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Journal of Clinical Microbiology, December 2007, p. 4039-4043, Vol. 45, No. 12
0095-1137/07/$08.00+0 doi:10.1128/JCM.01631-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

S. Manjulata Devi,1,
Irshad Ahmed,2
M. Abid Hussain,1
Mohammed Rizwan,1
Hérve Lamouliatte,3
Francis Mégraud,4,5 and
Niyaz Ahmed1,4*
Pathogen Evolution Laboratory, Centre for DNA Fingerprinting and Diagnostics, Hyderabad, India,1 Deccan College of Medical Sciences and Allied Hospitals, Hyderabad, India,2 Service Hépato-Gastroentérologie, Hôpital Saint André, Bordeaux, France,3 ISOGEM Working Group on Genetics of Helicobacters, International Society for Genomic and Evolutionary Microbiology (ISOGEM), Sassari, Italy,4 INSERM U853 and Université Victor Segalen Bordeaux 2, Laboratoire de Bactériologie, 33076 Bordeaux, France5
Received 15 August 2007/ Returned for modification 26 September 2007/ Accepted 27 September 2007
Helicobacter pylori cagA and vacA genotypes have been used for almost a decade as stable entities to link the severity of gastritis and ulcer disease. We describe here microevolution of the two genomic islands, cag pathogenicity island (cagPAI; 40 kb) and tfs3 (16 kb) from isolates obtained at inclusion (one subclone) and after a 10-year period (two subclones) from a duodenal ulcer patient. Our results indicate microevolution in cagA, cagE, and cag7 genes of the cagPAI and open reading frames G, P, and L in tfs3, which possibly leads to inactivation or pseudogenization of these genes. Interestingly, no significant reduction in the severity of gastroduodenal pathology was found. These results point to an obvious difficulty in correlating the continuously evolving virulence factors such as the cagPAI genes with disease characteristics that appear to remain stable.
Published ahead of print on 17 October 2007.
A.A. and S.M.D. contributed equally to this study.
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