Figure 3: Histologic findings in the respiratory tracts of ferrets inoculated with A/Anhui/1/2013 (H7N9) influenza virus.
From: Mammalian adaptation of influenza A(H7N9) virus is limited by a narrow genetic bottleneck
Representative features observed in tracheas (a–c), bronchi (d–f), bronchioles (g–i) and alveoli (j–o) on day 3 (a,d,g,h,i,j,k,n,o) and day 5 (b,c,e,f,l,m) post inoculation. Stains were hematoxylin and eosin (a,b,d,g,h,j,k) or immunohistochemical stains for influenza A virus nucleoprotein (c,e,f,i,l), pneumocyte type II cells (m; surfactant protein c), macrophages (n; ionized calcium-binding adapter molecule 1), and neutrophils (o; myeloperoxidase). Influenza A was detected in tracheas (c), bronchi (e), submucosal glands (f), bronchioles (i) and alveolar epithelial cells (l) (blue arrows). (a–c) Tracheas showed multifocal epithelial hyperplasia (b) and mucosal and submucosal (a,b) neutrophil and lymphocyte infiltration. (d–f) Bronchi showed multifocal epithelial hyperplasia, submucosal gland epithelial necrosis, macrophage and neutrophil infiltration, and luminal macrophages, neutrophils and cellular debris (d, black arrow). (g–i) Bronchioles showed epithelial necrosis (g, black arrowheads), regenerative hyperplasia (h, blue arrowhead), and marked luminal macrophage, neutrophil and lymphocyte infiltrates admixed with cellular debris (g,h, black arrows). (j–o) Peribronchiolar alveoli (j,k) had varying degrees of pneumocyte necrosis and regeneration (type II hyperplasia; m, black arrows), macrophage infiltration (n, black arrowheads), neutrophil infiltration (o, blue arrowheads), oedema (k, black arrow) and cellular debris. Scale bars, 20μ—h, m; 50μ—a,b,c,e,f,g,i,j,k,l,n,o; 100μ—d.
