Abstract
The present study was done to describe the mechanisms of the hematogenous spread of C. albicans from the lung.
ICR and BALB/c mice were administered anti-cancer drug and adrenocortic steroid hormone intraperitoneally to develop leukopenia of less than 4, 000/mm3. A spore suspension of 2×106 live cells of C. albicans was inoculated intratracheally into non treated and drug-treated mice. The drug-treated animals developed disseminated candidiasis from the lung soon after inoculation. The mechanical destruction of vessel walls by fungi was important for their vascular invasion. The dissemination appeared when the fungal cells invaded into veins of more than 50μm in diameter. On the other hand, no dissemination occurred when the fungal cells entered into capillarys lumens of less than 50μm in diameter, because fibrin thrombi enclosed the cells. The fungal cells were surrounded by the cytoplasm of I type alveolar cells in alveoli of the lung. While the high incidence of dissemination occured by additional administration of heparin, the intraveneous injection of anti-C. albicans antibody after inoculation of C. albicans decreased the incidence of the dissemination.
