We report herein a novel spontaneous chronic, progressive respiratory disease in domestic cats with the morphologic features of UIP; these features include the temporal heterogeneity, persistent, progressive proliferation of myofibroblasts/fibroblasts, and an association between IPF and the development of primary pulmonary neoplasia. The light microscopic and ultrastructure characteristics of the type II pneumocytes in spontaneous IPF of cats is similar to a familial form of IPF in humans, suggesting that the disease in cats may be genetically based, and providing an opportunity to develop the cat as a model to study the human disease. Based on these finding we conclude the following: (1) spontaneous chronic respiratory disease with both the clinical and pathology findings consistent with UIP/ IPF occurs in the domestic cat; (2) as with the human disease, hyperplastic type II pneumocytes and myofibroblasts are cellular constituents in feline IPF; (3) the changes in type II pneumocyte ultrastructure in feline IPF are similar to a familial form of human IPF associated with a mutation in the surfactant protein C gene; (4) the altered type II cell ultrastructure suggests spontaneous feline IPF is primarily a defect in the type II pneumocyte; and (5) understanding the cause(s) and pathogenesis of IPF in the cat holds promise for advancing our understanding of the disease in humans.
Tissue Collection and Preparation
Tissues were collected from either postmortem samples or open-lung biopsies of affected cats; normal feline lung was obtained from archived tissues at Michigan State University. Lung tissue samples from cats 1 to 4 and cats 13 to 15 were acquired through case material submitted to the Diagnostic Center for Population and Animal Health at Michigan State University. Cats 5 to 8 and cat 16 were submitted to the necropsy service at the North Carolina State University College of Veterinary Medicine; cats 9 to 12 were initially examined at the College of Veterinary Medicine, University of Missouri. All of the described tissues for histopathology were fixed in 10% neutral-buffered formalin and embedded in paraffin. The tissues were processed routinely for histopathology, with 6 |j,m sections placed on glass slides for hematoxylin-eosin (HE), Alcian blue/periodic acid Schiff (AB-PAS), and Masson trichrome staining. Unstained 6 |j,m sections were placed on glass slides for immunohistochem-istry.