BEAST analysis based on 1,425 core genome SNPs in 101 ST258 isolates with NJST258_1 reference genome, with the 215 kb region of recombination  masked, gives temporal context to the emergence of ST258, with key events and initial reports of KPC-producing K. pneumoniae in different countries plotted. Blue font indicates reports of KPC-producing K. pneumoniae, brown font is ST258. Green shading on the phylogeny shows lines of iterations of Bayesian analyses. The mean mutation rate of K. pneumoniae ST258 is 1.03 x 10−6 (95% HPD 8.09 x 10−7 to 1.24 x 10−6). The TMRCA for the ST258 clade is approximately 20 years ago, around 1995. The plot inset is a root-to-tip analysis of SNP accumulations for each isolate since the MRCA of ST258. The slope of the fit line is 4.66, which is close to the mutation rate calculated by BEAST ((1.03 x 10−6 substitutions per site per year) x (3.8 Mbp core genome size) = 3.9 SNPs per year).
Multidrug-resistant Klebsiella pneumoniae producing the KPC carbapenemase have rapidly spread throughout the world, causing severe healthcare-associated infections with limited antimicrobial treatment options. Dissemination of KPC-producing K. pneumoniae is largely attributed to expansion of a single dominant strain, ST258. In this study, we explore phylogenetic relationships and evolution within ST258 and its clonal group, CG258, using whole genome sequence analysis of 167 isolates from 20 countries collected over 17 years. Our results show a common ST258 ancestor emerged from its diverse parental clonal group around 1995 and likely acquired blaKPC prior to dissemination. Over the past two decades, ST258 has remained highly clonal despite diversity in accessory elements and divergence in the capsule polysaccharide synthesis locus. Apart from the large recombination event that gave rise to ST258, few mutations set it apart from its clonal group. However, one mutation occurs in a global transcription regulator. Characterization of outer membrane protein sequences revealed a profile in ST258 that includes a truncated OmpK35 and modified OmpK37. Our work illuminates potential genomic contributors to the pathogenic success of ST258, helps us better understand the global dissemination of this strain, and identifies genetic markers unique to ST258.
ver historia personal en: www.cerasale.com.ar [dado de baja por la Cancillería Argentina por temas políticos, propio de la censura que rige en nuestro medio]//
weblog.maimonides.edu/farmacia/archives/UM_Informe_Autoevaluacion_FyB.pdf - //
weblog.maimonides.edu/farmacia/archives/0216_Admin_FarmEcon.pdf - //
www.proz.com/kudoz/english_to_spanish/art_literary/523942-key_factors.html - 65k - // www.llave.connmed.com.ar/portalnoticias_vernoticia.php?codigonoticia=17715 // www.frusculleda.com.ar/homepage/espanol/activities_teaching.htm // http://www.on24.com.ar/nota.aspx?idNot=36331 ||
No hay comentarios:
Publicar un comentario