melitensis cells and fractions. Res Microbiol 1996,147(3):145–157.PubMedCrossRef 44. Cloeckaert A, Jacques I, Grillo MJ, Marin CM, Grayon M, Blasco JM, Verger JM: Development and evaluation as vaccines in mice of Brucella melitensis Rev.1 single and double deletion mutants of the bp26 and omp31 genes coding for antigens of diagnostic significance in ovine brucellosis. Vaccine 2004,22(21–22):2827–2835.PubMedCrossRef 45. Hydroxychloroquine in vitro Cloeckaert A, Verger JM, Grayon M, Grepinet O: Restriction site polymorphism of the genes encoding
the major 25 kDa and 36 kDa outer-membrane proteins of Brucella . Microbiology 1995,141(Pt 9):2111–2121.PubMedCrossRef 46. Kumar S, Nei M, Dudley J, Tamura K: MEGA: a biologist-centric software for evolutionary analysis of DNA and protein sequences. Brief Bioinform 2008,9(4):299–306.PubMedCrossRef 47. Whatmore AM, Perrett LL, MacMillan AP: Characterisation of the genetic diversity of Brucella by multilocus sequencing. BMC Microbiol 2007, 7:34.PubMedCrossRef 48. Huynh LY, Van Ert MN, Hadfield T, Probert WS, Bellaire BH, Dobson M, Burgess RJ, Weyant RS, Popovic T, Zanecki S, et al.: Multiple Locus Variable Number Tandem Repeat (VNTR) Analysis (MLVA) of Brucella spp. identifies species specific Copanlisib markers and insights into phylogenetic relatiohsips. National Institute of Allergy and Infectious Disease, NIH: Frontiers in Research 2008.
49. Tiller RV, De BK, Boshra M, Huynh LY, Van Ert MN, Wagner DM, Klena J, MT S, El-Shafie SS, Keim P, et al.: Comparison of two multiple locus variable number tandem repeat (VNTR) analysis (MLVA) methods for molecular strain typing human Brucella melitensis isolates from the Middle East. Journal of Clinical Microbiology 2009,47(7):2226–2231.PubMedCrossRef Authors’ contributions SG, SCB, AJ, JB CC participated in the clinical
diagnosis, isolation and initial characterization of the strain BO2 and also contributed in drafting the manuscript. RVT, JEG, DRL, ARH, only BKD performed both biochemical and molecular studies and drafted the manuscript. All authors read and approved the final manuscript.”
“Background Enteropathogenic Escherichia coli (EPEC) is an important cause of infantile diarrhea worldwide and particularly in developing countries [1, 2]. EPEC strains adhere intimately to the brush border of the intestinal epithelium and initiate a complex signaling cascade by virtue of a chromosomal pathogenicity island, the locus for enterocyte effacement (LEE) (reviewed by Clarke et al [3]). EPEC strains also carry an EPEC adherence factor (EAF) plasmid, which encodes the bundle forming pili, a plasmid-encoded regulator, and other putative virulence genes. The majority of EPEC isolates belong to classic serotypes derived from 12 classical O serogroups (O26, O55, O86, O111, O114, O119, O125, O126, O127, O128, O142, and O158) [4, 5].