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Article: Lung pathology of fatal severe acute respiratory syndrome

TitleLung pathology of fatal severe acute respiratory syndrome
Authors
Issue Date2003
PublisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/lancet
Citation
Lancet, 2003, v. 361 n. 9371, p. 1773-1778 How to Cite?
AbstractBackground: Severe acute respiratory syndrome (SARS) is a novel infectious disease with global impact. A virus from the family Coronaviridae has been identified as the cause, but the pathogenesis is still unclear. Methods: Post-mortem tissue samples from six patients who died from SARS in February and March, 2003, and an open lung biopsy from one of these patients were studied by histology and virology. Only one full autopsy was done. Evidence of infection with the SARS-associated coronavirus (SARS-CoV) and human metapneumovirus was sought by reverse-transcriptase PCR and serology. Pathological samples were examined by light and electron microscopy and immunohistochemistry. Findings: All six patients had serological evidence of recent infection with SARS-CoV. Diffuse alveolar damage was common but not universal. Morphological changes identified were bronchial epithelial denudation, loss of cilia, and squamous metaplasia. Secondary bacterial pneumonia was present in one case. A giant-cell infiltrate was seen in four patients, with a pronounced increase in macrophages in the alveoli and the interstitium of the lung. Haemophagocytosis was present in two patients. The alveolar pneumocytes also showed cytomegaly with granular amphophilic cytoplasm. The patient for whom full autopsy was done had atrophy of the white pulp of the spleen. Electron microscopy revealed viral particles in the cytoplasm of epithelial cells corresponding to coronavirus. Interpretation: SARS is associated with epithelial-cell proliferation and an increase in macrophages in the lung. The presence of haemophagocytosis supports the contention that cytokine dysregulation may account, at least partly, for the severity of the clinical disease. The case definition of SARS should acknowledge the range of lung pathology associated with this disease.
Persistent Identifierhttp://hdl.handle.net/10722/79196
ISSN
2015 Impact Factor: 44.002
2015 SCImago Journal Rankings: 14.638
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorPoon, LLMen_HK
dc.contributor.authorLee, KCen_HK
dc.contributor.authorNg, WFen_HK
dc.contributor.authorLai, STen_HK
dc.contributor.authorLeung, CYen_HK
dc.contributor.authorChu, CMen_HK
dc.contributor.authorHui, PKen_HK
dc.contributor.authorMak, KLen_HK
dc.contributor.authorLim, Wen_HK
dc.contributor.authorYan, KWen_HK
dc.contributor.authorChan, KHen_HK
dc.contributor.authorTsang, NCen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorYuen, KYen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.date.accessioned2010-09-06T07:51:46Z-
dc.date.available2010-09-06T07:51:46Z-
dc.date.issued2003en_HK
dc.identifier.citationLancet, 2003, v. 361 n. 9371, p. 1773-1778en_HK
dc.identifier.issn0140-6736en_HK
dc.identifier.urihttp://hdl.handle.net/10722/79196-
dc.description.abstractBackground: Severe acute respiratory syndrome (SARS) is a novel infectious disease with global impact. A virus from the family Coronaviridae has been identified as the cause, but the pathogenesis is still unclear. Methods: Post-mortem tissue samples from six patients who died from SARS in February and March, 2003, and an open lung biopsy from one of these patients were studied by histology and virology. Only one full autopsy was done. Evidence of infection with the SARS-associated coronavirus (SARS-CoV) and human metapneumovirus was sought by reverse-transcriptase PCR and serology. Pathological samples were examined by light and electron microscopy and immunohistochemistry. Findings: All six patients had serological evidence of recent infection with SARS-CoV. Diffuse alveolar damage was common but not universal. Morphological changes identified were bronchial epithelial denudation, loss of cilia, and squamous metaplasia. Secondary bacterial pneumonia was present in one case. A giant-cell infiltrate was seen in four patients, with a pronounced increase in macrophages in the alveoli and the interstitium of the lung. Haemophagocytosis was present in two patients. The alveolar pneumocytes also showed cytomegaly with granular amphophilic cytoplasm. The patient for whom full autopsy was done had atrophy of the white pulp of the spleen. Electron microscopy revealed viral particles in the cytoplasm of epithelial cells corresponding to coronavirus. Interpretation: SARS is associated with epithelial-cell proliferation and an increase in macrophages in the lung. The presence of haemophagocytosis supports the contention that cytokine dysregulation may account, at least partly, for the severity of the clinical disease. The case definition of SARS should acknowledge the range of lung pathology associated with this disease.en_HK
dc.languageengen_HK
dc.publisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/lanceten_HK
dc.relation.ispartofLanceten_HK
dc.subject.meshAdulten_HK
dc.subject.meshBiopsyen_HK
dc.subject.meshBronchi - pathologyen_HK
dc.subject.meshCell Nucleus - ultrastructureen_HK
dc.subject.meshFatal Outcomeen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGiant Cells - ultrastructureen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLung - pathology - virologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMetaplasiaen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshOrgan Sizeen_HK
dc.subject.meshSARS Virus - isolation & purificationen_HK
dc.subject.meshSevere Acute Respiratory Syndrome - complications - pathology - virologyen_HK
dc.titleLung pathology of fatal severe acute respiratory syndromeen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0140-6736&volume=361&issue=9371&spage=1773&epage=1778&date=2003&atitle=Lung+pathology+of+fatal+severe+acute+respiratory+syndromeen_HK
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hken_HK
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.identifier.authorityPoon, LLM=rp00484en_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0140-6736(03)13413-7en_HK
dc.identifier.pmid12781536-
dc.identifier.scopuseid_2-s2.0-0038024612en_HK
dc.identifier.hkuros81987en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038024612&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume361en_HK
dc.identifier.issue9371en_HK
dc.identifier.spage1773en_HK
dc.identifier.epage1778en_HK
dc.identifier.isiWOS:000183074800009-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK
dc.identifier.scopusauthoridPoon, LLM=7005441747en_HK
dc.identifier.scopusauthoridLee, KC=7501503975en_HK
dc.identifier.scopusauthoridNg, WF=7401613384en_HK
dc.identifier.scopusauthoridLai, ST=7402937038en_HK
dc.identifier.scopusauthoridLeung, CY=7402612388en_HK
dc.identifier.scopusauthoridChu, CM=7404345558en_HK
dc.identifier.scopusauthoridHui, PK=35869139500en_HK
dc.identifier.scopusauthoridMak, KL=35735787500en_HK
dc.identifier.scopusauthoridLim, W=7202378277en_HK
dc.identifier.scopusauthoridYan, KW=7102869279en_HK
dc.identifier.scopusauthoridChan, KH=7406034307en_HK
dc.identifier.scopusauthoridTsang, NC=36940414600en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK

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