[Pathogenesis, immunobiology and epidemiology of cryptococcosis]

Cryptococcus neoformans is taken up by the human host via the respiratory tract. The polysaccharide capsule is regarded as the pathogenetic principle inhibiting phagocytosis of the fungus by cells of the unspecific host defense. Unspecific opsonization of Cr. n. by early phase proteins causes a rapid and successful elimination in the non-compromised host. In case of non-elimination the presence of Cr. n. capsule antigen in excess results in a downregulation of antibody formation thereby inhibiting specific opsonization. Furthermore the blockade of specific T cells and cytotoxic cells by means of free antigen and/or immunocomplexes causes a downregulation of the cellular immunity: Cr. n. antigens of different character induce T suppressor cells inhibiting cellular immunity via a cascade of effector cells and soluble factors. The AIDS patient enters cryptococcosis in a state comparable to a Cr. n.-infected non-AIDS patient whose cellular immunity is already downregulated by this mycosis itself. Both phenomena--the mycosis-induced downregulation of cellular immunity as well as the AIDS-specific lack of CD4 helper cells and its consequences--act, therefore, synergistically in the same pathogenetic direction. This explains the fulminant development and sequel of cryptococcosis typical with AIDS patients. Most probably each exposition of an AIDS patient to Cr. n. results in clinically manifest cryptococcosis. The frequence of cryptococcosis in AIDS is, therefore, reflecting the general exposure of humans to Cr. n. in a given region. Cryptococcosis in AIDS is at least about 1000x more frequent than cryptococcosis in non-AIDS individuals.(ABSTRACT TRUNCATED AT 250 WORDS)