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Pulmonary pathology of severe acute respiratory syndrome in Toronto

Identifieur interne : 001552 ( Pmc/Checkpoint ); précédent : 001551; suivant : 001553

Pulmonary pathology of severe acute respiratory syndrome in Toronto

Auteurs : David M. Hwang ; Dean W. Chamberlain ; Susan M. Poutanen ; Donald E. Low ; Sylvia L. Asa ; Jagdish Butany

Source :

RBID : PMC:7100506

Abstract

The severe acute respiratory syndrome (SARS) pandemic in Toronto resulted in a large number of autopsies on its victims. We describe the pulmonary pathology of patients who died in the 2003 Toronto outbreak. Autopsy material from the lungs of 20 patients who died between March and July 2003 were characterized by histology, molecular biology, and immunohistochemistry for cytokeratins, thyroid transcription factor-1, CD68, Epstein–Barr virus, cytomegalovirus, and human herpes simplex viruses. Matched controls were obtained from patients who died of other causes over the same interval. The mean duration of illness was 27 days (range 5–108 days). Post-mortem lung tissues from 19 of 20 patients with probable SARS were positive for SARS-associated coronavirus by RT-PCR. Histologically, all patients showed varying degrees of exudative and proliferative phase acute lung injury, evidenced in conventional and immunohistochemical stains by edema, inflammatory infiltrate, pneumocyte hyperplasia, fibrinous exudates, and organization. Eight of 20 patients showed predominantly a diffuse alveolar damage pattern of acute lung injury, six showed predominantly an acute fibrinous and organizing pneumonia pattern, and the remainder showed an admixture of the two patterns. Squamous metaplasia and scattered multinucleate giant cells were present in most cases. Vascular fibrin thrombi were a common finding and were often associated with pulmonary infarcts. Special stains demonstrated vascular endothelial damage of both small- and mid-sized pulmonary vessels. Two cases were complicated by invasive fungal disease consistent with Aspergillosis, and another by coinfection with cytomegalovirus. Our findings indicate that the lungs of patients who die of SARS are almost always positive for the SARS-associated coronavirus by RT-PCR, and may show features of both diffuse alveolar damage and acute fibrinous and organizing pneumonia patterns of acute injury. Cases of SARS may be complicated by coexistent infections and therapy-related lung injury.


Url:
DOI: 10.1038/modpathol.3800247
PubMed: 15272286
PubMed Central: 7100506


Affiliations:


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PMC:7100506

Le document en format XML

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<p id="Par1">The severe acute respiratory syndrome (SARS) pandemic in Toronto resulted in a large number of autopsies on its victims. We describe the pulmonary pathology of patients who died in the 2003 Toronto outbreak. Autopsy material from the lungs of 20 patients who died between March and July 2003 were characterized by histology, molecular biology, and immunohistochemistry for cytokeratins, thyroid transcription factor-1, CD68, Epstein–Barr virus, cytomegalovirus, and human herpes simplex viruses. Matched controls were obtained from patients who died of other causes over the same interval. The mean duration of illness was 27 days (range 5–108 days). Post-mortem lung tissues from 19 of 20 patients with probable SARS were positive for SARS-associated coronavirus by RT-PCR. Histologically, all patients showed varying degrees of exudative and proliferative phase acute lung injury, evidenced in conventional and immunohistochemical stains by edema, inflammatory infiltrate, pneumocyte hyperplasia, fibrinous exudates, and organization. Eight of 20 patients showed predominantly a diffuse alveolar damage pattern of acute lung injury, six showed predominantly an acute fibrinous and organizing pneumonia pattern, and the remainder showed an admixture of the two patterns. Squamous metaplasia and scattered multinucleate giant cells were present in most cases. Vascular fibrin thrombi were a common finding and were often associated with pulmonary infarcts. Special stains demonstrated vascular endothelial damage of both small- and mid-sized pulmonary vessels. Two cases were complicated by invasive fungal disease consistent with Aspergillosis, and another by coinfection with cytomegalovirus. Our findings indicate that the lungs of patients who die of SARS are almost always positive for the SARS-associated coronavirus by RT-PCR, and may show features of both diffuse alveolar damage and acute fibrinous and organizing pneumonia patterns of acute injury. Cases of SARS may be complicated by coexistent infections and therapy-related lung injury.</p>
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<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Mod Pathol</journal-id>
<journal-id journal-id-type="iso-abbrev">Mod. Pathol</journal-id>
<journal-title-group>
<journal-title>Modern Pathology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0893-3952</issn>
<issn pub-type="epub">1530-0285</issn>
<publisher>
<publisher-name>Nature Publishing Group US</publisher-name>
<publisher-loc>New York</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">15272286</article-id>
<article-id pub-id-type="pmc">7100506</article-id>
<article-id pub-id-type="publisher-id">BF3800247</article-id>
<article-id pub-id-type="doi">10.1038/modpathol.3800247</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Pulmonary pathology of severe acute respiratory syndrome in Toronto</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Hwang</surname>
<given-names>David M</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Chamberlain</surname>
<given-names>Dean W</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Poutanen</surname>
<given-names>Susan M</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff3">3</xref>
<xref ref-type="aff" rid="Aff4">4</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Low</surname>
<given-names>Donald E</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff3">3</xref>
<xref ref-type="aff" rid="Aff4">4</xref>
<xref ref-type="aff" rid="Aff5">5</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Asa</surname>
<given-names>Sylvia L</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Butany</surname>
<given-names>Jagdish</given-names>
</name>
<address>
<email>jagdish.butany@uhn.on.ca</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<aff id="Aff1">
<label>1</label>
Toronto Medical Laboratories, Toronto, Ontario Canada</aff>
<aff id="Aff2">
<label>2</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.231844.8</institution-id>
<institution-id institution-id-type="ISNI">0000 0004 0474 0428</institution-id>
<institution>Department of Pathology,</institution>
<institution>University Health Network,</institution>
</institution-wrap>
Toronto, Ontario Canada</aff>
<aff id="Aff3">
<label>3</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.17063.33</institution-id>
<institution-id institution-id-type="ISNI">0000 0001 2157 2938</institution-id>
<institution>Department of Laboratory Medicine and Pathobiology,</institution>
</institution-wrap>
Toronto, Ontario Canada</aff>
<aff id="Aff4">
<label>4</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.416166.2</institution-id>
<institution-id institution-id-type="ISNI">0000 0004 0473 9881</institution-id>
<institution>Department of Microbiology,</institution>
<institution>Mount Sinai Hospital,</institution>
</institution-wrap>
Toronto, Ontario Canada</aff>
<aff id="Aff5">
<label>5</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.17063.33</institution-id>
<institution-id institution-id-type="ISNI">0000 0001 2157 2938</institution-id>
<institution>Department of Medicine,</institution>
<institution>University of Toronto,</institution>
</institution-wrap>
Toronto, Ontario Canada</aff>
</contrib-group>
<pub-date pub-type="epub">
<day>23</day>
<month>7</month>
<year>2004</year>
</pub-date>
<pub-date pub-type="ppub">
<year>2005</year>
</pub-date>
<volume>18</volume>
<issue>1</issue>
<fpage>1</fpage>
<lpage>10</lpage>
<history>
<date date-type="received">
<day>2</day>
<month>4</month>
<year>2004</year>
</date>
<date date-type="rev-recd">
<day>29</day>
<month>6</month>
<year>2004</year>
</date>
<date date-type="accepted">
<day>30</day>
<month>6</month>
<year>2004</year>
</date>
</history>
<permissions>
<copyright-statement>© United States and Canadian Academy of Pathology, Inc. 2005</copyright-statement>
<license>
<license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p>
</license>
</permissions>
<abstract id="Abs1">
<p id="Par1">The severe acute respiratory syndrome (SARS) pandemic in Toronto resulted in a large number of autopsies on its victims. We describe the pulmonary pathology of patients who died in the 2003 Toronto outbreak. Autopsy material from the lungs of 20 patients who died between March and July 2003 were characterized by histology, molecular biology, and immunohistochemistry for cytokeratins, thyroid transcription factor-1, CD68, Epstein–Barr virus, cytomegalovirus, and human herpes simplex viruses. Matched controls were obtained from patients who died of other causes over the same interval. The mean duration of illness was 27 days (range 5–108 days). Post-mortem lung tissues from 19 of 20 patients with probable SARS were positive for SARS-associated coronavirus by RT-PCR. Histologically, all patients showed varying degrees of exudative and proliferative phase acute lung injury, evidenced in conventional and immunohistochemical stains by edema, inflammatory infiltrate, pneumocyte hyperplasia, fibrinous exudates, and organization. Eight of 20 patients showed predominantly a diffuse alveolar damage pattern of acute lung injury, six showed predominantly an acute fibrinous and organizing pneumonia pattern, and the remainder showed an admixture of the two patterns. Squamous metaplasia and scattered multinucleate giant cells were present in most cases. Vascular fibrin thrombi were a common finding and were often associated with pulmonary infarcts. Special stains demonstrated vascular endothelial damage of both small- and mid-sized pulmonary vessels. Two cases were complicated by invasive fungal disease consistent with Aspergillosis, and another by coinfection with cytomegalovirus. Our findings indicate that the lungs of patients who die of SARS are almost always positive for the SARS-associated coronavirus by RT-PCR, and may show features of both diffuse alveolar damage and acute fibrinous and organizing pneumonia patterns of acute injury. Cases of SARS may be complicated by coexistent infections and therapy-related lung injury.</p>
</abstract>
<kwd-group xml:lang="en">
<title>Keywords</title>
<kwd>severe acute respiratory syndrome</kwd>
<kwd>diffuse alveolar damage</kwd>
<kwd>acute respiratory distress syndrome</kwd>
<kwd>lung pathology</kwd>
</kwd-group>
<custom-meta-group>
<custom-meta>
<meta-name>issue-copyright-statement</meta-name>
<meta-value>© United States & Canadian Academy of Pathology 2005</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<affiliations>
<list></list>
<tree>
<noCountry>
<name sortKey="Asa, Sylvia L" sort="Asa, Sylvia L" uniqKey="Asa S" first="Sylvia L" last="Asa">Sylvia L. Asa</name>
<name sortKey="Butany, Jagdish" sort="Butany, Jagdish" uniqKey="Butany J" first="Jagdish" last="Butany">Jagdish Butany</name>
<name sortKey="Chamberlain, Dean W" sort="Chamberlain, Dean W" uniqKey="Chamberlain D" first="Dean W" last="Chamberlain">Dean W. Chamberlain</name>
<name sortKey="Hwang, David M" sort="Hwang, David M" uniqKey="Hwang D" first="David M" last="Hwang">David M. Hwang</name>
<name sortKey="Low, Donald E" sort="Low, Donald E" uniqKey="Low D" first="Donald E" last="Low">Donald E. Low</name>
<name sortKey="Poutanen, Susan M" sort="Poutanen, Susan M" uniqKey="Poutanen S" first="Susan M" last="Poutanen">Susan M. Poutanen</name>
</noCountry>
</tree>
</affiliations>
</record>

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