Alveolar spaces are commonly filled with fibrin, neutrophils, macrophages or proteinic edema fluid with multiple, often coalescent, foci of alveolar septal necrosis, and septal microvascular thrombosis. Clusters of necrotic inflammatory cells are often in alveolar spaces. In less severely affected areas, alveolar septal thickening due to pneumocyte hypertrophy is evident. Bronchi and bronchioles display varying degree of epithelial necrosis, hypertrophy or hyperplasia, with occasional foci of squamous metaplasia in some sections. Peribronchiolar and perivascular lymphocytic infiltrates are evident in some sections.
Microvascular congestion is prominent throughout the sections.
These animals had rather characteristic clinical signs of swine influenza, but the severity was somewhat unusual. A variant of swine influenza which has recently been described causes proliferative and necrotizing pneumonia similar to the lesions seen in these cases. An acute fibrinohemorrhagic pneumonia caused by Streptococcus suis has also been recently described in which fibrinoid alveolar septal necrosis similar to that seen in these cases is a prominent feature. The extremely high morbidity and acute nature of the outbreak along with histologic features suggest swine influenza virus as the primary etiologic agent, but a dual infection with Streptococcus suis cannot be ruled out based upon the histologic lesions. Swine influenza is an acute contagious disease caused by type A orthomyxoviruses.