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Journal of Clinical Microbiology, June 2009, p. 1680-1688, Vol. 47, No. 6
0095-1137/09/$08.00+0 doi:10.1128/JCM.00273-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Pediatric Helicobacter pylori Isolates Display Distinct Gene Coding Capacities and Virulence Gene Marker Profiles
,
Sarah Talarico,1
Benjamin D. Gold,2
Jutta Fero,1
Dexter T. Thompson,2
Jeannette Guarner,3,4
Steven Czinn,5 and
Nina R. Salama1*
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington,1 Department of Pediatric Gastroenterology and Nutrition,2 Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia,3 Children's Healthcare of Atlanta, Atlanta, Georgia,4 Department of Pediatrics, University of Maryland, Baltimore, Maryland5
Received 6 February 2009/ Returned for modification 25 March 2009/ Accepted 18 April 2009
Helicobacter pylori strains display remarkable genetic diversity, and the presence of strains bearing the toxigenic vacA s1 allele, a complete cag pathogenicity island (PAI), cagA alleles containing multiple EPIYA phosphorylation sites, and expressing the BabA adhesin correlates with development of gastroduodenal disease in adults. To better understand the genetic variability present among pediatric strains and its relationship to disease, we characterized H. pylori strains infecting 47 pediatric North American patients. Prevalence of mixed infection was assessed by random amplified polymorphic DNA analysis of multiple H. pylori clones from each patient. Microarray-based comparative genomic hybridization was used to examine the genomic content of the pediatric strains. The cagA and vacA alleles were further characterized by allele-specific PCR. A range of EPIYA motif configurations were observed for the cagA gene, which was present in strains from 22 patients (47%), but only 19 (41%) patients contained a complete cag PAI. Thirty patients (64%) were infected with a strain having the vacA s1 allele, and 28 patients (60%) had the babA gene. The presence of a functional cag PAI was correlated with ulcer disease (P = 0.0095). In spite of declining rates of H. pylori infection in North America, at least 11% of patients had mixed infection. Pediatric strains differ in their spectrum of strain-variable genes and percentage of absent genes in comparison to adult strains. Most children were infected with H. pylori strains lacking the cag PAI, but the presence of a complete cag PAI, in contrast to other virulence markers, was associated with more severe gastroduodenal disease.
* Corresponding author. Mailing address: Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N, Mailstop C3-168, Seattle, WA 98109-1024. Phone: (206) 667-1540. Fax: (206) 667-6524. E-mail: nsalama{at}fhcrc.org
Published ahead of print on 22 April 2009.
Supplemental material for this article may be found at http://jcm.asm.org/.
Journal of Clinical Microbiology, June 2009, p. 1680-1688, Vol. 47, No. 6
0095-1137/09/$08.00+0 doi:10.1128/JCM.00273-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»