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dc.contributor.authorGarcía López, Ernesto
dc.contributor.authorMartin-Galiano, Antonio Javier 
dc.date.accessioned2020-04-23T07:10:10Z
dc.date.available2020-04-23T07:10:10Z
dc.date.issued2020
dc.identifier.citationFront Microbiol. 2020 Mar 31;11:524.es_ES
dc.identifier.issn1664-302Xes_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9702
dc.description.abstractThe molecular basis of the pathogenesis of the opportunistic invasive infections caused by isolates of the Gemella genus remains largely unknown. Moreover, inconsistencies in the current species assignation were detected after genome-level comparison of 16 public Gemella isolates. A literature search detected that, between the two most pathogenic species, Gemella morbillorum causes about twice the number of cases compared to Gemella haemolysans. These two species shared their mean diseases - sepsis and endocarditis - but differed in causing other syndromes. A number of well-known virulence factors were harbored by all species, such as a manganese transport/adhesin sharing 83% identity from oral endocarditis-causing streptococci. Likewise, all Gemellae carried the genes required for incorporating phosphorylcholine into their cell walls and encoded some choline-binding proteins. In contrast, other proteins were species-specific, which may justify the known epidemiological differences. G. haemolysans, but not G. morbillorum, harbor a gene cluster potentially encoding a polysaccharidic capsule. Species-specific surface determinants also included Rib and MucBP repeats, hemoglobin-binding NEAT domains, peptidases of C5a complement factor and domains that recognize extracellular matrix molecules exposed in damaged heart valves, such as collagen and fibronectin. Surface virulence determinants were associated with several taxonomically dispersed opportunistic genera of the oral microbiota, such as Granulicatella, Parvimonas, and Streptococcus, suggesting the existence of a horizontally transferrable gene reservoir in the oral environment, likely facilitated by close proximity in biofilms and ultimately linked to endocarditis. The identification of the Gemella virulence pool should be implemented in whole genome-based protocols to rationally predict the pathogenic potential in ongoing clinical infections caused by these poorly known bacterial pathogens.es_ES
dc.description.sponsorshipThis research was supported by grants MPY 509/19 from the Instituto de Salud Carlos III (ISCIII) and SAF2017-88664-R from the Spanish Ministerio de Economía, Industria y Competitividad (MEICOM). The Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES) is an initiative of the ISCIII. AM-G is the recipient of a Miguel Servet contract by the ISCIII.es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Mediaes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectGranulicatellaes_ES
dc.subjectParvimonases_ES
dc.subjectemergent pathogenes_ES
dc.subjecthorizontal gene transferes_ES
dc.subjectvirulence factores_ES
dc.titleThe Versatility of Opportunistic Infections Caused by Gemella Isolates Is Supported by the Carriage of Virulence Factors From Multiple Originses_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID32296407es_ES
dc.format.volume11es_ES
dc.format.page524es_ES
dc.identifier.doi10.3389/fmicb.2020.00524es_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España)
dc.contributor.funderCentro de Investigación Biomedica en Red - CIBER
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fmicb.2020.00524es_ES
dc.identifier.journalFrontiers in microbiologyes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/ MPY 509/19es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/SAF2017-88664-Res_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución 4.0 Internacional
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