A comparison of virulence of two strains ofLegionella pneumophilabased on experimental aerosol infection of guinea-pigs

Abstract

Two strains of Legionella pneumophila (LP) serogroup I, of differing virulence, were examined in terms of numbers of viable organisms in tissues, pyrexia and mortality following aerosol infection. The Corby strain was the more virulent, with pyrexia and deaths of guinea-pigs 3 to 6 days after infection. This strain multiplied very rapidly in the lungs to reach a peak of 5 X 10(11) viable organisms/lung. Organisms were present in the blood, liver, spleen and kidney. The Philadelphia-1 strain (NCTC 11192) was unable to replicate in the lung and was cleared between 14 and 21 days after infection. Pyrexia was not observed. No guinea-pigs died and viable LP was not found in any organ other than the lung. Lung lavages on aerosol infected animals were performed and the virulent Corby strain was found to be mainly intracellular. The avirulent Philadelphia-1 strain was found predominantly in the extracellular location. There were approximately 10 times the number of viable virulent LP in the lung macrophage fraction than in the lung PMNL fraction. In comparison, there were approximately equal numbers of the viable avirulent strain in the macrophages and the PMNL. Experimental evidence suggests that the macrophage preferentially supports the growth of the virulent Corby strain compared with the PMNL. The avirulent strain on the other hand appears to be destroyed by both the macrophages and the PMNL.

Cloning and Characterization of the Gene Encoding the Major Cell-Associated Phospholipase A of Legionella pneumophila , plaB , Exhibiting Hemolytic Activity

“…L. pneumophila sg1 strain Corby (33) was used to construct an expression library in Escherichia coli (30) for mutagenesis of the Legionella plaB gene and later served as a wild-type control. Legionella strains used for Southern blot analysis were L. pneumophila sg1 strain Philadelphia I (ATCC 33152), L. pneumophila sg1 strain Msp19 (7), L. pneumophila sg1 strain 685 (7), L. pneumophila sg3 strain Bloomington (ATCC 33155), L. pneumophila sg3 strain U22 (7), L. pneumophila sg4 strain Los Angeles (ATCC 33156), L. pneumophila sg6 strain Chicago-2 (ATCC 33215), L. pneumophila 664 sg6 (patient isolate) (7), L. pneumophila type strains (sg7, sg10, sg12, and sg13) (kindly provided by P. C. Lück, Dresden, Germany), L. pneumophila was routinely grown on buffered charcoal-yeast extract (BCYE) agar for 2 days at 37°C (19).…”

FliA expression analysis and influence of the regulatory proteins RpoN, FleQ and FliA on virulence and in vivo fitness in Legionella pneumophila

“…Experiments were done with L. pneumophila Sg1 strain Corby (Jepras et al 1985) and L. pneumophila Sg1 strain Paris (Cazalet et al 2004) and their isogenic ΔrpoN, ΔfleQ and ΔfliA mutant strains (Heuner et al 2002;Jacobi et al 2004;Albert-Weissenberger et al 2010;Brüggemann et al 2006). Further Corby strains used in this study were ΔflaA, ΔmotA and ΔfliD (Dietrich 2000;Heuner and Albert-Weissenberger 2008).…”

“…Sequence or relevant characteristics a Source or Reference Strains Escherichia coli DH5α K-12 DH5α F -Φ80d∆lacZM15 ∆(lacZYA-argF)U169 deoR recA1 endA1 hsdR17 glnV44 thi-1 gyrA96 relA1 (Hanahan 1983) L. pneumophila (Lp) Corby Virulent L. pneumophila serogroup 1, strain Corby (Jepras et al 1985 …”

“…It seems as if fliA belongs to the class III genes in strain Paris, but is not directly linked to the flagellar regulon in strain Corby (Albert-Weissenberger et al 2010;Jacobi et al 2004). Both strains are virulent L. pneumophila Sg1 isolates with only small differences within their genomes (Cazalet et al 2004;Jepras et al 1985;Glöckner et al 2008). Our intention was to clarify the regulation of fliA expression in L. pneumophila and to examine the differences between both strains.…”

Demonstration of the intracellular production of tissue-destructive protease by Legionella pneumophila multiplying within guinea-pig and human alveolar macrophages

“…A. Williams & R. B. Fitzgeorge (unpublished data) have shown that the strain used in this study was unable to grow in cellfree guinea-pig lung lavage, even when this was obtained from animals with experimental Legionnaires' disease. Since this strain is also killed by polymorphonuclear neutrophil leukocytes (Fitzgeorge et al, 1988 ;Jepras et al, 1985), it would suggest that the macrophage is the principal site of protease production in vivo. Immunocytochemical studies support this suggestion, since the protease was seen concentrated at the sites of lung lesions and only in association with specifically labelled L. pneumophila (Williams et al, 1987).…”