Antimicrobial Activity of Clinically Isolated Bacterial Species Against Staphylococcus aureus.
Identifieur interne : 000168 ( Main/Corpus ); précédent : 000167; suivant : 000169Antimicrobial Activity of Clinically Isolated Bacterial Species Against Staphylococcus aureus.
Auteurs : Britney L. Hardy ; Garima Bansal ; Katharine H. Hewlett ; Arshia Arora ; Scott D. Schaffer ; Edwin Kamau ; Jason W. Bennett ; D Scott MerrellSource :
- Frontiers in microbiology [ 1664-302X ] ; 2019.
Abstract
Bacteria often exist in polymicrobial communities where they compete for limited resources. Intrinsic to this competition is the ability of some species to inhibit or kill their competitors. This phenomenon is pervasive throughout the human body where commensal bacteria block the colonization of incoming microorganisms. In this regard, molecular epidemiological and microbiota-based studies suggest that species-specific interactions play a critical role in the prevention of nasal colonization of the opportunistic pathogen Staphylococcus aureus. Despite this, S. aureus exists as part of the microbiota of ∼25% of the population, suggesting that the interplay between S. aureus and commensals can be complex. Microbiota studies indicate that several bacterial genera are negatively correlated with S. aureus colonization. While these studies paint a broad overview of bacterial presence, they often fail to identify individual species-specific interactions; a greater insight in this area could aid the development of novel antimicrobials. As a proof of concept study designed to identify individual bacterial species that possess anti-S. aureus activity, we screened a small collection of clinical isolates from the Walter Reed National Military Medical Center for the ability to inhibit multiple S. aureus strains. We found that the majority of the isolates (82%) inhibited at least one S. aureus strain; 23% inhibited all S. aureus strains tested. In total, seven isolates mediated inhibitory activity that was independent of physical contact with S. aureus, and seven isolates mediated bactericidal activity. 16S rRNA based-sequencing revealed that the inhibitory isolates belonged to the Acinetobacter, Agromyces, Corynebacterium, Microbacteria, Mycobacterium, and Staphylococcus genera. Unexpectedly, these included seven distinct Acinetobacter baumannii isolates, all of which showed heterogeneous degrees of anti-S. aureus activity. Defined mechanistic studies on specific isolates revealed that the inhibitory activity was retained in conditioned cell free medium (CCFM) derived from the isolates. Furthermore, CCFM obtained from S. saprophyticus significantly decreased mortality of S. aureus-infected Galleria mellonella caterpillars. While future studies will seek to define the molecular mechanisms of the inhibitory activities, our current findings support the study of polymicrobial interactions as a strategy to understand bacterial competition and to identify novel therapeutics against S. aureus and other pathogens.
DOI: 10.3389/fmicb.2019.02977
PubMed: 32010080
PubMed Central: PMC6975196
Links to Exploration step
pubmed:32010080Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Antimicrobial Activity of Clinically Isolated Bacterial Species Against <i>Staphylococcus aureus</i>.</title><author><name sortKey="Hardy, Britney L" sort="Hardy, Britney L" uniqKey="Hardy B" first="Britney L" last="Hardy">Britney L. Hardy</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Bansal, Garima" sort="Bansal, Garima" uniqKey="Bansal G" first="Garima" last="Bansal">Garima Bansal</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Hewlett, Katharine H" sort="Hewlett, Katharine H" uniqKey="Hewlett K" first="Katharine H" last="Hewlett">Katharine H. Hewlett</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Arora, Arshia" sort="Arora, Arshia" uniqKey="Arora A" first="Arshia" last="Arora">Arshia Arora</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Schaffer, Scott D" sort="Schaffer, Scott D" uniqKey="Schaffer S" first="Scott D" last="Schaffer">Scott D. Schaffer</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Kamau, Edwin" sort="Kamau, Edwin" uniqKey="Kamau E" first="Edwin" last="Kamau">Edwin Kamau</name><affiliation><nlm:affiliation>Department of Clinical Microbiology, Walter Reed National Military Medical Center, Bethesda, MD, United States.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>U.S. Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Bennett, Jason W" sort="Bennett, Jason W" uniqKey="Bennett J" first="Jason W" last="Bennett">Jason W. Bennett</name><affiliation><nlm:affiliation>Multidrug-Resistant Organism Repository and Surveillance Network, Walter Reed Army Institute of Research, Silver Spring, MD, United States.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Medicine, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Merrell, D Scott" sort="Merrell, D Scott" uniqKey="Merrell D" first="D Scott" last="Merrell">D Scott Merrell</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Medicine, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:32010080</idno><idno type="pmid">32010080</idno><idno type="doi">10.3389/fmicb.2019.02977</idno><idno type="pmc">PMC6975196</idno><idno type="wicri:Area/Main/Corpus">000168</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000168</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Antimicrobial Activity of Clinically Isolated Bacterial Species Against <i>Staphylococcus aureus</i>.</title><author><name sortKey="Hardy, Britney L" sort="Hardy, Britney L" uniqKey="Hardy B" first="Britney L" last="Hardy">Britney L. Hardy</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Bansal, Garima" sort="Bansal, Garima" uniqKey="Bansal G" first="Garima" last="Bansal">Garima Bansal</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Hewlett, Katharine H" sort="Hewlett, Katharine H" uniqKey="Hewlett K" first="Katharine H" last="Hewlett">Katharine H. Hewlett</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Arora, Arshia" sort="Arora, Arshia" uniqKey="Arora A" first="Arshia" last="Arora">Arshia Arora</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Schaffer, Scott D" sort="Schaffer, Scott D" uniqKey="Schaffer S" first="Scott D" last="Schaffer">Scott D. Schaffer</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Kamau, Edwin" sort="Kamau, Edwin" uniqKey="Kamau E" first="Edwin" last="Kamau">Edwin Kamau</name><affiliation><nlm:affiliation>Department of Clinical Microbiology, Walter Reed National Military Medical Center, Bethesda, MD, United States.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>U.S. Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Bennett, Jason W" sort="Bennett, Jason W" uniqKey="Bennett J" first="Jason W" last="Bennett">Jason W. Bennett</name><affiliation><nlm:affiliation>Multidrug-Resistant Organism Repository and Surveillance Network, Walter Reed Army Institute of Research, Silver Spring, MD, United States.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Medicine, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Merrell, D Scott" sort="Merrell, D Scott" uniqKey="Merrell D" first="D Scott" last="Merrell">D Scott Merrell</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Medicine, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Frontiers in microbiology</title><idno type="ISSN">1664-302X</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Bacteria often exist in polymicrobial communities where they compete for limited resources. Intrinsic to this competition is the ability of some species to inhibit or kill their competitors. This phenomenon is pervasive throughout the human body where commensal bacteria block the colonization of incoming microorganisms. In this regard, molecular epidemiological and microbiota-based studies suggest that species-specific interactions play a critical role in the prevention of nasal colonization of the opportunistic pathogen <i>Staphylococcus aureus</i>. Despite this, <i>S. aureus</i> exists as part of the microbiota of ∼25% of the population, suggesting that the interplay between <i>S. aureus</i> and commensals can be complex. Microbiota studies indicate that several bacterial genera are negatively correlated with <i>S. aureus</i> colonization. While these studies paint a broad overview of bacterial presence, they often fail to identify individual species-specific interactions; a greater insight in this area could aid the development of novel antimicrobials. As a proof of concept study designed to identify individual bacterial species that possess anti<i>-S. aureus</i> activity, we screened a small collection of clinical isolates from the Walter Reed National Military Medical Center for the ability to inhibit multiple <i>S. aureus</i> strains. We found that the majority of the isolates (82%) inhibited at least one <i>S. aureus</i> strain; 23% inhibited all <i>S. aureus</i> strains tested. In total, seven isolates mediated inhibitory activity that was independent of physical contact with <i>S. aureus</i>, and seven isolates mediated bactericidal activity. 16S rRNA based-sequencing revealed that the inhibitory isolates belonged to the <i>Acinetobacter</i>, <i>Agromyces</i>, <i>Corynebacterium</i>, <i>Microbacteria</i>, <i>Mycobacterium</i>, and <i>Staphylococcus</i> genera. Unexpectedly, these included seven distinct <i>Acinetobacter baumannii</i> isolates, all of which showed heterogeneous degrees of anti-<i>S. aureus</i> activity. Defined mechanistic studies on specific isolates revealed that the inhibitory activity was retained in conditioned cell free medium (CCFM) derived from the isolates. Furthermore, CCFM obtained from <i>S. saprophyticus</i> significantly decreased mortality of <i>S. aureus</i>-infected <i>Galleria mellonella</i> caterpillars. While future studies will seek to define the molecular mechanisms of the inhibitory activities, our current findings support the study of polymicrobial interactions as a strategy to understand bacterial competition and to identify novel therapeutics against <i>S. aureus</i> and other pathogens.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">32010080</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>28</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-302X</ISSN><JournalIssue CitedMedium="Print"><Volume>10</Volume><PubDate><Year>2019</Year></PubDate></JournalIssue><Title>Frontiers in microbiology</Title><ISOAbbreviation>Front Microbiol</ISOAbbreviation></Journal><ArticleTitle>Antimicrobial Activity of Clinically Isolated Bacterial Species Against <i>Staphylococcus aureus</i>.</ArticleTitle><Pagination><MedlinePgn>2977</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fmicb.2019.02977</ELocationID><Abstract><AbstractText>Bacteria often exist in polymicrobial communities where they compete for limited resources. Intrinsic to this competition is the ability of some species to inhibit or kill their competitors. This phenomenon is pervasive throughout the human body where commensal bacteria block the colonization of incoming microorganisms. In this regard, molecular epidemiological and microbiota-based studies suggest that species-specific interactions play a critical role in the prevention of nasal colonization of the opportunistic pathogen <i>Staphylococcus aureus</i>. Despite this, <i>S. aureus</i> exists as part of the microbiota of ∼25% of the population, suggesting that the interplay between <i>S. aureus</i> and commensals can be complex. Microbiota studies indicate that several bacterial genera are negatively correlated with <i>S. aureus</i> colonization. While these studies paint a broad overview of bacterial presence, they often fail to identify individual species-specific interactions; a greater insight in this area could aid the development of novel antimicrobials. As a proof of concept study designed to identify individual bacterial species that possess anti<i>-S. aureus</i> activity, we screened a small collection of clinical isolates from the Walter Reed National Military Medical Center for the ability to inhibit multiple <i>S. aureus</i> strains. We found that the majority of the isolates (82%) inhibited at least one <i>S. aureus</i> strain; 23% inhibited all <i>S. aureus</i> strains tested. In total, seven isolates mediated inhibitory activity that was independent of physical contact with <i>S. aureus</i>, and seven isolates mediated bactericidal activity. 16S rRNA based-sequencing revealed that the inhibitory isolates belonged to the <i>Acinetobacter</i>, <i>Agromyces</i>, <i>Corynebacterium</i>, <i>Microbacteria</i>, <i>Mycobacterium</i>, and <i>Staphylococcus</i> genera. Unexpectedly, these included seven distinct <i>Acinetobacter baumannii</i> isolates, all of which showed heterogeneous degrees of anti-<i>S. aureus</i> activity. Defined mechanistic studies on specific isolates revealed that the inhibitory activity was retained in conditioned cell free medium (CCFM) derived from the isolates. Furthermore, CCFM obtained from <i>S. saprophyticus</i> significantly decreased mortality of <i>S. aureus</i>-infected <i>Galleria mellonella</i> caterpillars. While future studies will seek to define the molecular mechanisms of the inhibitory activities, our current findings support the study of polymicrobial interactions as a strategy to understand bacterial competition and to identify novel therapeutics against <i>S. aureus</i> and other pathogens.</AbstractText><CopyrightInformation>Copyright © 2020 Hardy, Bansal, Hewlett, Arora, Schaffer, Kamau, Bennett and Merrell.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hardy</LastName><ForeName>Britney L</ForeName><Initials>BL</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bansal</LastName><ForeName>Garima</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hewlett</LastName><ForeName>Katharine H</ForeName><Initials>KH</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arora</LastName><ForeName>Arshia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schaffer</LastName><ForeName>Scott D</ForeName><Initials>SD</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kamau</LastName><ForeName>Edwin</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Clinical Microbiology, Walter Reed National Military Medical Center, Bethesda, MD, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>U.S. Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, MD, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bennett</LastName><ForeName>Jason W</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Multidrug-Resistant Organism Repository and Surveillance Network, Walter Reed Army Institute of Research, Silver Spring, MD, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Merrell</LastName><ForeName>D Scott</ForeName><Initials>DS</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>01</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Microbiol</MedlineTA><NlmUniqueID>101548977</NlmUniqueID><ISSNLinking>1664-302X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">MRSA</Keyword><Keyword MajorTopicYN="N">Staphylococcus aureus</Keyword><Keyword MajorTopicYN="N">bacterial interaction</Keyword><Keyword MajorTopicYN="N">clinical isolates</Keyword><Keyword MajorTopicYN="N">polymicrobial interactions</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>08</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>12</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>2</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>2</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>2</Month><Day>6</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32010080</ArticleId><ArticleId IdType="doi">10.3389/fmicb.2019.02977</ArticleId><ArticleId IdType="pmc">PMC6975196</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Am J Infect Control. 2008 Sep;36(7):468-71</Citation><ArticleIdList><ArticleId IdType="pubmed">18786448</ArticleId></ArticleIdList></Reference><Reference><Citation>Appl Environ Microbiol. 2019 May 2;85(10):</Citation><ArticleIdList><ArticleId IdType="pubmed">30578265</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2010 May 20;465(7296):346-9</Citation><ArticleIdList><ArticleId IdType="pubmed">20485435</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2016 Oct 25;11(10):e0165491</Citation><ArticleIdList><ArticleId IdType="pubmed">27780238</ArticleId></ArticleIdList></Reference><Reference><Citation>J Bacteriol. 2015 Jul;197(14):2252-64</Citation><ArticleIdList><ArticleId IdType="pubmed">25917910</ArticleId></ArticleIdList></Reference><Reference><Citation>J Bacteriol. 2019 Oct 4;201(21):</Citation><ArticleIdList><ArticleId IdType="pubmed">31405914</ArticleId></ArticleIdList></Reference><Reference><Citation>Int J Med Microbiol. 2014 Jan;304(1):63-71</Citation><ArticleIdList><ArticleId IdType="pubmed">24119540</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Host Microbe. 2013 Dec 11;14(6):631-40</Citation><ArticleIdList><ArticleId IdType="pubmed">24331461</ArticleId></ArticleIdList></Reference><Reference><Citation>Elife. 2017 Jul 11;6:</Citation><ArticleIdList><ArticleId IdType="pubmed">28696203</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS Pathog. 2016 Jul 07;12(7):e1005633</Citation><ArticleIdList><ArticleId IdType="pubmed">27389401</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Microbiol. 2003 May;41(5):2242-6</Citation><ArticleIdList><ArticleId IdType="pubmed">12734292</ArticleId></ArticleIdList></Reference><Reference><Citation>Front Cell Infect Microbiol. 2016 Sep 27;6:104</Citation><ArticleIdList><ArticleId IdType="pubmed">27730096</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Invest. 2003 May;111(9):1265-73</Citation><ArticleIdList><ArticleId IdType="pubmed">12727914</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Microbiol. 2019 Jul;76(7):842-847</Citation><ArticleIdList><ArticleId IdType="pubmed">31053906</ArticleId></ArticleIdList></Reference><Reference><Citation>Front Microbiol. 2018 Oct 08;9:2419</Citation><ArticleIdList><ArticleId IdType="pubmed">30349525</ArticleId></ArticleIdList></Reference><Reference><Citation>Microbiology. 2019 May;165(5):503-515</Citation><ArticleIdList><ArticleId IdType="pubmed">30893029</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2005 Sep 15;175(6):3907-19</Citation><ArticleIdList><ArticleId IdType="pubmed">16148137</ArticleId></ArticleIdList></Reference><Reference><Citation>J Appl Microbiol. 2013 Sep;115(3):654-62</Citation><ArticleIdList><ArticleId IdType="pubmed">23758410</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Microbiol. 1982 Sep;16(3):427-31</Citation><ArticleIdList><ArticleId IdType="pubmed">6890071</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2013;8(2):e56846</Citation><ArticleIdList><ArticleId IdType="pubmed">23451098</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS Pathog. 2014 Jan;10(1):e1003862</Citation><ArticleIdList><ArticleId IdType="pubmed">24453967</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2002 Feb;70(2):631-41</Citation><ArticleIdList><ArticleId IdType="pubmed">11796592</ArticleId></ArticleIdList></Reference><Reference><Citation>mBio. 2019 Jan 8;10(1):</Citation><ArticleIdList><ArticleId IdType="pubmed">30622190</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Microbiol Rev. 2001 Apr;14(2):244-69</Citation><ArticleIdList><ArticleId IdType="pubmed">11292638</ArticleId></ArticleIdList></Reference><Reference><Citation>mBio. 2016 Jan 05;7(1):e01725-15</Citation><ArticleIdList><ArticleId IdType="pubmed">26733066</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2001 Apr 21;357(9264):1225-40</Citation><ArticleIdList><ArticleId IdType="pubmed">11418146</ArticleId></ArticleIdList></Reference><Reference><Citation>J Mol Biol. 2016 Aug 28;428(17):3355-71</Citation><ArticleIdList><ArticleId IdType="pubmed">27170548</ArticleId></ArticleIdList></Reference><Reference><Citation>J Invest Dermatol. 2017 Apr;137(4):976-979</Citation><ArticleIdList><ArticleId IdType="pubmed">27923738</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Microbiol. 2000 Feb;38(2):918-22</Citation><ArticleIdList><ArticleId IdType="pubmed">10655417</ArticleId></ArticleIdList></Reference><Reference><Citation>J Antimicrob Chemother. 2011 Aug;66(8):1785-90</Citation><ArticleIdList><ArticleId IdType="pubmed">21622972</ArticleId></ArticleIdList></Reference><Reference><Citation>Virulence. 2016 Apr 2;7(3):214-29</Citation><ArticleIdList><ArticleId IdType="pubmed">26730990</ArticleId></ArticleIdList></Reference><Reference><Citation>BMC Microbiol. 2008 Mar 06;8:43</Citation><ArticleIdList><ArticleId IdType="pubmed">18325110</ArticleId></ArticleIdList></Reference><Reference><Citation>Infection. 2005 Feb;33(1):3-8</Citation><ArticleIdList><ArticleId IdType="pubmed">15750752</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Microbiol Rev. 2012 Jan;25(1):193-213</Citation><ArticleIdList><ArticleId IdType="pubmed">22232376</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2013 Jan 15;110(3):1059-64</Citation><ArticleIdList><ArticleId IdType="pubmed">23277552</ArticleId></ArticleIdList></Reference><Reference><Citation>FEMS Microbiol Rev. 2001 May;25(3):285-308</Citation><ArticleIdList><ArticleId IdType="pubmed">11348686</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Microbiol. 2010;64:143-62</Citation><ArticleIdList><ArticleId IdType="pubmed">20825344</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2007 Oct 18;449(7164):804-10</Citation><ArticleIdList><ArticleId IdType="pubmed">17943116</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet Infect Dis. 2005 Dec;5(12):751-62</Citation><ArticleIdList><ArticleId IdType="pubmed">16310147</ArticleId></ArticleIdList></Reference><Reference><Citation>JAMA. 2007 Oct 17;298(15):1763-71</Citation><ArticleIdList><ArticleId IdType="pubmed">17940231</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2015 Jan 8;517(7533):205-8</Citation><ArticleIdList><ArticleId IdType="pubmed">25337874</ArticleId></ArticleIdList></Reference><Reference><Citation>Sci Transl Med. 2017 Feb 22;9(378):</Citation><ArticleIdList><ArticleId IdType="pubmed">28228596</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2016 Jul 27;535(7613):511-6</Citation><ArticleIdList><ArticleId IdType="pubmed">27466123</ArticleId></ArticleIdList></Reference><Reference><Citation>mBio. 2010 Jun 22;1(3):null</Citation><ArticleIdList><ArticleId IdType="pubmed">20802827</ArticleId></ArticleIdList></Reference><Reference><Citation>Appl Environ Microbiol. 2003 Jan;69(1):18-23</Citation><ArticleIdList><ArticleId IdType="pubmed">12513972</ArticleId></ArticleIdList></Reference><Reference><Citation>Front Microbiol. 2018 Oct 16;9:2458</Citation><ArticleIdList><ArticleId IdType="pubmed">30459722</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2011;6(11):e27317</Citation><ArticleIdList><ArticleId IdType="pubmed">22076151</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Terre/explor/SilverBacteriV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000168 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000168 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Terre
|area= SilverBacteriV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= pubmed:32010080
|texte= Antimicrobial Activity of Clinically Isolated Bacterial Species Against Staphylococcus aureus.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i -Sk "pubmed:32010080" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a SilverBacteriV1
| This area was generated with Dilib version V0.6.38. |  |