Pulmonary Lesions in Mice Inoculated with Actinobacillus pleuropneumoniae Hemolysin and Lipopolysaccharide

Abstract

Non-Swiss albino (CF1) male mice were used as a model to study the effects of specific toxic components of Actinobacillus pleuropneumoniae on the respiratory system. Mice were divided into five groups of ten each and were inoculated by the intranasal route with whole-cell Actinobacillus pleuropneumoniae serotype 1, cell-free culture supernatant fluid (CFCSF) containing hemolysin protein, purified lipopolysaccharide (LPS), heat-treated CFCSF, or phosphate-buffered saline solution. Pulmonary 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 observed in these three groups but was most consistent in the CFCSF-inoculated mice. Ultrastructurally, lungs from mice inoculated with whole cells, LPS, and CFCSF were characterized by severe degenerative changes in type I and type II pneumocytes. Alveolar spaces contained cellular debris and fibrin. Endothelial cells were swollen, and selected pulmonary capillaries were occluded with platelets and fibrin. Infiltrating neutrophils were often swollen, vacuolated, and degranulated. Although inoculation with relatively large numbers of A. pleuropneumoniae are required to kill mice, the mouse lung appears quite sensitive to the toxic components produced by these bacteria. The elaboration of these two toxic components by A. pleuropneumoniae may be responsible for the characteristic pulmonary inflammatory and necrotic lesions observed in infected swine.