Experimental basis for the clinical epidemiology of fungal infections. A review.
Based on the concept that the agents of deep fungal infections can be divided into primary pathogens and opportunists the experimental basis for the clinical epidemiology of mycoses is outlined. Kinetics of experimental infections with opportunists and primary pathogens discriminate between the two fungal categories. Natural resistance eliminates opportunists and prevents the establishment of progressive infection in the normal host. Primary pathogens call upon mechanisms of adoptive cell mediated immunity for their control. Therefore athymic mice which are not more susceptible to opportunists than control mice, cannot control infection with primary pathogens. In order to induce comparable overwhelming opportunistic mycoses with reasonable challenge doses, non-specific phagocytic resistance has to be eliminated. In agreement with in vivo studies, in vitro studies of the susceptibility of fungi to killing by phagocytes point out, that the susceptibility of the tissue phase of fungi to killing by "immunologically unarmed" phagocytes discriminates between opportunists and primary pathogens. In order to restrain primary pathogenic fungi, phagocytes have also in vitro to call upon adoptive, T cell-dependent immune mechanisms, which appear superfluous for control of opportunists. This difference explains the discrepant opportunistic proclivities of the two fungal categories. Patients with defective phagocytic defenses are prone to opportunistic mycoses, while deficient cell mediated immunity results in a greater vulnerability to primary pathogens.
Schaffner
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D000818:Animals; D005658:Fungi / Q000472:pathogenicity; D006801:Humans; D007111:Immunity, Cellular; D009181:Mycoses / Q000453:epidemiology* / Q000276:immunology; D009894:Opportunistic Infections / Q000453:epidemiology* / Q000276:immunology; D014774:Virulence