The Effects of Carbonate on Candida albicans Filamentation, Biofilm Formation, and Antifungal Resistance.

Candida albicans, a member of the normal microbial population of healthy humans, is an opportunistic pathogen that can cause serious disease in immunocompromised patients. An important virulence factor of C. albicans is the formation of biofilms.

Constitutive ALS3 expression in Candida albicans enhances adhesion and biofilm formation of efg1, but not cph1 mutant strains.

Adhesion to living and non-living surfaces is an important virulence trait of the fungal pathogen Candida albicans. Biofilm formation in this organism depends on the expression of a number of cell surface proteins including the hypha-specific protein Als3p. Loss of ALS3 impairs biofilm formation and decreases cell-cell adhesion.

Examining the effects of BRG1 over-expression on Candida albicans strains growing as pseudohyphae.

The pathogen Candida albicans is pleiomorphic and grows in yeast and filamentous forms but the relationship between the regulation of different filamentous forms is unclear. BRG1 encodes a DNA binding protein which is an important regulator of morphology. Mutants lacking BRG1 grow as yeast under all conditions tested and over-expressing BRG1 drives hyphal growth even in the absence of inducing signals.

Anaerobic conditions are a major influence on Candida albicans chlamydospore formation.

Candidiasis now represents the fourth most frequent nosocomial infection both in the USA and worldwide. Candida albicans is an increasingly common threat to human health as a consequence of AIDS, steroid therapy, organ and tissue transplantation, cancer therapy, broad-spectrum antibiotics, and other immune defects. Unfortunately, these infections carry unacceptably high morbidity, mortality rates and important economic repercussions (estimated total direct cost of approximately 2 billion dollars in 1998 in US hospitals alone).

Geldanamycin-Induced Morphological Changes Require Candida albicans Hyphal Growth Regulatory Machinery.

In Candida albicans, geldanamycin treatment inhibits the essential chaperone Hsp90 and induces a change from yeast to filamentous morphology, likely by impeding cell cycle progression and division. However, filaments formed by wild-type cells upon geldanamycin exposure are quite different in appearance from true hyphae. We have observed that effects on morphology caused by geldanamycin treatment appear to vary in strains with defects in different morphological regulators.