Changes in Antibody Levels during and following an Episode of Acute Adenolymphangitis (ADL) among Lymphedema Patients in Léogâne, Haiti
Identifieur interne : 001430 ( Pmc/Checkpoint ); précédent : 001429; suivant : 001431Changes in Antibody Levels during and following an Episode of Acute Adenolymphangitis (ADL) among Lymphedema Patients in Léogâne, Haiti
Auteurs : Katherine E. Mues [États-Unis] ; Patrick J. Lammie [États-Unis] ; Mitchel Klein [États-Unis] ; David G. Kleinbaum [États-Unis] ; David Addiss [États-Unis] ; Leanne M. Fox [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2015.
Abstract
Episodes of acute adenolymphangitis (ADL) are often the first clinical sign of lymphatic filariasis (LF). They are often accompanied by swelling of the affected limb, inflammation, fever, and general malaise and lead to the progression of lymphedema. Although ADL episodes have been studied for a century or more, questions still remain as to their etiology. We quantified antibody levels to pathogens that potentially contribute to ADL episodes during and after an episode among lymphedema patients in Léogâne, Haiti. We estimated the proportion of ADL episodes hypothesized to be attributed to specific pathogens.
We measured antibody levels to specific pathogens during and following an ADL episode among 41 lymphedema patients enrolled in a cohort study in Léogâne, Haiti. We calculated the absolute and relative changes in antibody levels between the ADL and convalescent time points. We calculated the proportion of episodes that demonstrated a two-fold increase in antibody level for several bacterial, fungal, and filarial pathogens.
Our results showed the greatest proportion of two-fold changes in antibody levels for the carbohydrate antigen
Although our results are limited by the lack of a control group and few antibody responses, they provide some evidence for infection with
Url:
DOI: 10.1371/journal.pone.0141047
PubMed: 26492462
PubMed Central: 4619626
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Mues</name><affiliation wicri:level="2"><nlm:aff id="aff001"><addr-line>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Lammie, Patrick J" sort="Lammie, Patrick J" uniqKey="Lammie P" first="Patrick J." last="Lammie">Patrick J. 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Mues</name><affiliation wicri:level="2"><nlm:aff id="aff001"><addr-line>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Lammie, Patrick J" sort="Lammie, Patrick J" uniqKey="Lammie P" first="Patrick J." last="Lammie">Patrick J. Lammie</name><affiliation wicri:level="2"><nlm:aff id="aff002"><addr-line>Parasitic Diseases Branch, Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Parasitic Diseases Branch, Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Klein, Mitchel" sort="Klein, Mitchel" uniqKey="Klein M" first="Mitchel" last="Klein">Mitchel Klein</name><affiliation wicri:level="2"><nlm:aff id="aff001"><addr-line>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Kleinbaum, David G" sort="Kleinbaum, David G" uniqKey="Kleinbaum D" first="David G." last="Kleinbaum">David G. Kleinbaum</name><affiliation wicri:level="2"><nlm:aff id="aff001"><addr-line>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Addiss, David" sort="Addiss, David" uniqKey="Addiss D" first="David" last="Addiss">David Addiss</name><affiliation wicri:level="2"><nlm:aff id="aff003"><addr-line>Task Force for Global Health, Decatur, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Task Force for Global Health, Decatur, Georgia</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Fox, Leanne M" sort="Fox, Leanne M" uniqKey="Fox L" first="Leanne M." last="Fox">Leanne M. Fox</name><affiliation wicri:level="2"><nlm:aff id="aff002"><addr-line>Parasitic Diseases Branch, Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Parasitic Diseases Branch, Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="sec001"><title>Introduction</title><p>Episodes of acute adenolymphangitis (ADL) are often the first clinical sign of lymphatic filariasis (LF). They are often accompanied by swelling of the affected limb, inflammation, fever, and general malaise and lead to the progression of lymphedema. Although ADL episodes have been studied for a century or more, questions still remain as to their etiology. We quantified antibody levels to pathogens that potentially contribute to ADL episodes during and after an episode among lymphedema patients in Léogâne, Haiti. We estimated the proportion of ADL episodes hypothesized to be attributed to specific pathogens.</p></sec><sec id="sec002"><title>Methods</title><p>We measured antibody levels to specific pathogens during and following an ADL episode among 41 lymphedema patients enrolled in a cohort study in Léogâne, Haiti. We calculated the absolute and relative changes in antibody levels between the ADL and convalescent time points. We calculated the proportion of episodes that demonstrated a two-fold increase in antibody level for several bacterial, fungal, and filarial pathogens.</p></sec><sec id="sec003"><title>Results</title><p>Our results showed the greatest proportion of two-fold changes in antibody levels for the carbohydrate antigen <italic>Streptococcus</italic> group A, followed by IgG2 responses to a soluble filarial antigen (BpG2), Streptococcal Pyrogenic Exotoxin B, and an antigen for the fungal pathogen <italic>Candida</italic>. When comparing the median antibody level during the ADL episode to the median antibody level at the convalescent time point, only the antigens for <italic>Pseudomonas</italic> species (P-value = 0.0351) and Streptolysin O (P-value = 0.0074) showed a significant result.</p></sec><sec id="sec004"><title>Conclusion</title><p>Although our results are limited by the lack of a control group and few antibody responses, they provide some evidence for infection with <italic>Streptococcus A</italic> as a potential contributing factor to ADL episodes. Our results add to the current evidence and illustrate the importance of determining the causal role of bacterial and fungal pathogens and immunological antifilarial response in ADL episodes.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Ramaiah, Kd" uniqKey="Ramaiah K">KD Ramaiah</name></author><author><name sortKey="Ottesen, Ea" uniqKey="Ottesen E">EA Ottesen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Nutman, Tb" uniqKey="Nutman T">TB Nutman</name></author><author><name sortKey="Kazura, Jw" uniqKey="Kazura J">JW Kazura</name></author><author><name sortKey="Guerrant, Rl" uniqKey="Guerrant R">RL Guerrant</name></author><author><name sortKey="Walker, Dh" uniqKey="Walker D">DH Walker</name></author><author><name sortKey="Weller, Pf" uniqKey="Weller P">PF Weller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dreyer, G" uniqKey="Dreyer G">G 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<front><journal-meta><journal-id journal-id-type="nlm-ta">PLoS One</journal-id><journal-id journal-id-type="iso-abbrev">PLoS ONE</journal-id><journal-id journal-id-type="publisher-id">plos</journal-id><journal-id journal-id-type="pmc">plosone</journal-id><journal-title-group><journal-title>PLoS ONE</journal-title></journal-title-group><issn pub-type="epub">1932-6203</issn><publisher><publisher-name>Public Library of Science</publisher-name><publisher-loc>San Francisco, CA USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26492462</article-id><article-id pub-id-type="pmc">4619626</article-id><article-id pub-id-type="doi">10.1371/journal.pone.0141047</article-id><article-id pub-id-type="publisher-id">PONE-D-15-32812</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Changes in Antibody Levels during and following an Episode of Acute Adenolymphangitis (ADL) among Lymphedema Patients in Léogâne, Haiti</article-title><alt-title alt-title-type="running-head">Antibody Levels Associated with Acute Adenolymphangitis in Haiti</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Mues</surname><given-names>Katherine E.</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref><xref rid="cor001" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Lammie</surname><given-names>Patrick J.</given-names></name><xref ref-type="aff" rid="aff002"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Klein</surname><given-names>Mitchel</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kleinbaum</surname><given-names>David G.</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Addiss</surname><given-names>David</given-names></name><xref ref-type="aff" rid="aff003"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Fox</surname><given-names>LeAnne M.</given-names></name><xref ref-type="aff" rid="aff002"><sup>2</sup></xref></contrib></contrib-group><aff id="aff001"><label>1</label><addr-line>Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia, United States of America</addr-line></aff><aff id="aff002"><label>2</label><addr-line>Parasitic Diseases Branch, Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America</addr-line></aff><aff id="aff003"><label>3</label><addr-line>Task Force for Global Health, Decatur, Georgia, United States of America</addr-line></aff><contrib-group><contrib contrib-type="editor"><name><surname>Deribe</surname><given-names>Kebede</given-names></name><role>Editor</role><xref ref-type="aff" rid="edit1"></xref></contrib></contrib-group><aff id="edit1"><addr-line>Brighton and Sussex Medical School, UNITED KINGDOM</addr-line></aff><author-notes><fn fn-type="conflict" id="coi001"><p><bold>Competing Interests: </bold>The authors have declared that no competing interests exist.</p></fn><fn fn-type="con" id="contrib001"><p>Conceived and designed the experiments: KEM MK PJL LMF DGK. Performed the experiments: PJL. Analyzed the data: KEM. Contributed reagents/materials/analysis tools: PJL DA LMF. Wrote the paper: KEM DGK LMF PJL DA.</p></fn><corresp id="cor001">* E-mail: <email>Katie.mues@gmail.com</email></corresp></author-notes><pub-date pub-type="epub"><day>22</day><month>10</month><year>2015</year></pub-date><pub-date pub-type="collection"><year>2015</year></pub-date><volume>10</volume><issue>10</issue><elocation-id>e0141047</elocation-id><history><date date-type="received"><day>27</day><month>7</month><year>2015</year></date><date date-type="accepted"><day>2</day><month>10</month><year>2015</year></date></history><permissions><license xlink:href="https://creativecommons.org/publicdomain/zero/1.0/"><license-p>This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the <ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/publicdomain/zero/1.0/">Creative Commons CC0</ext-link> public domain dedication</license-p></license></permissions><self-uri content-type="pdf" xlink:type="simple" xlink:href="pone.0141047.pdf"></self-uri><abstract><sec id="sec001"><title>Introduction</title><p>Episodes of acute adenolymphangitis (ADL) are often the first clinical sign of lymphatic filariasis (LF). They are often accompanied by swelling of the affected limb, inflammation, fever, and general malaise and lead to the progression of lymphedema. Although ADL episodes have been studied for a century or more, questions still remain as to their etiology. We quantified antibody levels to pathogens that potentially contribute to ADL episodes during and after an episode among lymphedema patients in Léogâne, Haiti. We estimated the proportion of ADL episodes hypothesized to be attributed to specific pathogens.</p></sec><sec id="sec002"><title>Methods</title><p>We measured antibody levels to specific pathogens during and following an ADL episode among 41 lymphedema patients enrolled in a cohort study in Léogâne, Haiti. We calculated the absolute and relative changes in antibody levels between the ADL and convalescent time points. We calculated the proportion of episodes that demonstrated a two-fold increase in antibody level for several bacterial, fungal, and filarial pathogens.</p></sec><sec id="sec003"><title>Results</title><p>Our results showed the greatest proportion of two-fold changes in antibody levels for the carbohydrate antigen <italic>Streptococcus</italic> group A, followed by IgG2 responses to a soluble filarial antigen (BpG2), Streptococcal Pyrogenic Exotoxin B, and an antigen for the fungal pathogen <italic>Candida</italic>. When comparing the median antibody level during the ADL episode to the median antibody level at the convalescent time point, only the antigens for <italic>Pseudomonas</italic> species (P-value = 0.0351) and Streptolysin O (P-value = 0.0074) showed a significant result.</p></sec><sec id="sec004"><title>Conclusion</title><p>Although our results are limited by the lack of a control group and few antibody responses, they provide some evidence for infection with <italic>Streptococcus A</italic> as a potential contributing factor to ADL episodes. Our results add to the current evidence and illustrate the importance of determining the causal role of bacterial and fungal pathogens and immunological antifilarial response in ADL episodes.</p></sec></abstract><funding-group><funding-statement>This study was funded by grants from the Office of Women’s Health (<ext-link ext-link-type="uri" xlink:href="http://www.cdc.gov/women/">http://www.cdc.gov/women/</ext-link>), U.S. Centers for Disease Control and Prevention, Atlanta, Georgia; and the WHO/UNDP/World Bank Special Programme for Research and Training in Tropical Diseases (Filariasis Operational Research Project No. 950568) (<ext-link ext-link-type="uri" xlink:href="http://apps.who.int/tdr/index.html">http://apps.who.int/tdr/index.html</ext-link>). KEM was supported in part by Emory University, Laney Graduate School. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Centers for Disease Control and Prevention. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.</funding-statement></funding-group><counts><fig-count count="2"></fig-count><table-count count="2"></table-count><page-count count="13"></page-count></counts><custom-meta-group><custom-meta id="data-availability"><meta-name>Data Availability</meta-name><meta-value>Data are available from the Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention. To access the data, contact Monica Parise, M.D., Deputy Director for Science and Program, Division of Parasitic Diseases and Malaria Center for Global Health, Center for Disease Control and Prevention, by emailing <email>mparise@cdc.gov.</email></meta-value></custom-meta></custom-meta-group></article-meta><notes><title>Data Availability</title><p>Data are available from the Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention. To access the data, contact Monica Parise, M.D., Deputy Director for Science and Program, Division of Parasitic Diseases and Malaria Center for Global Health, Center for Disease Control and Prevention, by emailing <email>mparise@cdc.gov.</email></p></notes></front></pmc><affiliations><list><country><li>États-Unis</li></country><region><li>Géorgie (États-Unis)</li></region></list><tree><country name="États-Unis"><region name="Géorgie (États-Unis)"><name sortKey="Mues, Katherine E" sort="Mues, Katherine E" uniqKey="Mues K" first="Katherine E." last="Mues">Katherine E. Mues</name></region><name sortKey="Addiss, David" sort="Addiss, David" uniqKey="Addiss D" first="David" last="Addiss">David Addiss</name><name sortKey="Fox, Leanne M" sort="Fox, Leanne M" uniqKey="Fox L" first="Leanne M." last="Fox">Leanne M. Fox</name><name sortKey="Klein, Mitchel" sort="Klein, Mitchel" uniqKey="Klein M" first="Mitchel" last="Klein">Mitchel Klein</name><name sortKey="Kleinbaum, David G" sort="Kleinbaum, David G" uniqKey="Kleinbaum D" first="David G." last="Kleinbaum">David G. Kleinbaum</name><name sortKey="Lammie, Patrick J" sort="Lammie, Patrick J" uniqKey="Lammie P" first="Patrick J." last="Lammie">Patrick J. Lammie</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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