Mammals are protected from fungal pathogens by two evolutionary pillars: adaptive immunity and elevated body temperature. Anthropogenic climate change is eroding this thermal barrier, while a concurrent decline in human basal body temperature accelerates convergence from both directions. Candida auris , a thermotolerant, multidrug-resistant pathogen, arose independently as genetically distinct clades on multiple continents, a pattern implicating shared selective pressures rather than clonal spread. Unlike its closest relatives, which grow poorly at mammalian temperatures, it thrives at 37°C, tolerates up to 47°C, persists on hospital surfaces, resists all three major antifungal classes, and causes invasive infections with 30–60% mortality. We review its evolutionary biology, ecology, and clinical significance, evaluating hypotheses for its origin, and the mechanisms underlying its thermotolerance and virulence. C. auris may be the first of many fungi adapting to breach mammalian thermal defenses, making predictive frameworks for fungal disease emergence an urgent priority.
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Schuh et al. (2026) studied this question.
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