About: Summary Aims The severe acute respiratory syndrome (SARS) caused a large outbreak of atypical pneumonia in Beijing, China from early March 2003. We report the pathological features from three patients who died of SARS. Methods Autopsies were performed on three patients who died 9–15 days after the onset of the illness, and the clinical and laboratory features reviewed. Tissue sections were stained with haematoxylin and eosin (H&E), and in situ reverse transcriptase polymerase chain reaction (RT–PCR) on lung sections was performed using SARS coronavirus-specific primers. Results The typical gross pathological change in the lungs was diffuse haemorrhage on the lung surface. Histopathological examination revealed serous, fibrinous and haemorrhagic inflammation in most pulmonary alveoli, with capillary engorgement and some capillary microthrombosis. The pulmonary alveoli were thickened with interstitial mononuclear inflammatory infiltrates, diffuse alveolar damage, desquamation of pneumocytes and hyaline-membrane formation; fibrinoid material and erythrocytes were present in alveolar spaces. There were thromboemboli in some bronchial arterioles. Haemorrhagic necrosis and reduced numbers of lymphocytes were observed in lymph nodes and spleen. In situ RT–PCR detected SARS coronavirus RNA in type II alveolar cells, interstitial cells and bronchiolar epithelial cells from all three patients Conclusions Severe immunological damage in lung tissue is responsible for the clinical features of SARS.   Goto Sponge  NotDistinct  Permalink

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  • Summary Aims The severe acute respiratory syndrome (SARS) caused a large outbreak of atypical pneumonia in Beijing, China from early March 2003. We report the pathological features from three patients who died of SARS. Methods Autopsies were performed on three patients who died 9–15 days after the onset of the illness, and the clinical and laboratory features reviewed. Tissue sections were stained with haematoxylin and eosin (H&E), and in situ reverse transcriptase polymerase chain reaction (RT–PCR) on lung sections was performed using SARS coronavirus-specific primers. Results The typical gross pathological change in the lungs was diffuse haemorrhage on the lung surface. Histopathological examination revealed serous, fibrinous and haemorrhagic inflammation in most pulmonary alveoli, with capillary engorgement and some capillary microthrombosis. The pulmonary alveoli were thickened with interstitial mononuclear inflammatory infiltrates, diffuse alveolar damage, desquamation of pneumocytes and hyaline-membrane formation; fibrinoid material and erythrocytes were present in alveolar spaces. There were thromboemboli in some bronchial arterioles. Haemorrhagic necrosis and reduced numbers of lymphocytes were observed in lymph nodes and spleen. In situ RT–PCR detected SARS coronavirus RNA in type II alveolar cells, interstitial cells and bronchiolar epithelial cells from all three patients Conclusions Severe immunological damage in lung tissue is responsible for the clinical features of SARS.
Subject
  • Dermatologic terminology
  • Membrane biology
  • Metropolitan areas of China
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