engleski

Rapid systemic progression of a local Legionella longbeachae infection in A/J mice

Introduction: For assessment of virulence of Legionella longbeachae serogroup 1 we established a mice model of experimental legionellosis. It was shown that mice intratracheally inoculated with 1000000 CFU L. longbeachae serogroup 1 developed an acute disease and died within 7 days. Pathohistological changes in the lungs of infected animals were typical for multifocal bronchopneumonia. Until recently, it was belived that Legionnaires disease is exclusively a lung disease and limited informations were available concerning the progression of the disease. 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 the liver, spleen and kidneys. Materials and Methods: Pathogen-free female 6- to 10-weeks-old A/J mice were infected by intratracheal inoculation with L. longbeache serogroup 1 using a dose of 1000000 CFU. We determined the CFU of bacteria in the lung, liver, spleen and kidneys 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. Results: The very first bacteria could be isolated from these organs than 24 hours post infection at a CFU concentration around the detection limit of the assay (100 CFU/organ). Multiplication of L. longbeachae in the lung was associated with increased colony counts in the analysed organs reaching the concentration between 10000 CFU (kidney) and 1000000 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 was seen in the lungs. Pathohistology of liver, spleen and kidney analysed 72 hours post infection showed degenerative and infiltrative changes. In the liver, degeneration of the hepatocytes and focal infiltrations within portal triads by mononuclear and polymorphonuclear leukocytes was observed. The architecture of the spleen showed all signs of severe splenitis. In kidney, glomerules were reduced in size, the juxtaglomerular apparatus showed decreased cellularity. Significant changes in the kidney tubular system were noted. Conclusion: 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 the product of a local bacterial multiplication, or they are the outcome of a certain virulent factor(s).

systemic disease; legionellosis; mice model

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