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23 gesichtete, geschützte Fragmente: Plagiat

[1.] Wfe/Fragment 001 01 - Diskussion
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Chapter 1

INTRODUCTION

1.1 Helicobacter pylori

1.1.1 History

Spiral organisms in the stomachs of mammals were first reported in 1893 in Turin by Bizzozero. By the end of 1940, two additional reports of spiral gastric bacteria had appeared (Marshall, 2001). Although it was noted in 1924 by Murray Luck that the human stomach contains abundant urease activity and it was shown in 1959 that this activity disappeared after antibiotic treatment (indicating that the enzyme was of bacterial origin), the connection between gastric urease and gastric spiral bacteria was not established until the culturing of H. pylori in 1982 (Marshall and Warren, 1984). Research on gastric bacteria was at first impeded by the general belief that bacteria could not live in the acidic environment of the stomach. It was not until 1982 that H. pylori was first cultured by a research scientist, Barry Marshall, through the encouragement of a pathologist, Robin Warren. The first successful culture occurred by chance when a biopsy was left in the incubator for 5 days over the Easter holidays. By 1984, other groups had independently reported the disease associations of the organism (Langenberg et al., 1984; McNulty and Watson, 1984). Marshall hypothesized that the new bacterium was a Campylobacter found in the pyloric region of the stomach and therefore called it Campylobacter pyloridis, even though the new organism had different flagellar morphology than campylobacters.


Langenberg, M., G. Tytgat, M. Schipper, P. Rietra, and H. Zanen, Campylobacter like organisms in the stomach of patients and healthy individuals, The Lancet, 323, 1348-1349, 1984.

Marshall, B. J., One hundred years of discovery and rediscovery of Helicobacter pylori and its association with peptic ulcer disease, chap. 3, pp. 19-24, Helicobacter pylori: Physiology and genetics; ASM, 2001.

Marshall, B. J., and J. R. Warren, Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration, Lancet, 1, 1311-1315, 1984.

McNulty, C. A., and D. M. Watson, Spiral bacteria of the gastric antrum, Lancet, 1, 1068-1069, 1984.

[Page 1]

CHAPTER 1

INTRODUCTION

History

Spiral organisms in the stomachs of mammals were discovered more than 125 years ago in 1874, and spiral bacteria were first reported in the human stomach in 1906. By the end of 1940, two additional reports of spiral gastric bacteria had appeared (64). Although it was noted in 1924 that the human stomach contains abundant urease activity (137) and it was shown in 1959 that this activity disappeared after antibiotic treatment (indicating that the enzyme was of bacterial origin), the connection between gastric urease and gastric spiral bacteria was not established until the culturing of H. pylori in 1983 (102, 103, 165).

Research on gastric bacteria was at first impeded by the general belief that bacteria could not live in the acidic environment of the stomach (64, 137). It was not until 1983 that H. pylori was first cultured by a research scientist, Barry Marshall, through the encouragement of a pathologist, Robin Warren (102).

[Page 2]

The first successful culture occurred by chance when a biopsy was left in the incubator for 5 days over the Easter holidays in April 1982 (64, 137). By 1984, two other groups had independently reported the disease associations of the organism (137). Marshall hypothesized that the new bacterium was a Campylobacter found in the pyloric region of the stomach and therefore called it Campylobacter pyloridis (102), even though the new organism had different flagellar morphology than campylobacters.


64. Goodwin, S. 1993. Historical and microbiological perspectives, p. 1-10. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection: Pathophysiology, epidemiology, and management. Kluwer Academic Publishers, Boston.

102. Marshall, B. J., H. Royce, D. I. Annear, C. S. Goodwin, J. W. Pearman, J. R. Warren, and J. A. Armstrong. 1984. Original isolation of Campylobacter pyloridis new species from human gastric mucosa. Microbios Lett. 25:83-88.

103. Marshall, B. J., and J. R. Warren. 1984. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1:1311-5.

137. Rathbone, B. J., and R. V. Heatley. 1992. The historical associations between bacteria and peptic ulcer disease, p. 1-4. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and gastroduodenal disease, 2nd ed. Blackwell Scientific Publications, Oxford.

165. Warren, J. R., and B. Marshall. 1983. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. The Lancet:1273-5.

Anmerkungen

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[2.] Wfe/Fragment 002 01 - Diskussion
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C. pyloridis became C. pylori when linguists pointed out that the former was grammatically incorrect (Marshall et al., 1987), and Campylobacter became Helicobacter when it was discovered that its 16S ribosomal RNA was clearly distinct from other Campylobacter species tested (Andersen and Wadström, 2001). In 2005, Warren and Marshall were awarded the Nobel Prize in Medicine for their work on H. pylori.

1.1.2 General characteristics

Helicobacter pylori is a gram-negative, curved or slightly spiral, microaerophilic, slow-growing organism. The most characteristic of it's [sic] enzymes is a potent multisubunit urease. H. pylori is motile and possesses five to seven sheathed polar flagella (Geis et al., 1989; Josenhans et al., 1995). The bacterium's unique feature is its ability to colonize the stomach.

Because of the relevance of this organism to human health, an effort was made to sequence the genome. H. pylori 26695, originally isolated from a gastritis patient in the United Kingdom, was the strain chosen for sequencing because it colonizes piglets and elicits immune and inflammatory responses (Tomb et al., 1997). Strain J99 was sequenced in order to permit within-species genome comparison (Alm et al., 1999). The H. pylori genomes consist of a circular chromosome approximately 1.7 Mb in size. Of the 1590 predicted coding sequences, 279 genes were H. pylori specific. Some of these species-specific genes are thought to play an important role in adaptation of H. pylori to the human stomach. The organism appears to have a limited metabolic and biosynthetic capacity. These characteristics are consistent with those of an organism that colonizes a restricted ecological niche (Tomb et al., 1997). One interesting feature of the genome is that many predicted proteins, including urease, are most closely related to corresponding proteins from gram-positive organisms, archaea, or eukaryotes, rather than from other gram-negative organisms (Tomb et al., 1997), suggesting horizontal gene transfer during the evolution of H. pylori (Garcia-Vallvé et al., 2002; Gressmann et al., 2005).


Alm, R. A., L. S. Ling, D. T. Moir, B. L. King, E. D. Brown, P. C. Doig, D. R. Smith, B. Noonan, B. C. Guild, B. L. deJonge, G. Carmel, P. J. Tummino, A. Caruso, M, Uria-Nickelsen, D. M, Mills, C. Ives, R. Gibson, D. Merberg, S. D. Mills, Q. Jiang, D. E. Taylor, G. F. Vovis, and T. J. Trust, Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori, Nature, 397, 176-180, 1999.

Andersen, L. P., and T. Wadstrom, Basic bacteriology and culture, chap, 4, pp, 27-38, Helicobacter pylori: Physiology and genetics; ASM. 2001,

Garcia-Vallve, S., P. J. Janssen, and C. A. Ouzounis, Genetic variation between Helicobacter pylori strains: gene acquisition or loss?, Trends Microbiol, 10, 445447, 2002.

Geis, G., H. Leying, S. Suerbaum, U. Mai, and W. Opferkuch, Ultrastrueture and chemical analysis of Campylobacter pylori flagella, J Clin Microbiol, 27, 436-441, 1989.

Gressmann, H., B. Linz, R. Ghai, K. P. Pleissner, R. Sehlapbach, Y. Yamaoka, C. Kraft, S. Suerbaum, T. F. Meyer, and M. Achtman, Gain and loss of multiple genes during the evolution of Helicobacter pylori, PLoS Genet, 1, 2005.

Josenhans, C., A. Labigne, and S. Suerbaum, Comparative ultrastruetural and functional studies of Helicobacter pylori and Helicobacter mustelae flagellin mutants: both flagellin subunits, flaA and flaB, are necessary for full motility in Helicobacter species, J Bacteriol, 177, 3010-3020, 1995.

Marshall, B. J., E. W. McCallum, and C. Prakash, Campylobacter pyloridis and gastritis, Gastroenterology, 92, 2051-2051, 1987.

Tomb, J. F., O. White, A. E. Kerlavage, E. A. Clayton, G. G. Sutton, E. D. Fleischmann, K. A. Ketchum, H. P. Klenk, S. Gill, B. A. Dougherty, K. Nelson, J. Quackenbush, L. Zhou, E. F. Kirkness, S. Peterson, B. Loftus, D. Eichardson, E. Dodson, H. G. Khalak, A. Glodek, K. McKenney, L. M. Fitzegerald, N. Lee, M. D. Adams, E. K. Hickey, D. E. Berg, J. D. Gocayne, T. E. Utterback, J. D. Peterson, J. M. Kelley, M. D. Cotton, J. M. Weidman, C. Fujii, C. Bowman, L. Watthey, E. Wallin, W. S. Hayes, M. Borodovsky, P. D. Karp, H. O. Smith, C. M. Fraser, and J. C. Venter, The complete genome sequence of the gastric pathogen Helicobacter pylori, Nature, 388, 539-547, 1997.

C. pyloridis became C. pylori when linguists pointed out that the former was grammatically incorrect (101), and Campylobacter became Helicobacter when it was discovered that its 16S ribosomal RNA was clearly distinct from other Campylobacter species tested (63).

General characteristics

Helicobacter pylori is a gram-negative, curved or slightly spiral, microaerophilic, slow-growing organism. Its most characteristic enzyme is a potent multi-subunit urease. H. pylori is motile and possesses four to six sheathed polar flagella (80, 150). The bacterium’s unique feature is its ability to colonize the stomach. [...]

Because of the relevance of this organism to human health, an effort was made to sequence the genome. H. pylori 26695, originally isolated from a gastritis patient in

[page 3]

the United Kingdom, was the strain chosen for sequencing because it colonizes piglets and elicits immune and inflammatory responses (157). Strain J99 was later sequenced (7). The H. pylori genomes consist of a circular chromosome approximately 1.7 Mb in size. Of the 1590 predicted coding sequences, 594 lack homology to E. coli or H. influenzae genes (76). 499 of these lacked obvious homology to any sequences in databases at the time of annotation, in 1997 (34). Some of these species-specific genes no doubt play an important role in adaptation of H. pylori to the human stomach.

[...] The organism appears to have a limited metabolic and biosynthetic capacity. These characteristics are consistent with those of an organism that colonizes a restricted ecological niche (157). One interesting feature of the genome is that many predicted proteins, including urease, are most closely related to corresponding proteins from Gram-positive organisms, Archaea, or eukaryotes, rather than from other Gram-negative organisms (157), suggesting horizontal gene transfer during the evolution of H. pylori.


7. Alm, R., L.-S. L. Ling, D. T. Moir, B. L. King, E. D. Brown, P. C. Doig, D. R. Smith, B. Noonan, B. C. Guild, B. L. deJonge, G. Carmel, P. J. Tummino, A. Caruso, M. Uria-Nickelsen, D. M. Mills, C. Ives, R. Gibson, D. Merberg, S. D. Mills, Q. Jiang, D. E. Taylor, G. F. Vovis, and T. J. Trust. 1999. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 397:176-180.

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.

63. Goodwin, C. S. 1994. How Helicobacter pylori acquired its name, and how it overcomes gastric defence mechanisms. Journal of Gastroenterology and Hepatology 9:S1-3.

76. Huynen, M., T. Dandelkar, and P. Bork. 1998. Differential genome analysis applied to the species-specific features of Helicobacter pylori. FEBS Letters 426:1-5.

80. Jones, D. M., A. Curry, and A. J. Fox. 1985. An ultrastructural study of the gastric Campylobacter-like organism 'Campylobacter pyloridis'. Journal of General Microbiology 131:2335-41.

101. Marshall, B. J., and C. S. Goodwin. 1987. Revised nomenclature of Campylobacter pyloridis. Int. J. Systematic Bacteriol. 37:68.

150. Stark, R. M., J. Greenman, and M. R. Millar. 1995. Physiology and biochemistry of Helicobacter pylori. British Journal of Biomedical Science 52:282-290.

157. Tomb, J.-F., others, and J. C. Venter. 1997. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature 388:539-547.

Anmerkungen

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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.

Anmerkungen

The source is not mentioned.

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Although most infections are asymptomatic, about 10% of cases of H. pylori colonization lead to illness. H. pylori is a major cause of chronic active gastritis and peptic ulcer disease and is also an early risk factor for gastric cancer. Infections are occasionally cleared spontaneously after a brief acute phase, but many last for years or decades, and it is these long-term infections that are most often implicated in disease (Kusters et al., 2006). The persistence of the H. pylori infection is surprising considering that the bacterium stimulates marked humoral and cellular immune responses in the human host, which are insufficient to clear the infection (Harry L. T. Mobley and Hazell , 2001; Suerbaum and Michetti , 2002).

1.1.4 Ecological niche

The means by which H. pylori occupies its gastric niche and the basis for its biochemical capabilities and requirements is of great fundamental interest. A thorough understanding of H. pylori physiology and metabolism could lead to new and better drug therapies, to the identification of potential targets for therapeutic intervention, or to an effective vaccine. Understanding how the organism colonizes and persists in the host is an important step in fully understanding its pathogenesis.

H. pylori have adapted to survive in the very specific and unique ecological niche of the human stomach (Lee and Josenhans, 2005; Sachs et al., 2003; Go, 2002). Because of the presence of gastric acid which rapidly destroys the majority of bacteria, the stomach is typically colonized only by transient oral flora. H. pylori appears to have evolved specific mechanisms to assist its survival in this hostile environment. These factors include the ability to swim well in the thick, protective mucus gel layer, the ability to transiently survive exposure to acid, and the ability to attach to the epithelial cell layer to prevent the bacteria from being washed out of the stomach through the mechanical action of peristalsis. As a result, other infectious agents do not appear to successfully compete with H. pylori in this environment (Sachs et al., 2003).

Major non-specific host defenses against microbial colonization of the stomach are gastric acid, peristalsis, and the continual shedding of the cells and mucus lining of the gastric surface.


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

Harry L. T. Mobley, G. L. M. and S. L. Hazell, Helicobacter pylori Physiology and Genetics, ASM Press, 2001,

Kusters, J. G., A. H. van Vliet, and E. J. Kuipers, Pathogenesis of Helicobacter pylori infection, Clin Microbiol Rev, 19, 449-490, 2006,

Lee, S. K,, and C. Josenhans, Helicobacter pylori and the innate immune system, Int J Med Microbiol, 295, 325-334, 2005,

Sachs, G., D. L. Weeks, K. Melchers, and D. R. Scott, The gastric biology of Helicobacter pylori, Annu Rev Physiol, 65, 349-369, 2003,

Suerbaum, S., and P. Michetti, Helicobacter pylori infection, N Engl J Med, 347, 1175-1186, 2002.

Although most infections are asymptomatic, about 10% of cases of H. pylori colonization lead to illness (34). H. pylori is a major cause of chronic active gastritis and peptic ulcer disease (80, 81, 141, 150) and is also an early risk factor for gastric cancer (127, 128). Infections are occasionally cleared spontaneously after a brief acute phase, but many last for years or decades, and it is these long-term infections that are most often implicated in disease (16, 159). The persistence of the H. pylori infection is surprising considering that the bacterium stimulates marked humoral and cellular immune responses in the human host, which are insufficient to clear the infection (26).

[page 6]

Ecological niche

The means by which H. pylori occupies its gastric niche and the basis for its biochemical capabilities and requirements is of great fundamental interest. A thorough understanding of H. pylori physiology and metabolism could lead to new and better drug therapies, to the identification of potential targets for therapeutic intervention, or to an effective vaccine. Understanding how the organism colonizes and persists in the host is an important step in fully understanding its pathogenesis.

H. pylori has adapted to survive in the very specific and unique ecological niche of the human stomach. Because of the presence of gastric acid, which rapidly destroys the majority of bacteria, the stomach is typically colonized only by transient oral flora (156). H. pylori appears to have evolved specific mechanisms to assist its survival in the hostile environment. These factors include the ability to swim well in the thick, protective mucus gel layer, the ability to transiently survive exposure to acid, and the ability to attach to the epithelial cell layer to prevent the bacteria from being washed out of the stomach through the mechanical action of peristalsis. As a result, other infectious agents do not appear to successfully compete with H. pylori in this environment.

Major non-specific host defenses against microbial colonization of the stomach are gastric acid, peristalsis, and the continual shedding of the cells and mucus lining the gastric surface (34).


16. Blaser, M. J. 1992. Perspectives on the pathogenesis of Helicobacter pylori infections, p. 276-280. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and Gastroduodenal Disease, 2nd ed. Blackwell Scientific Publishing, Oxford.

26. Chen, M., and A. Lee. 1993. Vaccination possibilities and probabilities, p. 158-169. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston.

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.

80. Jones, D. M., A. Curry, and A. J. Fox. 1985. An ultrastructural study of the gastric Campylobacter-like organism 'Campylobacter pyloridis'. Journal of General Microbiology 131:2335-41.

81. Jones, D. M., A. M. Lessells, and J. Eldridge. 1984. Campylobacter like organisms on the gastric mucosa: culture, histological, and serological studies. Journal of Clinical Pathology 37:1002-6.

127. Nomura, A., G. N. Stemmermann, P.-H. Chyou, I. Kato, G. I. Perez- Perez, and M. J. Blaser. 1991. Helicobacter pylori infection and gastric carcinoma among Japanese Americans in Hawaii. The New England Journal of Medicine 325:1132-6.

128. Parsonnet, J., G. D. Friedman, D. P. Vandersteen, Y. Chang, J. H. Vogelman, N. Orentreich, and R. K. Sibley. 1991. Helicobacter pylori infection and the risk of gastric carcinoma. The New England Journal of Medicine 325:1127-31.

141. Rollason, T. P., J. Stone, and J. M. Rhodes. 1984. Spiral organisms in endoscopic biopsies of the human stomach. Journal of Clinical Pathology 37:23- 6.

150. Stark, R. M., J. Greenman, and M. R. Millar. 1995. Physiology and biochemistry of Helicobacter pylori. British Journal of Biomedical Science 52:282-290.

156. Thompkins, D. S. 1992. Isolation and characterization of Helicobacter pylori, p. 19-28. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and Gastroduodenal Disease, 2 ed. Blackwell Scientific Publications, Oxford.

159. Tytgat, G., and M. Dixon. 1993. Overview: Role in peptic ulcer disease, p. 75-87. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston.

Anmerkungen

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[This layer of gastric mucus, about 0.2-0.6 mm thick, is secreted] by epithelial cells and plays an important protective role in the stomach, both as a lubricant and as part of the gastric mucosal barrier against acid and pepsin. H. pylori thrives in this mucus environment. The mucus layer forms a stable, continuous layer over the mucosa and provides an environment for the neutralization of luminal acid, maintaining a near neutral pH at the mucosal surface (Ferrero, 2005).

According to studies employing light and electron microscopy and examination of stained gastric biopsies, H. pylori can be found both in the gastric mucus and in close proximity to the mucosal epithelial cells where it is protected from the acidic environment of the stomach lumen (Hazell et al., 1986; Liu et al., 2006).


Ferrero, R. L., Innate immune recognition of the extracellular mucosal pathogen, Helicobacter pylori, Mol Immunol, 42, 879-885, 2005.

Hazell, S. L., A. Lee, L. Brady, and W. Hennessy, Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium, J Infect Dis, 153, 658-663, 1986.

Liu, Y., E. Hidaka, Y. Kaneko, T. Akamatsu, and H. Ota, Ultrastructure of Helicobacter pylori in human gastric mucosa and H. pylori-infected human gastric mucosa using transmission electron microscopy and the high-pressure freezing-freeze substitution technique, J Gastroenterol, 41, 569-574, 2006.

[Page 6]

This layer of gastric mucus, about 0.2-0.6 mm thick, is secreted by epithelial cells and plays an important protective role in the stomach, both as a lubricant and as part of the gastric mucosal barrier against acid and pepsin (62).

H. pylori thrives in a mucus environment.

[Page 7]

The mucus layer forms a stable, continuous layer over the mucosa and provides an environment for the neutralization of lumenal acid, maintaining a near neutral pH at the mucosal surface (5).

According to studies employing light and electron microscopy and examination of stained gastric biopsies, H. pylori can be found both in the gastric mucus and in close proximity to the mucosal epithelial cells where it is protected from the acidic environment of the stomach lumen (17, 68).


5. Allen, A. 1984. The structure and function of gastrointestinal mucous, p. 3-11. In E. C. Boedeker (ed.), Attachment of organisms to the gut mucosa, vol. II. CRC Press, Boca Raton.

17. Boren, T., S. Normark, and P. Faulk. 1994. Helicobacter pylori: Molecular basis for host recognition and bacterial adherence. Trends in Microbiology 2:221-8.

62. Goggin, P., and T. Northfield. 1993. Mucosal defence, p. 40-. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston.

68. Hazell, S. L., A. Lee, L. Brady, and W. Hennessy. 1986. Campylobacter pyloridis and gastritis: Association with intracellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium. The Journal of Infectious Diseases 153:658-663.

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In addition to point mutations that are unique to individual strains, large gene clusters are present in some strains but not in others (Gressmann et al., 2005). Early studies revealed that about 60% of H. pylori isolates produce an immunodominant 120-140 kDa protein of unknown function (CagA) (Cover et al., 1990; Crabtree et al., 1991). The cagA gene is located within an approximately 40 kb DNA segment called the cag pathogenicity island (PAI) (Akopyants et al., 1998; Censini et al., 1996). Many of the genes within the cag PAI help H. pylori activate proinflammatory signal transduction pathways in gastric epithelial cells (Segal et al., 1996, 1997), contributing to the host inflammatory response. Infection with strains that contain the cag PAI is more likely to result in clinical disease than is colonization with cag-negative strains (Covacci et al., 1993; Cover et al., [1990; Crabtree et al., 1991).]

Akopvants, N. S,, S. W, Clifton, D. Kersulvte, J. E. Crabtree, B. E. Youree, C. A. Reece, N. O. Bukanov, E. S. Drazek, B. A. Roe, and D. E. Berg, Analyses of the eag pathogenicity island of Helicobacter pylori, Mol Microbiol, 28, 37-53, 1998.

Censini, S,, C, Lange, Z, Xiang, J, E, Crabtree, P, Ghiara, M, Borodovskv, R, Rap- puoli, and A, Covaeei, cag, a pathogenicity island of Helicobacter pylori, encodes type I-speeihe and disease-associated virulence factors, Proc Natl Acad Sci U S A, 93, 14,648-14,653, 1996.

Covacci, A,, S, Censini, M, Bugnoli, E, Petracca, D, Burroni, G, Macchia, A, Mas- sone, E, Papini, Z, Xiang, and N, Figura, Molecular characterization of the 128- kda immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer, Proc Natl Acad Sci U S A, 90, 5791-5795, 1993,

Cover, T, L,, C, P, Dooley, and M, J, Blaser, Characterization of and human serologic response to proteins in Helicobacter pylori broth culture supernatants with vacuolizing cytotoxin activity, Infect Immun, 58, 603-610, 1990,

Crabtree, J, E,, J, D, Taylor, J, I, Wyatt, E, V, Heatlev, T, M, Shalleross, D, S, Tompkins, and B, J, Eathbone, Mucosal iga recognition of Helicobacter pylori 120 kda protein, peptic ulceration, and gastric pathology, Lancet, 338, 332-335, 1991,

Gressmann, H,, B, Linz, R, Ghai, K, P, Pleissner, R, Sehlapbaeh, Y, Yamaoka, C. Kraft, S. Suerbaum, T, F, Meyer, and M, Aehtman, Gain and loss of multiple genes during the evolution of Helicobacter pylori, PLoS Genet, 1, 2005.

Segal, E. D,, S. Falkow, and L. S. Tompkins, Helicobacter pylori attachment to gastric cells induces evtoskeletal rearrangements and tyrosine phosphorylation of host cell proteins, Proc Natl Acad Sci U S A, 93, 1259-1264, 1996.

Segal, E. D,, C. Lange, A. Covaeei, L. S. Tompkins, and S. Falkow, Induction of host signal transduction pathways by Helicobacter pylori, Proc Natl Acad Sci U S A, 94, 7595-7599, 1997.

In addition to point mutations that are unique to individual strains, large gene clusters are present in some strains but not in others. Early studies revealed that about 60% of H. pylori isolates produce an immunodominant 120-140 kDa protein of unknown function (CagA) (35, 36). The cagA gene is located within an approximately 40 kb DNA segment called the cag pathogenicity island (PAI) (2, 23). Many of the genes within the cag PAI help H. pylori activate proinflammatory signal transduction pathways in gastric epithelial cells (145, 146), contributing to the host inflammatory response. Infection with strains that contain the cag PAI is more likely to result in clinical disease than is colonization with cag-negative strains (33, 35, 36). Therefore, the presence or absence of the cag PAI is an important characteristic among H. pylori strains.

2. Akopyants, N. S., S. W. Clifton, D. Kersulyte, J. E. Crabtree, B. E. Youree, C. A. Reece, N. O. Bukanov, E. S. Drazek, B. A. Roe, and D. E. Berg. 1998. Analyses of the cag pathogenicity island of Helicobacter pylori. Mol. Microbiol. 28:37-53.

23. Censini, S., C. Lange, Z. Xiang, J. E. Crabtree, P. Ghiara, M. Borodovsky, R. Rappuoli, and A. Covacci. 1996. cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc. Natl. Acad. Sci. U.S.A. 93:14648-14653.

33. Covacci, A., S. Censini, M. Bugnoli, R. Petracca, D. Burroni, G. Macchia, A. Massone, E. Papini, Z. Xiang, N. Figura, and e. al. 1993. Molecular characterization of the 128-kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc. Natl. Acad. Sci. U.S.A. 90:5791-5795.

35. Cover, T. L., C. P. Dooley, and M. J. Blaser. 1990. Characterization of and human serologic response to proteins in Helicobacter pylori broth culture supernatants with vacuolizing cytotoxin activity. Infect. Immun. 58:603-610.

36. Crabtree, J. E., J. D. Taylor, J. I. Wyatt, R. V. Heatley, T. M. Shallcross, L. S. Tompkins, and B. J. Rathbone. 1991. Mucosal IgA recognition of Helicobacter pylori 120 kDa protein, peptic ulceration, and gastric pathology. Lancet 338:332-335.

145. Segal, E. D., S. Falkow, and L. S. Tompkins. 1995. Helicobacter pylori attachment to gastric cells induces cytoskeletal rearrangements and tyrosine phosphorylation of host cell proteins. Proc. Natl. Acad. Sci. U.S.A. 93:1259-1264.

146. Segal, E. D., C. Lange, A. Covacci, L. S. Tompkins, and S. Falkow. 1997. Induction of host signal transduction pathways by Helicobacter pylori. Proc. Natl. Acad. Sci. U.S.A. 94:7595-7599.

Anmerkungen

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Therefore, the presence or absence of the cag PAI is an important characteristic among H. pylori strains.

Additional strain-specific genes have been identified by comparing the complete genome sequences of H. pylori 26695 with H. pylori J99 (Alm and Trust , 1999). The overall genomic organization, gene order and predicted proteomes (sets of proteins encoded by the genome) were found to be quite similar. Both strains contained the complete cag PAI flanked by the same chromosomal genes and a previously described 31-bp repeat (Akopyants et al., 1998; Censini et al., 1996). The DNA-sequence differences between orthologues from the two strains are found mainly in the third position of coding triplets, consistent with the variation seen between H. pylori strains identified by methods dependent on the nucleotide sequence or on the sequencing of specific loci in different strains (Akopyanz [sic] et al., 1992). This nucleotide variation however does not translate into a highly divergent proteome. A total of 275 (18.4%) J99 and 290 (18.7%) 26695 gene products have orthologues of unknown function in other species, and 346 (23.1%) J99 and 367 (23.6%) 26695 genes are H. pylori specific, showing no sequence similarity with genes available in public databases. Of these H. pylori specific genes, 56 and 69 are specific to strains J99 and 26995, respectively (Alm et al., 1999).

The fact that strain-specific DNA-restriction/modification genes have a lower (G+C) content than the remainder of the genome and are associated with regions that are organized differently in the J99 and 26695 genomes indicates that these genes may have been acquired horizontally from other bacterial species or transferred more recently from other H. pylori strains by natural transformation (Alm et al., 1999).


Alm, R. A., and T. J. Trust, Analysis of the genetic diversity of Helicobacter pylori: the tale of two genomes, J Mol Med, 77, 834-846, 1999.

Alm, R. A., L. S. Ling, D. T. Moir, B. L. King, E. D. Brown, P. C. Doig, D. R. Smith, B. Noonan, B. C. Guild, B. L. deJonge, G. Carmel, P. J. Tummino, A. Caruso, M. Uria-Nickelsen, D. M. Mills, C. Ives, R. Gibson, D. Merberg, S. D. Mills, Q. Jiang, D. E. Taylor, G. F. Vovis, and T. J. Trust, Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori, Nature, 397, 176-180, 1999.

Akopyanz, N., N. O. Bukanov, T. U. Westblom, S. Kresovich, and D. E. Berg, DNA diversity among clinical isolates of Helicobacter pylori detected by PCR-based rapd fingerprinting, Nucleic Acids Res, 20, 5137-5142, 1992.

Akopyants, N. S., S. W. Clifton, D. Kersulyte, J. E. Crabtree, B. E. Youree, C. A. Reece, N. O. Bukanov, E. S. Drazek, B. A. Roe, and D. E. Berg, Analyses of the cag pathogenicity island of Helicobacter pylori, Mol Microbiol, 28, 37-53, 1998.

Censini, S., C. Lange, Z. Xiang, J. E. Crabtree, P. Ghiara, M. Borodovsky, R. Rappuoli, and A. Covaeci, cag. a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors, Proc Natl Acad Sci USA, 93, 14,648-14,653, 1996.

Therefore, the presence or absence of the cag PAI is an important characteristic among H. pylori strains.

[page 12]

Additional strain-specific genes have been identified by comparing the complete genome sequences of H. pylori 26695 with H. pylori J99 (7). The overall genomic organization, gene order and predicted proteomes (sets of proteins encoded by the genome) were found to be quite similar. Both strains contained the complete cag PAI flanked by the same chromosomal genes and a previously described 31-bp repeat (2). The DNA-sequence differences between orthologues from the two strains are found mainly in the third position of coding triplets, consistent with the variation seen between H. pylori strains identified by methods dependent on the nucleotide sequence or on the sequencing of specific loci in different strains (1). However, this nucleotide variation does not translate into a highly divergent proteome. A total of 275 (18.4%) J99 and 290 (18.7%) 26695 gene products have orthologues of unknown function in other species, and 346 (23.1%) J99 and 367 (23.6%) 26695 genes are H. pylori specific, showing no sequence similarity with genes available in public databases. Of these H. pylori specific genes, 56 and 69 are specific to stains J99 and 26995, respectively (7).

[page 13]

The fact that strain-specific DNA-restriction/modification genes have a lower (G+C) content than the remainder of the genome and are associated with regions that are organized differently in the J99 and 26695 genomes indicates that these genes may have been acquired horizontally from other bacterial species or transferred more recently from other H. pylori strains by natural transformation (7).


1. Akopyants, N., N. O. Bukanov, T. U. Westblom, S. Kresovich, and D. E. Berg. 1992. DNA diversity among clinical isolates of Helicobacter pylori deteted [sic] by PCR-based RAPD fingerprinting. Nucleic Acids Res. 20:5137-5142.

2. Akopyants, N. S., S. W. Clifton, D. Kersulyte, J. E. Crabtree, B. E. Youree, C. A. Reece, N. O. Bukanov, E. S. Drazek, B. A. Roe, and D. E. Berg. 1998. Analyses of the cag pathogenicity island of Helicobacter pylori. Mol. Microbiol. 28:37-53.

7. Alm, R., L.-S. L. Ling, D. T. Moir, B. L. King, E. D. Brown, P. C. Doig, D. R. Smith, B. Noonan, B. C. Guild, B. L. deJonge, G. Carmel, P. J. Tummino, A. Caruso, M. Uria-Nickelsen, D. M. Mills, C. Ives, R. Gibson, D. Merberg, S. D. Mills, Q. Jiang, D. E. Taylor, G. F. Vovis, and T. J. Trust. 1999. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 397:176-180.

Anmerkungen

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There is increasing evidence that recombination occurs between different H. pylori strains (Kraft et al., 2006; Kraft and Suerbaum, 2005; Suerbaum and Achtman, 2004). Simultaneous colonization of human stomachs with more than one strain of H. pylori is detectable in about 5-10% of patients in the United States (Fujimoto et al., 1994), and may occur even more commonly in other populations (Jorgensen et al., 1996). Mixed infections, even those that are transient, provide an opportunity for genetic exchange between strains. Analysis of single cell clones from a patient who was naturally infected with two different H. pylori strains, one of which was cag+ and the other cag-, revealed evidence for at least six different genetic exchanges. One of these exchanges resulted in the replacement of the entire cag PAI with DNA containing the empty site allele from the cag-negative strain. Several others involved a region encoding putative outer membrane proteins that could be involved in interactions with the host (Kersulyte et al., 1999). Genetic exchange may play an important role in the biology of H. pylori by generating new genotypes much more rapidly than is possible by mutation alone, therefore allowing cells to rapidly adapt to new sites in the gastric environment or to new hosts. For several genes, including flaA, flaB, and portions of vacA, phylogenetic analyses of orthologous sequences from different strains have yielded a bush-like rather than a tree-like pattern, indicating considerable interstrain recombination. Recombination is thought to occur more commonly in H. pylori than in any other bacterial species analyzed thus far (Suerbaum et al., 1998). Thus, the high level of allelic variation observed in H. pylori can be attributed to at least two factors. First, large populations of H. pylori have probably evolved within millions of individual human stomachs over thousands of years, resulting in considerable mutational diversity. Second, additional diversity has accumulated as a result of extensive intragenic recombination due to mixed infections (Kraft and Suerbaum, 2005).

Fujimoto, S., B. Marshall, and M. J. Blaser, PCR-based restriction fragment length polymorphism typing of Helicobacter pylori, J Clin Microbiol, 32, 331-334, 1994.

Jorgensen, M., G. Daskalopoulos, V. Warburton, H. M. Mitchell, and S. L. Hazell, Multiple strain colonization and metronidazole resistance in Helicobacter pylori-infected patients: identification from sequential and multiple biopsy specimens, J Infect Dis, 174, 631-635, 1996.

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

Kraft, C., and S. Suerbaum, Mutation and recombination in Helicobacter pylori: mechanisms and role in generating strain diversity, Int J Med Microbiol, 295, 299-305, 2005.

Kraft, C., A. Stack, C. Josenhans, E. Niehus, G. Dietrich, P. Correa, J. G. Fox, D. Falush, and S. Suerbaum, Genomic changes during chronic Helicobacter pylori infection, J Bacteriol, 188, 249-254, 2006.

Suerbaum, S., and M. Achtman, Helicobacter pylori: recombination, population structure and human migrations, Int J Med Microbiol, 294, 133.139, 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 Sci U S A, 95, 12,619-12,624, 1998.

[Page 13]

There is increasing evidence that recombination occurs between different H. pylori strains (10, 58, 61). Simultaneous colonization of human stomachs with more than one strain of H. pylori is detectable in about 5-10% of patients in the United States (57), and may occur even more commonly in other populations (82). Mixed infections, even those that are transient, provide an opportunity for genetic exchange between strains. Analysis of single cell clones from a patient who was naturally infected with two different H. pylori strains, one of which was cag+ and the other cag-, revealed evidence for at least six different genetic exchanges. One of these exchanges resulted in the replacement of the entire cag PAI with DNA containing the “empty site allele” from the cag-negative strain. Several others involved a region encoding putative outer membrane proteins that could be involved in interactions with the host (86). Genetic exchange may play an important role in the biology of H. pylori by generating new genotypes much more rapidly than is possible by mutation alone, therefore allowing cells to rapidly adapt to new sites in the gastric environment or to new hosts.

For several genes, including flaA, flaB, and portions of vacA, phylogenetic analyses of orthologous sequences from different strains have yielded a “bush”-like rather than a “tree”-like pattern, indicating considerable interstrain recombination. Recombination is thought to occur more commonly in H. pylori than in any other

[Page 14]

bacterial species analyzed thus far (153). Thus, the high level of allelic variation observed in H. pylori can be attributed to at least two factors. First, large populations of H. pylori have probably evolved within millions of individual human stomachs over thousands of years, resulting in considerable mutational diversity. Second, additional diversity has accumulated as a result of extensive intragenic recombination due to mixed infections (34).


10. Atherton, J. C., P. Cao, J. R. M. Peek, M. K. R. Tummuru, M. J. Blaser, and T. L. Cover. 1995. Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J. Biol. Chem. 270:17771-17777.

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.

57. Fujimoto, S., B. Marshall, and M. J. Blaser. 1994. PCR-based restriction fragment length polymorphism typing of Helicobacter pylori. J. Clin. Microbiol. 34:331-334.

58. Garner, J. A., and T. L. Cover. 1995. Analysis of genetic diversity in cytotoxin-producing and non-cytotoxin-producing Helicobacter pylori strains. J. Infect. Dis. 172:290-293.

61. Go, M. F., V. Kapur, D. Y. Graham, and J. M. Musser. 1996. Population genetic analysis of Helicobacter pylori by multilocus enzyme electrophoresis: Extensive allelic diversity and recombinational population structure. J. Bacteriol. 178:3934-3938.

82. Jorgensen, M., G. Daskalopoulos, V. Warburton, H. M. Mitchell, and S. L. Hazell. 1996. Multiple strain colonization and metronidazole resistance in Helicobacter pylori-infected patients: Identification from sequential and multiple biopsy specimens. J. Infect. Dis. 174:631-635.

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.

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.

Anmerkungen

Although identical, nothing has been marked as a citation; the source is not given.

S. Suerbaum has been the advisor for this PhD-Thesis, thus the preference for literary references with him as author or co-author instead of the original references.

Sichter
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As with several other bacterial species, including Neisseria spp. and Streptococcus pneumoniae, H. pylori is naturally competent for genetic transformation in vitro (Nedenskov-Sorensen et al., 1990). This property allows for the uptake of exogenous DNA, which may subsequently replicate, in the case of plasmids, or incorporate into the chromosome by homologous recombination. In addition to genetic exchange via transformation, H. pylori strains may exchange DNA via a contact-dependent mechanism resembling bacterial conjugation.

Nedenskov-Sorensen, P., G. Bukholm, and K. Bovre, Natural competence for genetic transformation in Campylobacter pylori, J Infect Dis, 161, 365-366, 1990.

As with several other bacterial species, including Neisseria spp. and Streptococcus pneumoniae, H. pylori is naturally competent for genetic transformation in vitro (125). This property allows for the uptake of exogenous DNA, which may subsequently replicate, in the case of plasmids, or incorporate into the chromosome by homologous recombination. In addition to genetic exchange via transformation, H. pylori strains may exchange DNA via a contact-dependent mechanism resembling bacterial conjugation (89).

89. Kuipers, E. J., D. A. Israel, J. G. Kusters, and M. J. Blaser. 1998. Evidence for a conjugation-like mechanism of DNA transfer in Helicobacter pylori. J. Bacteriol. 180:2901-2905.

125. Nedenskov-Sorensen, P., G. Bukholm, and K. Bovre. 1990. Natural competence for genetic transformation in Campylobacter pylori. J. Infect. Dis. 161:365-366.

Anmerkungen

Although identical, nothing has been marked as a citation; the source is not given.

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(Graf Isolan), Hindemith

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Ahmed and Sechi 2005, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung, Wfe

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H. pylori is usually acquired during childhood, with transmission occurring predominantly within families (Tindberg et al., 2001; Kivi et al., 2003; Kivi and Tindberg, 2006). Some studies have demonstrated the possible co-existence of a large array of clonal lineages within H. pylori populations evolving within each individual in isolation from one another (Suerbaum et al., 1998; Han et al., 2000; Owen and Xerry, 2003).

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.

Han, S. R., H. C. Zschausch, H. G. Meyer, T. Schneider, M. Loos, S. Bhakdi, and M. J. Maeurer, Helicobacter pylori: clonal population structure and restricted transmission within families revealed by molecular typing, J Clin Microbiol, 38, 3646-3651, 2000.

Kivi, M., and Y. Tindberg, Helicobacter pylori occurrence and transmission: a family affair?, Scand J Infect Dis, 38, 407-417, 2006.

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

Owen, R. J., and J. Xerry, Tracing clonality of Helicobacter pylori infecting family members from analysis of DNA sequences of three housekeeping genes (ureI, atpA and ahpC), deduced amino acid sequences, and pathogenicity-associated markers (cagA and vacA), J Med Microbiol, 52, 515-524, 2003.

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 Sci U S A, 95, 12,619-12,624, 1998.

Tindberg, Y., C. Bengtsson, F. Granath, M. Blennow, O. Nyrén, and M. Granström, Helicobacter pylori infection in Swedish school children: lack of evidence of child-to-child transmission outside the family, Gastroenterology, 121, 310-316, 2001.

H. pylori infection is usually acquired during childhood, where transmission occurs predominantly within families [13]. A couple of recent studies demonstrated the possible co-existence of a large array of clonal lineages within H. pylori populations that are evolving in each individual separately from one another [14,10].

10. Owen RJ, Xerry J: Tracing clonality of Helicobacter pylori infecting family members from analysis of DNA sequences of three housekeeping genes (ureI, atpA and ahpC), deduced amino acid sequences, and pathogenicity-associated markers (cagA and vacA). J Med Microbiol 2003, 52:515-524.

13. Drumm B, Perez-Perez GI, Blaser MJ, Sherman PM: Intrafamilial clustering of Helicobacter pylori infection. N Engl J Med 1990, 322:359-363.

14. Han SR, Zschausch HC, Meyer HG, Schneider T, Loos M, Bhakdi S, Maeurer MJ: Helicobacter pylori: clonal population structure and restricted transmission within families revealed by molecular typing. J Clin Microbiol 2000, 38:3646-3651.

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World-wide studies of H. pylori isolates from different geographical regions demonstrated weak clonal groupings and geographical partitioning of H. pylori isolates (Achtman et al., 1999; Carroll et al., 2003). [...] Should recombination only occur between a resident H. pylori population, exchange of genetic sequences can homogenise this population. The introduction of polymorphisms and sequence variants from one H. pylori population specific to a particular geographical region to another H. pylori population from a different geographical region via human migration makes the association of particular genotypes with specific geographical locations more difficult. Although this introduction of new polymorphisms into a particular H. pylori population poses a problem with identifying specific genotypes within certain geographical locales, it may, provide information on the ancestry of the hosts. Different studies have been aimed at identifying whether H. pylori was introduced to Latin America via European or Asian migrant populations (Kersulyte et al., 2000; Ghose et al., 2002). However, a recent study by Falush et al. (Falush et al., 2003b) showed that sequence analysis of H. pylori isolates obtained from 27 countries displayed geographical partitioning.

Achtman, M., T. Azuma, D. E. Berg, Y. Ito, G. Morelli, Z. J. Pan, S. Suerbaum, S. A. Thompson, A. van der Ende, and L. J. van Doorn, Recombination and clonal groupings within Helicobacter pylori from different geographical regions, Mol Microbiol, 32, 459-470, 1999.

Carroll, I. M., N. Ahmed, S. M. Beesley, A. A. Khan, S. Ghousunnissa, C. A. Moráin, and C. J. Smyth, Fine-structure molecular typing of Irish Helicobacter pylori isolates and their genetic relatedness to strains from four different continents, J Clin Microbiol, 41, 5755-5759, 2003.

Falush, D., T. Wirth, B. Linz, J. K. Pritchard, M. Stephens, M. Kidd, M. J. Blaser, D. Y. Graham, S. Vacher, G. I. Perez-Perez, Y. Yamaoka, F. Mégraud, K. Otto, U. Reichard, E. Katzowitsch, X. Wang, M. Achtman, and S. Suerbaum, Traces of human migrations in Helicobacter pylori populations, Science, 299, 1582-1585, 2003b.

Ghose, C., G. I. Perez-Perez, M. G. Dominguez-Bello, D. T. Pride, C. M. Bravi, and M. J. Blaser, East Asian genotypes of Helicobacter pylori strains in Amerindians provide evidence for its ancient human carriage, Proc Natl Acad Sci U S A, 99, 15,107-15,111, 2002.

Kersulyte, D., A. K. Mukhopadhyay, B. Velapatiño, W. Su, Z. Pan, C. Garcia, V. Hernandez, Y. Valdez, R. S. Mistry, R. H. Gilman, Y. Yuan, H. Gao, T. Alarcón, M. López-Brea, G. Balakrish Nair, A. Chowdhury, S. Datta, M. Shirai, T. Nakazawa, R. Ally, I. Segal, B. C. Wong, S. K. Lam, F. O. Olfat, T. Borén, L. Engstrand, O. Torres, R. Schneider, J. E. Thomas, S. Czinn, and D. E. Berg, Differences in genotypes of Helicobacter pylori from different human populations, J Bacteriol, 182, 3210-3218, 2000.

In addition, worldwide studies encompassing H. pylori isolates from many geographic regions have demonstrated weak clonal groupings and geographic partitioning of H. pylori isolates [9,17]. If recombination only occurs between a resident H. pylori population, exchange of genetic sequences can genetically homogenise this population. [...]

Introduction of polymorphisms and sequence variants from one H. pylori population from a particular geographic region to another H. pylori population from another geographic region via human migration makes the association of particular genotypes with specific geographic locations more difficult. Although the introduction of new polymorphisms into a particular H. pylori population poses a problem with identifying specific genotypes within certain geographic locales, it may, however, provide information on the ancestry of the hosts in whose stomachs the strains were carried. Studies have been aimed at demonstrating the path of human migration to Latin America with conflicting results regarding whether European or Asian populations brought H. pylori to South America [16,11]. However, a recent and comprehensive study by Flaush [sic] et al. [19] demonstrated that sequence analysis of H. pylori isolates recovered from twenty-seven countries displayed geographic partitioning.


9. Achtman M, Azuma T, Berg DE, Ito Y, Morelli G, Pan ZJ, Suerbaum S, Thompson SA, van der Ende A, van Doorn LJ: Recombination and clonal groupings within Helicobacter pylori from different geographical regions. Mol Microbiol 1999, 32:459-470.

11. Go MF: Helicobacter pylori: its role in ulcer disease and gastric cancer and how to detect the infection. Acta Gastroenterol Latinoam 1996, 26:45-49.

16. Kersulyte D, Mukhopadhyay AK, Velapatino B, Su W, Pan Z, Garcia C, Hernandez V, Valdez Y, Mistry RS, Gilman RH, Yuan Y, Gao H, Alarcon T, Lopez-Brea M, Balakrish Nair G, Chowdhury A, Datta S, Shirai M, Nakazawa T, Ally R, Segal I, Wong BC, Lam SK, Olfat FO, Boren T, Engstrand L, Torres O, Schneider R, Thomas JE, Czinn S, Berg DE: Differences in genotypes of Helicobacter pylori from different human populations. J Bacteriol 2000, 182:3210-3218.

17. Ahmed N, Khan AA, Alvi A, Tiwari S, Jyothirmayee CS, Kauser F, Ali M, Habibullah CM: Genomic analysis of Helicobacter pylori from Andhra Pradesh, South India: Molecular evidence for three major genetic clusters. Curr Sci 2003, 85:101-108.

19. Falush D, Wirth T, Linz B, Pritchard JK, Stephens M, Kidd M, Blaser MJ, Graham DY, Vacher S, Perez-Perez GI, Yamaoka Y, Megraud F, Otto K, Reichard U, Katzowitsch E, Wang X, Achtman M, Suerbaum S: Traces of human migrations in Helicobacter pylori populations. Science 2003, 299:1582-1585.

40. Carroll IM, Ahmed N, Beesley SM, Khan AA, Ghousunnissa S, O'Morain CA, Smyth CJ: Fine-structure molecular typing of Irish Helicobacter pylori isolates and their genetic relatedness to strains from four different continents. J Clin Microbiol 2003, 41:5755-5759.

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Thus, polymorphisms within the H. pylori genome can be utilised as useful markers for studying ancient and recent human migrations. Albeit, recombination between H. pylori strains from migrant and native populations can sometimes complicate analysis. Therefore, the study of migrated populations that have remained in isolation from the native populations is essential (Carroll et al., 2004).

Carroll, I. M., A. A. Khan, and N. Ahmed, Revisiting the pestilence of helicobacter pylori: insights into geographical genomics and pathogen evolution, Infect Genet Evol, 4, 81-90, 2004.

Thus, polymorphisms within the H. pylori genome can serve as useful markers for studying ancient human migrations. However, a mix up of H. pylori strains between migrated and native populations can sometimes complicate analysis. Accordingly, the study of migrated populations that have remained isolated from the native populations is

essential.

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In paleoanthropology, the recent single-origin hypothesis (RSOH, or Out-of-Africa model, or Replacement Hypothesis) is one of two influential accounts of the origin of anatomically modern humans, Homo sapiens. According to the RSOH, anatomically modern humans evolved in Africa between 200,000 and 100,000 years ago, with members of one branch leaving Africa between 55000 to 80,000 years ago. In paleoanthropology, the recent single-origin hypothesis (RSOH, or Out-of-Africa model, or Replacement Hypothesis) is one of two accounts of the origin of anatomically modern humans, Homo sapiens. According to the RSOH, anatomically modern humans evolved in Africa before 200,000 to 100,000 years ago, with members of one branch leaving Africa about 80,000 years ago.
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The three main haplogroups, which are found only in Africa are L1, L2, and L3. Of interest and greater prevalence in East Africa is L3, where it accounts for about half of all types from this region. This frequency profile suggests an origin for L3 in East Africa (Watson et al., 1997; Forster, 2004). This is supported by the evidence that the out-of-Africa migration, which took place from a source in East Africa 60,000–80,000 years ago, gave rise only to L3 lineages outside Africa.

Forster, P., Ice ages and the mitochondrial DNA chronology of human dispersals: a review, Philos Trans R Soc Lond B Biol Sci, 359, 255-264, 2004.

Watson, E., P. Forster, M. Richards, and H. J. Bandelt, Mitochondrial footprints of human expansions in Africa, Am J Hum Genet, 61, 691-704, 1997.

We here define two previously unlabeled subclades of L3A, L3f, and L3g. The lineages remaining within L3* represent ∼20% of all L3A types in Africa. Although they are distributed throughout the continent, they reach the highest frequencies in East Africa, where they account for about half of all types from this region. This frequency profile suggests an origin for L3 in East Africa (Watson et al. 1997). This is supported by the evidence that the out-of-Africa migration, which took place from a source in East Africa 60,000–80,000 years ago, gave rise only to L3 lineages outside Africa.

Watson E, Forster P, Richards M, Bandelt H-J (1997) Mitochondrial footprints of human expansions in Africa. Am J Hum Genet 61:691–704

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The macro-Haplogroups M and N are a branch of the African haplogroup L3 and span many continents. They are believed to have originated in Africa some 80,000 years before present. Both haplogroups are believed to represent the initial migration by modern humans out of Africa. Haplogroup M particularly represents the dispersal of modern human into Eurasia some 60,000 years ago along the Southern Asian coastline. Owing to its old age, haplogroup M is one of those mtDNA lineages which does not correspond well to present-day racial groups, as it spans East Asian, South-East Asian, South Asian, Amerindian, as well as Ethiopian and various Middle Eastern groups in lesser frequency (Salas et al., 2002).

Salas, A., M. Richards, T. De la Fe, M. V. Lareu, B. Sobrino, P. Sánchez-Diz, V. Macaulay, and A. Carracedo, The making of the African mtDNA landscape, Am J Hum Genet, 71, 1082-1111, 2002.

An enormous haplogroup spanning many continents, the macro-Haplogroup M is a branch of the African haplogroup L3, and is believed to have originated in Africa some 80,000 years before present.

The two haplogroups M and N are believed to represent the initial migration by modern humans out of Africa. Haplogroup M in particular represents the dispersal of modern human into Eurasia some 60,000 years ago along the southern Asian coastline.

[...]

Owing to its great age, haplogroup M is one of those mtDNA lineages which does not correspond well to present-day racial groups, as it spans East Asian, South-East Asian, South Asian, Amerindian, as well as Ethiopian and various Middle Eastern groups in lesser frequency.

Anmerkungen

Though nearly identical, nothing has been marked as a citation; the source is not given. Strangely enough, the source named here has been used earlier on this page of W.F.E.'s thesis (cf. Fragment 014 11) but was not named there. Furthermore this passage is not to be found in Salas et al (2002).

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Underhill et al (Underhill et al., 2000), comparing the NR Y of 1062 individuals from different regions, have found three mutually reinforcing mutations (two transversions and a 1-bp deletion), distinguishing a haplogroup, which is represented today by a minority of Africans, mainly Sudanese, Ethiopians and Khoisans. All non-Africans, except a single Sardinian, and most African males sampled carried only the derived alleles at the three sites. This implies that modern extant human Y chromosomes trace ancestry to Africa and that the descendants of the derived lineage left Africa and eventually replaced archaic human Y chromosomes in Eurasia. Three mutually reinforcing mutations, M42, M94 and M139 (two transversions and a 1-bp deletion), distinguish haplogroup I, which is represented today by a minority of Africans—mainly Sudanese, Ethiopians and Khoisans (Table 1). All non-Africans, except a single Sardinian, and most African males sampled carry only the derived alleles at the three sites. This implies that modern extant human Y chromosomes trace ancestry to Africa and that the descendants of the derived lineage left Africa and eventually replaced archaic human Y chromosomes in Eurasia5.

5. Hammer, M.F. et al. Out of Africa and back again: nested cladistic analysis of human Y chromosome variation. Mol. Biol. Evol. 15, 427–441 (1998).

Anmerkungen

The source is given, but nothing has been marked as a citation.

The conclusion ("This implies [...]") is not clearly attributed to Underhill et al. (2000), or in fact Hammer et al. (1998) to who it is attributed by Underhill et al. (2000).

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Assuming only relatively recent migrants from Africa gave rise to today's non- African humans, there could have been more than one migration that left descendants. Two routes for the migration out of Africa have been assumed (Forster and Matsumura, 2005). The first and most obvious route is from Egypt, across the Sinai into the Levant. This route is confronted by the major obstruction of the arid zone of the Sahara and Sinai deserts, and thus tends to be only passable during the short periods of interglacial optimum when the Sahara is covered by fresh water lakes, rivers and abundant game. The second route only opened when sea levels fell; it is across the Bab-el-Mandeb, between Yemen and Djibouti. This route too is obstructed by a barrier, the Red Sea and its hazardous reefs, and so is usually only opened when there is a major fall in sea levels. At the times at which sea levels were low, this area is also one of high aridity, probably keeping a beachcombing human population close to the ancient shorelines, which are now well below sea-level, making the finding of early human fossils there very difficult.

Forster, P., and S. Matsumura, Evolution. Did early humans go north or south?, Science, 308 , 965-966, 2005.

Assuming only relatively recent migrants from Africa gave rise to today's non-African humans, was there more than one migration that left descendants? (for example, one each via the north and south ends of the Red Sea)

There are two possible routes out of Africa.

1. The first and most obvious one is from Egypt, across the Sinai into the Levant. This route is confronted by the major impediment of the arid zone of the Sahara and Sinai deserts, and thus tends to be only passable during the short periods of interglacial optimum when the Sahara is covered by fresh water lakes, rivers and abundant game.
2. The second route, only opened when sea levels fall is across the Bab-el-Mandeb, between Yemen and Djibouti/Eritrea. This route too is confronted by a barrier, this time the Red Sea and its hazardous reefs, and so is usually only opened when there is a major fall in sea levels. Although, humans must have had ocean-going vessels at least 60,000 years ago to reach Australia, which was separated by a minimum of 80 miles of ocean even at the ocean's lowest level, so it is also possible that humans had vessels capable of crossing a gap of ocean at the strait of Aden not long earlier. This area, at the times at which sea levels were low, is also an area of high aridity, probably keeping a beachcombing human population close to the ancient shorelines, now well below sea-level, making the finding of early human fossils here very difficult.
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Genetic evidence suggests that humans departed Africa only once. The mtDNA M and N haplogroups are derived from haplogroup L3, and they both suggest a single exit from Africa. The distribution of the M158 Y chromosome haplotype of the "Eurasian Adam" indicates a similar history, dating the period between 30-79,000 years ago. During the period in which it is thought (on genetic evidence) humans left Africa, between 55,000 and 85,000 years ago, paleoclimatological evidence suggests that a vast belt of desert stretched from the West African Atlantic border to the Eastern Siberian Pacific border. These deserts confined humans south of that line, and reduced the food returns to cultures based exclusively on grassland and woodland based hunter gatherer technologies. The M haplogroups seems to support the existence of this barrier. The fall in sea levels at the time opened up the second route out of Africa, and the growth of a beachcombing lifestyle, confirmed at the perched coastline shell-middens at Zuli Bay, allowed additional dietary supplements, in the form of hunting large game and with highly nutritious shellfish.

Low glacial sea levels at this period would have been the first time in millennia that permitted a dry crossing from the Gulf of Aden to the islands East of Java facing Australia. Among Y-chromosomal haplogroups, the M130 and the M174 YAP gene haplogroups in particular support this hypothesis as their path follows a great arc along the shorelines of Saudi Arabia, India, South East Asia and Australia. This beachcomber society moved on through Southern China and Taiwan to Japan and Eastern Siberia. Approximately 8-10,000 years ago the M130 haplogroup was carried by Na-Dené speaking peoples into the North West Pacific coast of America (Forster, 2004).


Forster, P., Ice ages and the mitochondrial DNA chronology of human dispersals: a review, Philos Trans R Soc Lond B Biol Sci , 359 , 255-264, 2004.

Genetic evidence suggests Homo sapiens left Africa in prehistoric times only once. The mtDNA M* and N* haplogroups derive from haplogroup L3, and suggest a single exit from Africa. The distribution of the M158 Y chromosome haplotype of the "Eurasian Adam" shows a similar history, dating to the period between 30,000 - 79,000 years ago. In the period in which it is thought, on genetic evidence, humans left Africa, between 75,000 and 85,000 years ago, paleoclimatological evidence suggests a vast belt of desert stretched from the West African Atlantic to the Eastern Siberian Pacific. These deserts kept AMH humans confined south of that line, and reduced the food returns to cultures based exclusively on grassland and woodland based hunter gatherer technologies. The M* haplogroups seems to support the existence of this barrier. The drop in sea levels at the time did open up the second route out of Africa, and the growth of a beachcombing lifestyle, confirmed at the perched coastline shell-middens at Zuli Bay, did allow dietary supplementing of hunting of large game with highly nutritious shellfish.

Low glacial sea levels at this period would have been the first time in millennia permitting a dry walk from the Gulf of Aden to the islands East of Java facing Australia.(citation needed) Among Y-chromosomal haplogroups, the M130 and the M174 YAP gene haplogroups in particular confirm this hypothesis as their path traces a great arc along the shorelines of Saudi Arabia, India, South East Asia and Australia. This beachcomber culture moved on through southern China, and Taiwan to Japan and Eastern Siberia. There about 8-10,000 years ago the M130 haplogroup was carried by Na-Dené speaking peoples into the North West Pacific coast of America.

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1.3.1 Geography

Sudan is located in Northeastern Africa. It borders the Red Sea between Egypt on the North and Eritrea and Ethiopia on the Southeast; while Chad and the Central [African Republic are located on the West.]

GEOGRAPHY

Location: Sudan is located in northeastern Africa. It borders the Red Sea between Egypt on the north and Eritrea and Ethiopia on the southeast; it borders Chad and the Central African Republic on the west.

Anmerkungen

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To be continued on the next page, see Fragment 018 01.

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The total area of the country is 2,505,813 square kilometers. The length of Sudans borders is 7,687 kilometers. The bordering countries are the Central African Republic, Chad, Democratic Republic of the Congo, Egypt, Eritrea, Ethiopia, Kenya, Libya, and Uganda.

The country in general is a broad, flat plain, with low mountains in the Northeast (near the Red Sea coast), in the West, and on the Southeast. A group of low mountains in the south-central region are known as the Nuba Mountains. The Nile River divides the Eastern third from the Western two-thirds of the country. In the North, the Nubian Desert lies to the east of the Nile and the Libyan Desert to the West. The two areas are stony, virtually rainless, and dune-covered. South of the central area, vegetation gradually changes from dry grassland and woodland to verdant savannah.

The Nile is the dominant geographic feature of Sudan, flowing for approximately 3,000 kilometers from Uganda in the South to Egypt in the North. Most of the country lies within the Nile's catchment basin. The Blue Nile originating in the Ethiopian higlands and the White Nile from the Central African lakes, join at Khartoum to form the Nile River proper that flows to Egypt. Other major tributaries of the Nile include Bahr al Ghazal, Sobat, and Atbarah rivers.

There has been no comprehensive census in Sudan since 1983. The most recent survey occurred in 1993, which produced a population figure of 24.9 million, but it omitted the South because of insecurity. In 2003 the United Nations Population Division estimated Sudans population at 33.6 million, a figure similar to other estimates. According to the United Nations, the annual growth rate was 2.8 percent. The United Nations estimated the population density at 13.4 persons per square kilometer, which is a misleading measurement since half of the population lives on approximately 15 percent of the land, and the Northern third of the country is quite thinly populated. Estimates of urbanisation ranged from 31 percent to 37 percent, with the highest concentration in the greater Khartoum area.

Size: The total area of the country is 2,505,813 square kilometers.

Land Boundaries: The length of Sudan’s borders is 7,687 kilometers. Border countries are: Central African

[page 4]

Republic (1,165 kilometers), Chad (1,360 kilometers), Democratic Republic of the Congo (628 kilometers), Egypt (1,273 kilometers), Eritrea (605 kilometers), Ethiopia (1,606 kilometers), Kenya (232 kilometers), Libya (383 kilometers), and Uganda (435 kilometers).

[...]

Topography: The country is generally a broad, flat plain, with low mountains in the northeast near the Red Sea coast, in the west, and on the southeast. An outcropping of low mountains in the south-central region is known as the Nuba Mountains. The Nile River system divides the eastern third from the western two-thirds of the country. In the North, the Nubian Desert lies to the east of the Nile, the Libyan Desert to the west. Both are stony, virtually rainless, and dune-covered. South of Khartoum, the vegetation gradually changes from dry grassland and woodland to verdant savannah.

Principal Rivers: The Nile is the dominant geographic feature of Sudan, flowing 3,000 kilometers from Uganda in the south to Egypt in the north. Most of the country lies within its catchment basin. The Blue Nile and the White Nile, originating in the Ethiopian highlands and the Central African lakes, respectively, join at Khartoum to form the Nile River proper that flows to Egypt. Other major tributaries of the Nile are the Bahr al Ghazal, Sobat, and Atbarah rivers.

[page 5]

Population: Sudan has not had a comprehensive census since 1983. The most recent survey occurred in 1993, which produced a population figure of 24.9 million, but it omitted the South because of insecurity. As a result, most if not all demographic and social statistics are based on dated and incomplete information. In 2003 the United Nations Population Division estimated Sudan’s population at 33.6 million, a figure compatible with other estimates, although one or two estimates were higher by several million. According to the United Nations, the annual growth rate was 2.8 percent. The United Nations estimated the population density at 13.4 persons per square kilometer, a misleading measurement because half of the population lives on approximately 15 percent of the land, and the northern third of the country is quite thinly populated. Estimates of urbanization ranged from 31 percent to 37 percent, with the greatest concentration in the greater Khartoum area.

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[21.] Wfe/Fragment 019 02 - Diskussion
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1.3.2 History

Northern Sudan was inhabited by hunter-gatherers by at least 60,000 years ago. With the advent of pastoralists, these people had given way to them and probably to agriculturalists at least by the fourth millennium B.C. Sudan's subsequent culture and history have largely revolved around relations to the South with tropical Africa, and to the North with Egypt, the Nile River forming a bridge through the Sahara Desert between the two. The Ancient Egyptians sent military expeditions into Nubia, and at times occupied it as well as Cush, the land between the second and sixth cataracts, influencing the population of the North. From the early eighth century to the mid-seventh century B. C., the Cushites conquered and ruled Egypt. By the early sixth century B.C., the Cushitic state of Meroe had emerged and it eventually extended southward almost to present-day Khartoum. Meroe was in a good position for trade, as trade passing North to Egypt stopped there. The Meroites also had a route to and from the Red Sea, and, on the Red Sea, trade was increasing to and from India and East Asia. Meroe also maintained commercial relations with the Roman world, developed a distinctive culture and written language, and became the locale of an iron-working industry. It succumbed to invasion in the mid-fourth century A.D., their Conquerors being the neighboring Aksum kingdom, based in Ethiopia. By the sixth century, three states emerged as the political and cultural heirs of the Meroitic kingdom. They were all ruled by warrior aristocracies who converted to Christianity, accepting the Monophysite rite of Egypt. The use of Greek in liturgy was encouraged by the church and eventually gave way to the Nubian language. Arabic, however, gained importance after the seventh century, especially as a medium for commerce, after the expansion of the Muslim empire. With the disintegration of the Christian Nubian kingdoms by the fifteenth century, Islamic culture and religion spread throughout Northern and Eastern Sudan. Pastoralists from Egypt advanced into the land, gradually giving rise to a new population composed of local Nubians and Muslim Arabs (Fadlalla, 2004).


Fadlalla, M, H,, Short History of Sudan, i universe, 2004,

HISTORICAL BACKGROUND

Prehistory and Early History: Northern Sudan was inhabited by hunting and gathering peoples by at least 60,000 years ago. These peoples had given way to pastoralists and probably agriculturalists at least by the fourth millennium B.C. Sudan’s subsequent culture and history have largely revolved around relations to the north with Egypt and to the south with tropical Africa, the Nile River forming a “bridge” through the Sahara Desert between the two. The Ancient Egyptians sent military expeditions into Nubia, the region between the first and second Nile cataracts, and at times occupied Nubia as well as Cush, the land between the second and sixth cataracts, the population becoming partially Egyptianized. From the early eighth century to the mid-seventh century B. C., the Cushites conquered and ruled Egypt. By the early sixth

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century B.C., a Cushitic state, Meroe, had emerged that eventually extended southward almost to present-day Khartoum. Meroe maintained commercial relations with the Roman world, developed a distinctive culture and written language, and became the locale of an iron-working industry. It succumbed to invasion in the mid-fourth century A. D.

By the sixth century, three states had emerged as the political and cultural heirs of the Meroitic kingdom. All were ruled by warrior aristocracies who converted to Christianity, accepting the Monophysite rite of Egypt. The church encouraged literacy, the use of Greek in liturgy eventually giving way to the Nubian language. Arabic, however, gained importance after the seventh century, especially as a medium for commerce. With the disintegration of the Christian Nubian kingdoms by the fifteenth century, Islamic civilization and religion spread throughout northern and eastern Sudan. Pastoralists from Egypt filtered into the land, gradually giving rise to a new population composed of local Nubians and Muslim Arabs.

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[22.] Wfe/Fragment 020 01 - Diskussion
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1.3.3.1 Ethnic groups

Ethnic identity is highly fluid in Sudan and depends upon the criteria by which individual groups of Sudanese distinguish themselves from other groups. The largest and most commonly recognized ethnic groups are the Arabs, Nubians, Beja, and Fur (all Northerners and Muslims), and the Dinka, Nuer, Shilluk, and Nuba, all Nilotic peoples of the South. The Arabs and Dinka represent the largest groups within their respective regions. All of these ethnic groups are further subdivided into tribal or other units. In rough percentages, Sudans population is composed of 50 percent black Africans, 40 percent Arabs, 6 percent Beja, and 34 [sic!] percent other.

Ethnic Groups: Ethnic identity is highly fluid in Sudan and depends upon the criteria by which individual groups of Sudanese distinguish themselves from other groups. The largest commonly recognized ethnic groups are Arabs, Nubians, Beja, and Fur (all Northerners and Muslims), and the Dinka, Nuer, Shilluk, and Nuba, all Nilotic peoples of the South. The Arabs and Dinka are the largest groups within their respective regions. All of these ethnic groups are subdivided into tribal or other units. In rough percentages, Sudan’s population is composed of 50 percent black Africans, 40 percent Arabs, 6 percent Beja, and 3–4 percent other.
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[23.] Wfe/Fragment 041 20 - Diskussion
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The sets of sequences were also tested by the homoplasy test. This test analyses the apparent homoplasies among informative, synonymous polymorphic sites. When the same site changes twice in the ancestry of a set of sequences homoplasies occur. The frequency of apparent homoplasies, as measured by the homoplasy ratio, indicates the frequency of recombination (Maynard Smith and Smith, 1998). The homoplasy ratio varies between 0, indicating completely clonal descent by the accumulation of mutations and 1, indicating free recombination where all sequence polymorphisms are found repeatedly in independent sequences that are in different branches of a maximal parsimony tree (apparent homoplasies).

Maynard Smith, J., and N. H. Smith, Detecting recombination from gene trees, Mol Biol Evol , 15 , 590-599, 1998.

The sets of sequences were tested with the homoplasy test (21), which analyzes the apparent homoplasies among informative, synonymous polymorphic sites. The frequency of apparent homoplasies, as measured by the homoplasy ratio, H, is an indicator of the frequency of recombination. The homoplasy ratio can vary between 0, indicating completely clonal descent by the accumulation of mutations, and 1, indicating free recombination where all sequence polymorphisms are found repeatedly in independent sequences that are in different branches of a maximal parsimony tree (apparent homoplasies).

21. Maynard Smith, J., and N. H. Smith. 1998. Detecting recombination from gene trees. Mol. Biol. Evol. 15:590–599.

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