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Journal of Clinical Microbiology, November 2004, p. 5302-5308, Vol. 42, No. 11
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.11.5302-5308.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The cag Pathogenicity Island of Helicobacter pylori Is Disrupted in the Majority of Patient Isolates from Different Human Populations

Farhana Kauser,1,{dagger} Aleem A. Khan,2,{dagger} M. Abid Hussain,1,{dagger} Ian M. Carroll,3 Naheed Ahmad,4 Santosh Tiwari,2 Yogesh Shouche,5 Bimal Das,6 Mahfooz Alam,1 S. Mahaboob Ali,2 C. M. Habibullah,2 Rafaela Sierra,7 Francis Megraud,8 Leonardo A. Sechi,9 and Niyaz Ahmed1*

Pathogen Evolution Group, Centre for DNA Fingerprinting and Diagnostics,1 Centre for Liver Research and Diagnostics, Deccan College of Medical Sciences and Allied Hospitals, Hyderabad,2 Department of Botany, Patna University, Patna,4 National Centre for Cell Science, Pune,5 Department of Microbiology, All India Institute of Medical Sciences, New Delhi, India,6 The Moyne Institute of Preventive Medicine, Trinity College, Dublin, Ireland,3 Instituto de Investigaciones en Salud, Universidad de Costa Rica, San José, Costa Rica,7 Laboratoire de Bacteriologie-C.H.U. Pellegrin, Bordeaux, France,8 Department of Biomedical Sciences, University of Sassari, Sassari, Italy9

Received 7 May 2004/ Returned for modification 1 June 2004/ Accepted 25 June 2004

The cag pathogenicity island (cag-PAI) is one of the major virulence determinants of Helicobacter pylori. The chromosomal integrity of this island or the lack thereof is speculated to play an important role in the progress of the gastroduodenal pathology caused by H. pylori. We determined the integrity of the cag-PAI by using specific flanking and internally anchored PCR primers to know the biogeographical distribution of strains carrying fully integral cag-PAI with proinflammatory behavior in vivo. Genotypes based on eight selected loci were studied in 335 isolates obtained from eight different geographic regions. The cag-PAI appeared to be disrupted in the majority of patient isolates throughout the world. Conservation of cag-PAI was highest in Japanese isolates (57.1%). However, only 18.6% of the Peruvian and 12% of the Indian isolates carried an intact cag-PAI. The integrity of cag-PAI in European and African strains was minimal. All 10 strains from Costa Rica had rearrangements. Overall, a majority of the strains of East Asian ancestry were found to have intact cag-PAI compared to strains of other descent. We also found that the cagE and cagT genes were less often rearranged (18%) than the cagA gene (27%). We attempted to relate cag-PAI rearrangement patterns to disease outcome. Deletion frequencies of cagA, cagE, and cagT genes were higher in benign cases than in isolates from severe ulcers and gastric cancer. Conversely, the cagA promoter and the left end of the cag-PAI were frequently rearranged or deleted in isolates linked to severe pathology. Analysis of the cag-PAI genotypes with a different biogeoclimatic history will contribute to our understanding of the pathogen-host interaction in health and disease.

* Corresponding author. Mailing address: Pathogen Evolution Group, CDFD, ECIL Rd., Nacharam, Hyderabad 500 076, India. Phone: 91 40 27150008. Fax: 91 40 27155610. E-mail: niyaz{at}cdfd.org.in.

{dagger} F.K., A.A.K., and M.A.H. contributed equally to this study.

Journal of Clinical Microbiology, November 2004, p. 5302-5308, Vol. 42, No. 11
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.11.5302-5308.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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