Pathogenicity island <it>cag</it>, <it>vacA </it>and IS<it>605 </it>genotypes in Mexican strains of <it>Helicobacter pylori </it>associated with peptic ulcers

• Main Authors: Tabche-Barrera María L, Aguilar-Gutiérrez Germán R, Ponce-de-León Sergio, Lazcano-Ponce Eduardo C, Castillo-Rojas Gonzalo, López-Vidal Yolanda, Antonio-Rincón Fernando
• Format: Article
• Language: English
• Published: BMC 2011-05-01
• Series: Annals of Clinical Microbiology and Antimicrobials
• Subjects: <it>Helicobacter pylori</it>; <it>cag </it>PAI; <it>vacA</it>; peptic ulcers; Mexico
• Online Access: http://www.ann-clinmicrob.com/content/10/1/18

<p>Abstract</p> <p>Background</p> <p><it>Helicobacter pylori </it>is associated with chronic gastritis, peptic ulcers, and gastric cancer. Two major virulence factors of <it>H. pylori </it>have been described: the pathogenicity island <it>cag </it>(<it>cag </it>PAI) and the vacuolating cytotoxin gene (<it>vacA</it>). Virtually all strains have a copy of <it>vacA</it>, but its genotype varies. The <it>cag </it>PAI is a region of 32 genes in which the insertion of IS<it>605 </it>elements in its middle region has been associated with partial or total deletions of it that have generated strains with varying virulence. Accordingly, the aim of this work was to determine the <it>cag </it>PAI integrity<it>, vacA </it>genotype and IS<it>605 </it>status in groups of isolates from Mexican patients with non-peptic ulcers (NPU), non-bleeding peptic ulcers (NBPU), and bleeding peptic ulcers (BPU).</p> <p>Methods</p> <p>The <it>cag </it>PAI integrity was performed by detection of eleven targeted genes along this locus using dot blot hybridization and PCR assays. The <it>vacA </it>allelic, <it>cag </it>PAI genotype 1 and IS<it>605 </it>status were determined by PCR analysis.</p> <p>Results</p> <p>Groups of 16-17 isolates (n = 50) from two patients with NPU, NBPU, and BPU, respectively, were studied. 90% (45/50) of the isolates harbored a complete <it>cag </it>PAI. Three BPU isolates lacked the <it>cag </it>PAI, and two of the NBPU had an incomplete <it>cag </it>PAI: the first isolate was negative for three of its genes, including deletion of the <it>cagA </it>gene, whereas the second did not have the <it>cagM </it>gene. Most of the strains (76%) had the <it>vacA </it>s1b/m1 genotype; meanwhile the IS<it>605 </it>was not present within the <it>cag </it>PAI of any strain but was detected elsewhere in the genome of 8% (4/50).</p> <p>Conclusion</p> <p>The patients had highly virulent strains since the most of them possessed a complete <it>cag </it>PAI and had a <it>vacA </it>s1b/m1 genotype. All the isolates presented the <it>cag </it>PAI without any IS<it>605 </it>insertion (genotype 1). Combined <it>vacA </it>genotypes showed that 1 NPU, 2 NBPU, and 1 BPU patients (66.6%) had a mixed infection; coexistence of <it>H. pylori </it>strains with different <it>cag </it>PAI status was observed in 1 NBPU and 2 BPU (50%) of the patients, but only two of these patients (NBPU and BPU) had different <it>vacA </it>genotypes.</p>