Rapid systemic propagation of Legionella longbeachae lung infection in A/J mice

Legionnaire's disease was considered to be exclusively a lung disease and limited informations were available concerning the progression of the disease. It was shown that mice intratracheally inoculated with 105 CFU L. longbeachae serogroup 1 developed an acute disease and died within six days. Pathohistological changes in the lungs of infected animals were typical for multifocal bronchopneumonia. Therefore, we were interested to explore whether a systematisation of the primary process in the lungs may occur. In this study we analysed the intensity of bacterial multiplication and pathohistological changes in liver, spleen and kidney. Pathogen-free female 6- to 10-weeks-old A/J mice were infected by intratracheal inoculation with L. longbeachae serogroup 1 using a dose of 105 CFU. We determined the CFU of bacteria in the lung, liver, spleen and kidney of A/J mice 2, 24, 48 and 72 hours post infection. We also followed the patohistological changes in these organs 72 hours post infection (HE, PAS, Mallory and Gomory stain). Increasing multiplication of L. longbeachae in the lung was associated with increased colony counts in analysed organs reaching the concentration between 103 CFU (kidney) and 105 CFU (liver) at 72 hours post infection. We never detected an excessive proliferation of bacteria in these organs, which would be independent of the bacterial proliferation that has been seen in the lungs. Pathohistology of liver, spleen and kidney analysed 72 hours post infection showed mainly mild inflammatory cellular infiltrates and degenerative changes. In the liver, beyond the degeneration of the hepatocytes, the most prominent observation was focal infiltrations within portal triads by mononuclear and polymorphonuclear leukocytes. The architecture of the white and red pulp of the spleen showed all signs of severe destructive splenitis. In kidney the glomerules were reduced in size and the juxtaglomerular apparatus showed decreased cellularity. Additionally, a significant degeneration of particular proximal tubule and collagen increase in the intertubular spaces was observed. We confirmed that L. longbeachae serogroup 1 rapidly disseminate in the liver, spleen and kidney causing severe systemic disease in mice. At the moment we do not know if the observed pathohistological changes are caused by local bacterial multiplication and their virulent factor(s) or by uncontrolled host immune response.