Overview of porcine interstitial and bronchointerstitial pneumonia: infectious and non-infectious causes

Abstract

Interstitial pneumonia in swine is an important respiratory condition in which inflammation and thickening of the pulmonary interstitium result in impaired gas exchange and respiratory distress. The multifactorial etiology of the disease includes viral, bacterial, and parasitic pathogens, as well as environmental or toxic insults. Clinical signs range from acute respiratory distress and fever to chronic weight loss and reduced growth performance, contributing to economic losses due to decreased productivity and increased mortality. Pathogenesis typically begins with a primary insult, commonly viral infection, septicemia, parasitic migration, or toxic exposure, triggering inflammation and immune cell infiltration within the lung parenchyma. This process may progress to alveolar septal thickening and impaired pulmonary function. Gross lesions vary depending on the etiologic agent and chronicity, ranging from rubbery-to-firm lungs that appear bright-red to tan with a patchy, lobular, or diffuse distribution. Histologically, lesions include interstitial septal thickening, mononuclear inflammatory cell infiltration, and type II pneumocyte hyperplasia. Several infectious agents are associated with interstitial pneumonia. Viral pathogens such as porcine reproductive and respiratory syndrome virus, porcine circovirus 2, swine influenza A virus, porcine parainfluenza virus, porcine hemagglutinating encephalomyelitis virus, and porcine astrovirus 4 may induce interstitial or bronchointerstitial pneumonia. Bacterial pathogens such as Escherichia coli, Actinobacillus suis, Streptococcus suis, and Erysipelothrix rhusiopathiae, and parasites including Ascaris suum and Metastrongylus spp., may contribute through septicemia or larval migration. Accurate diagnosis requires integration of gross and histopathologic findings with ancillary techniques such as PCR, immunohistochemistry, and in situ hybridization.