Histopathologic Changes and SARS-CoV-2 Immunostaining in the Lung of a Patient With COVID-19

Abstract

Histopathologic Changes and SARS–CoV-2 Immunostaining in the Lung of a Patient With COVID-19 Background: Although many studies have demonstrated the epidemiologic characteristics of SARS–CoV-2 disease (COVID-19), details of pathologic changes in the lung are still lacking. Objective: To describe the histopathologic changes in the lung of a patient with COVID-19. Case Report: A 72-year-old man with a history of diabetes and hypertension presented with fever and cough. His throat and pharyngeal swabs were positive for SARS–CoV-2 by day 6 after the initial symptoms. Rapidly progressive respiratory failure required endotracheal intubation and mechanical ventilation 1 week after presentation. Lung tissue was obtained by transthoracic 14-gauge needle biopsy from the left upper anterior segment (Figure 1, A, arrow), left upper lingular segment (Figure 1, B, arrow), and left lower lobe (Figure 1, C, arrow), coinciding with groundglass opacities on chest computed tomography (CT). Two throat swab samples were collected from the tonsils and posterior pharyngeal wall. Biopsy lung sections were analyzed with hematoxylin– eosin staining, and immunostaining for SARS–CoV-2 was conducted as reported elsewhere (1). Throat swabs were assessed for SARS–CoV-2 by using real-time reverse transcriptase polymerase chain reaction assays (2). The CT scans revealed patchy bilateral ground glass–like opacifications (Figure 1A-C, arrows). Despite antiviral therapies, respiratory and hemodynamic instability continued and the patient died 3 weeks after diagnosis. Permission for postmortem transthoracic needle biopsy, but not autopsy, was obtained from the patient's family. Histopathologic examination of lung biopsy tissues revealed diffuse alveolar damage, organizing phase. Denuded alveolar lining cells (Figure 2, A-1, arrow 1), with reactive type II pneumocyte hyperplasia, were noted (Figure 2, A-1, arrow 2). Intra-alveolar fibrinous exudates were present (Figure 2, A-2, arrow 3), along with loose interstitial fibrosis and chronic inflammatory infiltrates (Figure 2, A-2, arrow 4). Intra-alveolar loose fibrous plugs of organizing pneumonia were noted (Figure 2, A-3, arrow 5), with presence of intra-alveolar organizing fibrin seen in most foci (Figure 2, A-4, arrow 6). Immunostaining of lung sections with an antibody to the Rp3 NP protein of SARS–CoV-2 revealed prominent expression on alveolar epithelial cells (Figure 2, B, top panel), including damaged, desquamated cells within the alveolar space