Further studies on experimental bacterial pneumonia: ultrastructural changes produced in the lungs by Salmonella cholerae-suis

Abstract

The development of ultrastructural changes in the lungs of pigs was examined at intervals from 6 hours to 14 days after intranasal infection with virulent Salm. cholerae-suis. Most bacteria were phagocytosed by PMN and pulmonary macrophages immediately after arrival in distal airways and alveoli. During the first few days after infection oedema fluid formed in interalveolar septa and alveoli, there was exudation of fibrin and degenerative changes of a mild nature occurred in epithelial cells. Bacteria laden phagocytic cells migrated through the tissues to pulmonary lymphatics and capillaries. Many bacteria survived and multiplied in phagocytes, causing necrosis of the cells from the fifth to the seventh day, when large numbers of organisms were liberated into the tissues. This phase coincided with widespread exudation and maximum destruction of lung tissue. Although necrosis appeared to be caused by free organisms, at no stage did bacteria become attached to, or penetrate, pulmonary cells, and it is suggested that injury is mediated by a toxin produced by Salm. cholerae-suis. Many alveoli were distended by osmiophilic lamellar material released by degenerating type II pneumonocytes. This appearance and later hyperplasia of type II epithelial cells and excessive secretion of lamellar bodies was typical of the changes in human alveolar lipoproteinosis. From the ninth day onwards the number of bacteria in the lung fell dramatically, organisms were confined to circumscribed abscesses and lymphoid tissue developed throughout the lungs.