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Legionella pneumophila is the most frequent species among the Legionellaceae. In the environment it infects protozoa. When transmitted to humans it can cause influenza-like infection called Pontiac-fever or pneumonia, especially in immunocompromised patients. In cases of human infection it enters alveolar macrophages by coiling or conventional phagocytosis and replicates within a so called replicative phagosom that did not fuse with the endosome and lysosome. Legionella strains isolated from different water systems may vary in the capability to infect macrophages. Therefore the assessment of the risk at least for immunocompetent persons is difficult on the basis of the number of Legionellae present in a given water system. Various factors enables Legionella to productively infect protozoa and macrophages.
The role of the lipopolysaccharide (LPS) of Legionella in the course of the infection is still not elucidated. Mutants expressing a changed LPS are not different in the capability to infect and multiply within the natural hosts (amoebae) and macrophages.
Several proteins like Mip, OmpS, pili and the outer membrane protein OmpM are important for the uptake into both amoebae and macrophages.
While inside of the host cells Legionella recruits cell organelles that surround the bacterium –laden phagosom. During this time Legionella is associated with the endoplasmic reticulum. This close association presumably facilitates the entry of nutrients into the endosomal lumen. The gene cluster containing the icm and dot genes are responsible for the synthesis of a type IV secretion apparatus by which Legionella acquire these nutrients and possibly influence the cellular metabolism of the host cells i.e. amoebae and macrophages.