Abstract
Twenty-seven six-week-old cesarean-derived, colostrum-deprived pigs were inoculated intratracheally with an isolate of Haemophilus pleuropneumoniae serotype 5 (principles) of high virulence (I-200) or low virulence (B-8) or phosphate buffered saline (controls). Pigs given I-200 had severe serofibrinous pleuropneumonia at three hours after inoculation; two of three pigs were dead by 24 hours after inoculation. Interalveolar septa in the caudal lung lobes were 41% thicker than septa from control pigs at three hours after inoculation and 79% thicker by 24 hours after inoculation. Interalveolar septal capillaries in caudal lung lobes were 10.2% larger than control capillaries at three hours after inoculation and 25.6% larger by 24 hours after inoculation. Interalveolar septal capillary platelet volume was greater than the platelet volume of controls; 70% of these platelets were aggregated. There was severe diffuse alveolar, interalveolar septal, and interlobular septal edema at three hours after inoculation with fibrin, neutrophils, and macrophages present in later samples. Thirty-three percent of the lung parenchyma was necrotic at 24 hours after inoculation. Endothelial cell degeneration was generally mild, but necrotic in regions of pulmonary infarction. Pigs inoculated with the B-8 isolate did not develop marked macroscopic lesions at any sampling time. Interalveolar septa were 18% thicker than controls nine hours after inoculation and 5% thicker at six and 24 hours after inoculation. Capillary platelet volume was greatest at nine hours after inoculation with 50% of these platelets aggregated; 30% of the platelet volume was aggregated at the 24-hour sample period. Moderate diffuse pulmonary and interlobular septal edema was present at three, six, and nine hours after inoculation, but absent 24 hours after inoculation. Intravascular macrophages were present in the six, nine, and 24-hour lung samples in both B-8 and I-200 inoculated pigs. These cells were adherent to interalveolar septal capillary endothelial cells and contained phagocytized cellular debris and fibrin. These results indicate the early effects of H., pleuropneumoniae infection involve macrophage and platelet activation, and a marked increase in interalveolar septal capillary permeability.