Genome-wide association study of hemolytic uremic syndrome causing Shiga toxin-producing Escherichia coli from Sweden, 1994–2018

Shiga toxin-producing Esc herichia coli (STEC) infection can cause clinical manifestations ranging from diarrhea to potentially fatal hemolytic uremic syndrome (HUS). This study is aimed at identifying STEC genetic factors associated with the development of HUS in Sweden. A total of 238 STEC genomes...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:European journal of clinical microbiology & infectious diseases 2023-06, Vol.42 (6), p.771-779
Hauptverfasser: Matussek, Andreas, Mernelius, Sara, Chromek, Milan, Zhang, Ji, Frykman, Anne, Hansson, Sverker, Georgieva, Valya, Xiong, Yanwen, Bai, Xiangning
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 779
container_issue 6
container_start_page 771
container_title European journal of clinical microbiology & infectious diseases
container_volume 42
creator Matussek, Andreas
Mernelius, Sara
Chromek, Milan
Zhang, Ji
Frykman, Anne
Hansson, Sverker
Georgieva, Valya
Xiong, Yanwen
Bai, Xiangning
description Shiga toxin-producing Esc herichia coli (STEC) infection can cause clinical manifestations ranging from diarrhea to potentially fatal hemolytic uremic syndrome (HUS). This study is aimed at identifying STEC genetic factors associated with the development of HUS in Sweden. A total of 238 STEC genomes from STEC-infected patients with and without HUS between 1994 and 2018 in Sweden were included in this study. Serotypes, Shiga toxin gene ( stx ) subtypes, and virulence genes were characterized in correlation to clinical symptoms (HUS and non-HUS), and pan-genome wide association study was performed. Sixty-five strains belonged to O157:H7, and 173 belonged to non-O157 serotypes. Our study revealed that strains of O157:H7 serotype especially clade 8 were most commonly found in patients with HUS in Sweden. stx2a and stx2a  +  stx2c subtypes were significantly associated with HUS. Other virulence factors associated with HUS mainly included intimin ( eae ) and its receptor ( tir ), adhesion factors, toxins, and secretion system proteins. Pangenome wide-association study identified numbers of accessory genes significantly overrepresented in HUS-STEC strains, including genes encoding outer membrane proteins, transcriptional regulators, phage-related proteins, and numerous genes related to hypothetical proteins. Whole-genome phylogeny and multiple correspondence analysis of pangenomes could not differentiate HUS-STEC from non-HUS-STEC strains. In O157:H7 cluster, strains from HUS patients clustered closely; however, no significant difference in virulence genes was found in O157 strains from patients with and without HUS. These results suggest that STEC strains from different phylogenetic backgrounds may independently acquire genes determining their pathogenicity and confirm that other non-bacterial factors and/or bacteria-host interaction may affect STEC pathogenesis.
doi_str_mv 10.1007/s10096-023-04600-1
format Article
fullrecord <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_446264</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2806994691</sourcerecordid><originalsourceid>FETCH-LOGICAL-c614t-b9fccaeb0712b24ac4064a1b92400d67ae907894eaf9b409440f12207c6251863</originalsourceid><addsrcrecordid>eNp9ksFu1DAQhiMEotuFF-CALHHh0IDteO34hKpSClIlDgWuluM4WZfEXuyYZW-IV-ANeRJm2W2hHPYQ25r5_plx_BfFE4JfEIzFywSr5CWmVYkZx7gk94oZYdWiZJWo7hczLCtWSkGro-I4pWsMolqIh8VRJQiGj8-KHxfWh9GWa9dapFMKxunJBY_SlNsNCh1a2jEMm8kZlKMdYUsb30bQIKNzcr5HV0vXazSFb86XqxjabLbR82SWNjqzdBqZMDjUgQhdrW1r_QkiUrJf339STOpHxYNOD8k-3u_z4uOb8w9nb8vL9xfvzk4vS8MJm8pGdsZo22BBaEOZNgxzpkkjKcO45UJbCdeTzOpONgxLxnBHKMXCcLogNa_mRbmrm9Z2lRu1im7UcaOCdmof-gwnqxjjlLODfJ9XCkJ93vIV5YKTg_xr9-lUhdirwWVFZLUQEvhXOx7g0bbG-inq4Y7sbsa7perDV0UwEZTWAiqgXQUTXZqcVz5EDel6QWEVMBcgz_dNYviSbZrU6JKxw6C9DTkpWmMOT8Hldv5n_6HXIUcPTwIUIYKzGqw0L-hNz5BStN3twASrrS3VzpYKbKn-2FJtSz_996q3khsfAlDt_x2kfG_j394Hyv4GzynugA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2811764872</pqid></control><display><type>article</type><title>Genome-wide association study of hemolytic uremic syndrome causing Shiga toxin-producing Escherichia coli from Sweden, 1994–2018</title><source>MEDLINE</source><source>NORA - Norwegian Open Research Archives</source><source>SWEPUB Freely available online</source><source>SpringerLink Journals - AutoHoldings</source><creator>Matussek, Andreas ; Mernelius, Sara ; Chromek, Milan ; Zhang, Ji ; Frykman, Anne ; Hansson, Sverker ; Georgieva, Valya ; Xiong, Yanwen ; Bai, Xiangning</creator><creatorcontrib>Matussek, Andreas ; Mernelius, Sara ; Chromek, Milan ; Zhang, Ji ; Frykman, Anne ; Hansson, Sverker ; Georgieva, Valya ; Xiong, Yanwen ; Bai, Xiangning</creatorcontrib><description>Shiga toxin-producing Esc herichia coli (STEC) infection can cause clinical manifestations ranging from diarrhea to potentially fatal hemolytic uremic syndrome (HUS). This study is aimed at identifying STEC genetic factors associated with the development of HUS in Sweden. A total of 238 STEC genomes from STEC-infected patients with and without HUS between 1994 and 2018 in Sweden were included in this study. Serotypes, Shiga toxin gene ( stx ) subtypes, and virulence genes were characterized in correlation to clinical symptoms (HUS and non-HUS), and pan-genome wide association study was performed. Sixty-five strains belonged to O157:H7, and 173 belonged to non-O157 serotypes. Our study revealed that strains of O157:H7 serotype especially clade 8 were most commonly found in patients with HUS in Sweden. stx2a and stx2a  +  stx2c subtypes were significantly associated with HUS. Other virulence factors associated with HUS mainly included intimin ( eae ) and its receptor ( tir ), adhesion factors, toxins, and secretion system proteins. Pangenome wide-association study identified numbers of accessory genes significantly overrepresented in HUS-STEC strains, including genes encoding outer membrane proteins, transcriptional regulators, phage-related proteins, and numerous genes related to hypothetical proteins. Whole-genome phylogeny and multiple correspondence analysis of pangenomes could not differentiate HUS-STEC from non-HUS-STEC strains. In O157:H7 cluster, strains from HUS patients clustered closely; however, no significant difference in virulence genes was found in O157 strains from patients with and without HUS. These results suggest that STEC strains from different phylogenetic backgrounds may independently acquire genes determining their pathogenicity and confirm that other non-bacterial factors and/or bacteria-host interaction may affect STEC pathogenesis.</description><identifier>ISSN: 0934-9723</identifier><identifier>ISSN: 1435-4373</identifier><identifier>EISSN: 1435-4373</identifier><identifier>DOI: 10.1007/s10096-023-04600-1</identifier><identifier>PMID: 37103716</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Bacteria ; Biomedical and Life Sciences ; Biomedicine ; Diarrhea ; E coli ; Escherichia coli ; Escherichia coli Infections - complications ; Escherichia coli Infections - epidemiology ; Escherichia coli Infections - microbiology ; Escherichia coli Proteins - genetics ; Genes ; Genetic factors ; Genome-wide association studies ; Genome-Wide Association Study ; Genomes ; Hemolytic uremic syndrome ; Hemolytic-Uremic Syndrome - epidemiology ; Hemolytic-Uremic Syndrome - microbiology ; Humans ; Infectious Medicine ; Infektionsmedicin ; Internal Medicine ; Intimin ; Medical Microbiology ; Membrane proteins ; Original ; Original Article ; Outer membrane proteins ; Pathogenesis ; Pathogenicity ; Pathogens ; Phages ; Phylogeny ; Proteins ; Serotypes ; Shiga toxin ; Shiga toxin-producing Escherichia coli ; Shiga-Toxigenic Escherichia coli ; Strains (organisms) ; Sweden - epidemiology ; Toxins ; Virulence ; Virulence factors ; Whole genome sequencing</subject><ispartof>European journal of clinical microbiology &amp; infectious diseases, 2023-06, Vol.42 (6), p.771-779</ispartof><rights>The Author(s) 2023</rights><rights>2023. The Author(s).</rights><rights>The Author(s) 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>info:eu-repo/semantics/openAccess</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c614t-b9fccaeb0712b24ac4064a1b92400d67ae907894eaf9b409440f12207c6251863</citedby><cites>FETCH-LOGICAL-c614t-b9fccaeb0712b24ac4064a1b92400d67ae907894eaf9b409440f12207c6251863</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10096-023-04600-1$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10096-023-04600-1$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,552,780,784,885,26566,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37103716$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-193579$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/326761$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:152482931$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Matussek, Andreas</creatorcontrib><creatorcontrib>Mernelius, Sara</creatorcontrib><creatorcontrib>Chromek, Milan</creatorcontrib><creatorcontrib>Zhang, Ji</creatorcontrib><creatorcontrib>Frykman, Anne</creatorcontrib><creatorcontrib>Hansson, Sverker</creatorcontrib><creatorcontrib>Georgieva, Valya</creatorcontrib><creatorcontrib>Xiong, Yanwen</creatorcontrib><creatorcontrib>Bai, Xiangning</creatorcontrib><title>Genome-wide association study of hemolytic uremic syndrome causing Shiga toxin-producing Escherichia coli from Sweden, 1994–2018</title><title>European journal of clinical microbiology &amp; infectious diseases</title><addtitle>Eur J Clin Microbiol Infect Dis</addtitle><addtitle>Eur J Clin Microbiol Infect Dis</addtitle><description>Shiga toxin-producing Esc herichia coli (STEC) infection can cause clinical manifestations ranging from diarrhea to potentially fatal hemolytic uremic syndrome (HUS). This study is aimed at identifying STEC genetic factors associated with the development of HUS in Sweden. A total of 238 STEC genomes from STEC-infected patients with and without HUS between 1994 and 2018 in Sweden were included in this study. Serotypes, Shiga toxin gene ( stx ) subtypes, and virulence genes were characterized in correlation to clinical symptoms (HUS and non-HUS), and pan-genome wide association study was performed. Sixty-five strains belonged to O157:H7, and 173 belonged to non-O157 serotypes. Our study revealed that strains of O157:H7 serotype especially clade 8 were most commonly found in patients with HUS in Sweden. stx2a and stx2a  +  stx2c subtypes were significantly associated with HUS. Other virulence factors associated with HUS mainly included intimin ( eae ) and its receptor ( tir ), adhesion factors, toxins, and secretion system proteins. Pangenome wide-association study identified numbers of accessory genes significantly overrepresented in HUS-STEC strains, including genes encoding outer membrane proteins, transcriptional regulators, phage-related proteins, and numerous genes related to hypothetical proteins. Whole-genome phylogeny and multiple correspondence analysis of pangenomes could not differentiate HUS-STEC from non-HUS-STEC strains. In O157:H7 cluster, strains from HUS patients clustered closely; however, no significant difference in virulence genes was found in O157 strains from patients with and without HUS. These results suggest that STEC strains from different phylogenetic backgrounds may independently acquire genes determining their pathogenicity and confirm that other non-bacterial factors and/or bacteria-host interaction may affect STEC pathogenesis.</description><subject>Bacteria</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Diarrhea</subject><subject>E coli</subject><subject>Escherichia coli</subject><subject>Escherichia coli Infections - complications</subject><subject>Escherichia coli Infections - epidemiology</subject><subject>Escherichia coli Infections - microbiology</subject><subject>Escherichia coli Proteins - genetics</subject><subject>Genes</subject><subject>Genetic factors</subject><subject>Genome-wide association studies</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Hemolytic uremic syndrome</subject><subject>Hemolytic-Uremic Syndrome - epidemiology</subject><subject>Hemolytic-Uremic Syndrome - microbiology</subject><subject>Humans</subject><subject>Infectious Medicine</subject><subject>Infektionsmedicin</subject><subject>Internal Medicine</subject><subject>Intimin</subject><subject>Medical Microbiology</subject><subject>Membrane proteins</subject><subject>Original</subject><subject>Original Article</subject><subject>Outer membrane proteins</subject><subject>Pathogenesis</subject><subject>Pathogenicity</subject><subject>Pathogens</subject><subject>Phages</subject><subject>Phylogeny</subject><subject>Proteins</subject><subject>Serotypes</subject><subject>Shiga toxin</subject><subject>Shiga toxin-producing Escherichia coli</subject><subject>Shiga-Toxigenic Escherichia coli</subject><subject>Strains (organisms)</subject><subject>Sweden - epidemiology</subject><subject>Toxins</subject><subject>Virulence</subject><subject>Virulence factors</subject><subject>Whole genome sequencing</subject><issn>0934-9723</issn><issn>1435-4373</issn><issn>1435-4373</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>3HK</sourceid><sourceid>D8T</sourceid><recordid>eNp9ksFu1DAQhiMEotuFF-CALHHh0IDteO34hKpSClIlDgWuluM4WZfEXuyYZW-IV-ANeRJm2W2hHPYQ25r5_plx_BfFE4JfEIzFywSr5CWmVYkZx7gk94oZYdWiZJWo7hczLCtWSkGro-I4pWsMolqIh8VRJQiGj8-KHxfWh9GWa9dapFMKxunJBY_SlNsNCh1a2jEMm8kZlKMdYUsb30bQIKNzcr5HV0vXazSFb86XqxjabLbR82SWNjqzdBqZMDjUgQhdrW1r_QkiUrJf339STOpHxYNOD8k-3u_z4uOb8w9nb8vL9xfvzk4vS8MJm8pGdsZo22BBaEOZNgxzpkkjKcO45UJbCdeTzOpONgxLxnBHKMXCcLogNa_mRbmrm9Z2lRu1im7UcaOCdmof-gwnqxjjlLODfJ9XCkJ93vIV5YKTg_xr9-lUhdirwWVFZLUQEvhXOx7g0bbG-inq4Y7sbsa7perDV0UwEZTWAiqgXQUTXZqcVz5EDel6QWEVMBcgz_dNYviSbZrU6JKxw6C9DTkpWmMOT8Hldv5n_6HXIUcPTwIUIYKzGqw0L-hNz5BStN3twASrrS3VzpYKbKn-2FJtSz_996q3khsfAlDt_x2kfG_j394Hyv4GzynugA</recordid><startdate>20230601</startdate><enddate>20230601</enddate><creator>Matussek, Andreas</creator><creator>Mernelius, Sara</creator><creator>Chromek, Milan</creator><creator>Zhang, Ji</creator><creator>Frykman, Anne</creator><creator>Hansson, Sverker</creator><creator>Georgieva, Valya</creator><creator>Xiong, Yanwen</creator><creator>Bai, Xiangning</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>3HK</scope><scope>5PM</scope><scope>ABXSW</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>DG8</scope><scope>ZZAVC</scope><scope>F1U</scope></search><sort><creationdate>20230601</creationdate><title>Genome-wide association study of hemolytic uremic syndrome causing Shiga toxin-producing Escherichia coli from Sweden, 1994–2018</title><author>Matussek, Andreas ; Mernelius, Sara ; Chromek, Milan ; Zhang, Ji ; Frykman, Anne ; Hansson, Sverker ; Georgieva, Valya ; Xiong, Yanwen ; Bai, Xiangning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c614t-b9fccaeb0712b24ac4064a1b92400d67ae907894eaf9b409440f12207c6251863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Bacteria</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Diarrhea</topic><topic>E coli</topic><topic>Escherichia coli</topic><topic>Escherichia coli Infections - complications</topic><topic>Escherichia coli Infections - epidemiology</topic><topic>Escherichia coli Infections - microbiology</topic><topic>Escherichia coli Proteins - genetics</topic><topic>Genes</topic><topic>Genetic factors</topic><topic>Genome-wide association studies</topic><topic>Genome-Wide Association Study</topic><topic>Genomes</topic><topic>Hemolytic uremic syndrome</topic><topic>Hemolytic-Uremic Syndrome - epidemiology</topic><topic>Hemolytic-Uremic Syndrome - microbiology</topic><topic>Humans</topic><topic>Infectious Medicine</topic><topic>Infektionsmedicin</topic><topic>Internal Medicine</topic><topic>Intimin</topic><topic>Medical Microbiology</topic><topic>Membrane proteins</topic><topic>Original</topic><topic>Original Article</topic><topic>Outer membrane proteins</topic><topic>Pathogenesis</topic><topic>Pathogenicity</topic><topic>Pathogens</topic><topic>Phages</topic><topic>Phylogeny</topic><topic>Proteins</topic><topic>Serotypes</topic><topic>Shiga toxin</topic><topic>Shiga toxin-producing Escherichia coli</topic><topic>Shiga-Toxigenic Escherichia coli</topic><topic>Strains (organisms)</topic><topic>Sweden - epidemiology</topic><topic>Toxins</topic><topic>Virulence</topic><topic>Virulence factors</topic><topic>Whole genome sequencing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matussek, Andreas</creatorcontrib><creatorcontrib>Mernelius, Sara</creatorcontrib><creatorcontrib>Chromek, Milan</creatorcontrib><creatorcontrib>Zhang, Ji</creatorcontrib><creatorcontrib>Frykman, Anne</creatorcontrib><creatorcontrib>Hansson, Sverker</creatorcontrib><creatorcontrib>Georgieva, Valya</creatorcontrib><creatorcontrib>Xiong, Yanwen</creatorcontrib><creatorcontrib>Bai, Xiangning</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>NORA - Norwegian Open Research Archives</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SWEPUB Linköpings universitet full text</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Linköpings universitet</collection><collection>SwePub Articles full text</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>European journal of clinical microbiology &amp; infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matussek, Andreas</au><au>Mernelius, Sara</au><au>Chromek, Milan</au><au>Zhang, Ji</au><au>Frykman, Anne</au><au>Hansson, Sverker</au><au>Georgieva, Valya</au><au>Xiong, Yanwen</au><au>Bai, Xiangning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome-wide association study of hemolytic uremic syndrome causing Shiga toxin-producing Escherichia coli from Sweden, 1994–2018</atitle><jtitle>European journal of clinical microbiology &amp; infectious diseases</jtitle><stitle>Eur J Clin Microbiol Infect Dis</stitle><addtitle>Eur J Clin Microbiol Infect Dis</addtitle><date>2023-06-01</date><risdate>2023</risdate><volume>42</volume><issue>6</issue><spage>771</spage><epage>779</epage><pages>771-779</pages><issn>0934-9723</issn><issn>1435-4373</issn><eissn>1435-4373</eissn><abstract>Shiga toxin-producing Esc herichia coli (STEC) infection can cause clinical manifestations ranging from diarrhea to potentially fatal hemolytic uremic syndrome (HUS). This study is aimed at identifying STEC genetic factors associated with the development of HUS in Sweden. A total of 238 STEC genomes from STEC-infected patients with and without HUS between 1994 and 2018 in Sweden were included in this study. Serotypes, Shiga toxin gene ( stx ) subtypes, and virulence genes were characterized in correlation to clinical symptoms (HUS and non-HUS), and pan-genome wide association study was performed. Sixty-five strains belonged to O157:H7, and 173 belonged to non-O157 serotypes. Our study revealed that strains of O157:H7 serotype especially clade 8 were most commonly found in patients with HUS in Sweden. stx2a and stx2a  +  stx2c subtypes were significantly associated with HUS. Other virulence factors associated with HUS mainly included intimin ( eae ) and its receptor ( tir ), adhesion factors, toxins, and secretion system proteins. Pangenome wide-association study identified numbers of accessory genes significantly overrepresented in HUS-STEC strains, including genes encoding outer membrane proteins, transcriptional regulators, phage-related proteins, and numerous genes related to hypothetical proteins. Whole-genome phylogeny and multiple correspondence analysis of pangenomes could not differentiate HUS-STEC from non-HUS-STEC strains. In O157:H7 cluster, strains from HUS patients clustered closely; however, no significant difference in virulence genes was found in O157 strains from patients with and without HUS. These results suggest that STEC strains from different phylogenetic backgrounds may independently acquire genes determining their pathogenicity and confirm that other non-bacterial factors and/or bacteria-host interaction may affect STEC pathogenesis.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>37103716</pmid><doi>10.1007/s10096-023-04600-1</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0934-9723
ispartof European journal of clinical microbiology & infectious diseases, 2023-06, Vol.42 (6), p.771-779
issn 0934-9723
1435-4373
1435-4373
language eng
recordid cdi_swepub_primary_oai_swepub_ki_se_446264
source MEDLINE; NORA - Norwegian Open Research Archives; SWEPUB Freely available online; SpringerLink Journals - AutoHoldings
subjects Bacteria
Biomedical and Life Sciences
Biomedicine
Diarrhea
E coli
Escherichia coli
Escherichia coli Infections - complications
Escherichia coli Infections - epidemiology
Escherichia coli Infections - microbiology
Escherichia coli Proteins - genetics
Genes
Genetic factors
Genome-wide association studies
Genome-Wide Association Study
Genomes
Hemolytic uremic syndrome
Hemolytic-Uremic Syndrome - epidemiology
Hemolytic-Uremic Syndrome - microbiology
Humans
Infectious Medicine
Infektionsmedicin
Internal Medicine
Intimin
Medical Microbiology
Membrane proteins
Original
Original Article
Outer membrane proteins
Pathogenesis
Pathogenicity
Pathogens
Phages
Phylogeny
Proteins
Serotypes
Shiga toxin
Shiga toxin-producing Escherichia coli
Shiga-Toxigenic Escherichia coli
Strains (organisms)
Sweden - epidemiology
Toxins
Virulence
Virulence factors
Whole genome sequencing
title Genome-wide association study of hemolytic uremic syndrome causing Shiga toxin-producing Escherichia coli from Sweden, 1994–2018
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-12T02%3A04%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Genome-wide%20association%20study%20of%20hemolytic%20uremic%20syndrome%20causing%20Shiga%20toxin-producing%20Escherichia%20coli%20from%20Sweden,%201994%E2%80%932018&rft.jtitle=European%20journal%20of%20clinical%20microbiology%20&%20infectious%20diseases&rft.au=Matussek,%20Andreas&rft.date=2023-06-01&rft.volume=42&rft.issue=6&rft.spage=771&rft.epage=779&rft.pages=771-779&rft.issn=0934-9723&rft.eissn=1435-4373&rft_id=info:doi/10.1007/s10096-023-04600-1&rft_dat=%3Cproquest_swepu%3E2806994691%3C/proquest_swepu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2811764872&rft_id=info:pmid/37103716&rfr_iscdi=true