Abstract
The experimental results of the relationship between iron and a fungal infection were obtained and tissue reactin for deep-seated mycosis was evaluated.
1) Increased susceptibility to infection in iron overload: When experimental candidiasis was induced in ICR mice with iron overload, the mice had renal abscesses containing candidial pseudohyphae in the eraly stage after the inoculation. By contrast, in mice with Candida albicans and without iron overload, no fungal elements were detected in renal abscesses in the same early stage. The excess iron thus promoted the growth of Candida; however, there was no significant histological difference when iron was loaded or not. The same results were gained when leukemic mice were employed.
2) Resistance to infection due to decreased serum iron: The decreased serum iron induced by lipopolysaccharides or muramyl dipeptide had a deterrent effect on the growth of Aspergillus, so that production of the fungal lesion occurred later.
3) Increased susceptibility to infection by decreased UIBC (unbound iron binding capacity): Decreased UIBC produced by diabetic ketoacidosis enhanced the growth of Rhizopus oryzae.
4) Increased susceptibility to infection due to decreased amount of transferrin: A decreased transferrin level in D(+) galactosamine-induced liver injury accelearted the growth of Candida.
From these results, the following was concluded; there was no significant difference in tissue reaction for deep-seated mycosis between the group with deranged iron metabolism and the control group; however, the deranged iron metabolism influenced the growth speed of the fungi and the extent of the fungal lesion.
