Emerging Fungal Pathogen Candida Auris Evades Neutrophil Attack

has recently emerged as the first fungal pathogen to cause a global public health threat. The reason this species is causing hospital-associated outbreaks of invasive candidiasis with high mortality is unknown. In this study, we examine the interaction of with neutrophils, leukocytes critical for control of invasive fungal infections. We show that human neutrophils do not effectively kill Compared to , neutrophils poorly recruited to and failed to form neutrophil extracellular traps (NETs), which are structures of DNA, histones, and proteins with antimicrobial activity. In mixed cultures, neutrophils preferentially engaged and killed over Imaging of neutrophils in a zebrafish larval model of invasive candidiasis revealed the recruitment of approximately 50% fewer neutrophils in response to compared to Upon encounter with in the zebrafish hindbrain, neutrophils produced clouds of histones, suggesting the formation of NETs. These structures were not observed in infection. Evasion of neutrophil attack and innate immunity offers an explanation for the virulence of this pathogen. The emerging fungal pathogen has produced numerous outbreaks of invasive disease in hospitals worldwide. Why this species causes deadly disease is unknown. Our findings reveal a failure of neutrophils to kill compared to the most commonly encountered species, While neutrophils produce neutrophil extracellular traps (NETs) upon encounter with , these antimicrobial structures are not formed in response to Using human neutrophils and a zebrafish model of invasive candidiasis, we show that poorly recruits neutrophils and evades immune attack. Identification of this impaired innate immune response to sheds light on the dismal outcomes for patients with invasive disease.