Histopathological study of experimental poststreptococcal pneumonia in mice. Group A, type 50, streptococcal infection of murine nares controls with Staphylococcus aureus and E. coli.
Microscopic methods (light and electron microscopy, histochemistry, immunohistochemistry) have been used to assess previously unknown pulmonary inflammatory responses of specific pathogen-free (SPF) mice secondary to infection via the nares by group A, type 50, streptococci suspended in saline ("strep group mice"). As controls for the strep group mice, the animals were either injected with saline alone via nares (no lesions were seen), or with Staphylococcus aureus in saline ("staph group mice") or with E. coli ("E. coli group mice"). The three different bacterial species caused clearly different histological changes in the lung. In the strep group mice, the microscopic findings were consistent with the diagnosis of lymphocytic interstitial pneumonia of bronchiolovascular bundles, secondary to exaggerated pulmonary recirculation of lymphocytes, concomitant with vasoconstrictive angiopathy of encased pulmonary artery branches and nodular inflammatory cell aggregates in lung parenchyma. These aggregates either consisted predominantly of lymphocytes, or of mixed cells (neutrophils, lymphocytes, macrophages) or of activated macrophages only. In 18 of 22 inflamed lungs of strep group mice, no bacteria could be cultured from lung tissue. In staph group mice the microscopic findings are consistent with the diagnosis of lymphocytic interstitial pneumonia of bronchiolovascular bundles, secondary to exaggerated pulmonary recirculation of lymphocytes only. In 12 of 17 inflamed lungs of staph group mice, no bacteria could be cultured from lung tissue. In E. coli group mice the microscopic findings were consistent with the diagnosis of distal terminal bronchiolitis and early pleural-based pneumonitis, in which lymphocytes and neutrophils mingled with macrophages. In 10 of 11 inflamed lungs of E. coli group mice, no bacteria could be cultured from lung tissue. The morphologic approaches described here may have potential for unravelling the complex inflammatory processes underlying different forms of interstitial and parenchymal pneumonia.