The simultaneous and independent worldwide outbreaks of Candida auris invasive infections seem to be a puzzling paradox [1, 2]. Since its first isolation, C. auris has risen several questions on how it could have appeared, survived, and thrived [1]. Several speculative hypotheses have been proposed. Although misuse of antimicrobials and over-abuse of azoles have been considered the main contributors to C. auris emergence [2, 3], these do not completely justify its spreading. One of the most recent theories considers changes in climate conditions as a causative factor altering infectious disease ecology [4, 5] (Fig. 1). Humans and microbes had been influencing each other for decades. Global warming is one of the major components of climate change connected to human activities, having considerable impact on health and indirectly boosting infectious diseases. Only few fungal species can be considered as pathogenetic for humans, as the majority of mammals are remarkably resistant to invasive fungal diseases. Besides immunological responses, humans are characterized by a “thermal restriction zone” that protects against infections. Human-induced climate changes may be responsible for the progressive narrowing of this thermal restriction zone, defined as the difference between human basal temperature and environmental temperature. As C. auris is more thermotolerant if compared to other yeasts, global warming might have played an important role in its emergence [4]. Although the specific ecological niche has not been identified yet, the climatic oscillations effect on wetlands might have contributed to enrich this potential habitat, conferring thermal and salinity tolerance to C. auris non-pathogenetic naïve strains. Acquisition of virulence factors might be explained considering the potential transfer of virulence genes from other pathogenetic Candida spp. to C. auris naïve strains, or by the combination of global warming and UV radiations that might have induced genetic mutations. The upgrade of C. auris strains, from saprophyte to pathogenetic yeasts, has witnessed an intermediate avian host, thus permitting its transmission to humans. Overtime, genetic and epigenetic changes have led to an extreme adaptability of C. auris to different ecological niches, leading to the development of persistent outbreaks in healthcare settings [4, 5]. Although global warming seems to be an appealing theory, it is not possible to ignore other factors which might explain C. auris rise. High population densities, poor hygiene, migrations, international travels, and pollution might indeed have contributed to the persistence of C. auris and acquisition of antifungal resistance [4]. Future studies are needed to identify its evolutionary reservoirs and validate the climate changes theory.

中文翻译：

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全球变暖通过耳念珠菌感染“加热”ICU：气候变化理论

耳念珠菌侵袭性感染在世界范围内同时独立爆发似乎是一个令人费解的悖论 [1, 2]。自第一次分离以来，C. auris 提出了几个关于它如何出现、生存和繁衍的问题[1]。已经提出了几种推测性假设。尽管滥用抗菌素和过度滥用唑类被认为是耳念珠菌出现的主要原因 [2, 3]，但这些并不能完全证明其传播是合理的。最新的理论之一将气候条件的变化视为改变传染病生态的致病因素 [4, 5]（图 1）。几十年来，人类和微生物一直在相互影响。全球变暖是与人类活动相关的气候变化的主要组成部分之一，对健康有相当大的影响，并间接助长了传染病。只有少数真菌物种可以被认为是人类的致病菌，因为大多数哺乳动物对侵袭性真菌病具有显着的抵抗力。除了免疫反应，人类还有一个“热限制区”，可以防止感染。人类引起的气候变化可能是导致这一热限制区逐渐变窄的原因，该限制区定义为人类基础温度和环境温度之间的差异。由于 C. auris 比其他酵母更耐热，因此全球变暖可能在其出现中发挥了重要作用 [4]。虽然尚未确定具体的生态位，气候波动对湿地的影响可能有助于丰富这个潜在的栖息地，赋予耳念珠菌非致病性幼稚菌株耐热和耐盐性。考虑到毒力基因从其他致病念珠菌属的潜在转移，可以解释毒力因子的获得。到 C. auris naïve 菌株，或通过可能诱导基因突变的全球变暖和紫外线辐射的组合。C. auris 菌株的升级，从腐生菌到致病酵母，见证了一个中间鸟类宿主，从而允许其传播给人类。随着时间的推移，遗传和表观遗传的变化导致 C. auris 对不同生态位的极端适应性，导致在医疗保健环境中持续爆发 [4, 5]。尽管全球变暖似乎是一个吸引人的理论，但也不能忽视其他可能解释 C. auris 上升的因素。人口密度高、卫生条件差、迁移、国际旅行和污染可能确实导致了耳念珠菌的持续存在和抗真菌耐药性的获得 [4]。未来的研究需要确定其进化储层并验证气候变化理论。