Ulcer bed infection
Identifieur interne : 000B59 ( Istex/Corpus ); précédent : 000B58; suivant : 000B60Ulcer bed infection
Auteurs : Lis Danielsen ; Eva Balslev ; Gerd Döring ; Niels H Iby ; S Ren Munk Madsen ; Magnus Gren ; Henrik Klem Thomsen ; Henrik H. Steen Fos ; Henrik WesthSource :
- APMIS [ 0903-4641 ] ; 1998-07.
English descriptors
Abstract
We report a case of ulcer bed infection in an enlarging venous leg ulcer without clinical signs of cellulitis in the surrounding tissues. Signs of infection in the leg ulcer were: 1) cocci‐like structures and bacteria‐like rods around vessel walls in the viable ulcer bed, 2) vasculitis‐like inflammation of deeply situated vessels of the viable tissue, 3) Pseudomonas aeruginosa‐specific antibodies in the serum (other than against exotoxin A), 4) extensive epidermolysis of normal human skin by the wound exudate in vitro, and 5) P. aeruginosa exotoxin A in the wound exudate (23 ng/ml). In an in vitro cell assay, the wound exudate was cytotoxic and rabbit antibodies to exotoxin A, but not a serine proteinase inhibitor, inhibited this cytotoxicity. P. aeruginosa exotoxin A might contribute to the pathogenesis of the ulcer enlargement. The ulcer improved after the third skin graft, probably mainly due to effective treatment with a long‐stretch compression bandage.
Url:
DOI: 10.1111/j.1699-0463.1998.tb00218.x
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ISTEX:99C25EA57BC41D9FEDF8DB9C4036554668E820B9Le document en format XML
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Steen" last="Fos">Henrik H. Steen Fos</name><affiliation><mods:affiliation>Division of Diagnostics, Statens Serum Institut, Copenhagen, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Westh, Henrik" sort="Westh, Henrik" uniqKey="Westh H" first="Henrik" last="Westh">Henrik Westh</name><affiliation><mods:affiliation>Division of Diagnostics, Statens Serum Institut, Copenhagen, Denmark</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">APMIS</title><idno type="ISSN">0903-4641</idno><idno type="eISSN">1600-0463</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-07">1998-07</date><biblScope unit="volume">106</biblScope><biblScope unit="issue">7‐12</biblScope><biblScope unit="page" from="721">721</biblScope><biblScope unit="page" to="726">726</biblScope></imprint><idno type="ISSN">0903-4641</idno></series><idno type="istex">99C25EA57BC41D9FEDF8DB9C4036554668E820B9</idno><idno type="DOI">10.1111/j.1699-0463.1998.tb00218.x</idno><idno type="ArticleID">APM721</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0903-4641</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Pseudomonas aeruginosa exotoxin A</term><term>Wound exudate</term><term>cytotoxicity</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We report a case of ulcer bed infection in an enlarging venous leg ulcer without clinical signs of cellulitis in the surrounding tissues. Signs of infection in the leg ulcer were: 1) cocci‐like structures and bacteria‐like rods around vessel walls in the viable ulcer bed, 2) vasculitis‐like inflammation of deeply situated vessels of the viable tissue, 3) Pseudomonas aeruginosa‐specific antibodies in the serum (other than against exotoxin A), 4) extensive epidermolysis of normal human skin by the wound exudate in vitro, and 5) P. aeruginosa exotoxin A in the wound exudate (23 ng/ml). In an in vitro cell assay, the wound exudate was cytotoxic and rabbit antibodies to exotoxin A, but not a serine proteinase inhibitor, inhibited this cytotoxicity. P. aeruginosa exotoxin A might contribute to the pathogenesis of the ulcer enlargement. The ulcer improved after the third skin graft, probably mainly due to effective treatment with a long‐stretch compression bandage.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>LIS DANIELSEN</name><affiliations><json:string>Departments of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark</json:string><json:string>Lis Danielsen, Department of Dermatology, Bispebjerg Hospital, Bispebjerg Bakke 23, DK‐2400 Copenhagen NV, Denmark.</json:string></affiliations></json:item><json:item><name>EVA BALSLEV</name><affiliations><json:string>Department of Pathology, Roskilde County Hospital, Denmark</json:string></affiliations></json:item><json:item><name>GERD DÖRING</name><affiliations><json:string>University of Tübingen, Germany</json:string></affiliations></json:item><json:item><name>NIELS HØIBY</name><affiliations><json:string>Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark</json:string></affiliations></json:item><json:item><name>SØREN MUNK MADSEN</name><affiliations><json:string>Klaus Trier Research Laboratory ApS, Frederiksberg Hospital, Copenhagen</json:string></affiliations></json:item><json:item><name>MAGNUS ÅGREN</name><affiliations><json:string>Departments of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark</json:string></affiliations></json:item><json:item><name>HENRIK KLEM THOMSEN</name><affiliations><json:string>Departments of Pathology, Bispebjerg Hospital, Copenhagen, Denmark</json:string></affiliations></json:item><json:item><name>HENRIK H. STEEN FOS</name><affiliations><json:string>Division of Diagnostics, Statens Serum Institut, Copenhagen, Denmark</json:string></affiliations></json:item><json:item><name>HENRIK WESTH</name><affiliations><json:string>Division of Diagnostics, Statens Serum Institut, Copenhagen, Denmark</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Wound exudate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Pseudomonas aeruginosa exotoxin A</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cytotoxicity</value></json:item></subject><articleId><json:string>APM721</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>We report a case of ulcer bed infection in an enlarging venous leg ulcer without clinical signs of cellulitis in the surrounding tissues. Signs of infection in the leg ulcer were: 1) cocci‐like structures and bacteria‐like rods around vessel walls in the viable ulcer bed, 2) vasculitis‐like inflammation of deeply situated vessels of the viable tissue, 3) Pseudomonas aeruginosa‐specific antibodies in the serum (other than against exotoxin A), 4) extensive epidermolysis of normal human skin by the wound exudate in vitro, and 5) P. aeruginosa exotoxin A in the wound exudate (23 ng/ml). In an in vitro cell assay, the wound exudate was cytotoxic and rabbit antibodies to exotoxin A, but not a serine proteinase inhibitor, inhibited this cytotoxicity. P. aeruginosa exotoxin A might contribute to the pathogenesis of the ulcer enlargement. The ulcer improved after the third skin graft, probably mainly due to effective treatment with a long‐stretch compression bandage.</abstract><qualityIndicators><score>4.638</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>972</abstractCharCount><pdfWordCount>2826</pdfWordCount><pdfCharCount>17824</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>151</abstractWordCount></qualityIndicators><title>Ulcer bed infection</title><refBibs><json:item><author><json:item><name>L. Danielsen</name></json:item><json:item><name>H. Westh</name></json:item><json:item><name>E. Balslev</name></json:item><json:item><name>V. T. Rosdahl</name></json:item><json:item><name>G. 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Rev.</title></host><title>Bacterial toxins: cellular mechanisms of action</title></json:item><json:item><author><json:item><name>R. E. Morris</name></json:item><json:item><name>M. D. Manhart</name></json:item><json:item><name>C. B. Saelinger</name></json:item></author><host><volume>48</volume><pages><last>811</last><first>806</first></pages><author></author><title>Infect. Immun.</title></host><title>Receptor‐mediated entry of Pseudomonas toxin: methylamine blocks clustering step</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>106</volume><publisherId><json:string>APM</json:string></publisherId><pages><total>6</total><last>726</last><first>721</first></pages><issn><json:string>0903-4641</json:string></issn><issue>7‐12</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1600-0463</json:string></eissn><title>APMIS</title><doi><json:string>10.1111/(ISSN)1600-0463</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>pathology</json:string><json:string>microbiology</json:string><json:string>immunology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>oncology & carcinogenesis</json:string></scienceMetrix></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1111/j.1699-0463.1998.tb00218.x</json:string></doi><id>99C25EA57BC41D9FEDF8DB9C4036554668E820B9</id><score>0.21744806</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/99C25EA57BC41D9FEDF8DB9C4036554668E820B9/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/99C25EA57BC41D9FEDF8DB9C4036554668E820B9/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/99C25EA57BC41D9FEDF8DB9C4036554668E820B9/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Ulcer bed infection</title><title level="a" type="sub" xml:lang="en">Report of a case of enlarging venous leg ulcer colonized by Pseudomonas aeruginosa</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>© 1998 APMIS</p></availability><date>1998</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Ulcer bed infection</title><title level="a" type="sub" xml:lang="en">Report of a case of enlarging venous leg ulcer colonized by Pseudomonas aeruginosa</title><author xml:id="author-1"><persName><forename type="first">LIS</forename><surname>DANIELSEN</surname></persName><affiliation>Departments of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark</affiliation><affiliation>Lis Danielsen, Department of Dermatology, Bispebjerg Hospital, Bispebjerg Bakke 23, DK‐2400 Copenhagen NV, Denmark.</affiliation></author><author xml:id="author-2"><persName><forename type="first">EVA</forename><surname>BALSLEV</surname></persName><affiliation>Department of Pathology, Roskilde County Hospital, Denmark</affiliation></author><author xml:id="author-3"><persName><forename type="first">GERD</forename><surname>DÖRING</surname></persName><affiliation>University of Tübingen, Germany</affiliation></author><author xml:id="author-4"><persName><forename type="first">NIELS</forename><surname>HØIBY</surname></persName><affiliation>Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark</affiliation></author><author xml:id="author-5"><persName><forename type="first">SØREN MUNK</forename><surname>MADSEN</surname></persName><affiliation>Klaus Trier Research Laboratory ApS, Frederiksberg Hospital, Copenhagen</affiliation></author><author xml:id="author-6"><persName><forename type="first">MAGNUS</forename><surname>ÅGREN</surname></persName><affiliation>Departments of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark</affiliation></author><author xml:id="author-7"><persName><forename type="first">HENRIK KLEM</forename><surname>THOMSEN</surname></persName><affiliation>Departments of Pathology, Bispebjerg Hospital, Copenhagen, Denmark</affiliation></author><author xml:id="author-8"><persName><forename type="first">HENRIK H. STEEN</forename><surname>FOS</surname></persName><affiliation>Division of Diagnostics, Statens Serum Institut, Copenhagen, Denmark</affiliation></author><author xml:id="author-9"><persName><forename type="first">HENRIK</forename><surname>WESTH</surname></persName><affiliation>Division of Diagnostics, Statens Serum Institut, Copenhagen, Denmark</affiliation></author></analytic><monogr><title level="j">APMIS</title><idno type="pISSN">0903-4641</idno><idno type="eISSN">1600-0463</idno><idno type="DOI">10.1111/(ISSN)1600-0463</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-07"></date><biblScope unit="volume">106</biblScope><biblScope unit="issue">7‐12</biblScope><biblScope unit="page" from="721">721</biblScope><biblScope unit="page" to="726">726</biblScope></imprint></monogr><idno type="istex">99C25EA57BC41D9FEDF8DB9C4036554668E820B9</idno><idno type="DOI">10.1111/j.1699-0463.1998.tb00218.x</idno><idno type="ArticleID">APM721</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We report a case of ulcer bed infection in an enlarging venous leg ulcer without clinical signs of cellulitis in the surrounding tissues. Signs of infection in the leg ulcer were: 1) cocci‐like structures and bacteria‐like rods around vessel walls in the viable ulcer bed, 2) vasculitis‐like inflammation of deeply situated vessels of the viable tissue, 3) Pseudomonas aeruginosa‐specific antibodies in the serum (other than against exotoxin A), 4) extensive epidermolysis of normal human skin by the wound exudate in vitro, and 5) P. aeruginosa exotoxin A in the wound exudate (23 ng/ml). In an in vitro cell assay, the wound exudate was cytotoxic and rabbit antibodies to exotoxin A, but not a serine proteinase inhibitor, inhibited this cytotoxicity. P. aeruginosa exotoxin A might contribute to the pathogenesis of the ulcer enlargement. The ulcer improved after the third skin graft, probably mainly due to effective treatment with a long‐stretch compression bandage.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>Wound exudate</term></item><item><term>Pseudomonas aeruginosa exotoxin A</term></item><item><term>cytotoxicity</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/99C25EA57BC41D9FEDF8DB9C4036554668E820B9/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0463</doi><issn type="print">0903-4641</issn><issn type="electronic">1600-0463</issn><idGroup><id type="product" value="APM"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="APMIS">APMIS</title></titleGroup></publicationMeta><publicationMeta level="part" position="07007"><doi origin="wiley">10.1111/apm.1998.106.issue-7-12</doi><numberingGroup><numbering type="journalVolume" number="106">106</numbering><numbering type="journalIssue">7‐12</numbering></numberingGroup><coverDate startDate="1998-07">July 1998</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="9" status="forIssue"><doi origin="wiley">10.1111/j.1699-0463.1998.tb00218.x</doi><idGroup><id type="unit" value="APM721"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">Original Article</title></titleGroup><copyright>© 1998 APMIS</copyright><eventGroup><event type="firstOnline" date="2009-08-15"></event><event type="publishedOnlineFinalForm" date="2009-08-15"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:HeaderRef result:HeaderRef" date="2010-04-21"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-04"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="721">721</numbering><numbering type="pageLast" number="726">726</numbering></numberingGroup><correspondenceTo>Lis Danielsen, Department of Dermatology, Bispebjerg Hospital, Bispebjerg Bakke 23, DK‐2400 Copenhagen NV, Denmark.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:APM.APM721.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received November 27, 1997. 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Signs of infection in the leg ulcer were: 1) cocci‐like structures and bacteria‐like rods around vessel walls in the viable ulcer bed, 2) vasculitis‐like inflammation of deeply situated vessels of the viable tissue, 3) <i>Pseudomonas aeruginosa</i>‐specific antibodies in the serum (other than against exotoxin A), 4) extensive epidermolysis of normal human skin by the wound exudate <i>in vitro</i>, and 5) <i>P. aeruginosa</i> exotoxin A in the wound exudate (23 ng/ml). In an <i>in vitro</i> cell assay, the wound exudate was cytotoxic and rabbit antibodies to exotoxin A, but not a serine proteinase inhibitor, inhibited this cytotoxicity. <i>P. aeruginosa</i> exotoxin A might contribute to the pathogenesis of the ulcer enlargement. The ulcer improved after the third skin graft, probably mainly due to effective treatment with a long‐stretch compression bandage.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Ulcer bed infection</title><subTitle>Report of a case of enlarging venous leg ulcer colonized by Pseudomonas aeruginosa</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Ulcer bed infection</title></titleInfo><name type="personal"><namePart type="given">LIS</namePart><namePart type="family">DANIELSEN</namePart><affiliation>Departments of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark</affiliation><affiliation>Lis Danielsen, Department of Dermatology, Bispebjerg Hospital, Bispebjerg Bakke 23, DK‐2400 Copenhagen NV, Denmark.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">EVA</namePart><namePart type="family">BALSLEV</namePart><affiliation>Department of Pathology, Roskilde County Hospital, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GERD</namePart><namePart type="family">DÖRING</namePart><affiliation>University of Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NIELS</namePart><namePart type="family">HØIBY</namePart><affiliation>Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SØREN MUNK</namePart><namePart type="family">MADSEN</namePart><affiliation>Klaus Trier Research Laboratory ApS, Frederiksberg Hospital, Copenhagen</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MAGNUS</namePart><namePart type="family">ÅGREN</namePart><affiliation>Departments of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HENRIK KLEM</namePart><namePart type="family">THOMSEN</namePart><affiliation>Departments of Pathology, Bispebjerg Hospital, Copenhagen, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HENRIK H. STEEN</namePart><namePart type="family">FOS</namePart><affiliation>Division of Diagnostics, Statens Serum Institut, Copenhagen, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HENRIK</namePart><namePart type="family">WESTH</namePart><affiliation>Division of Diagnostics, Statens Serum Institut, Copenhagen, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1998-07</dateIssued><edition>Received November 27, 1997. Accepted February 6, 1998</edition><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">21</extent></physicalDescription><abstract lang="en">We report a case of ulcer bed infection in an enlarging venous leg ulcer without clinical signs of cellulitis in the surrounding tissues. Signs of infection in the leg ulcer were: 1) cocci‐like structures and bacteria‐like rods around vessel walls in the viable ulcer bed, 2) vasculitis‐like inflammation of deeply situated vessels of the viable tissue, 3) Pseudomonas aeruginosa‐specific antibodies in the serum (other than against exotoxin A), 4) extensive epidermolysis of normal human skin by the wound exudate in vitro, and 5) P. aeruginosa exotoxin A in the wound exudate (23 ng/ml). In an in vitro cell assay, the wound exudate was cytotoxic and rabbit antibodies to exotoxin A, but not a serine proteinase inhibitor, inhibited this cytotoxicity. P. aeruginosa exotoxin A might contribute to the pathogenesis of the ulcer enlargement. The ulcer improved after the third skin graft, probably mainly due to effective treatment with a long‐stretch compression bandage.</abstract><subject lang="en"><genre>keywords</genre><topic>Wound exudate</topic><topic>Pseudomonas aeruginosa exotoxin A</topic><topic>cytotoxicity</topic></subject><relatedItem type="host"><titleInfo><title>APMIS</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0903-4641</identifier><identifier type="eISSN">1600-0463</identifier><identifier type="DOI">10.1111/(ISSN)1600-0463</identifier><identifier type="PublisherID">APM</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>106</number></detail><detail type="issue"><caption>no.</caption><number>7‐12</number></detail><extent unit="pages"><start>721</start><end>726</end><total>6</total></extent></part></relatedItem><identifier type="istex">99C25EA57BC41D9FEDF8DB9C4036554668E820B9</identifier><identifier type="DOI">10.1111/j.1699-0463.1998.tb00218.x</identifier><identifier type="ArticleID">APM721</identifier><accessCondition type="use and reproduction" contentType="copyright">© 1998 APMIS</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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