Lung pathology of fatal severe acute respiratory syndrome

By J. Nicholls, L. Poon, Kam‐cheong Lee, Wai-fu Ng, S. Lai, C. Leung, C. Chu, Pak‐Kwan Hui, K. Mak, W. Lim and 6 more. The Lancet, 2003

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Summary Background 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. Published online May 16, 2003 http://image.thelancet.com/extras/03art4347web.pdf

Subfields: Infectious Diseases, Neurology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/c80e5480c3532c6eac348aba94aca49c1e280d79

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Citations in the corpus

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Effects of chloroquine on viral infections: an old drug against today's diseases (2003, background): “57 PRCV induces severe lung damage through immune-mediated mechanisms-ie, probably through an increase in the concentrations of proinflammatory cytokines such as TNF␣ and interleukin 6, whose role in inducing lung damage has been proved using adenoviral vectors in animal models.”
ACE2 Receptor Expression and Severe Acute Respiratory Syndrome Coronavirus Infection Depend on Differentiation of Human Airway Epithelia (2005, background): “Limited human pathological studies demonstrate that the respiratory tract is a major site of SARS-CoV infection and morbidity (8, 30).”
Severe Acute Respiratory Syndrome Coronavirus as an Agent of Emerging and Reemerging Infection (2007, background): “During the epidemic in 2003, 8,096 cases with 774 deaths had occurred in over 30 countries among five continents (89, 117, 144, 180, 182, 197, 236, 250, 259, 260, 270, 290, 292, 303, 336, 377).”
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Enteric involvement of severe acute respiratory syndrome-associated coronavirus infection (2003, background): “21 It is suggested that cytokine dysregulation plays an instrumental role in the determination of severity of lung disease.”
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