ROLE OF THE PULMONARY INTRAVASCULAR MACROPHAGE IN INFLAMMATORY LUNG DISEASE OF CATS AND DOGS.
A.R.Dillona, A. Warner,b J. Hudsona, R Molinab; College of Veterinary Medicinea, Auburn University, Auburn, AL; Animal Resources Centerb, Harvard Medical School, Boston, MA.
The differing clinical syndromes associated with D. Immitis infection in dogs and cats may result from between-species differences in pulmonary response to infection. To evaluate and compare the changes in pulmonary pathology arising from infection with D. Immitis, dead heartworms and live heartworms (2/cat and 14/dog) were surgically transplanted into 4 cats and 4 dogs. Radiographic evaluation and gamma reticuloendothelial scintigraphy with Tc99 sulfa-colloid were performed before and after transplantation. Lung lobes were collected for light and electron microscopic evaluation. Macrophage activity was evaluated by measuring Tc99 radioactivity in tissue samples of lung, liver, spleen, kidney, heart, skeletal M, bone marrow, and blood. Single Photon Emission Computer Tomography (SPECT) after Tc99 was used to determine the 3 dimensional distribution of PIMs.
In dogs 1 week after transplantation of dead heartworms, there was severe Type 1 Cell edema and focal damage with marked fibrosis. In cats 1 week after transplantation of dead heartworms, there was marked Type II cell hyperplasia with less fibrosis and elastin deposition than in the dogs. Glycocalix surface changes in PIMs of cats showed evidence of stimulation. PIM activity was absent in the dogs with live or dead heartworms. Phagocytic activity was greater in the lung that in the liver of all cats studied. Total lung PIM activity was decreased in cats with live heartworms as compared to normal cats and cats with dead heartworms. The suppression of PIM activity with live heartworms was not as significant as that induced by gadolinium chloride (GdCl3) administration. The PIM suppression by D. immitis and GdCl3 would appear to be uniform in all areas of the lung. These data would suggest that live heartworms may elaborate a macrophage inhibiting factor that suppresses PIM activity in cats and the loss of this inhibiting factor may contribute to the acute inflammatory lung changes associated with heartworm death in cats.