• Helena Andreson, Toomas Sillakivi, Margot Peetsalu, Ants Peetsalu, and Marika Mikelsaar.
• Department of Microbiology, University of Tartu, Tartu, Estonia. Helena.Andreson@ut.ee
• Scand. J. Gastroenterol. 2007 Mar 1; 42 (3): 324-9.

ObjectiveIn patients with perforated peptic ulcer (PPU) the convergence between the high eradication rate of Helicobacter pylori infection and low rates of ulcer relapse after treatment has been associated with reinfection by non-virulent strains. The objective of this study was to evaluate the persistence of infection by virulent H. pylori strains and ulcer recurrence in 33 patients with PPU one year after surgery and antimicrobial treatment.Material And MethodsThe histological evaluation and molecular detection of H. pylori cagA and ureA genes, vacA allelic types and the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analyses of the glmM gene products from antral mucosa specimens were performed initially, 2-5 months and 1 year after therapy.ResultsThe density of H. pylori colonization was temporarily decreased (p<0.05) 2-5 months after therapy. After one year, complete eradication was achieved in only 7 patients (23%) at histological examination and recurrent ulcers were found in 3/33 (9%) patients. The vacA s1a allelic type of cagA-positive strains persisted in 19/33 (58%) PPU patients with identical PCR-RFLP fingerprints in 8/9 (89%) of the patients.ConclusionsIn PPU patients with a low eradication rate of H. pylori infection after surgical and antimicrobial treatment, the frequent recrudescence of the infection is mostly caused by the persisting virulent strains of the cagA and vacA s1a subtypes. In the 1-year follow-up period the recurrent ulceration can be postponed just by the lowered colonization density of H. pylori after eradicative therapy.

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