The clinical pathology of severe acute respiratory syndrome (SARS): a report from China

Abstract

In order to investigate the clinical pathology of severe acute respiratory syndrome (SARS), the autopsies of three patients who died from SARS in Nan Fang Hospital Guangdong, China were studied retrospectively. Routine haematoxylin and eosin (H&E) staining was used to study all of the tissues from the three cases. The lung tissue specimens were studied further with Macchiavello staining, viral inclusion body staining, reticulin staining, PAS staining, immunohistochemistry, ultrathin sectioning and staining, light microscopy, and transmission electron microscopy. The first symptom was hyperpyrexia in all three cases, followed by progressive dyspnoea and lung field shadowing. The pulmonary lesions included bilateral extensive consolidation, localized haemorrhage and necrosis, desquamative pulmonary alveolitis and bronchitis, proliferation and desquamation of alveolar epithelial cells, exudation of protein and monocytes, lymphocytes and plasma cells in alveoli, hyaline membrane formation, and viral inclusion bodies in alveolar epithelial cells. There was also massive necrosis of splenic lymphoid tissue and localized necrosis in lymph nodes. Systemic vasculitis included oedema, localized fibrinoid necrosis, and infiltration of monocytes, lymphocytes, and plasma cells into vessel walls in the heart, lung, liver, kidney, adrenal gland, and the stroma of striated muscles. Thrombosis was present in small veins. Systemic toxic changes included degeneration and necrosis of the parenchyma cells in the lung, liver, kidney, heart, and adrenal gland. Electron microscopy demonstrated clusters of viral particles, consistent with coronavirus, in lung tissue. SARS is a systemic disease that injures many organs. The lungs, immune organs, and systemic small vessels are the main targets of virus attack, so that extensive consolidation of the lung, diffuse alveolar damage with hyaline membrane formation, respiratory distress, and decreased immune function are the main causes of death.

Figure 1

Gross morphology of the lung

Figure 2

Alveoli filled with desquamated epithelial cells. (A) H&E (original magnification ×400). (B) Cytokeratin (streptavidin peroxidase, original magnification ×400)

Figure 3

Exudation of monocytes into alveoli. (A) H&E, original magnification ×400. (B) CD 68 (streptavidin peroxidase, original magnification ×400)

Figure 4

(A, B) Formation of hyaline membranes (H&E, original magnification ×200)

Figure 5

(A, B) Intracytoplasmic viral inclusion bodies in alveolar epithelial cells (H&E, original magnification ×400). (C) Purple viral inclusion bodies (Macchiavello staining, original magnification ×1000)

Figure 6

(A) There is no change in the width of the walls of abnormal alveoli (Ag, original magnification ×200). (B) Organization of alveolar exudates (A3, duration of 20 days) (H&E, original magnification ×200). (C) Organization of alveolar exudates (A3, duration of 20 days) (Ag, original magnification ×400)

Figure 7

(A–C) Mononuclear and multinucleate epithelial giant cells in alveoli (H&E, original magnification ×540)

Figure 8

(A) Thrombosis and local necrosis of a vein wall in the lung (H&E, original magnification ×200). (B) Vasculitis of small veins in the brain (H&E, original magnification ×200)

Figure 9

(A) Disappearance of a splenic corpuscle and (B) massive necrosis of lymphatic tissue (H&E, original magnification ×200)

Figure 10

(A) Dissociation of hepatocyte cords. (H&E, original magnification ×400). (B) Patchy necrosis of hepatocytes (H&E, original magnification ×200)

Figure 11

(A) Dilatation of SER and clusters of viral particles in smooth endoplasmic reticulin of type 2 alveolar pneumocyte (bar = 500 nm). (B) Amplified clusters of viral particles shown in A (bar = 200 nm)