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Abstract Body

Legionella pneumophila is an environmental bacterium present in most natural and man-made water sources, where it is present as planktonic, in biofilms or within various protozoan hosts. While protozoa graze on most bacteria as a source of food, L. pneumophila has co-evolved with protozoan species as its natural hosts. Bacterial residence within protozoa is essential for the long term survival of L. pneumophila and its protection from anti-bacterial agents, such as chlorine. Although L. pneumophila replicate within the trophozoite form of amoeba, the cyst from of amoeba is non-permissive for bacterial proliferation but is highly protective for the bacterium for a long period. Upon nutrient depletion in the water system or within dormant amoebic cysts, L. pneumophila becomes dormant but it remains viable but non-culturable (VBNC). The dormant VBNC L. pneumophila can become metabolically active and is resuscitated upon entry into an amoeba host in the trophozoite form. It is not surprising that L. pneumophila has evolved to interfere with encystation of the amoeba host to maintain it in the permissive trophozoite form. This is achieved by the secretion of a Legionella amylase A (LamA) by intra-vacuolar L. pneumophila into the amoeba cytosol. The injected LamA degrades most of the amoeba stored glycogen, which is the main resource for amoeba to synthesize the double-layer cellulose cell wall of the cyst form. Upon transmission to humans as the accidental host, L. pneumophila proliferate within alveolar macrophages causing pneumonia. Secretion of the amoeba host-adapted LamA by intracellular L. pneumophila into the macrophage cytosol results in an accidental and paradoxical pro-inflammatory macrophage response with a modest decrease in bacterial proliferation. Therefore, L. pneumophila is resuscitated from the VBNC dormant stage upon entry into amoeba natural host and the bacterium has evolved to interfere with encystation of the amoeba host.