Margarit I

References (4)

Title : Serotype IV Streptococcus agalactiae ST-452 has arisen from large genomic recombination events between CC23 and the hypervirulent CC17 lineages - Campisi_2016_Sci.Rep_6_29799
Author(s) : Campisi E , Rinaudo CD , Donati C , Barucco M , Torricelli G , Edwards MS , Baker CJ , Margarit I , Rosini R
Ref : Sci Rep , 6 :29799 , 2016
Abstract : Streptococcus agalactiae (Group B Streptococcus, GBS) causes life-threatening infections in newborns and adults with chronic medical conditions. Serotype IV strains are emerging both among carriers and as cause of invasive disease and recent studies revealed two main Sequence Types (STs), ST-452 and ST-459 assigned to Clonal Complexes CC23 and CC1, respectively. Whole genome sequencing of 70 type IV GBS and subsequent phylogenetic analysis elucidated the localization of type IV isolates in a SNP-based phylogenetic tree and suggested that ST-452 could have originated through genetic recombination. SNPs density analysis of the core genome confirmed that the founder strain of this lineage originated from a single large horizontal gene transfer event between CC23 and the hypervirulent CC17. Indeed, ST-452 genomes are composed by two parts that are nearly identical to corresponding regions in ST-24 (CC23) and ST-291 (CC17). Chromosome mapping of the major GBS virulence factors showed that ST-452 strains have an intermediate yet unique profile among CC23 and CC17 strains. We described unreported large recombination events, involving the cps IV operon and resulting in the expansion of serotype IV to CC23. This work sheds further light on the evolution of GBS providing new insights on the recent emergence of serotype IV.
ESTHER : Campisi_2016_Sci.Rep_6_29799
PubMedSearch : Campisi_2016_Sci.Rep_6_29799
PubMedID: 27411639

Title : Genomic Analysis Reveals Multi-Drug Resistance Clusters in Group B Streptococcus CC17 Hypervirulent Isolates Causing Neonatal Invasive Disease in Southern Mainland China - Campisi_2016_Front.Microbiol_7_1265
Author(s) : Campisi E , Rosini R , Ji W , Guidotti S , Rojas-Lopez M , Geng G , Deng Q , Zhong H , Wang W , Liu H , Nan C , Margarit I , Rinaudo CD
Ref : Front Microbiol , 7 :1265 , 2016
Abstract : Neonatal invasive disease caused by group B Streptococcus (GBS) represents a significant public health care concern globally. However, data related to disease burden, serotype distribution, and molecular epidemiology in China and other Asian countries are very few and specifically relative to confined regions. The aim of this study was to investigate the genetic characteristics of GBS isolates recovered from neonates with invasive disease during 2013-2014 at Guangzhou and Changsha hospitals in southern mainland China. We assessed the capsular polysaccharide type, pilus islands (PIs) distribution and hvgA gene presence in a panel of 26 neonatal clinical isolates, of which 8 were recovered from Early Onset Disease and 18 from Late Onset Disease (LOD). Among 26 isolates examined, five serotypes were identified. Type III was the most represented (15 cases), particularly among LOD strains (n = 11), followed by types Ib (n = 5), V (n = 3), Ia (n = 2) and II (n = 1). We performed whole-genome sequencing analysis and antimicrobial susceptibility testing on the 14 serotype III isolates belonging to the hypervirulent Clonal Complex 17 (serotype III-CC17). The presence of PI-2b alone was associated with 13 out of 14 serotype III-CC17 strains. Genome analysis led us to identify two multi-drug resistance gene clusters harbored in two new versions of integrative and conjugative elements (ICEs), carrying five or eight antibiotic resistance genes, respectively. These ICEs replaced the 16 kb-locus that normally contains the PI-1 operon. All isolates harboring the identified ICEs showed multiple resistances to aminoglycoside, macrolide, and tetracycline antibiotic classes. In conclusion, we report the first whole-genome sequence analysis of 14 GBS serotype III-CC17 strains isolated in China, representing the most prevalent lineage causing neonatal invasive disease. The acquisition of newly identified ICEs conferring multiple antibiotic resistance could in part explain the spread of this specific clone among Chinese neonatal isolates and underlines the need for a constant epidemiological surveillance.
ESTHER : Campisi_2016_Front.Microbiol_7_1265
PubMedSearch : Campisi_2016_Front.Microbiol_7_1265
PubMedID: 27574519

Title : Genomic analysis reveals the molecular basis for capsule loss in the group B Streptococcus population - Rosini_2015_PLoS.One_10_e0125985
Author(s) : Rosini R , Campisi E , De Chiara M , Tettelin H , Rinaudo D , Toniolo C , Metruccio M , Guidotti S , Sorensen UB , Kilian M , Ramirez M , Janulczyk R , Donati C , Grandi G , Margarit I
Ref : PLoS ONE , 10 :e0125985 , 2015
Abstract : The human and bovine bacterial pathogen Streptococcus agalactiae (Group B Streptococcus, GBS) expresses a thick polysaccharide capsule that constitutes a major virulence factor and vaccine target. GBS can be classified into ten distinct serotypes differing in the chemical composition of their capsular polysaccharide. However, non-typeable strains that do not react with anti-capsular sera are frequently isolated from colonized and infected humans and cattle. To gain a comprehensive insight into the molecular basis for the loss of capsule expression in GBS, a collection of well-characterized non-typeable strains was investigated by genome sequencing. Genome based phylogenetic analysis extended to a wide population of sequenced strains confirmed the recently observed high clonality among GBS lineages mainly containing human strains, and revealed a much higher degree of diversity in the bovine population. Remarkably, non-typeable strains were equally distributed in all lineages. A number of distinct mutations in the cps operon were identified that were apparently responsible for inactivation of capsule synthesis. The most frequent genetic alterations were point mutations leading to stop codons in the cps genes, and the main target was found to be cpsE encoding the portal glycosyl transferase of capsule biosynthesis. Complementation of strains carrying missense mutations in cpsE with a wild-type gene restored capsule expression allowing the identification of amino acid residues essential for enzyme activity.
ESTHER : Rosini_2015_PLoS.One_10_e0125985
PubMedSearch : Rosini_2015_PLoS.One_10_e0125985
PubMedID: 25946017
Gene_locus related to this paper: strag-a0a076z217 , strag-a0a0h1ywg1

Title : Complete genome sequence and comparative genomic analysis of an emerging human pathogen, serotype V Streptococcus agalactiae - Tettelin_2002_Proc.Natl.Acad.Sci.U.S.A_99_12391
Author(s) : Tettelin H , Masignani V , Cieslewicz MJ , Eisen JA , Peterson S , Wessels MR , Paulsen IT , Nelson KE , Margarit I , Read TD , Madoff LC , Wolf AM , Beanan MJ , Brinkac LM , Daugherty SC , DeBoy RT , Durkin AS , Kolonay JF , Madupu R , Lewis MR , Radune D , Fedorova NB , Scanlan D , Khouri H , Mulligan S , Carty HA , Cline RT , Van Aken SE , Gill J , Scarselli M , Mora M , Iacobini ET , Brettoni C , Galli G , Mariani M , Vegni F , Maione D , Rinaudo D , Rappuoli R , Telford JL , Kasper DL , Grandi G , Fraser CM
Ref : Proc Natl Acad Sci U S A , 99 :12391 , 2002
Abstract : The 2,160,267 bp genome sequence of Streptococcus agalactiae, the leading cause of bacterial sepsis, pneumonia, and meningitis in neonates in the U.S. and Europe, is predicted to encode 2,175 genes. Genome comparisons among S. agalactiae, Streptococcus pneumoniae, Streptococcus pyogenes, and the other completely sequenced genomes identified genes specific to the streptococci and to S. agalactiae. These in silico analyses, combined with comparative genome hybridization experiments between the sequenced serotype V strain 2603 V/R and 19 S. agalactiae strains from several serotypes using whole-genome microarrays, revealed the genetic heterogeneity among S. agalactiae strains, even of the same serotype, and provided insights into the evolution of virulence mechanisms.
ESTHER : Tettelin_2002_Proc.Natl.Acad.Sci.U.S.A_99_12391
PubMedSearch : Tettelin_2002_Proc.Natl.Acad.Sci.U.S.A_99_12391
PubMedID: 12200547
Gene_locus related to this paper: strag-ESTA , strag-GBS0040 , strag-GBS1828 , strag-pepx , strag-SAG0108 , strag-SAG0246 , strag-SAG0383 , strag-SAG0521 , strag-SAG0679 , strag-SAG0680 , strag-SAG0681 , strag-SAG0785 , strag-SAG0912 , strag-SAG1040 , strag-SAG1562 , strag-SAG2132