Lesions of Pulmonary Pleura Associated with Canine Heartworm Disease

One important aspect of canine heartworm disease caused by Dirofiluriu immitis is the damage that occurs in the lungs. This includes not only pulmonary arterial disease, manifested by intimal villous hyperplasia, subintimal fibrosis, parasitic thromboembolism and periarterial disease, but also interalveolar fibrosis, alveolar epithelialization, and hemosideroPulmonary pleural lesions, either in association with sis. I. 3.4.7 or separate from underlying lung pathology, have never been reported. Lung tissue was collected from dogs with heartworm disease which were submitted for routine necropsy. Tissues were fixed, embedded in parafin, and stained with hematoxylin and eosin (HE). Selected tissues were stained for hemosiderin with Perk’ Prussian blue, for elastic fibers with Miller’s modification of Weigert’s stain, and for collagen by Heidenhain’s azan. Not all dogs with heartworms had clinical or pathological evidence of heartworm disease. Only dogs with moderate or severe clinical disease had pleural changes. Dogs with mild disease had pulmonary arterial intimal proliferation, but there was no gross or histological evidence of parenchymal or pleural involvement. The most severely affected lungs had a generalized mottled appearance as a result of diffuse hemosiderosis, congestion, scattered focal, and sometimes extensive, hemorrhage and focal areas of fibrosis. The latter changes involved the pleura (fig. 1). There were areas of prominent neovascularization on the pleural surface, which were either associated with pulmonary hemorrhage (fig. l) or were present with no other apparent focal abnormality (fig. 2). Where diffuse hemosiderosis was a prominent feature, there was a reduction in the intensity of hemosiderin in the neovascularized areas. The lesions were generalized but were more severe, particularly in the right caudal lobe; they were also present in the left caudal and right middle lobes. An exception to this was ventral consolidation, consistent with bronchopneumonia in the cranial and middle lobes of some lungs. In moderate cases, the visible gross lesions in the lungs were confined to the caudal lobes with the right lobe affected more frequently. The pulmonary artery had scattered focal areas of intimal proliferation and blockage or partial blockage of the distal branches by parasitic thrombi. The latter were more frequent in the caudal lobes, particularly the right. The lung parenchyma that surrounded the thrombi frequently had hemorrhage that usually extended to the pleural surface. The histological association between lung changes and pleural changes in the sections examined varied. One prominent change was cuboidal transformation of the mesothelium (fig. 3), but this could not be related to any consistent pathological changes in the submesothelium. The most widespread lesion in the pulmonary pleura was separation between the mesothelium and the elastic fibers, due most frequently to the formation of fibrous tissue. This varied from being dense and well organized to active proliferation-often with a heavy infiltration of inflammatory cells and capillary proliferation (fig. 4). Pleural lesions usually were associated with a marked interstitial inflammatory reaction of the adjacent alveolar septa. Where the fibrous tissue extended beneath the elastic