Pathogenicity of Legionella pneumophila

The bacterium Legionella pneumophila is the principal etiologic agent of Le gionnaires' disease, a form of lobar pneumonia. Ubiquitous in aquatic envir onments, the gram-negative Legionella organism is a facultative, intracellu lar parasite of protozoa. The pathogenesis of legionellosis is largely due to the ability of L. pneumophila to invade and grow within alveolar macroph ages, and it is widely believed that this ability results from a prior adap tation to intracellular niches in nature. Indeed, intracellular legionellae display a remarkable capacity to avoid endosomal and lysosomal bactericida l activities and to establish a unique replicative phagosome. In recent yea rs, much progress has been made toward identifying the bacterial factors th at promote intracellular infection and virulence. Surface structures that e nhance infection include LPS, flagella, type IV pili, an outer membrane por in, and the Mip propyl-proline isomerase. Both type II and type IV protein secretion systems are critical for L. pneumophila pathogenesis. Whereas the type II (Lsp) system secretes a collection of degradative enzymes, the typ e IV (Dot/Icm) system likely exports effector proteins that are especially critical for trafficking of the Legionella phagosome. In addition to facili tating pilus formation and type II secretion, the inner membrane prepilin p eptidase (Pill)) of L. pneumophila appears to mediate a third, potentially novel pathway that is operative in the mammalian host. Periplasmic and cyto solic infectivity determinants include a catalase-peroxidase and the HtrA a nd Hsp60 stress-response proteins. The stationary phase response and the ir on acquisition functions of L. pneumophila also play key roles in pathogene sis, as do a number of other loci, including the pts, mil and enh genes.