J Clin Microbiol 2011,49(9):3114–3121.PubMedCrossRef 53. Borch K, Jonsson KA, Petersson F, Redeen S, Mardh S, Franzen LE: Prevalence of gastroduodenitis and Helicobacter pylori infection in a general population sample: relations to symptomatology and life-style. Dig Dis Sci 2000,45(7):1322–1329.PubMedCrossRef 54. Monstein HJ, Olsson C, Nilsson I, Grahn N, Benoni C, Ahrne S: find more Multiple displacement

amplification of DNA from human colon and rectum biopsies: bacterial profiling and identification of Helicobacter pylori-DNA by means of 16S rDNA-based TTGE and pyrosequencing analysis. J Microbiol Methods 2005,63(3):239–247.PubMedCrossRef 55. CLC bio; http://​wwwclcbiocom 56. NCBI-Entrez Nucleotide; http://​wwwncbinlmnihgov​/​nucleotide Competing selleck products interests The authors declare that they have no competing interests. Authors’ contributions AK, AR, KB and HJM participated in the conception, design

and data interpretation and drafting of the manuscript. AK, AR, MND performed the practical molecular biology procedures. KB collected and selected the biopsy specimens. All authors have been involved in drafting of the manuscript and approved the final version.”
“Background Over the past decade, Clostridium difficile has emerged as an important gut pathogen, causing hospital- and community-acquired diarrhea. The number of patients and the severity of disease have increased dramatically, due to the emergence of two hypervirulent PCR ribotype, 027 [1] and 078 [2, 3]. Traditionally, PCR ribotype 027 has been linked to nosocomial outbreaks. In contrast, PCR ribotype 078 has been detected frequently in farming animals, especially pigs [2, 4], and is found more during community acquired infection. The increase in C. difficile infections (CDI) of humans

has boosted interest in C. difficile biology, diagnostics and pathogenesis. In the past few years, multiple genome sequences of several Forskolin nmr PCR ribotypes have been determined [5–8]. The analyses of the genomes, aided by comparative genomics of DNA-DNA microarrays [9, 10] has shown that the genomes of C. difficile are highly variable with inserts of mobile DNA from phage, plasmid or transposon origin. These mobile DNA elements are actively moving within C. difficile genomes and are frequently passed on to neighboring bacteria, harboring mosaic genomes [7, 11]. It is unclear what role the mobile elements play in the virulence of C. difficile. Some virulence linked genes, for example the holin-like tcdE, have a phage origin [12]. In fact, it has been suggested that the whole pathogenicity locus (PaLoc), encoding the major C. difficile virulence factors TcdA and TcdB, is of phage origin [13, 14]. Recently, phages have been shown to upregulate toxin production in C. difficile, thereby increasing the virulence [15]. C.