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. 1972 Oct;69(1):55–70.

Experimental Visceral Aspergillosis

Herschel Sidransky, Sheldon M Epstein, Ethel Verney, Claire Horowitz
PMCID: PMC2032775  PMID: 4628112

Abstract

Studies conducted to gain insight into the pathogenesis of experimental aspergillosis indicated that mice pretreated with cortisone acetate and then injected intraperitoneally with nongerminating spores of Aspergillus flavus developed a high incidence of lethal visceral hyphal aspergillosis. A similar, high incidence of fatal infections was observed in cortisone-treated animals in which the number of peritoneal macrophages had been increased by prior injection of thioglycollate. To determine whether germination of spores within the host was important to the subsequent development of disseminated hyphal aspergillosis, germinating spores of A flavus were injected intraperitoneally into normal animals. While a similar dose of nongerminating spores, administered intraperitoneally into normal mice, induced a low incidence of lethal injection, germinating spores induced a high incidence of fatal disease associated with widely disseminated visceral hyphal aspergillosis. Our studies indicate that phagocytic cells in the peritoneal cavity of normal mice are able to ingest nonperminating spores of A flavus and kill them, preventing germination. However, the phagocytic cells are unable to cope with early germinating spores, which then continue to proliferate, leading to extensive hyphal invasion of visceral organs and death.

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