136 Clinical Presentation and Diagnosis

progressive decrease in rates of viral shedding from the nasopharynx, stool, and urine from day 10 to 21 after the onset of symptoms. In addition, nearly half the patients had shifting radiographic shadows. If viral-induced damage was the primary pathological mechanism, such a flitting pattern of radiological change is difficult to explain (Peiris 2003b).

Taken together, these findings suggest that the lung damage at this phase is related to immunopathological damage as a result of an overexuberant host response, rather than uncontrolled viral replication (Peiris 2003b).

Histopathology

Lung Biopsy

The histopathological examination of a lung biopsy specimen from a patient with SARS showed a mild interstitial inflammation with scattered alveolar pneumocytes showing cytomegaly, granular amphophilic cytoplasm, and enlarged nuclei with prominent nucleoli. No cells showed inclusions typical of herpes virus or adenovirus infection (Peiris 2003a).

Postmortem Findings

Postmortem histopathological evaluations of lung tissue from patients who died from SARS showed diffuse alveolar damage at various levels of progression and severity, consistent with the pathologic manifestations of acute respiratory distress syndrome (Ksiazek, Tsang, Poutanen).

The changes included hyaline membrane formation, interstitial mononuclear inflammatory infiltrates, and desquamation of pneumocytes in alveolar spaces (Ksiazek, Nicholls). There were also scattered foci of alveolar myxoid fibroblastic tissue, a finding consistent with the early organizational phase of progressive pneumonia. Interalveolar septa were mildly thickened, with a mild mononuclear infiltrate (Tsang). Bronchial epithelial denudation, loss of cilia, and squamous metaplasia were early features (Nicholls). The presence of hemophagocytosis

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