Pseudomonas pneumonia of mink: pathogenesis, vaccination, and serologic studies.

Fulminating pneumonia was produced in mink by the intratracheal administration of Pseudomonas aeruginosa. The sequence of pulmonary lesions was focal inflammation, focal necrosis, and widespread inflammation and necrosis. Secondary lesions of peracute hemorrhage and necrosis were the result of bacterial spread via the airways. Invasion of vessel walls by P aeruginosa was a terminal event and was secondary to bacillary invasion and necrosis of adjacent tissues. Regional (lymphatic) and systemic spread of bacteria followed the development of pulmonary lesions, but there was little morphologic evidence of tissue damage in other organs. Immunofluorescence studies showed that P aeruginosa antigen was dispersed within pulmonary cells and was free in the lung parenchyma. Mink surviving beyond postinfection hour 60 had a macrophage infiltration into limited pulmonary lesions. A vaccine trial was conducted with P aeruginosa lipopolysaccharides (LPS) used as antigen, and an enzyme-linked immunosorbent assay was used to detect antibody. Antibody was detected in mink after vaccination with LPS or natural exposure. Mink with antibody to LPS, from vaccination or naturally acquired, were resistant to experimental infection.