PULMONARY-LESIONS IN MICE INOCULATED WITH ACTINOBACILLUS-PLEUROPNEUMONIAE HEMOLYSIN AND LIPOPOLYSACCHARIDE

Non-Swiss albino (CF1) male mice were used as a model to study the eff ects of specific toxic components of Actinobacillus pleuropneumoniae o n the respiratory system. Mice were divided into five groups of ten ea ch and were inoculated by the intranasal route with whole-cell Actinob acillus pleuropneumoniae serotype 1, cell-free culture supernatant flu id (CFCSF) containing hemolysin protein, purified lipopolysaccharide ( LPS), heat-treated CFCSF, or phosphate-buffered saline solution. Pulmo nary lesions were evaluated at 6 and 12 hours after inoculation. Mice inoculated with whole cells, CFCSF, and LPS developed severe purulent bronchiolitis and alveolitis. Focal pulmonary necrosis was also observ ed in these three groups but was most consistent in the CFCSF-inoculat ed mice. Ultrastructurally, lungs from mice inoculated with whole cell s, LPS, and CFCSF were characterized by severe degenerative changes in type I and type II pneumocytes. Alveolar spaces contained cellular de bris and fibrin. Endothelial cells were swollen, and selected pulmonar y capillaries were occluded with platelets and fibrin. Infiltrating ne utrophils were often swollen, vacuolated, and degranulated. Although i noculation with relatively large numbers of A. pleuropneumoniae are re quired to kill mice, the mouse lung appears quite sensitive to the tox ic components produced by these bacteria. The elaboration of these two toxic components by A. pleuropneumoniae may be responsible for the ch aracteristic pulmonary inflammatory and necrotic lesions observed in i nfected swine.