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      Serotype III Streptococcus agalactiae from Bovine Milk and Human Neonatal Infections 1

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          Abstract

          Although largely unrelated, many bovine type III GBS appear to share a common ancestor with an important human clone.

          Abstract

          Streptococcus agalactiae (group B streptococcus [GBS]) causes invasive human infections and bovine mastitis. This study examined the genetic relationship between bovine and human serotype III GBS by using molecular techniques that classify human serotype III GBS into four distinct phylogenetic lineages. Bovine serotype III GBS were largely contained in two lineages, which are distinct from the two major lineages (restriction digest types III-2 and III-3) that infect human neonates. One of the bovine lineages closely resembles the human III-1 lineage, whose members occasionally cause human neonatal infections. The bovine strains in the other lineage characteristically have an initiation factor IF2 gene ( infB) H allele and multilocus sequence types that are not found in human GBS strains. Evidence suggests that this “H allele” lineage is related to the human III-3 lineage. These results support the assertion that human and bovine GBS are largely unrelated and provide further insight into the genetic relation between human and bovine GBS.

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          Complete genome sequence of Neisseria meningitidis serogroup B strain MC58.

          The 2,272,351-base pair genome of Neisseria meningitidis strain MC58 (serogroup B), a causative agent of meningitis and septicemia, contains 2158 predicted coding regions, 1158 (53.7%) of which were assigned a biological role. Three major islands of horizontal DNA transfer were identified; two of these contain genes encoding proteins involved in pathogenicity, and the third island contains coding sequences only for hypothetical proteins. Insights into the commensal and virulence behavior of N. meningitidis can be gleaned from the genome, in which sequences for structural proteins of the pilus are clustered and several coding regions unique to serogroup B capsular polysaccharide synthesis can be identified. Finally, N. meningitidis contains more genes that undergo phase variation than any pathogen studied to date, a mechanism that controls their expression and contributes to the evasion of the host immune system.
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            Genome sequence of Streptococcus agalactiae, a pathogen causing invasive neonatal disease.

            Streptococcus agalactiae is a commensal bacterium colonizing the intestinal tract of a significant proportion of the human population. However, it is also a pathogen which is the leading cause of invasive infections in neonates and causes septicaemia, meningitis and pneumonia. We sequenced the genome of the serogroup III strain NEM316, responsible for a fatal case of septicaemia. The genome is 2 211 485 base pairs long and contains 2118 protein coding genes. Fifty-five per cent of the predicted genes have an ortholog in the Streptococcus pyogenes genome, representing a conserved backbone between these two streptococci. Among the genes in S. agalactiae that lack an ortholog in S. pyogenes, 50% are clustered within 14 islands. These islands contain known and putative virulence genes, mostly encoding surface proteins as well as a number of genes related to mobile elements. Some of these islands could therefore be considered as pathogenicity islands. Compared with other pathogenic streptococci, S. agalactiae shows the unique feature that pathogenicity islands may have an important role in virulence acquisition and in genetic diversity.
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              Identification of a high-virulence clone of type III Streptococcus agalactiae (group B Streptococcus) causing invasive neonatal disease.

              Chromosomal genotypes of 128 isolates of six serotypes (Ia, Ib, Ic, II, Ic/II, and III) of Streptococcus agalactiae (group B Streptococcus) recovered predominantly from human infants in the United States were characterized by an analysis of electrophoretically demonstrable allelic profiles at 11 metabolic enzyme loci. Nineteen distinctive electrophoretic types (ETs), representing multilocus clonal genotypes, were identified. Mean genetic diversity per locus among ETs of isolates of the same serotype was, on average, nearly equal to that in all 19 ETs. Cluster analysis of the ETs revealed two primary phylogenetic divisions at a genetic distance of 0.65. A single clone (ET 1) represented by 40 isolates expressing type III antigen formed division I. Division II was composed of 18 ETs in three major lineages diverging from one another at distances greater than 0.35 and included strains of all six antigenic classes. The type III organisms in division I produce more extracellular neuraminidase and apparently are more virulent than the type III strains in division II, which are related to strains of other serotypes that cause disease much less frequently. The existence of this unusually virulent clone accounts, in major part, for the high morbidity and mortality associated with infection by type III organisms.
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                Author and article information

                Journal
                Emerg Infect Dis
                Emerging Infect. Dis
                EID
                Emerging Infectious Diseases
                Centers for Disease Control and Prevention
                1080-6040
                1080-6059
                August 2004
                : 10
                : 8
                : 1412-1419
                Affiliations
                [* ]University of Utah Health Sciences Center, Salt Lake City, Utah, USA;
                []Faculté de Médicine Vétérinaire, Université de Montréal, Saint-Hyacinthe, Québec, Canada;
                []John Radcliffe Hospital, Oxford, United Kingdom;
                [§ ]St. Jude Children's Research Hospital, Memphis, Tennessee, USA
                [1 ]Presented in part at the XVth Lancefield International Symposium on Streptococci and Streptococcal Diseases, October 6–11, 2002, Goa, India.
                Author notes
                Address for correspondence: John F. Bohnsack, Department of Pediatrics, University of Utah Health Sciences Center, 50 North Medical Drive, Salt Lake City, UT 84132, USA; fax: 801-585-9314; email: john.bohnsack@ 123456hsc.utah.edu
                Article
                03-0917
                10.3201/eid1008.030917
                3320405
                15496242
                be28875c-02b3-46d7-b45b-bb186df77efb
                History
                Categories
                Research
                Research

                Infectious disease & Microbiology
                infb,bovine mastitis,group b streptococcus,phylogeny,streptococcus agalactiae,neonatal sepsis

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