1986 Volume 48 Issue 2 Pages 377-387
Specific-pathogen-free (SPF) neonatal pigs were intranasally inoculated with serotype D strains of Pasteurella multocida and/or strain L3 of Bordetella bronchiseptica, and their lesions were studied. Marked inflammatory changes were observed only after the infection with B. bronchiseptica. Both organisms were constantly recovered from the nasal cavities of the pigs during the experimental period; B. bronchiseptica was recovered in higher numbers than P. multocida. Degeneration and resorption of trabeculae in varying grades were observed in all the inoculated pigs. The turbinate bone lesions induced by P. multocida were characterized by the following changes: slight resorption of trabeculae by osteocytic osteolysis, active osteoid synthesis near trabeculae and periosteum due to increase of osteoblasts, and enhanced new bone formation. In many areas of the trabeculae, the trabeculae had been replaced by the proliferative osteoblasts and osteoids, thus, none of the pigs showed gross signs of swine atrophic rhinitis (AR). In contrast, the lesions induced by B. bronchiseptica were severe resorption of trabeculae by osteoclastic osteolysis, perforating resorption, increase of fibrous tissue near trabeculae, and impaired osteogenesis due to the damage to the osteoblasts. Thus, all the pigs showed severe gross signs of AR. Hence, quality and severity of the lesions observed between the 2 species of the bacteria were apparently different. Co-infection of the pigs with the 2 spites of the bacteria apparently enhanced the turbinate lesion formation. Our observations are consistent with the hypothesis that B. bronchiseptica alone is responsible for pathogenesis of swine AR. The different mechanisms in pathogenesis by the 2 species of the bacteria in relation to the production of characteristic turbinate lesions are discussed.
