Encephalitis, Not Cerebral Malaria, Is Likely Cause of Coma with Negative Blood Smears

C. albicans cultured from the internal organs of these mice regardless of whether they were treated with control sera or sera from mice with numerous antibodies to C. albicans antigens.All but 2 of the iv-challenged mice were dead by 14 days after challenge.The surviving mice (1 control-treated bg/bg nulnu and I monoassociated sera-treated bg/bg nul+) had --7 logs of C. albicans in their kidneys.The mean time of death for mice that died during the experiment was also interesting since mice that received GF sera appear to have had slightly longer mean survival times.We have not yet done a passive transfer experiment to see if the Candida-"immune" sera will protect bg/bg nulnu mice against mucosal infection or to systemic candidiasis of endogenous origin.The alternative explanation offered by Matthews and Burney [ II] is insightful but, in our estimation, premature.Before we are convinced that antibodies to the 47-kDa antigen (or possibly hsp 90) are protective, it would be useful to know the following: Do bg/bg nu/+ or nu/+ mice make antibodies to hsp 90 after an iv injection or intestinal tract colonization (monoassociation) with C. albicans?Can antibodies to hsp 90 increase the resistance ofGF bg/bg nulnu mice to systemic or mucosal candidiasis and to systemic candidiasis of endogenous origin?The role ofantibody in defense against systemic and mucosal candidiasis is important as we have indicated (see abstract (l0] and [7,8]).Further experimentation in our gnotobiotic model will clarify of the role of antibodies in murine resistance to mucosal and systemic candidiasis.Maybe then we can formulate hypotheses that might be applicable to candidiasis in humans.