Loading…

Staphylococcus aureus CC30 Lineage and Absence of sed , j , r -Harboring Plasmid Predict Embolism in Infective Endocarditis

induces severe infective endocarditis (IE) where embolic complications are a major cause of death. Risk factors for embolism have been reported such as a younger age or larger IE vegetations, while methicillin resistance conferred by the gene appeared as a protective factor. It is unclear, however,...

Full description

Saved in:
Bibliographic Details
Published in:Frontiers in cellular and infection microbiology 2018-06, Vol.8, p.187-187
Main Authors: Rasigade, Jean-Philippe, Leclère, Amélie, Alla, François, Tessier, Adrien, Bes, Michèle, Lechiche, Catherine, Vernet-Garnier, Véronique, Laouénan, Cédric, Vandenesch, François, Leport, Catherine
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c496t-66101cd315f05bc8caf72e8f8d5fb343a75bb08f69b9243a0a6db6747bc568e83
cites cdi_FETCH-LOGICAL-c496t-66101cd315f05bc8caf72e8f8d5fb343a75bb08f69b9243a0a6db6747bc568e83
container_end_page 187
container_issue
container_start_page 187
container_title Frontiers in cellular and infection microbiology
container_volume 8
creator Rasigade, Jean-Philippe
Leclère, Amélie
Alla, François
Tessier, Adrien
Bes, Michèle
Lechiche, Catherine
Vernet-Garnier, Véronique
Laouénan, Cédric
Vandenesch, François
Leport, Catherine
description induces severe infective endocarditis (IE) where embolic complications are a major cause of death. Risk factors for embolism have been reported such as a younger age or larger IE vegetations, while methicillin resistance conferred by the gene appeared as a protective factor. It is unclear, however, whether embolism is influenced by other characteristics such as clonal complex (CC) or virulence pattern. We examined clinical and microbiological predictors of embolism in a prospective multicentric cohort of 98 French patients with monomicrobial IE. The genomic contents of causative isolates were characterized using DNA array. To preserve statistical power, genotypic predictors were restricted to CC, secreted virulence factors and virulence regulators. Multivariate regularized logistic regression identified three independent predictors of embolism. Patients at higher risk were younger than the cohort median age of 62.5 y (adjusted odds ratio [OR] 0.14; 95% confidence interval [CI] 0.05-0.36). characteristics predicting embolism were a CC30 genetic background (adjusted OR 9.734; 95% CI 1.53-192.8) and the absence of pIB485-like plasmid-borne enterotoxin-encoding genes , and ( ; adjusted OR 0.07; 95% CI 0.004-0.457). CC30 has been repeatedly reported to exhibit enhanced fitness in bloodstream infections, which might impact its ability to cause embolism. -encoded enterotoxins, whose superantigenic activity is unlikely to protect against embolism, possibly acted as a proxy to others genes of the pIB485-like plasmid found in genetically unrelated isolates from mostly embolism-free patients. did not independently predict embolism but was strongly associated with . This - association might have driven previous reports of a negative association of and embolism. Collectively, our results suggest that the influence of genotypic features on the risk of embolism may be stronger than previously suspected and independent of clinical risk factors.
doi_str_mv 10.3389/fcimb.2018.00187
format article
fullrecord <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_e3f07d201143496884db691e77fef272</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_e3f07d201143496884db691e77fef272</doaj_id><sourcerecordid>2059042506</sourcerecordid><originalsourceid>FETCH-LOGICAL-c496t-66101cd315f05bc8caf72e8f8d5fb343a75bb08f69b9243a0a6db6747bc568e83</originalsourceid><addsrcrecordid>eNpdktuLEzEUxgdR3GXdd58kjwpOzWUuyYtQSrWFggvqc8jlpE2ZmdRkprDsP2_arsuugeQkJ-f7HRK-onhP8IwxLr4443s9o5jwGc5L-6q4ppTVJRWcv362vypuU9rjPFpMuWBviysqBONZeV08_BzVYXffBROMmRJSU4QcFguG0cYPoLaA1GDRXCcYDKDgUAKLPqN9nhGVKxV1iH7YortOpd5bdBfBejOiZa9D51OP_IDWgwMz-iOg5WCDUdH60ad3xRunugS3j_Gm-P1t-WuxKjc_vq8X801pKtGMZdMQTIxlpHa41oYb5VoK3HFbO80qptpaa8xdI7Sg-YhVY3XTVq02dcOBs5tifeHaoPbyEH2v4r0MystzIsStVHH0pgMJzOHW5p8hFcvNOa8yShBoWweOtjSzvl5Yh0n3YA0MY1TdC-jLm8Hv5DYcZYMxozXJgE8XwO4_2Wq-kaccJiJ3J_h4qv342CyGPxOkUfY-Geg6NUCYkqS4FriiNW5yKb6UmhhSiuCe2ATLk13k2S7yZBd5tkuWfHj-lCfBP3Owv37huq8</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2059042506</pqid></control><display><type>article</type><title>Staphylococcus aureus CC30 Lineage and Absence of sed , j , r -Harboring Plasmid Predict Embolism in Infective Endocarditis</title><source>PubMed Central</source><creator>Rasigade, Jean-Philippe ; Leclère, Amélie ; Alla, François ; Tessier, Adrien ; Bes, Michèle ; Lechiche, Catherine ; Vernet-Garnier, Véronique ; Laouénan, Cédric ; Vandenesch, François ; Leport, Catherine</creator><creatorcontrib>Rasigade, Jean-Philippe ; Leclère, Amélie ; Alla, François ; Tessier, Adrien ; Bes, Michèle ; Lechiche, Catherine ; Vernet-Garnier, Véronique ; Laouénan, Cédric ; Vandenesch, François ; Leport, Catherine ; AEPEI Study Group ; The AEPEI Study Group</creatorcontrib><description>induces severe infective endocarditis (IE) where embolic complications are a major cause of death. Risk factors for embolism have been reported such as a younger age or larger IE vegetations, while methicillin resistance conferred by the gene appeared as a protective factor. It is unclear, however, whether embolism is influenced by other characteristics such as clonal complex (CC) or virulence pattern. We examined clinical and microbiological predictors of embolism in a prospective multicentric cohort of 98 French patients with monomicrobial IE. The genomic contents of causative isolates were characterized using DNA array. To preserve statistical power, genotypic predictors were restricted to CC, secreted virulence factors and virulence regulators. Multivariate regularized logistic regression identified three independent predictors of embolism. Patients at higher risk were younger than the cohort median age of 62.5 y (adjusted odds ratio [OR] 0.14; 95% confidence interval [CI] 0.05-0.36). characteristics predicting embolism were a CC30 genetic background (adjusted OR 9.734; 95% CI 1.53-192.8) and the absence of pIB485-like plasmid-borne enterotoxin-encoding genes , and ( ; adjusted OR 0.07; 95% CI 0.004-0.457). CC30 has been repeatedly reported to exhibit enhanced fitness in bloodstream infections, which might impact its ability to cause embolism. -encoded enterotoxins, whose superantigenic activity is unlikely to protect against embolism, possibly acted as a proxy to others genes of the pIB485-like plasmid found in genetically unrelated isolates from mostly embolism-free patients. did not independently predict embolism but was strongly associated with . This - association might have driven previous reports of a negative association of and embolism. Collectively, our results suggest that the influence of genotypic features on the risk of embolism may be stronger than previously suspected and independent of clinical risk factors.</description><identifier>ISSN: 2235-2988</identifier><identifier>EISSN: 2235-2988</identifier><identifier>DOI: 10.3389/fcimb.2018.00187</identifier><identifier>PMID: 29938201</identifier><language>eng</language><publisher>Switzerland: Frontiers</publisher><subject>Bacteriology ; CC30 ; enterotoxin ; Immunology ; infective endocarditis ; Life Sciences ; Microbiology ; Microbiology and Parasitology ; MRSA ; S. aureus ; stroke ; Virology</subject><ispartof>Frontiers in cellular and infection microbiology, 2018-06, Vol.8, p.187-187</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright © 2018 Rasigade, Leclère, Alla, Tessier, Bes, Lechiche, Vernet-Garnier, Laouénan, Vandenesch, Leport and The AEPEI Study Group. 2018 Rasigade, Leclère, Alla, Tessier, Bes, Lechiche, Vernet-Garnier, Laouénan, Vandenesch, Leport and The AEPEI Study Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-66101cd315f05bc8caf72e8f8d5fb343a75bb08f69b9243a0a6db6747bc568e83</citedby><cites>FETCH-LOGICAL-c496t-66101cd315f05bc8caf72e8f8d5fb343a75bb08f69b9243a0a6db6747bc568e83</cites><orcidid>0000-0002-3681-6314 ; 0000-0001-9412-7106</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6003251/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6003251/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29938201$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01911410$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Rasigade, Jean-Philippe</creatorcontrib><creatorcontrib>Leclère, Amélie</creatorcontrib><creatorcontrib>Alla, François</creatorcontrib><creatorcontrib>Tessier, Adrien</creatorcontrib><creatorcontrib>Bes, Michèle</creatorcontrib><creatorcontrib>Lechiche, Catherine</creatorcontrib><creatorcontrib>Vernet-Garnier, Véronique</creatorcontrib><creatorcontrib>Laouénan, Cédric</creatorcontrib><creatorcontrib>Vandenesch, François</creatorcontrib><creatorcontrib>Leport, Catherine</creatorcontrib><creatorcontrib>AEPEI Study Group</creatorcontrib><creatorcontrib>The AEPEI Study Group</creatorcontrib><title>Staphylococcus aureus CC30 Lineage and Absence of sed , j , r -Harboring Plasmid Predict Embolism in Infective Endocarditis</title><title>Frontiers in cellular and infection microbiology</title><addtitle>Front Cell Infect Microbiol</addtitle><description>induces severe infective endocarditis (IE) where embolic complications are a major cause of death. Risk factors for embolism have been reported such as a younger age or larger IE vegetations, while methicillin resistance conferred by the gene appeared as a protective factor. It is unclear, however, whether embolism is influenced by other characteristics such as clonal complex (CC) or virulence pattern. We examined clinical and microbiological predictors of embolism in a prospective multicentric cohort of 98 French patients with monomicrobial IE. The genomic contents of causative isolates were characterized using DNA array. To preserve statistical power, genotypic predictors were restricted to CC, secreted virulence factors and virulence regulators. Multivariate regularized logistic regression identified three independent predictors of embolism. Patients at higher risk were younger than the cohort median age of 62.5 y (adjusted odds ratio [OR] 0.14; 95% confidence interval [CI] 0.05-0.36). characteristics predicting embolism were a CC30 genetic background (adjusted OR 9.734; 95% CI 1.53-192.8) and the absence of pIB485-like plasmid-borne enterotoxin-encoding genes , and ( ; adjusted OR 0.07; 95% CI 0.004-0.457). CC30 has been repeatedly reported to exhibit enhanced fitness in bloodstream infections, which might impact its ability to cause embolism. -encoded enterotoxins, whose superantigenic activity is unlikely to protect against embolism, possibly acted as a proxy to others genes of the pIB485-like plasmid found in genetically unrelated isolates from mostly embolism-free patients. did not independently predict embolism but was strongly associated with . This - association might have driven previous reports of a negative association of and embolism. Collectively, our results suggest that the influence of genotypic features on the risk of embolism may be stronger than previously suspected and independent of clinical risk factors.</description><subject>Bacteriology</subject><subject>CC30</subject><subject>enterotoxin</subject><subject>Immunology</subject><subject>infective endocarditis</subject><subject>Life Sciences</subject><subject>Microbiology</subject><subject>Microbiology and Parasitology</subject><subject>MRSA</subject><subject>S. aureus</subject><subject>stroke</subject><subject>Virology</subject><issn>2235-2988</issn><issn>2235-2988</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpdktuLEzEUxgdR3GXdd58kjwpOzWUuyYtQSrWFggvqc8jlpE2ZmdRkprDsP2_arsuugeQkJ-f7HRK-onhP8IwxLr4443s9o5jwGc5L-6q4ppTVJRWcv362vypuU9rjPFpMuWBviysqBONZeV08_BzVYXffBROMmRJSU4QcFguG0cYPoLaA1GDRXCcYDKDgUAKLPqN9nhGVKxV1iH7YortOpd5bdBfBejOiZa9D51OP_IDWgwMz-iOg5WCDUdH60ad3xRunugS3j_Gm-P1t-WuxKjc_vq8X801pKtGMZdMQTIxlpHa41oYb5VoK3HFbO80qptpaa8xdI7Sg-YhVY3XTVq02dcOBs5tifeHaoPbyEH2v4r0MystzIsStVHH0pgMJzOHW5p8hFcvNOa8yShBoWweOtjSzvl5Yh0n3YA0MY1TdC-jLm8Hv5DYcZYMxozXJgE8XwO4_2Wq-kaccJiJ3J_h4qv342CyGPxOkUfY-Geg6NUCYkqS4FriiNW5yKb6UmhhSiuCe2ATLk13k2S7yZBd5tkuWfHj-lCfBP3Owv37huq8</recordid><startdate>20180608</startdate><enddate>20180608</enddate><creator>Rasigade, Jean-Philippe</creator><creator>Leclère, Amélie</creator><creator>Alla, François</creator><creator>Tessier, Adrien</creator><creator>Bes, Michèle</creator><creator>Lechiche, Catherine</creator><creator>Vernet-Garnier, Véronique</creator><creator>Laouénan, Cédric</creator><creator>Vandenesch, François</creator><creator>Leport, Catherine</creator><general>Frontiers</general><general>Frontiers Media S.A</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-3681-6314</orcidid><orcidid>https://orcid.org/0000-0001-9412-7106</orcidid></search><sort><creationdate>20180608</creationdate><title>Staphylococcus aureus CC30 Lineage and Absence of sed , j , r -Harboring Plasmid Predict Embolism in Infective Endocarditis</title><author>Rasigade, Jean-Philippe ; Leclère, Amélie ; Alla, François ; Tessier, Adrien ; Bes, Michèle ; Lechiche, Catherine ; Vernet-Garnier, Véronique ; Laouénan, Cédric ; Vandenesch, François ; Leport, Catherine</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-66101cd315f05bc8caf72e8f8d5fb343a75bb08f69b9243a0a6db6747bc568e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Bacteriology</topic><topic>CC30</topic><topic>enterotoxin</topic><topic>Immunology</topic><topic>infective endocarditis</topic><topic>Life Sciences</topic><topic>Microbiology</topic><topic>Microbiology and Parasitology</topic><topic>MRSA</topic><topic>S. aureus</topic><topic>stroke</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rasigade, Jean-Philippe</creatorcontrib><creatorcontrib>Leclère, Amélie</creatorcontrib><creatorcontrib>Alla, François</creatorcontrib><creatorcontrib>Tessier, Adrien</creatorcontrib><creatorcontrib>Bes, Michèle</creatorcontrib><creatorcontrib>Lechiche, Catherine</creatorcontrib><creatorcontrib>Vernet-Garnier, Véronique</creatorcontrib><creatorcontrib>Laouénan, Cédric</creatorcontrib><creatorcontrib>Vandenesch, François</creatorcontrib><creatorcontrib>Leport, Catherine</creatorcontrib><creatorcontrib>AEPEI Study Group</creatorcontrib><creatorcontrib>The AEPEI Study Group</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in cellular and infection microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rasigade, Jean-Philippe</au><au>Leclère, Amélie</au><au>Alla, François</au><au>Tessier, Adrien</au><au>Bes, Michèle</au><au>Lechiche, Catherine</au><au>Vernet-Garnier, Véronique</au><au>Laouénan, Cédric</au><au>Vandenesch, François</au><au>Leport, Catherine</au><aucorp>AEPEI Study Group</aucorp><aucorp>The AEPEI Study Group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Staphylococcus aureus CC30 Lineage and Absence of sed , j , r -Harboring Plasmid Predict Embolism in Infective Endocarditis</atitle><jtitle>Frontiers in cellular and infection microbiology</jtitle><addtitle>Front Cell Infect Microbiol</addtitle><date>2018-06-08</date><risdate>2018</risdate><volume>8</volume><spage>187</spage><epage>187</epage><pages>187-187</pages><issn>2235-2988</issn><eissn>2235-2988</eissn><abstract>induces severe infective endocarditis (IE) where embolic complications are a major cause of death. Risk factors for embolism have been reported such as a younger age or larger IE vegetations, while methicillin resistance conferred by the gene appeared as a protective factor. It is unclear, however, whether embolism is influenced by other characteristics such as clonal complex (CC) or virulence pattern. We examined clinical and microbiological predictors of embolism in a prospective multicentric cohort of 98 French patients with monomicrobial IE. The genomic contents of causative isolates were characterized using DNA array. To preserve statistical power, genotypic predictors were restricted to CC, secreted virulence factors and virulence regulators. Multivariate regularized logistic regression identified three independent predictors of embolism. Patients at higher risk were younger than the cohort median age of 62.5 y (adjusted odds ratio [OR] 0.14; 95% confidence interval [CI] 0.05-0.36). characteristics predicting embolism were a CC30 genetic background (adjusted OR 9.734; 95% CI 1.53-192.8) and the absence of pIB485-like plasmid-borne enterotoxin-encoding genes , and ( ; adjusted OR 0.07; 95% CI 0.004-0.457). CC30 has been repeatedly reported to exhibit enhanced fitness in bloodstream infections, which might impact its ability to cause embolism. -encoded enterotoxins, whose superantigenic activity is unlikely to protect against embolism, possibly acted as a proxy to others genes of the pIB485-like plasmid found in genetically unrelated isolates from mostly embolism-free patients. did not independently predict embolism but was strongly associated with . This - association might have driven previous reports of a negative association of and embolism. Collectively, our results suggest that the influence of genotypic features on the risk of embolism may be stronger than previously suspected and independent of clinical risk factors.</abstract><cop>Switzerland</cop><pub>Frontiers</pub><pmid>29938201</pmid><doi>10.3389/fcimb.2018.00187</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-3681-6314</orcidid><orcidid>https://orcid.org/0000-0001-9412-7106</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 2235-2988
ispartof Frontiers in cellular and infection microbiology, 2018-06, Vol.8, p.187-187
issn 2235-2988
2235-2988
language eng
recordid cdi_doaj_primary_oai_doaj_org_article_e3f07d201143496884db691e77fef272
source PubMed Central
subjects Bacteriology
CC30
enterotoxin
Immunology
infective endocarditis
Life Sciences
Microbiology
Microbiology and Parasitology
MRSA
S. aureus
stroke
Virology
title Staphylococcus aureus CC30 Lineage and Absence of sed , j , r -Harboring Plasmid Predict Embolism in Infective Endocarditis
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T21%3A01%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Staphylococcus%20aureus%20CC30%20Lineage%20and%20Absence%20of%20sed%20,%20j%20,%20r%20-Harboring%20Plasmid%20Predict%20Embolism%20in%20Infective%20Endocarditis&rft.jtitle=Frontiers%20in%20cellular%20and%20infection%20microbiology&rft.au=Rasigade,%20Jean-Philippe&rft.aucorp=AEPEI%20Study%20Group&rft.date=2018-06-08&rft.volume=8&rft.spage=187&rft.epage=187&rft.pages=187-187&rft.issn=2235-2988&rft.eissn=2235-2988&rft_id=info:doi/10.3389/fcimb.2018.00187&rft_dat=%3Cproquest_doaj_%3E2059042506%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c496t-66101cd315f05bc8caf72e8f8d5fb343a75bb08f69b9243a0a6db6747bc568e83%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2059042506&rft_id=info:pmid/29938201&rfr_iscdi=true