Halotolerance of gut yeasts as a potential virulence factor

Despite the substantial significance of yeasts in biotechnology and medicine, the number of well-described fungal species remains limited, with their ecological and pathogenic roles still being uncovered. Halotolerance, a key aspect of osmotolerance, is considered a potential virulence factor that promotes microbial survival in the environment and within the host, particularly by resisting phagocytic oxidative and ionic stress. This study aimed to investigate and quantitatively compare the halotolerance of the most common gut-associated yeasts. There were analyzed 78 clinical strains of six species: Candida albicans, Pichia kudriavzevii, Geotrichum candidum, Trichosporon asahii, Trichosporon ovoides, and Rhodotorula mucilaginosa. Strains were cultivated in Sabouraud broth with NaCl concentrations ranging from 0.5% to 20% at two temperatures, 25°C and 35°C. Growth was measured spectrophotometrically at 450 nm after 96 hours of incubation. A second-degree polynomial regression model, implemented using Python programming language, was applied to analyze the non-linear growth response to salinity and to identify precise inflection points, indicating critical tolerance thresholds where growth inhibition dynamics shifted. The results revealed significant species-specific differences. G. candidum and P. kudriavzevii were the least tolerant (inflection points ~6.2% and ~8.5% NaCl at 25°C, respectively). C. albicans and R. mucilaginosa exhibited moderate tolerance, while Trichosporon spp. demonstrated exceptional halotolerance, maintaining growth potential at concentrations exceeding 15% NaCl. A notable synergistic effect of combined osmotic and temperature stress was observed for most species, with reduced tolerance at physiological temperature. These findings indicate that pronounced halotolerance may serve as an important virulence factor for opportunistic pathogens, likely enhancing their persistence in the host environment and potentially contributing to cross-resistance mechanisms against antifungal agents through shared adaptive responses to cellular stress.