GUT 1998;43:752-758 ( December )

Clinical outcome after infection with Helicobacter pylori does not appear to be reliably predicted by the presence of any of the genes of the cag pathogenicity island

P J Jenks,^a F Mégraud,^b A Labigne^a

^a Unité de Pathogénie Bactérienne des Muqueuses, Pasteur Institute, Paris, France, ^b Laboratory of Bacteriology, Pellegrin Hospital, Bordeaux, France

Correspondence to: Dr P J Jenks, Unité de Pathogénie Bactérienne des Muqueuses, Institut Pasteur, 25-28 Rue du Dr Roux, 75724 Paris Cedex 15, France (email: pjenks{at}pasteur.fr).

Accepted for publication 14 April 1998

BackgroundThe development of clinical disease after infection with Helicobacter pylori has been reported to be associated with expression of the cagA gene. Recently, it has been shown that cagA is part of a multigene locus, described as the cag pathogenicity island (PAI). The role of this region in determining clinical outcome remains to be established.
AimsTo investigate whether the presence of cagA is always associated with the presence of the complete cag PAI and to evaluate the distribution of selected cag genes in 73 H pylori strains isolated from patients in France.
MethodsClinical strains of H pylori were screened for selected genes of the cag PAI by polymerase chain reaction and colony hybridisation.
ResultsOf 64 strains that harboured the cagA gene, 57 (89%) also contained the entire cag PAI. The entire cag PAI was found in 85% (48/56) and 53% (9/17) of duodenal ulcer and non-ulcer dyspepsia isolates, respectively. Eight strains had deletions within the cag PAI, including deletion of the cagA gene in one isolate; the deletions were not associated with the insertion sequence IS605. Of eight strains lacking the cag PAI, four were isolated from patients with duodenal ulcer.
ConclusionThe cag PAI is not a uniform, conserved entity. Although the presence of the cag PAI is highly associated with duodenal ulcer, the clinical outcome of infection with H pylori is not reliably predicted by any gene of the cag PAI.
(GUT 1998;43:752-758)

Keywords: duodenal ulcer;  Helicobacter pylori;  cag pathogenicity island;  non-ulcer dyspepsia.

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© 1998 by Gut
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