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of Staphylococcus aureus and Staphylococcus epidermidis. Antimicrob Agents Chemother 2000, 44:231–238.PubMedCrossRef 20. Hiramatsu K, Aritaka N, Hanaki H, Kawasaki S, Hosoda Y, Hori S, Fukuchi Y, Kobayashi I: Dissemination in Japanese hospitals of strains of Staphylococcus aureus heterogeneously resistant to vancomycin. Lancet 1997, 350:1670–1673.PubMedCrossRef 21. Kuroda M, Ohota T, Uchiyama I, Baba T, Yuzawa H, Kobayasi I, Cui L, Oguchi A, Aoki K, Nagai Y, et al.: Whole genome sequencing of meticillin-resistant Staphylococcus aureus. Lancet 2001, 357:1225–1240.PubMedCrossRef

22. Hanaki H, Yamaguchi Y, Nomura S, Haraga I, Nagayama A, Sunakawa K: Method of detecting ß-lactam antibiotic induced vancomycin resistant MRSA (BIVR). Intl J Antimicrob Agents 2004, 23:1–5.CrossRef SGC-CBP30 mouse 23. O’Callaghan CH, Morris A, Kirby SM, Shingler AH: Novel method for detection do β-lactamases by using a chromogenic chephalosporin substrate. Antimicrob Agents Chemother 1972, 1:283–288.PubMedCrossRef 24. Pregnenolone Clinical and Laboratory Standards Institute: Performance standards for antimicrobial susceptibility testing; 15th informantional supplement. CLSI/NCCLS document M100-S15 Wayne, PA. Clinical and Laboratory Standards Institute, Wayne PA, USA; 2005. Authors’ contributions YH carried out the PCR experiments, ß-lactamase assay and the BIVR test. YI-D contributed to the nucleotide

sequencing and the pulse-field gel electrophoresis. HM carried out computer-aided nucleotide and amino acid alignments. MY, SH and KS contributed to the MDV3100 purchase collection of clinical isolates of MRSA. TN consulted with the investigators on the data acquisition and wrote the draft paper. HH conducted this study and gave final approval of the version of the paper to be submitted. All authors read and approved the final manuscript.”
“Background The human stomach pathogen Helicobacter pylori infects approximately 50% of the world population, usually from childhood until old age [1]. H. pylori exhibits exceptionally high genetic diversity, such that almost every infected human carries one or multiple unique H. pylori strains [2, 3]. This diversity is the result of the combination of a high mutation rate with very efficient recombination during mixed infections with multiple strains [4–7], for reviews see [8–11]. The specific mechanisms that are responsible for the high mutation rate of H.

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