Candida albicans

Candida albicans demonstrates that the stress-response machinery studied in Saccharomyces cerevisiae for longevity has been repurposed for pathogenesis. This yeast is a normal human commensal—most people carry it without harm—but it becomes a dangerous pathogen when host immunity weakens. The switch from commensal to pathogen involves morphological transformation from yeast to filamentous hyphal forms, regulated by many of the same stress-response pathways that control longevity in S. cerevisiae.

The yeast-to-hypha transition illustrates phenotypic plasticity in response to environmental signals. Temperature, pH, nutrient availability, and host immune factors all influence morphology. Hyphal forms invade tissues, resist phagocytosis, and form biofilms on medical devices. The transition involves signaling through pathways including TOR and protein kinase A—the same pathways implicated in yeast longevity. What promotes survival and longevity in one context enables virulence in another.

C. albicans biofilms represent a major clinical challenge. These structured communities on catheters and implants resist both antifungal drugs and immune clearance. Biofilm formation involves quorum sensing-like communication, morphological heterogeneity, and extracellular matrix production. The biofilm lifestyle—protective community formation under stress—parallels bacterial biofilm strategies, suggesting convergent evolution of community-based stress responses across kingdoms. Understanding C. albicans illuminates both fungal pathogenesis and general principles of microbial stress adaptation.