engleski

Multiple Organ Disfunction in Mice Inoculated with Legionella longbeachae

Legionella longbeachae is the predominant cause of legionellosis in Australia and is an emerging pathogen in the United States. The clinical picture of L. longbeachae infection ranges from mild illness to severe pneumonia and multisystem failure. We earlier showed that mice intratracheally inoculated with 10^5 CFU L. longbeachae develope an acute disease and die within 7 days. In this study we explore the dissemination of L. longbeachae lung infection in mice. Precisely, we analysed metabolic changes, intensity of bacterial multiplication, pathohistological and immunohistological changes in different mice organs. Pathogen-free female 6- to 10-weeks-old A/J mice were infected by intratracheal inoculation with L. longbeachae (10^5 CFU). We determined the CFU of bacteria in different organs during the first three days of infection. We also followed the patohistological (HE, PAS, Mallory). and immunohistological (CD11b, GR-1, CD8 antibody) changes in these organs 72 hours p.i, as well as, the level of serum aminotransferases. In parallel with the multiplication of L. longbeachae in the lungs an increased colony count in the analysed organs was seen ranging between 10^3 CFU (kidney) and 10^5 CFU (liver) at 72 hours p.i. In the liver, besides the degeneration of hepatocytes, the most prominent observation was focal infiltration within the portal triads by mononuclear and PMN leukocytes. Elevated levels of serum aminotransferases (AST, ALT) imply on liver disfunction. The architecture of the spleen showed signs of severe destructive splenitis. In the spleen we also detected a depletion of CD8+ cells 48 hours p.i. followed by prompt repopulation in the following days. Infiltration of CD11b+ and GR-1+ cells can also be seen 72 hours p.i. In the kidneys a significant degeneration in particular of the proximal tubules, as well as, collagen deposition in the intertubular spaces was observed. L. longbeachae causes a severe multiorgan disease in mice. However, it is not clear whether the observed pathohistological changes in the liver, spleen and kidneys are due to the effect of bacterial multiplication and their virulence factors or eventually the result of immunopathological reactions. Further studies would be necessary to answer this question.

legionellosis; systemic diseases; animal model

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