Lung pathology of fatal severe acute respiratory syndrome

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. Post-mortem tissue samples from six patients who died from SARS in February and March, 2003, and a...

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Published in:	The Lancet (British edition) Vol. 361; no. 9371; pp. 1773 - 1778
Main Authors:	Nicholls, John M, Poon, Leo LM, Lee, Kam C, Ng, Wai F, Lai, Sik T, Leung, Chung Y, Chu, Chung M, Hui, Pak K, Mak, Kong L, Lim, Wilna, Yan, Kin W, Chan, Kwok H, Tsang, Ngai C, Guan, Yi, Yuen, Kwok Y, Malik Peiris, JS
Format:	Journal Article
Language:	English
Published:	London Elsevier Ltd 24-05-2003 Lancet Elsevier Limited
Subjects:	Adult Alveoli Atrophy Autopsies Autopsy Biological and medical sciences Biopsy Bronchi - pathology Cell Nucleus - ultrastructure Cell proliferation Cilia Coronaviridae Coronaviruses COVID-19 Cytoplasm Damage detection Denudation Electron microscopy Epidemics Epithelial cells Fatal Outcome Fatalities Female Fever Giant Cells - ultrastructure Histology Hospitals Human viral diseases Humans Hypertension Identification methods Illnesses Immunohistochemistry Infectious diseases Influenza Lung - pathology Lung - virology Lungs Macrophages Male Medical research Medical sciences Metaplasia Microscopy Middle Aged Morphology Organ Size Pathogenesis Pathology Patients Pneumocytes Pneumonia Respiratory distress syndrome SARS Virus - isolation & purification Serology Severe acute respiratory syndrome Severe Acute Respiratory Syndrome - complications Severe Acute Respiratory Syndrome - pathology Severe Acute Respiratory Syndrome - virology Spleen Tropical medicine Viral diseases Viral diseases of the respiratory system and ent viral diseases Viruses White pulp Hong Kong China China Immunohistochemistry Electron microscope Lung disease Respiratory disease Acute Lung Serology Syndrome Infection Virus Pathology Coronavirus Autopsy Viral disease Evolution Death Molecular biology Coronaviridae Pneumopathy Reverse transcription polymerase chain reaction Nidovirales
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Summary:	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. 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. 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. 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. Published online May 16, 2003 http://image.thelancet.com/extras/03art4347web.pdf
Bibliography:	ObjectType-Case Study-3 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-4 content type line 23 ObjectType-Report-2
ISSN:	0140-6736 1474-547X
DOI:	10.1016/S0140-6736(03)13413-7