Nat Methods 2005,2(6):443–448.CrossRefPubMed 48. Choi KH, Mima T, Casart Y, Rholl D, Kumar A, Beacham IR, Schweizer HP: Genetic tools for select-agent-compliant

manipulation of Burkholderia pseudomallei. Appl Environ Microbiol 2008,74(4):1064–1075.CrossRefPubMed #Selleckchem NVP-LDE225 randurls[1|1|,|CHEM1|]# 49. Lépine F, Déziel E, Milot S, Rahme LG: A stable isotope dilution assay for the quantification of the Pseudomonas quinolone signal in Pseudomonas aeruginosa cultures. Biochim Biophys Acta 2003,1622(1):36–41.PubMed 50. du Noüy PL: Spontaneous Decrease Of The Surface Tension Of Serum. I. J Exp Med 1922, xxxw:575–597.CrossRef Authors’ contributions ED and DD designed the experiments. DD carried out all experimental procedures and analyzed the data. FL provided critical knowledge in LC/MS experimentation. DEW provided B. pseudomallei samples for LC/MS analysis. DD wrote the manuscript. FL and ED corrected the manuscript. All authors read and approved the final manuscript.”
“Background Yersinia enterocolitica, an important food- and water-borne human enteropathogen is known to cause a variety of gastrointestinal problems. Most commonly, it causes acute diarrhea, terminal ileitis and mesenteric lymphadenitis [1]. Long-term sequelae following infection include reactive arthritis and erythema nodosum [1]. Blood transfusion associated septicemia due to Y. enterocolitica has been reported

to have high mortality [2]. Currently, Y. enterocolitica is represented by six biovars (1A, 1B, 2, 3, 4 and 5) and more click here than 30 distinct serovars. The virulence of known pathogenic biovars namely 1B and 2-5 is attributed to pYV (plasmid for Yersinia virulence) plasmid [3] and chromosomally borne virulence factors [4]. The biovar 1A strains however lack pYV plasmid and have generally been regarded as avirulent. But several clinical, epidemiological and experimental evidences indicate their potential pathogeniCity [5]. Some biovar 1A strains have been reported to produce disease symptoms resembling that produced 17-DMAG (Alvespimycin) HCl by pathogenic biovars [6, 7]. These have been implicated in nosocomial [8] and food-borne [9] outbreaks

and isolated from extra-intestinal sites [10]. The biovar 1A strains also invade epithelial cells [11, 12], resist killing by macrophages [13] and carry virulence-associated genes such as ystB (enterotoxin), inv (invasin), myfA (fimbriae), hreP (subtilisin/kexin-like protease) and tccC (insecticidal-toxin like complex) [5, 14]. In the past, enterotoxin has been thought to be the only major virulence factor produced by biovar 1A strains. Recently insecticidal-toxin complex [15] and flagella [16] have been identified as virulence factors of Y. enterocolitica biovar 1A strains. However the exact mechanisms underlying the pathogenesis by biovar 1A strains remains unclear and there is need to investigate the role of other putative virulence factors. Urease (urea amidohydrolase; EC 3.5.1.