Diffuse alveolar damage in cats induced by nitrogen dioxide or feline calicivirus.
The ultrastructural morphogenesis of pulmonary lesions was studied in cats exposed to either aerosols of feline calicivirus (FCV) or high concentrations of NO2. Both directly injured alveolar lining cells, particularly type I cells. Necrosis of pneumocytes attended by an acute exudative response in the air exchange tissues was evident from 0 through 24 hours after exposure of cats to NO2 and from 12 through 96 hours after infection with FCV. The reparative process following alveolar injury was characterized by regenerative hyperplasia of type II pneumocytes, proliferation of stromal cells, and infiltration of mononuclear cells. Differences in the lesions produced by NO2 and FCV also were encountered. Endothelial necrosis was detected only after NO2 injury, whereas a marked infiltration of neutrophils and immunocytes was observed only after FCV injury. The FCV/NO2 experimental system in cats is well suited for studies of diffuse alveolar damage of toxic and viral etiology.
D000818:Animals; D001980:Bronchi / Q000473:pathology; D002139:Caliciviridae; D002415:Cats; D007249:Inflammation; D008171:Lung Diseases / Q000139:chemically induced / Q000473:pathology*; D009336:Necrosis; D009585:Nitrogen Dioxide / Q000633:toxicity*; D011650:Pulmonary Alveoli / Q000473:pathology*; D014777:Virus Diseases / Q000473:pathology*
D009585:Nitrogen Dioxide