Endocarditis caused by Candida albicans has been studied using a rabbit model. Endocarditis is established by infecting rabbits with C. albicans following transaortic catheterization. Candida yeast cells adhere to the trauma-induced clot and propagate within the clot because the host immune responses are unable to eradicate the fungus. We have found that rabbits with endocarditis make a classical cell-mediated immune response but the response is not sufficient to eradicate the organism. In vitro studies have demonstrated that C. albicans adheres to clot tissue. Adherence is inhibited partially by treating cells with proteases, formaldehyde or heat-killing, and completely inhibited by anti-Candida gamma globulin. C. albicans adheres to clot tissue much better than C. krusei, a relative non-pathogen. These in vitro studies are supported by in vivo data which have demonstrated that the infectious dose (I.D.50) for C. albicans is 105.2 while for C. krusei it is 107.4. Other in vitro studies have demonstrated that C. albicans cell wall aggregates platelets through a complement-mediated reaction. We believe that this induced aggregation is at least partially responsible for the continued growth of the clot (vegetation) on the heart valve during disease development. We have also constructed an indirect ELISA inhibition assay for quantitating fungal antigens during the early course of the disease. The preliminary observations look promising for developing a procedure which would be useful for the early diagnosis of the disease.
