DETECTION AND TYPING OF THE VIRULENCE DETERMINANTS CAGA AND VACA OF HELICOBACTER-PYLORI DIRECTLY FROM BIOPSY DNA - ARE IN-VITRO STRAINS REPRESENTATIVE OF IN-VIVO STRAINS

Background The relationship of Helicobacter pylori genotypes to gastro intestinal disease has relied on cultured isolates, This assumes that cultured strains are representative of in vivo strains. Objective To d etect and type the cagA status and the vacA genotypes directly from bi opsy DNA without the need for culture, and to further define the relat ionship between H. pylori genotypes and gastroduodenal pathology. Meth ods Fifty-two Caucasian patients undergoing routine endoscopy for dysp epsia had additional biopsies taken from four gastric sites and one du odenal site for biopsy DNA preparation, An antral sample was taken for biopsy culture, All recruited patients were H. pylori-positive on rap id urease test for Campylobacter-like organisms (CLO test) and/or hist ology, By polymerase chain reaction (PCR), the cagA status and the vac A s and m types were detected directly from biopsy DNA. Results H. pyl ori isolates were cultured from 28/52 patients in whom infection was d etected by PCR. Two isolate types differed from biopsy types. Fifty of the 52 patients, strains were typable from all four gastric sites and in 51/52 the same strain predominated throughout. The cancer strains were all cagA-positive/vacA s1 type. There was a correlation between c agA positivity and vacA s1 (41/43). There was no difference between th e cagA-positive/vacA s1 strains and the presence or absence of ulcers, There were only 5/52 vacA s2 m2 and four were in the non-ulcer dyspep tic group. Conclusion cagA status and the vacA genotyping was successf ul with tissue samples taken directly from gastric and duodenal biopsi es, Discrepancies between isolate and biopsy strain types stress the n eed for caution when interpreting in vitro strain types and suggest th at direct PCR of biopsies is the preferred typing technique, The cagA status and the st vacA allele are unreliable as single markers in dete rmining the risk of developing peptic ulcer disease. (C) 1998 Lippinco tt Williams & Wilkins.