About: Pulmonary pathology of severe acute respiratory syndrome in Toronto

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Pulmonary pathology of severe acute respiratory syndrome in Toronto
Creator	Butany, Jagdish Hwang, David Poutanen, Susan Asa, Sylvia Low, Donald Chamberlain, Dean
topic	covid:2e3b61da2cfd48b52834db5e8d624fb9b0d21fd5#this
Source	Medline; PMC
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.
has issue date	2004-07-23(xsd:dateTime)
bibo:doi	10.1038/modpathol.3800247
bibo:pmid	15272286
has license	no-cc
sha1sum (hex)	2e3b61da2cfd48b52834db5e8d624fb9b0d21fd5
schema:url	https://doi.org/10.1038/modpathol.3800247
resource representing a document's title	Pulmonary pathology of severe acute respiratory syndrome in Toronto
has PubMed Central identifier	PMC7100506
has PubMed identifier	15272286
schema:publication	Mod Pathol
resource representing a document's body	covid:2e3b61da2cfd48b52834db5e8d624fb9b0d21fd5#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/2e3b61da2cfd48b52834db5e8d624fb9b0d21fd5
is schema:about of	named entity 'material' named entity 'SARS-associated coronavirus' named entity 'RT-PCR' named entity 'histology' named entity 'mid-sized' named entity 'acute' named entity 'DIE' named entity 'SIZED' named entity 'A COMMON' named entity 'CASES' named entity 'MATERIAL' named entity 'HYPERPLASIA' named entity 'CHARACTERIZED' named entity 'THERAPY' named entity 'FEATURES' named entity 'FIBRIN' named entity 'EDEMA' named entity 'VASCULAR' named entity 'STAINS' named entity 'PNEUMOCYTE' named entity 'INFECTIONS' named entity '108' named entity 'ACUTE LUNG INJURY' named entity 'DIFFUSE ALVEOLAR DAMAGE' named entity 'TORONTO' named entity 'RELATED' named entity 'PULMONARY PATHOLOGY' named entity 'DURATION OF ILLNESS' named entity 'ALMOST ALWAYS' named entity 'THYROID TRANSCRIPTION FACTOR' named entity 'REMAINDER' named entity 'SARS-ASSOCIATED CORONAVIRUS' named entity 'OUTBREAK' named entity 'PULMONARY VESSELS' named entity 'LUNG TISSUES' named entity 'DIED' named entity 'ASPERGILLOSIS' named entity 'AUTOPSY' named entity 'SCATTERED' named entity 'LARGE' named entity 'DESCRIBE' named entity 'POST-MORTEM' named entity 'INTERVAL' named entity 'MID' named entity 'PROLIFERATIVE' named entity 'ORGANIZING PNEUMONIA' named entity 'THROMBI' named entity 'MAY BE' named entity 'PROBABLE' named entity 'SPECIAL' named entity 'ENDOTHELIAL' named entity 'ASSOCIATED WITH' named entity 'INVASIVE FUNGAL DISEASE' named entity 'CONVENTIONAL' named entity 'LUNG INJURY' named entity 'POSITIVE FOR' named entity 'MOLECULAR BIOLOGY' named entity 'IMMUNOHISTOCHEMISTRY' named entity 'FIBRINOUS' named entity 'ACUTE INJURY' named entity 'SMALL' named entity 'COINFECTION' named entity 'VARYING' named entity 'PULMONARY INFARCTS' named entity 'DEMONSTRATED' named entity 'CYTOKERATINS' named entity 'SQUAMOUS METAPLASIA' named entity 'HISTOLOGICALLY' named entity 'ADMIXTURE' named entity 'EXUDATIVE' named entity 'CONSISTENT WITH' named entity 'CYTOMEGALOVIRUS' named entity 'HUMAN' named entity 'HERPES SIMPLEX VIRUSES'

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