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AuthorShabayek, Sarahdc.contributor.author
AuthorSpellerberg, Barbaradc.contributor.author
Date of accession2021-03-29T13:54:14Zdc.date.accessioned
Available in OPARU since2021-03-29T13:54:14Zdc.date.available
Date of first publication2018-03-14dc.date.issued
AbstractStreptococcus agalactiae or group B streptococcus (GBS) is a leading cause of serious neonatal infections. GBS is an opportunistic commensal constituting a part of the intestinal and vaginal physiologic flora and maternal colonization is the principal route of GBS transmission. GBS is a pathobiont that converts from the asymptomatic mucosal carriage state to a major bacterial pathogen causing severe invasive infections. At present, as many as 10 serotypes (Ia, Ib, and II–IX) are recognized. The aim of the current review is to shed new light on the latest epidemiological data and clonal distribution of GBS in addition to discussing the most important colonization determinants at a molecular level. The distribution and predominance of certain serotypes is susceptible to variations and can change over time. With the availability of multilocus sequence typing scheme (MLST) data, it became clear that GBS strains of certain clonal complexes possess a higher potential to cause invasive disease, while other harbor mainly colonizing strains. Colonization and persistence in different host niches is dependent on the adherence capacity of GBS to host cells and tissues. Bacterial biofilms represent well-known virulence factors with a vital role in persistence and chronic infections. In addition, GBS colonization, persistence, translocation, and invasion of host barriers are largely dependent on their adherence abilities to host cells and extracellular matrix proteins (ECM). Major adhesins mediating GBS interaction with host cells include the fibrinogen-binding proteins (Fbs), the laminin-binding protein (Lmb), the group B streptococcal C5a peptidase (ScpB), the streptococcal fibronectin binding protein A (SfbA), the GBS immunogenic bacterial adhesin (BibA), and the hypervirulent adhesin (HvgA). These adhesins facilitate persistent and intimate contacts between the bacterial cell and the host, while global virulence regulators play a major role in the transition to invasive infections. This review combines for first time epidemiological data with data on adherence and colonization for GBS. Investigating the epidemiology along with understanding the determinants of mucosal colonization and the development of invasive disease at a molecular level is therefore important for the development of strategies to prevent invasive GBS disease worldwide.dc.description.abstract
Languageendc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseCC BY 4.0 Internationaldc.rights
Link to license texthttps://creativecommons.org/licenses/by/4.0/dc.rights.uri
KeywordColonizationdc.subject
KeywordMolecular characteristicsdc.subject
KeywordEpidemiology, serotypedc.subject
Dewey Decimal GroupDDC 610 / Medicine & healthdc.subject.ddc
MeSHStreptococcus agalactiaedc.subject.mesh
MeSHStreptococcal infectionsdc.subject.mesh
TitleGroup B streptococcal colonization,molecular characteristics, and epidemiologydc.title
Resource typeWissenschaftlicher Artikeldc.type
VersionpublishedVersiondc.description.version
DOIhttp://dx.doi.org/10.18725/OPARU-36422dc.identifier.doi
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-oparu-36484-9dc.identifier.urn
GNDStreptokokkeninfektiondc.subject.gnd
InstitutionUKU. Institut für Medizinische Mikrobiologie und Hygieneuulm.affiliationSpecific
Peer reviewjauulm.peerReview
DCMI TypeTextuulm.typeDCMI
CategoryPublikationenuulm.category
In cooperation withSuez Canal Universityuulm.cooperation
DOI of original publication10.3389/fmicb.2018.00437dc.relation1.doi
Source - Title of sourceFrontiers in Microbiologysource.title
Source - Place of publicationFrontiers Mediasource.publisher
Source - Volume9source.volume
Source - Year2018source.year
Source - Article number437source.articleNumber
Source - eISSN1664-302Xsource.identifier.eissn
University Bibliographyjauulm.unibibliographie


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CC BY 4.0 International
Except where otherwise noted, this item's license is described as CC BY 4.0 International