Candida auris is a recently emerged global fungal pathogen, which causes life threatening infections, often in healthcare settings and with immunocompromised patients. C. auris infections are particularly worrisome because the fungus is often resistant to multiple classes of antifungal drugs. Furthermore, the fungus forms durable biofilms that are difficult to remove from surfaces. Due to the relatively recent, resilient, and resistant nature of this fungal pathogen, we investigated whether C. auris made common fungal virulence factor melanin. Melanin is a black-brown pigment that enables microbes to evade the mammalian immune response due to its strong antioxidant properties, ability to inactivate antimicrobial peptides, shielding of pathogen-associated molecular patterns, and inactivation of antifungal drugs. We found that certain strains of C. auris , predominantly from Clade I and IV, oxidized catecholamines into melanin pigment. The formation of this melanin occurred extracellularly, resulting in granule-like melanin structures that are deposited on the surface of the fungus. This melanization was primarily chemically driven and mediated by alkalinization of the extracellular environment. The C. auris strains had relatively high cell surface hydrophobicity, but we did not find a correlation between hydrophobicity and ability to melanize. Melanin protected the fungus from oxidative damage but we did not observe a protective role in vitro or in vivo during infection of macrophages or Galleria mellonella, respectively. In summary, C. auris alkalinizes the extracellular medium, which promotes the chemical autooxidation of the L-DOPA to melanin that then attaches to its surface, thus illustrating a different mechanism for fungal melanization.