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      Epidemiology of and prenatal molecular distinction between invasive and colonizing group B streptococci in The Netherlands and Taiwan

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          Abstract

          The identification of markers for virulent group B streptococci (GBS) could guide prenatal prevention and intervention strategies. We compared the distribution of serotypes and potential pathogenicity islands (PPIs) between invasive and colonizing GBS. Colonizing and invasive strains from The Netherlands and Taiwan were serotyped. We used polymerase chain reaction (PCR) for the amplification of several new PPI markers. Several combinations of PPI-specific markers and serotypes were associated with invasiveness. For Dutch neonatal strains, a receiver operating characteristic (ROC) curve with serotype and five PPI markers showed an area under the curve (AUC) of 0.963 (95% confidence interval [CI] 0.935–0.99). For Taiwanese neonatal strains, serotype and four different PPI markers resulted in an ROC curve with an AUC of 0.894 (95% CI 0.826–0.963). PPI-specific and serological markers can distinguish local neonatal invasive GBS strains from colonizing ones. Apparently, there are clear regional differences in the GBS epidemiology and infection potential of clones.

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          Most cited references29

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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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            Pathogenicity islands in bacterial pathogenesis.

            In this review, we focus on a group of mobile genetic elements designated pathogenicity islands (PAI). These elements play a pivotal role in the virulence of bacterial pathogens of humans and are also essential for virulence in pathogens of animals and plants. Characteristic molecular features of PAI of important human pathogens and their role in pathogenesis are described. The availability of a large number of genome sequences of pathogenic bacteria and their benign relatives currently offers a unique opportunity for the identification of novel pathogen-specific genomic islands. However, this knowledge has to be complemented by improved model systems for the analysis of virulence functions of bacterial pathogens. PAI apparently have been acquired during the speciation of pathogens from their nonpathogenic or environmental ancestors. The acquisition of PAI not only is an ancient evolutionary event that led to the appearance of bacterial pathogens on a timescale of millions of years but also may represent a mechanism that contributes to the appearance of new pathogens within a human life span. The acquisition of knowledge about PAI, their structure, their mobility, and the pathogenicity factors they encode not only is helpful in gaining a better understanding of bacterial evolution and interactions of pathogens with eukaryotic host cells but also may have important practical implications such as providing delivery systems for vaccination, tools for cell biology, and tools for the development of new strategies for therapy of bacterial infections.
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              Complete genome sequence and comparative genomic analysis of an emerging human pathogen, serotype V Streptococcus agalactiae.

              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.
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                Author and article information

                Contributors
                e.vanelzakker@hagaziekenhuis.nl
                Journal
                Eur J Clin Microbiol Infect Dis
                European Journal of Clinical Microbiology & Infectious Diseases
                Springer-Verlag (Berlin/Heidelberg )
                0934-9723
                1435-4373
                31 March 2009
                August 2009
                : 28
                : 8
                : 921-928
                Affiliations
                [1 ]Department of Microbiology, Haga Hospital, PO Box 40551, 2504 LN The Hague, The Netherlands
                [2 ]Department of Microbiology, Academic Medical Center, Amsterdam, The Netherlands
                [3 ]Department of Microbiology Medical Center Haaglanden, The Hague, The Netherlands
                [4 ]Department of Microbiology and Infectious Diseases, Erasmus Medical Center, Rotterdam, The Netherlands
                [5 ]Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, Tainan, Taiwan
                Article
                726
                10.1007/s10096-009-0726-4
                2723670
                19333631
                e280227d-95d4-47ba-9890-5c8c4f83f00a
                © The Author(s) 2009
                History
                : 17 February 2009
                : 23 February 2009
                Categories
                Article
                Custom metadata
                © Springer-Verlag 2009

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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