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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Ultrastructure of pulmonary alveoli and macrophages in experimental Legionnaires' disease.

Guinea pigs, rhesus monkeys and marmosets infected with Legionella pneumophila in small particle aerosols developed an acute fibrinopurulent bronchopneumonia. Changes from 24 hr included exudation into alveoli of protein-rich, often fibrinous fluid and many polymorphonuclear leucocytes (PMN) and macrophages. Damage to alveolar capillary endothelium consisted of widespread cytoplasmic swelling and vesiculation, but necrosis of endothelium and the associated alveolar epithelium was focal and less common. Phagocytosis of L. pneumophila organisms was predominantly by macrophages, but the bacteria were also seen in PMN. Free organisms were present in alveoli and capillary lumina at all stages of the infection but were not observed in lung parenchymal cells. Some infected macrophages and PMN became necrotic and lysed to release intact bacteria. In all species of experimental animal, intracytoplasmic aggregations of granular material, believed to be glycogen, were seen frequently in macrophages and PMN which had phagocytosed L. pneumophila. These deposits of glycogen may reflect either an increased energy demand by the host cell or an interference with its carbohydrate metabolism.[1]


  1. Ultrastructure of pulmonary alveoli and macrophages in experimental Legionnaires' disease. Baskerville, A., Dowsett, A.B., Fitzgeorge, R.B., Hambleton, P., Broster, M. J. Pathol. (1983) [Pubmed]
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