulcers were thought to be stress-related and caused by hyperchlorhydria (Yoshida et al., 1977). The discovery that H. pylori is associated with gastric inflammation and peptic ulcer disease was initially met with skepticism. However, this discovery and following studies on H. pylori have revolutionized our opinion of the gastric environment, the diseases associated with it, and the appropriate treatment methods.

H. pylori is probably the most common human chronic infection and is distributed worldwide, infecting both males and females (Parkin, 2006). More than half of the world's population is persistently colonized with H. pylori. The prevalence of H. pylori is much higher in developing countries than in the Western world, although it increases with age in all populations studied (Perez-Perez et al., 2004). The incidence of H. pylori infection declines with increasing standards of socioeconomic development, including sewage disposal, water chlorination, hygienic food preparation, decreased crowding, and education (Ford et al., 2006). Natural acquisition of H. pylori infection usually occurs during childhood (Mourad-Baars and Chong, 2006). Once established, H. pylori generally persists for decades unless eradicated by anti-microbial therapy (Go, 2002; Magalhães Queiroz and Luzza , 2006). Because of the worldwide prevalence of infection, transmission of the organism from person to person is a major concern. Early studies demonstrated intra-familial clustering of infection, and more recently, DNA analyses of isolates have confirmed that most transmission occurs locally within families or small population groups ( Suerbaum et al., 1998; Drumm et al., 1990; Kivi et al., 2003). These results are consistent with an apparent inability of H. pylori to proliferate or survive for long periods in the environment. The mode of transmission from person to person has not been proven definitively. Oral-fecal, oral-oral, and gastro-oral routes are all considered possible (Magalhães Queiroz and Luzza , 2006). The study of the mode of transmission is made difficult by the fact that, unlike other infectious diseases, there is no well-defined clinical syndrome associated with its acquisition, and expression of chronic H. pylori infection in humans is highly variable. Hence, the usual approach of identifying cases and determining important exposures with infectious diseases [is not possible.]


Drumm, B., G. I. Perez-Perez, M. J. Blaser, and P. M. Sherman, Intrafamilial clustering of Helicobacter pylori infection, N Engl J Med, 322, 359-363, 1990,

Ford, A. C., D. Forman, A. G. Bailey, A. T. Axon, and P. Moavvedi, Initial poor quality of life predicts the new onset of dyspepsia: results from a longitudinal ten-year follow-up study, Gut, 2006,

Go, M. F., Review article: Natural history and epidemiology of Helicobacter pylori infection, Aliment Pharmacol Ther, 16 Suppl 1, 3-15, 2002.

Kivi, M., Y. Tindberg, M. Sorberg, T. H. Casswall, R. Befrits, P. M. Hellstrom, C. Bengtsson, L. Engstrand, and M. Granstrom, Concordance of Helicobacter pylori strains within families, J Clin Microbiol, 41, 5604-5608, 2003,

Magalhaes Queiroz, D. M., and F. Luzza, Epidemiology of Helicobacter pylori infection, Helicobacter, 11 Suppl 1, 1-5, 2006,

Parkin, D. M., The global health burden of infection-associated cancers in the year 2002, Int J Cancer, 118, 3030-3044, 2006.

Perez-Perez, G. I., D. Rothenbacher, and H. Brenner, Epidemiology of Helicobacter pylori infection, Helicobacter, 9 Suppl 1, 1-6, 2004.

Suerbaum, S., J. M. Smith, K. Bapumia, G. Morelli, N. H. Smith, E. Kunstmann, I. Dyrek, and M. Achtman, Free recombination within Helicobacter pylori, Proc Natl Acad Set USA, 95, 12,619-12,624, 1998.

Yoshida, T., H. Kubo, H. Murata, K. Ando, H. Ishii, and F. Miyagi, Acute multiple gastric ulcers in the pyloric antrum, Endoscopy, 9, 223-228, 1977,

Disease and Epidemiology

For most of the twentieth century, peptic ulcers were thought to be stress-related and caused by hyperchlorhydria. The discovery that H. pylori is associated with gastric inflammation and peptic ulcer disease was initially met with skepticism. However, this discovery and subsequent studies on H. pylori have revolutionized our view of the gastric environment, the diseases associated with it, and the appropriate treatment regimens.

H. pylori is probably the most common human chronic infection and is distributed worldwide. More than half of the world’s population is persistently colonized with H. pylori (34). The prevalence of H. pylori is much higher in emergent countries than in the Western world, although it increases with age in all populations studied (54). The incidence of H. pylori infection declines with increasing standards of socioeconomic development, including sewage disposal, water chlorination, hygienic food preparation, decreased crowding, and education (134). Once established, H. pylori generally persists for decades unless eradicated by anti-microbial therapy.

Because of the worldwide prevalence of infection, transmission of the organism from person to person is a major concern. Early studies demonstrated intrafamilial clustering of infection (42) and, more recently, DNA analyses of isolates have confirmed that most transmission occurs locally within families or small population groups (86, 153). These results are consistent with an apparent inability of H. pylori to proliferate or survive for long periods in the environment.

The mode of transmission from person to person has not been proven definitively. Oral-fecal, oral-oral, and gastro-oral routes have all been considered

[page 5]

possible (109). The study of the mode of transmission is made difficult by the fact that, unlike other infectious diseases, there is no well-defined clinical syndrome associated with its acquisition, and expression of chronic H. pylori infection in humans is highly variable. Hence, the usual approach of identifying cases and determining important exposures with infectious diseases is not possible.


34. Cover, T. L., D. E. Berg, M. J. Blaser, and H. L. T. Mobley. 2001. H. pylori pathogenesis, p. 509-558. In E. A. Groisman (ed.), Principles of Bacterial Pathogenesis. Academic Press, San Diego.

42. Drumm, B., G. I. Perez-Perez, M. J. Blaser, and P. M. Sherman. 1990. Intrafamilial clustering of Helicobacter pylori infection. New Engl. J. Med. 322:359-363.

54. Forman, D., and P. Webb. 1993. Geographic distribution and association with gastric cancer, p. 11-20. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston.

86. Kersulyte, D., H. Chalkauskas, and D. E. Berg. 1999. Emergence of recombinant strains of Helicobacter pylori during human infection. Mol. Microbiol. 31:31-43.

109. Megraud, F. 1992. Epidemiology of Helicobacter pylori infection, p. 107-123. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and Gastroduodenal Disease, 2 ed. Blackwell Scientific Publications, Oxford.

134. Pounder, R. E., and D. Ng. 1995. The prevalence of Helicobacter pylori in different countries. Aliment. Pharmacol. Ther. 9:S33-S39.

153. Suerbaum, S., J. M. Smith, K. Bapumia, G. Morelli, N. H. Smith, E. Kunstmann, I. Dyrek, and M. Achtman. 1998. Free recombination within Helicobacter pylori. Proc. Natl. Acad. Sci. U.S.A. 95:12619-12624.

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