Diagn Microbiol Infect Dis 2002, 44:383–386.CrossRefPubMed Authors’ contributions AAR participated in the preparation of the manuscript, designed and performed EMSA experiments selleck chemicals with the Et probes, cloned, assembled and analyzed the expanded 5′ flanking region, performed RT-PCR experiments; FVM designed and performed EMSA experiments with Bs probes, sequenced and analyzed polymorphisms of the 3′ flanking region; RP gained funds to develop the projects, wrote the manuscript, analyzed data and

supervised the development of the Ph.D. projects from AAR and FVM, whose partial data are contained in this manuscript. All authors read and approved the final manuscript.”
“Background In humans, Escherichia coli strains can be commensal (part of the normal intestinal microbiota) and/or the cause of various infectious diseases (intestinal and Vorinostat molecular weight extraintestinal infections) [1]. The extent of commensal or virulent properties displayed by a strain is determined by a complex balance between the status Tucidinostat manufacturer of

the host and the production of virulence factors in the bacteria. The role of the intrinsic virulence of the isolates needs to be clarified and molecular markers of virulence are required to predict the invasiveness of clinical strains isolated during the course of extraintestinal infection or patient colonization. E. coli has a clonal genetic structure and exhibits a low level of recombination [2]. E. coli strains can be categorised into four main phylogenetic groups,

A, B1, B2, and D. These groups have been defined based on proteic (multi-locus enzyme electrophoresis including the electrophoresis of esterases [3]) and genetic markers (restriction fragment length polymorphism [4], random amplified polymorphic DNA [4] and multi-locus sequence typing (MLST) [5, 6]). Seven types of esterases (A, B, Tangeritin C, D, I, F and S), differing in their ability to hydrolyse synthetic substrates and their sensitivity to di-isopropyl fluorophosphate, have been identified by separation on polyacrylamide agarose gels [7–9]. The most frequently observed type in this group of enzymes corresponds to esterase B (EC 3.1.1.1). This protein shows two types of electrophoretic mobility: B1 from Mf = 74 to Mf = 66 and B2 from Mf = 63 to Mf = 57 [9]. Strains with type B2 esterase belong to the phylogenetic group B2, whereas those with type B1 esterase belong to the non-B2 phylogenetic groups [10]. Several studies have shown a correlation between long-term evolutionary history (strain phylogeny) and virulence in E. coli, with most extraintestinal E. coli pathogens (including urinary tract infection strains) belonging to just one of the four main E. coli phylogenetic groups, the phylogenetic group B2 [11–13]. This correlation suggests a possible link between esterase polymorphism and extraintestinal virulence in an asexual species with a low level of recombination.