Fungal Cell Biology: Candida albicans Pathogenesis
Concept Name
Candida albicans Pathogenesis
Genetic Loci
EFG1 (enhanced filamentous growth) regulates yeast‑to‑hyphal transition. SAP gene family (secreted aspartyl proteinases) facilitates tissue invasion. ERG11 encodes lanosterol 14α‑demethylase – target of azoles.
Intracellular Cascade
Environmental cues (pH, temperature, serum) → Ras‑cAMP‑PKA pathway → activation of Efg1 → hyphal morphogenesis. Adhesins (Als family) mediate adhesion to host cells. Biofilm formation via quorum sensing (farnesol/tyrosol).
Required Cofactors
Iron is essential for growth; Candida uses iron‑acquisition systems (hemoglobin receptors, siderophores). Zinc is required for secreted aspartyl proteinase activity.
Histology Stains
PAS (Periodic Acid‑Schiff) and GMS (Gomori Methenamine Silver) stain fungal cell walls magenta‑red or black, respectively. Mucicarmine stains Cryptococcus capsule but not Candida.
EM Findings
Yeast cells show a thick cell wall (100‑200 nm) composed of mannoproteins, β‑glucans, and chitin. Hyphae have parallel cell walls with septa at regular intervals.
Knockout Phenotype
Deletion of EFG1 in C. albicans abolishes hyphal formation and significantly attenuates virulence in a murine model of disseminated candidiasis.
Specific Toxins
Azole antifungals (Fluconazole) inhibit Erg11, blocking ergosterol synthesis. Echinocandins (Caspofungin) inhibit β‑1,3‑glucan synthase. Amphotericin B binds ergosterol, forming membrane pores.