Ines Zollner-Schwetz1, Eva Leitner2, Wolfgang Plieschnegger3, Georg Semlitsch4, Vinzenz Stepan5, Lukas Reiter6, Gerhard Reicht6, Eduard Mörth7, Jörg Pavek8, Peter Parsché9, Christina Betterklieber10, Denise Atzmüller11, Robert Krause11, Christoph Högenauer12. 1. Section of Infectious Diseases and Tropical Medicine, Department of Internal Medicine, Medical University of Graz, Austria. Electronic address: ines.schwetz@medunigraz.at. 2. Institute of Hygiene, Microbiology and Environmental Medicine, Medical University of Graz, Austria. 3. Department of Internal Medicine, Barmherzige Brüder Krankenhaus St. Veit/Glan, Austria. 4. MedCenter Judenburg, Austria. 5. Department of Internal Medicine, Krankenhaus der Elisabethinen, Graz, Austria. 6. Department of Internal Medicine, Brothers of St. John of God Hospital, Graz, Austria. 7. Lassnitzhöhe, Austria. 8. Weiz, Austria. 9. Kapfenberg, Austria. 10. Department of Internal Medicine, Landeskrankenhaus Rottenmann, Rottenmann, Austria. 11. Section of Infectious Diseases and Tropical Medicine, Department of Internal Medicine, Medical University of Graz, Austria. 12. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Austria.
Abstract
OBJECTIVES: We determined primary and secondary resistance rates of H. pylori in different regions of Austria and potential bacterial and host factors associated with resistance. METHODS: In a prospective multicentre study H. pylori was cultivated from biopsies and susceptibility testing was performed according to EUCAST. Resistance to clarithromycin and levofloxacin was determined by sequencing of the resistance-determining regions of 23S rRNA and gyrA genes. cagA, vacA and babA2 genotypes were determined. RESULTS: A total of 1266 patients were included. 178 isolates were cultured: 128 from patients without prior eradication therapy, 50 from patients after failed eradication. Primary resistance to clarithromycin, levofloxacin and metronidazole were 17.2%, 9.4% and 10.2%, respectively. Secondary resistance to clarithromycin, levofloxacin and metronidazole were 64%, 18% and 44%, respectively. Prior eradication was associated with a higher risk of clarithromycin as well as metronidazole resistance (OR=8.1; 95% CI 3.8-17.1 and OR 5.7; 95% CI 2.5-13, respectively). CONCLUSION: Primary resistance to both clarithromycin and levofloxacin was markedly lower in Southern Austria than recently reported.
OBJECTIVES: We determined primary and secondary resistance rates of H. pylori in different regions of Austria and potential bacterial and host factors associated with resistance. METHODS: In a prospective multicentre study H. pylori was cultivated from biopsies and susceptibility testing was performed according to EUCAST. Resistance to clarithromycin and levofloxacin was determined by sequencing of the resistance-determining regions of 23S rRNA and gyrA genes. cagA, vacA and babA2 genotypes were determined. RESULTS: A total of 1266 patients were included. 178 isolates were cultured: 128 from patients without prior eradication therapy, 50 from patients after failed eradication. Primary resistance to clarithromycin, levofloxacin and metronidazole were 17.2%, 9.4% and 10.2%, respectively. Secondary resistance to clarithromycin, levofloxacin and metronidazole were 64%, 18% and 44%, respectively. Prior eradication was associated with a higher risk of clarithromycin as well as metronidazole resistance (OR=8.1; 95% CI 3.8-17.1 and OR 5.7; 95% CI 2.5-13, respectively). CONCLUSION: Primary resistance to both clarithromycin and levofloxacin was markedly lower in Southern Austria than recently reported.