1887

Abstract

Sequence variations located at the signal sequence and mid-region within the gene, the 3′-end of the gene, the indel motifs at the 3′-end of the pathogenicity island and the regions upstream of the and genes were determined by PCR in 19 paired antral or antrum and corpus isolates obtained at the same endoscopic session, and three antral pairs taken sequentially. Random amplification of polymorphic DNA (RAPD)-PCR and fluorescent amplified fragment length polymorphism (FAFLP)-PCR fingerprinting were applied to these paired clinical isolates. The FAFLP-PCR profiles generated were phylogenetically analysed. For the 22 paired isolates there were no differences within pairs at five of the genetic loci studied. However, six pairs of isolates (27 %), of which four were antrum and corpus pairs, showed differences in the numbers of repeats located at the 3′-end of the gene. RAPD-PCR fingerprinting showed that 16 (73 %) pairs, nine of which were antrum and corpus pairs, possessed identical profiles, while six (27 %) displayed distinctly different profiles, indicating mixed infections. Three of the six pairs showing differences at the 3′-end of the gene yielded identical RAPD-PCR fingerprints. FAFLP-PCR fingerprinting and phylogenetic analysis revealed that all 16 pairs that displayed identical RAPD-PCR profiles had highly similar, but not identical, fingerprints, demonstrating that these pairs were ancestrally related but had undergone minor genomic alterations. Two antrum and corpus pairs of isolates, within the latter group, were isolates obtained from two siblings from the same family. This analysis demonstrated that each sibling was colonized by ancestrally related strains that exhibited differences in genotype characteristics.

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2004-07-01
2019-11-14
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References

  1. Ahmed, N., Khan, A., Berg, D. E. & Habibullah, C. M. ( 2001;). Genomic analysis reveals distinct biogeographic partitioning of H. pylori from South Indians and other world populations. Int J Med Microbiol 291, S31 (abstract D11).
  2. Ahmed, N., Bal, A., Khan, A. A. & 9 other authors ( 2002;). Whole genome fingerprinting and genotyping of multiple drug resistant (MDR) isolates of Pseudomonas aeruginosa from endophthalmitis patients in India. Infect Genet Evol 1, 237–242.[CrossRef]
    [Google Scholar]
  3. Ahmed, N., Alam, M., Abdul Majeed, A., Asad Rahman, S., Cataldi, A., Cousins, D. & Hasnain, S. E. ( 2003;). Genome sequence based, comparative analysis of the fluorescent amplified fragment length polymorphisms (FAFLP) of tubercle bacilli from seals provides molecular evidence for a new species within the Mycobacterium tuberculosis complex. Infect Genet Evol 2, 193–199.[CrossRef]
    [Google Scholar]
  4. Akada, J. K., Ogura, K., Dailidiene, D., Dailide, G., Cheverud, J. M. & Berg, D. E. ( 2003;). Helicobacter pylori tissue tropism: mouse-colonizing strains can target different gastric niches. Microbiology 149, 1901–1909.[CrossRef]
    [Google Scholar]
  5. Akopyants, N. S., Eaton, K. A. & Berg, D. E. ( 1995;). Adaptive mutation and cocolonization during Helicobacter pylori infection of gnotobiotic piglets. Infect Immun 63, 116–121.
    [Google Scholar]
  6. Atherton, J. C., Cao, P., Peek, R. M., Jr, Tummuru, M. K., Blaser, M. J. & Cover, T. L. ( 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.[CrossRef]
    [Google Scholar]
  7. Bereswill, S., Schonenberger, R., Thies, C., Stahler, F., Strobel, S., Pfefferle, P., Wille, L. & Kist, M. ( 2000;). New approaches for genotyping of Helicobacter pylori based on amplification of polymorphisms in intergenic DNA regions and at the insertion site of the cag pathogenicity island. Med Microbiol Immunol 189, 105–113.[CrossRef]
    [Google Scholar]
  8. Bijlsma, J. J., Lie-A-Ling, M., Nootenboom, I. C., Vandenbroucke-Grauls, C. M. & Kusters, J. G. ( 2000;). Identification of loci essential for the growth of Helicobacter pylori under acidic conditions. J Infect Dis 182, 1566–1569.[CrossRef]
    [Google Scholar]
  9. Blaser, M. J. & Berg, D. E. ( 2001;). Helicobacter pylori genetic diversity and risk of human disease. J Clin Invest 107, 767–773.[CrossRef]
    [Google Scholar]
  10. Carroll, I. M., Ahmed, N., Beesley, S. M., Khan, A. A., Ghousunnissa, S., Ó Moráin, C. A. & Smyth, C. J. ( 2003;). 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.[CrossRef]
    [Google Scholar]
  11. Desai, M., Tanna, A., Wall, R., Efstratiou, A., George, R. & Stanley, J. ( 1998;). Fluorescent amplified-fragment length polymorphism analysis of an outbreak of group A streptococcal invasive disease. J Clin Microbiol 36, 3133–3137.
    [Google Scholar]
  12. Go, M. F., Kapur, V., Graham, D. Y. & Musser, J. M. ( 1996;). Population genetic analysis of Helicobacter pylori by multilocus enzyme electrophoresis: extensive allelic diversity and recombinational population structure. J Bacteriol 178, 3934–3938.
    [Google Scholar]
  13. Goulding, J. N., Hookey, J. V., Stanley, J., Olver, W., Neal, K. R., Ala'Aldeen, D. A. & Arnold, C. ( 2000;). Fluorescent amplified-fragment length polymorphism genotyping of Neisseria meningitidis identifies clones associated with invasive disease. J Clin Microbiol 38, 4580–4585.
    [Google Scholar]
  14. Grady, R., O'Neill, G., Cookson, B. & Stanley, J. ( 2000;). Fluorescent amplified-fragment length polymorphism analysis of the MRSA epidemic. FEMS Microbiol Lett 187, 27–30.[CrossRef]
    [Google Scholar]
  15. Karita, M. & Blaser, M. J. ( 1998;). Acid-tolerance response in Helicobacter pylori and differences between cagA + and cagA strains. J Infect Dis 178, 213–219.[CrossRef]
    [Google Scholar]
  16. Kersulyte, D., Chalkauskas, H. & Berg, D. E. ( 1999;). Emergence of recombinant strains of Helicobacter pylori during human infection. Mol Microbiol 31, 31–43.[CrossRef]
    [Google Scholar]
  17. Kersulyte, D., Mukhopadhyay, A. K., Velapatino, B. & 28 other authors ( 2000;). Differences in genotypes of Helicobacter pylori from different human populations. J Bacteriol 182, 3210–3218.[CrossRef]
    [Google Scholar]
  18. Kuipers, E. J., Israel, D. A., Kusters, J. G. & 8 other authors ( 2000;). Quasispecies development of Helicobacter pylori observed in paired isolates obtained years apart from the same host. J Infect Dis 181, 273–282.[CrossRef]
    [Google Scholar]
  19. Marshall, D. G., Chua, A., Keeling, P. W., Sullivan, D. J., Coleman, D. C. & Smyth, C. J. ( 1995;). Molecular analysis of Helicobacter pylori populations in antral biopsies from individual patients using randomly amplified polymorphic DNA (RAPD) fingerprinting. FEMS Immunol Med Microbiol 10, 317–323.[CrossRef]
    [Google Scholar]
  20. Marshall, D. G., Coleman, D. C., Sullivan, D. J., Xia, H., Ó Moráin, C. A. & Smyth, C. J. ( 1996;). Genomic DNA fingerprinting of clinical isolates of Helicobacter pylori using short oligonucleotide probes containing repetitive sequences. J Appl Bacteriol 81, 509–517.
    [Google Scholar]
  21. Marshall, D. G., Dundon, W. G., Beesley, S. M. & Smyth, C. J. ( 1998;). Helicobacter pylori – a conundrum of genetic diversity. Microbiology 144, 2925–2939.[CrossRef]
    [Google Scholar]
  22. Nordman, H., Borén, T., Davies, J. R., Engstrand, L. & Carlstedt, I. ( 1999;). pH-dependent binding of Helicobacter pylori to pig gastric mucins. FEMS Immunol Med Microbiol 24, 175–181.[CrossRef]
    [Google Scholar]
  23. Nordman, H., Davies, J. R., Lindell, G., de Bolos, C., Real, F. & Carlstedt, I. ( 2002;). Gastric MUC5AC and MUC6 are large oligomeric mucins that differ in size, glycosylation and tissue distribution. Biochem J 364, 191–200.
    [Google Scholar]
  24. Owen, R. J. & Xerry, J. ( 2003;). 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.[CrossRef]
    [Google Scholar]
  25. Park, S., Choue, R. W., Cho, Y. & Ziboh, V. A. ( 2003;). Regional biosynthesis of prostaglandins and hydroxyeicosatetraenoic acids from arachidonic acid in the rat stomach tissue. Prostaglandins Leukot Essent Fatty Acids 68, 35–42.[CrossRef]
    [Google Scholar]
  26. Pride, D. T., Meinersmann, R. J. & Blaser, M. J. ( 2001;). Allelic variation within Helicobacter pylori babA and babB. Infect Immun 69, 1160–1171.[CrossRef]
    [Google Scholar]
  27. Salaün, L., Audibert, C., Le Lay, G., Burucoa, C., Fauchere, J. L. & Picard, B. ( 1998;). Panmictic structure of Helicobacter pylori demonstrated by the comparative study of six genetic markers. FEMS Microbiol Lett 161, 231–239.[CrossRef]
    [Google Scholar]
  28. Taddei, F., Matic, I., Godelle, B. & Radman, M. ( 1997;). To be a mutator, or how pathogenic and commensal bacteria can evolve rapidly. Trends Microbiol 5, 427–428; discussion 428–429.[CrossRef]
    [Google Scholar]
  29. Tanaka, S., Meiselman, H. H., Engel, E., Guth, P. H., Furukawa, O., Wenby, R. B., Lee, J. & Kaunitz, J. D. ( 2002;). Regional differences of H+, HCO 3, and CO2 diffusion through native porcine gastroduodenal mucus. Dig Dis Sci 47, 967–973.[CrossRef]
    [Google Scholar]
  30. Thompson, F. L., Thompson, C. C., Vicente, A. C., Theophilo, G. N., Hofer, E. & Swings, J. ( 2003;). Genomic diversity of clinical and environmental Vibrio cholerae strains isolated in Brazil between 1991 and 2001 as revealed by fluorescent amplified fragment length polymorphism analysis. J Clin Microbiol 41, 1946–1950.[CrossRef]
    [Google Scholar]
  31. Wang, J. T., Sheu, J. C., Lin, J. T., Wang, T. H. & Wu, M. S. ( 1993;). Direct DNA amplification and restriction pattern analysis of Helicobacter pylori in patients with duodenal ulcer and their families. J Infect Dis 168, 1544–1548.[CrossRef]
    [Google Scholar]
  32. Wilson, K. ( 1995;). Preparation of genomic DNA from bacteria. In Current Protocols in Molecular Biology, vol. 1, pp. 2.4.1–2.4.5. Edited by F. M. Ausubel, R. Brent, R. E. Kingston, D. D. Moore, J. G. Seidman, J. A. Smith & K. Struhl. New York: Wiley.
  33. Yamaoka, Y., Kodama, T., Kashima, K., Graham, D. Y. & Sepulveda, A. R. ( 1998;). Variants of the 3′-region of the cagA gene in Helicobacter pylori isolates from patients with different H.pylori-associated diseases. J Clin Microbiol 36, 2258–2263.
    [Google Scholar]
  34. Yamaoka, Y., Kodama, T., Gutierrez, O., Kim, J. G., Kashima, K. & Graham, D. Y. ( 1999;). Relationship between Helicobacter pylori iceA, cagA, and vacA status and clinical outcome: studies in four different countries. J Clin Microbiol 37, 2274–2279.
    [Google Scholar]
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