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The Molecular Virulence Of Legionnaires' Disease Bacterium

3056 words - 13 pages

Legionella pneumophila, a facultative intracellular pathogen is responsible for almost 85% of cases of the legionelloses Legionnaires' disease and Pontiac fever (Dowling et al., 1992; Fields, 1997). These are a consequence of the fact that man has created additional environmental reservoirs for these opportunistic pathogens, providing them with a means by which they can be disseminated in aerosols and exposed to humans (Fields, 1997; Shuman et al., 1998). While both forms of legionellosis are caused by inhalation of adequate numbers of aerosolised legionellae by a susceptible host (Fields 1997), Pontiac fever which is the non pneumonic and less severe kind of illness is not provoked by ...view middle of the document...

When nutrients become limiting, virulence factors are expressed to depart from the abused host and ultimately infect another susceptible host (Byrne and Swanson, 1998). So, it is likely that expression of DNA-repair mechanisms from the UV plasmid (Tully, 1993) occurs just prior to the organism withdrawing from freshwater protozoa. Also in line with this proposal is the fact that one of the investigated virulence traits, flagellar expression, (Byrne and Swanson, 1998) seems to be related to the ability of L. pneumophila to infect both amoeba and human phagocytes (Pruckler et al., 1995). Another contributor to virulence is the L. pneumophila LPS (Lipopolysaccharide), whose expression switched from the LPS-ve to LPS+ve phenotype when LPS mutants were transferred from an in vitro to in vivo environment (Lüneberg et al., 1998). Expression of proteins by Legionella may thus be induced by switching from one type of environment to another (Abu Kwaik, 1998) or if of critical importance for viability, then expression may be constitutive (Sadosky et al., 1994).Many putative virulence factors in this species have been suggested (Dowling et al., 1992). Of major interest though, is that of the organism to multiply intracellularly, in their natural hosts protozoa (Fields, 1997), plus when the opportunity arises, in polymorphonuclear leukocytes, alveolar macrophages and peripheral blood monocytes (Dowling et al., 1992). The macrophage-like cell lines: HL-60 (Brand et al., 1994; Segal and Shuman, 1997; Lüneberg et al., 1998; Purcell and Shuman, 1998) and U937 (Gibson and Rodgers, 1993; Berger et al., 1994; Pruckler et al., 1995; Abu Kwaik, 1998; Andrews et al., 1998; Roy et al., 1998; Stone and Abu Kwaik, 1998), have been shown to be a useful substitute in research. Virulent legionellae also have the ability to invade non-phagocytic cells: HeLa cells (Garduño et al., 1998a) and alveolar epithelial cells (Cianciotto et al., 1995), the main use of which has been the study of L. pneumophila invasiveness and biology (Cianciotto et al., 1995; Garduño et al., 1998a; Garduño et al., 1998b).Virulent strains of L. pneumophila must therefore have a means of evading the cellular defence mechanisms. A key aspect is the ability of the pathogen to inhibit phagosome-lysosome fusion. Viable legionellae, once phagocytosed by coiling phagocytosis (Halablab et al., 1990; Dowling et al., 1992; Bozue and Johnson, 1996; Rittig et al., 1998), are encompassed in unique ribosome-studded phagosomes. Following engulfment, the replicative phagosomes interact with host cell smooth vesicles, mitochondria and ribosomes (Halablab et al., 1990; Dowling et al., 1992; Shuman et al., 1998), the latter of which are associated with the host endoplasmic reticulum (Swanson and Isberg, 1995). These legionella-specific phagosomes or LSPs (Shuman et al., 1998) fail to acidify or fuse with primary or secondary lysosomes of the phagocyte (Halablab et al., 1990).Current...

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