Ultrastructural morphogenesis of acute viral pneumonia produced by feline calicivirus.
The ultrastructural morphogenesis of acute viral pneumonia was studied in pathogen-free cats exposed to aerosols of a virulent strain of feline calicivirus. Electron microscopy and fluorescence microscopy indicated that the virus had a marked tropism for alveolar pneumocytes. Viral-induced necrosis of pneumocytes was observed as early as 12 hours after exposure and was associated with acute serofibrinous and neutrophilic inflammation in the distal air exchange tissue. The acute exudative phase abated by 168 hours after exposure. The regenerative phase that followed was characterized by hyperplasia of type II pneumocytes; influx of monocytes, lymphocytes, and plasma cells; and interalveolar and intraalveolar proliferation of fibroblasts. The decrease in pneumocyte injury coincided with the increase in alveolar macrophages and immunocytes. With minor exceptions, feline calicivirus-induced alveolar damage and the subsequent repair resembled toxic alveolar injury produced by oxidant gases. Feline caliciviral pneumonia, therefore, is a naturally occurring example of viral-induced diffuse alveolar damage.
D000818:Animals; D002139:Caliciviridae / Q000648:ultrastructure; D002371:Cat Diseases / Q000473:pathology*; D002415:Cats; D005260:Female; D008168:Lung / Q000648:ultrastructure*; D008297:Male; D011024:Pneumonia, Viral / Q000473:pathology / Q000662:veterinary*; D011650:Pulmonary Alveoli / Q000648:ultrastructure