A mouse model of dual infection with influenza virus and Streptococcus pneumoniae
Identifieur interne : 001342 ( Istex/Corpus ); précédent : 001341; suivant : 001343A mouse model of dual infection with influenza virus and Streptococcus pneumoniae
Auteurs : Jonathan A. Mccullers ; Robert G. WebsterSource :
- International congress series [ 0531-5131 ] ; 2001.
English descriptors
- Teeft :
- Additive process, Bacteremic, Blood cultures, Chinchilla model, Clinical illness, Congress series, Difco laboratories, Dos, Dual infection, Elsevier science, Excess mortality, Further study, Infection, Infectious agent, Infectious diseases, Infectious doses, Influenza, Influenza epidemics, Influenza virus, Influenza virus infection, Jude research hospital, Lauderdale street, Lethal synergism, Lethal synergy, Mice sequentially, Mock infection, Morbidity, Mouse, Mouse model, Otitis media, Overwhelming sepsis, Pathogenic mechanisms, Pneumococcal, Pneumococcal challenge, Pneumococcal infection, Pneumococcus, Pneumoniae, Pneumoniae strain, Sepsis, Sequential, Sequential infection, Sequentially, Sheep erythrocytes, Small animal model, Synergism, Synergistic, Synergistic interaction, Synergistic lethality, Weight loss.
Abstract
Abstract: Background: A lethal synergism exists between influenza virus and Streptococcus pneumoniae accounting for excess mortality during influenza epidemics. A small animal model of dual infection with these organisms would be useful for study of pathogenic mechanisms underlying this interaction. Methods: Groups of mice were infected with either mouse adapted influenza virus A/Puerto Rico/8/34 (H1N1), S. pneumoniae strain D39, both simultaneously, or pneumococcus following influenza virus. Weight loss, as a measure of morbidity, and mortality were followed. Blood cultures were collected 24 h after infection. Results: Mice infected simultaneously with both influenza virus and pneumococcus exhibited gradual weight loss and mortality commensurate with expectations for an additive process. In contrast, mice infected with pneumococcus 7 days following infection with influenza virus uniformly died in less than 24 h and were highly bacteremic. Discussion: A mouse model of sequential infection with influenza virus and S. pneumoniae has been developed. Mice infected with pneumococcus seven days after infection with influenza virus exhibit a synergistic lethality caused by overwhelming sepsis. This model will be useful for study of the mechanisms involved in pathogenic interactions between influenza virus and pneumococcus.
Url:
DOI: 10.1016/S0531-5131(01)00631-8
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ISTEX:009A5F10ABF1E6723029F6FB0CBCBF76C1D78CB9Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>A mouse model of dual infection with influenza virus and Streptococcus pneumoniae</title><author><name sortKey="Mccullers, Jonathan A" sort="Mccullers, Jonathan A" uniqKey="Mccullers J" first="Jonathan A" last="Mccullers">Jonathan A. Mccullers</name><affiliation><mods:affiliation>E-mail: jon.mccullers@stjude.org</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Infectious Diseases, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Webster, Robert G" sort="Webster, Robert G" uniqKey="Webster R" first="Robert G" last="Webster">Robert G. Webster</name><affiliation><mods:affiliation>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:009A5F10ABF1E6723029F6FB0CBCBF76C1D78CB9</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1016/S0531-5131(01)00631-8</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-X0VH0QCR-0/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001342</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001342</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">A mouse model of dual infection with influenza virus and Streptococcus pneumoniae</title><author><name sortKey="Mccullers, Jonathan A" sort="Mccullers, Jonathan A" uniqKey="Mccullers J" first="Jonathan A" last="Mccullers">Jonathan A. Mccullers</name><affiliation><mods:affiliation>E-mail: jon.mccullers@stjude.org</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Infectious Diseases, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</mods:affiliation></affiliation></author><author><name sortKey="Webster, Robert G" sort="Webster, Robert G" uniqKey="Webster R" first="Robert G" last="Webster">Robert G. Webster</name><affiliation><mods:affiliation>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">International congress series</title><title level="j" type="abbrev">ICS</title><idno type="ISSN">0531-5131</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">1219</biblScope><biblScope unit="supplement">C</biblScope><biblScope unit="page" from="601">601</biblScope><biblScope unit="page" to="607">607</biblScope></imprint><idno type="ISSN">0531-5131</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0531-5131</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Additive process</term><term>Bacteremic</term><term>Blood cultures</term><term>Chinchilla model</term><term>Clinical illness</term><term>Congress series</term><term>Difco laboratories</term><term>Dos</term><term>Dual infection</term><term>Elsevier science</term><term>Excess mortality</term><term>Further study</term><term>Infection</term><term>Infectious agent</term><term>Infectious diseases</term><term>Infectious doses</term><term>Influenza</term><term>Influenza epidemics</term><term>Influenza virus</term><term>Influenza virus infection</term><term>Jude research hospital</term><term>Lauderdale street</term><term>Lethal synergism</term><term>Lethal synergy</term><term>Mice sequentially</term><term>Mock infection</term><term>Morbidity</term><term>Mouse</term><term>Mouse model</term><term>Otitis media</term><term>Overwhelming sepsis</term><term>Pathogenic mechanisms</term><term>Pneumococcal</term><term>Pneumococcal challenge</term><term>Pneumococcal infection</term><term>Pneumococcus</term><term>Pneumoniae</term><term>Pneumoniae strain</term><term>Sepsis</term><term>Sequential</term><term>Sequential infection</term><term>Sequentially</term><term>Sheep erythrocytes</term><term>Small animal model</term><term>Synergism</term><term>Synergistic</term><term>Synergistic interaction</term><term>Synergistic lethality</term><term>Weight loss</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Background: A lethal synergism exists between influenza virus and Streptococcus pneumoniae accounting for excess mortality during influenza epidemics. A small animal model of dual infection with these organisms would be useful for study of pathogenic mechanisms underlying this interaction. Methods: Groups of mice were infected with either mouse adapted influenza virus A/Puerto Rico/8/34 (H1N1), S. pneumoniae strain D39, both simultaneously, or pneumococcus following influenza virus. Weight loss, as a measure of morbidity, and mortality were followed. Blood cultures were collected 24 h after infection. Results: Mice infected simultaneously with both influenza virus and pneumococcus exhibited gradual weight loss and mortality commensurate with expectations for an additive process. In contrast, mice infected with pneumococcus 7 days following infection with influenza virus uniformly died in less than 24 h and were highly bacteremic. Discussion: A mouse model of sequential infection with influenza virus and S. pneumoniae has been developed. Mice infected with pneumococcus seven days after infection with influenza virus exhibit a synergistic lethality caused by overwhelming sepsis. This model will be useful for study of the mechanisms involved in pathogenic interactions between influenza virus and pneumococcus.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>pneumococcus</json:string><json:string>influenza virus</json:string><json:string>influenza</json:string><json:string>pneumoniae</json:string><json:string>sepsis</json:string><json:string>pneumococcal</json:string><json:string>influenza virus infection</json:string><json:string>congress series</json:string><json:string>morbidity</json:string><json:string>weight loss</json:string><json:string>jude research hospital</json:string><json:string>blood cultures</json:string><json:string>sequential</json:string><json:string>sequential infection</json:string><json:string>sequentially</json:string><json:string>influenza epidemics</json:string><json:string>excess mortality</json:string><json:string>bacteremic</json:string><json:string>lethal synergism</json:string><json:string>pneumococcal infection</json:string><json:string>synergism</json:string><json:string>pathogenic mechanisms</json:string><json:string>clinical illness</json:string><json:string>mouse model</json:string><json:string>pneumoniae strain</json:string><json:string>dual infection</json:string><json:string>additive process</json:string><json:string>overwhelming sepsis</json:string><json:string>mice sequentially</json:string><json:string>infectious diseases</json:string><json:string>lethal synergy</json:string><json:string>infectious agent</json:string><json:string>synergistic</json:string><json:string>dos</json:string><json:string>infection</json:string><json:string>mouse</json:string><json:string>elsevier science</json:string><json:string>difco laboratories</json:string><json:string>further study</json:string><json:string>chinchilla model</json:string><json:string>otitis media</json:string><json:string>synergistic interaction</json:string><json:string>sheep erythrocytes</json:string><json:string>pneumococcal challenge</json:string><json:string>synergistic lethality</json:string><json:string>mock infection</json:string><json:string>small animal model</json:string><json:string>lauderdale street</json:string><json:string>infectious doses</json:string></teeft></keywords><author><json:item><name>Jonathan A McCullers</name><affiliations><json:string>E-mail: jon.mccullers@stjude.org</json:string><json:string>Department of Infectious Diseases, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</json:string></affiliations></json:item><json:item><name>Robert G Webster</name><affiliations><json:string>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Sepsis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Pneumonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Bacteria</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Mortality</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Synergism</value></json:item></subject><arkIstex>ark:/67375/6H6-X0VH0QCR-0</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Background: A lethal synergism exists between influenza virus and Streptococcus pneumoniae accounting for excess mortality during influenza epidemics. A small animal model of dual infection with these organisms would be useful for study of pathogenic mechanisms underlying this interaction. Methods: Groups of mice were infected with either mouse adapted influenza virus A/Puerto Rico/8/34 (H1N1), S. pneumoniae strain D39, both simultaneously, or pneumococcus following influenza virus. Weight loss, as a measure of morbidity, and mortality were followed. Blood cultures were collected 24 h after infection. Results: Mice infected simultaneously with both influenza virus and pneumococcus exhibited gradual weight loss and mortality commensurate with expectations for an additive process. In contrast, mice infected with pneumococcus 7 days following infection with influenza virus uniformly died in less than 24 h and were highly bacteremic. Discussion: A mouse model of sequential infection with influenza virus and S. pneumoniae has been developed. Mice infected with pneumococcus seven days after infection with influenza virus exhibit a synergistic lethality caused by overwhelming sepsis. This model will be useful for study of the mechanisms involved in pathogenic interactions between influenza virus and pneumococcus.</abstract><qualityIndicators><score>6.3</score><pdfWordCount>2068</pdfWordCount><pdfCharCount>12938</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>544 x 743 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>186</abstractWordCount><abstractCharCount>1337</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>A mouse model of dual infection with influenza virus and Streptococcus pneumoniae</title><pii><json:string>S0531-5131(01)00631-8</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>International congress series</title><language><json:string>unknown</json:string></language><publicationDate>2001</publicationDate><issn><json:string>0531-5131</json:string></issn><pii><json:string>S0531-5131(00)X0003-9</json:string></pii><volume>1219</volume><pages><first>601</first><last>607</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2001</json:string><json:string>1918</json:string><json:string>3000</json:string></date><geogName></geogName><orgName><json:string>ALSAC</json:string><json:string>Jackson Laboratory, Bar Harbor, ME</json:string><json:string>Animal Resource Center</json:string><json:string>Jude Children’s Research Hospital</json:string><json:string>American Lebanese Syrian Associated Charities</json:string><json:string>Difco Laboratories, Detroit</json:string><json:string>National Institute of Allergy and Infectious Diseases</json:string><json:string>Cancer Center Support</json:string><json:string>Difco Laboratories</json:string><json:string>Jude Children’s Research Hospital, Memphis, TN</json:string><json:string>International Congress Series</json:string><json:string>CORE</json:string><json:string>Department of Virology and Molecular Biology</json:string><json:string>Wampole Laboratories</json:string><json:string>Department of Infectious Diseases, St</json:string><json:string>Public Health</json:string></orgName><orgName_funder><json:string>Public Health</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>A. McCullers</json:string><json:string>Robert G. Websterb</json:string><json:string>Elaine Tuomanen</json:string><json:string>J.A. McCullers</json:string><json:string>Madison Avenue</json:string><json:string>R.G. Webster</json:string></persName><placeName><json:string>Cranbury</json:string><json:string>Puerto Rico</json:string><json:string>USA</json:string><json:string>TN</json:string><json:string>NJ</json:string><json:string>Memphis</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[4]</json:string><json:string>Department of Pathology, University of Tennessee, Memphis, 8000</json:string><json:string>[6]</json:string><json:string>[8]</json:string><json:string>[3]</json:string><json:string>[5]</json:string><json:string>[7]</json:string><json:string>[1,2]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-X0VH0QCR-0</json:string></ark><categories><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1016/S0531-5131(01)00631-8</json:string></doi><id>009A5F10ABF1E6723029F6FB0CBCBF76C1D78CB9</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-X0VH0QCR-0/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-X0VH0QCR-0/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-X0VH0QCR-0/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">A mouse model of dual infection with influenza virus and Streptococcus pneumoniae</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©2001 Elsevier Science B.V.</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>2001</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Fig. 1: Groups of mice were weighed daily after infection with either S. pneumoniae strain D39, influenza virus A/PR/8/34, both, or diluent as a control at day 0. Error bars represent the standard deviation between groups of four mice.</note><note type="content">Fig. 2: Mice were infected with either S. pneumoniae strain D39, influenza virus A/PR/8/34 and pneumococcus simultaneously, or influenza virus followed 7 days later by pneumococcus. Blood cultures were collected 24 h after infection with pneumococcus and quantitated. Titers beyond the limits of the assay are expressed as either >7 if greater than 1×107 CFU/ml or <2 if less than 100 CFU/ml.</note><note type="content">Table 1: Infection with pneumococcus following influenza is lethal in mice</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">A mouse model of dual infection with influenza virus and Streptococcus pneumoniae</title><author xml:id="author-0000"><persName><forename type="first">Jonathan A</forename><surname>McCullers</surname></persName><email>jon.mccullers@stjude.org</email><note type="correspondence"><p>Corresponding author. Tel.: +1-901-495-3486; fax: +1-901-495-3099</p></note><affiliation>Department of Infectious Diseases, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Robert G</forename><surname>Webster</surname></persName><affiliation>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</affiliation></author><idno type="istex">009A5F10ABF1E6723029F6FB0CBCBF76C1D78CB9</idno><idno type="ark">ark:/67375/6H6-X0VH0QCR-0</idno><idno type="DOI">10.1016/S0531-5131(01)00631-8</idno><idno type="PII">S0531-5131(01)00631-8</idno></analytic><monogr><title level="j">International congress series</title><title level="j" type="abbrev">ICS</title><idno type="pISSN">0531-5131</idno><idno type="PII">S0531-5131(00)X0003-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">1219</biblScope><biblScope unit="supplement">C</biblScope><biblScope unit="page" from="601">601</biblScope><biblScope unit="page" to="607">607</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Background: A lethal synergism exists between influenza virus and Streptococcus pneumoniae accounting for excess mortality during influenza epidemics. A small animal model of dual infection with these organisms would be useful for study of pathogenic mechanisms underlying this interaction. Methods: Groups of mice were infected with either mouse adapted influenza virus A/Puerto Rico/8/34 (H1N1), S. pneumoniae strain D39, both simultaneously, or pneumococcus following influenza virus. Weight loss, as a measure of morbidity, and mortality were followed. Blood cultures were collected 24 h after infection. Results: Mice infected simultaneously with both influenza virus and pneumococcus exhibited gradual weight loss and mortality commensurate with expectations for an additive process. In contrast, mice infected with pneumococcus 7 days following infection with influenza virus uniformly died in less than 24 h and were highly bacteremic. Discussion: A mouse model of sequential infection with influenza virus and S. pneumoniae has been developed. Mice infected with pneumococcus seven days after infection with influenza virus exhibit a synergistic lethality caused by overwhelming sepsis. This model will be useful for study of the mechanisms involved in pathogenic interactions between influenza virus and pneumococcus.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Sepsis</term></item><item><term>Pneumonia</term></item><item><term>Bacteria</term></item><item><term>Mortality</term></item><item><term>Synergism</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-X0VH0QCR-0/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>ICS</jid><aid>333</aid><ce:pii>S0531-5131(01)00631-8</ce:pii><ce:doi>10.1016/S0531-5131(01)00631-8</ce:doi><ce:copyright type="full-transfer" year="2001">Elsevier Science B.V.</ce:copyright></item-info><head><ce:title>A mouse model of dual infection with influenza virus and <ce:italic>Streptococcus pneumoniae</ce:italic></ce:title><ce:author-group><ce:author><ce:given-name>Jonathan A</ce:given-name><ce:surname>McCullers</ce:surname><ce:cross-ref refid="COR1">*</ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:e-address>jon.mccullers@stjude.org</ce:e-address></ce:author><ce:author><ce:given-name>Robert G</ce:given-name><ce:surname>Webster</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Infectious Diseases, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Department of Pathology, University of Tennessee, Memphis, 8000 Madison Avenue, Memphis, TN 38163, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1-901-495-3486; fax: +1-901-495-3099</ce:text></ce:correspondence></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para><ce:italic>Background</ce:italic>: A lethal synergism exists between influenza virus and <ce:italic>Streptococcus pneumoniae</ce:italic> accounting for excess mortality during influenza epidemics. A small animal model of dual infection with these organisms would be useful for study of pathogenic mechanisms underlying this interaction. <ce:italic>Methods</ce:italic>: Groups of mice were infected with either mouse adapted influenza virus A/Puerto Rico/8/34 (H1N1), <ce:italic>S. pneumoniae</ce:italic> strain D39, both simultaneously, or pneumococcus following influenza virus. Weight loss, as a measure of morbidity, and mortality were followed. Blood cultures were collected 24 h after infection. <ce:italic>Results</ce:italic>: Mice infected simultaneously with both influenza virus and pneumococcus exhibited gradual weight loss and mortality commensurate with expectations for an additive process. In contrast, mice infected with pneumococcus 7 days following infection with influenza virus uniformly died in less than 24 h and were highly bacteremic. <ce:italic>Discussion</ce:italic>: A mouse model of sequential infection with influenza virus and <ce:italic>S. pneumoniae</ce:italic> has been developed. Mice infected with pneumococcus seven days after infection with influenza virus exhibit a synergistic lethality caused by overwhelming sepsis. This model will be useful for study of the mechanisms involved in pathogenic interactions between influenza virus and pneumococcus.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Sepsis</ce:text></ce:keyword><ce:keyword><ce:text>Pneumonia</ce:text></ce:keyword><ce:keyword><ce:text>Bacteria</ce:text></ce:keyword><ce:keyword><ce:text>Mortality</ce:text></ce:keyword><ce:keyword><ce:text>Synergism</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>A mouse model of dual infection with influenza virus and Streptococcus pneumoniae</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>A mouse model of dual infection with influenza virus and</title></titleInfo><name type="personal"><namePart type="given">Jonathan A</namePart><namePart type="family">McCullers</namePart><affiliation>E-mail: jon.mccullers@stjude.org</affiliation><affiliation>Department of Infectious Diseases, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</affiliation><description>Corresponding author. Tel.: +1-901-495-3486; fax: +1-901-495-3099</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert G</namePart><namePart type="family">Webster</namePart><affiliation>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Background: A lethal synergism exists between influenza virus and Streptococcus pneumoniae accounting for excess mortality during influenza epidemics. A small animal model of dual infection with these organisms would be useful for study of pathogenic mechanisms underlying this interaction. Methods: Groups of mice were infected with either mouse adapted influenza virus A/Puerto Rico/8/34 (H1N1), S. pneumoniae strain D39, both simultaneously, or pneumococcus following influenza virus. Weight loss, as a measure of morbidity, and mortality were followed. Blood cultures were collected 24 h after infection. Results: Mice infected simultaneously with both influenza virus and pneumococcus exhibited gradual weight loss and mortality commensurate with expectations for an additive process. In contrast, mice infected with pneumococcus 7 days following infection with influenza virus uniformly died in less than 24 h and were highly bacteremic. Discussion: A mouse model of sequential infection with influenza virus and S. pneumoniae has been developed. Mice infected with pneumococcus seven days after infection with influenza virus exhibit a synergistic lethality caused by overwhelming sepsis. This model will be useful for study of the mechanisms involved in pathogenic interactions between influenza virus and pneumococcus.</abstract><note type="content">Fig. 1: Groups of mice were weighed daily after infection with either S. pneumoniae strain D39, influenza virus A/PR/8/34, both, or diluent as a control at day 0. Error bars represent the standard deviation between groups of four mice.</note><note type="content">Fig. 2: Mice were infected with either S. pneumoniae strain D39, influenza virus A/PR/8/34 and pneumococcus simultaneously, or influenza virus followed 7 days later by pneumococcus. Blood cultures were collected 24 h after infection with pneumococcus and quantitated. Titers beyond the limits of the assay are expressed as either >7 if greater than 1×107 CFU/ml or <2 if less than 100 CFU/ml.</note><note type="content">Table 1: Infection with pneumococcus following influenza is lethal in mice</note><subject><genre>Keywords</genre><topic>Sepsis</topic><topic>Pneumonia</topic><topic>Bacteria</topic><topic>Mortality</topic><topic>Synergism</topic></subject><relatedItem type="host"><titleInfo><title>International congress series</title></titleInfo><titleInfo type="abbreviated"><title>ICS</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued></originInfo><identifier type="ISSN">0531-5131</identifier><identifier type="PII">S0531-5131(00)X0003-9</identifier><part><date>2001</date><detail type="volume"><number>1219</number><caption>vol.</caption></detail><detail type="supplement"><number>C</number><caption>Suppl.</caption></detail><extent unit="issue-pages"><start>1</start><end>1048</end></extent><extent unit="pages"><start>601</start><end>607</end></extent></part></relatedItem><identifier type="istex">009A5F10ABF1E6723029F6FB0CBCBF76C1D78CB9</identifier><identifier type="ark">ark:/67375/6H6-X0VH0QCR-0</identifier><identifier type="DOI">10.1016/S0531-5131(01)00631-8</identifier><identifier type="PII">S0531-5131(01)00631-8</identifier><accessCondition type="use and reproduction" contentType="copyright">©2001 Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Elsevier Science B.V., ©2001</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-X0VH0QCR-0/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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