The genus Trichosporon includes approximately 30 species, of which at least six are associated with infection (trichosporonosis): T. asahii, T. mucoides, T. asteroides, T. cutaneum, T. inkin, and T. ovoides (7, 9). The first two species are responsible for deep-seated infection, and the last four are involved in superficial infection, including white piedra. More than 90% of deep-seated trichosporonosis is caused by T. asahii. Most patients with deep-seated trichosporonosis have an underlying hematological malignancy or neoplastic disease, and neutropenia due to cytotoxic chemotherapy is the most common apparent risk factor for this infection. Deep-seated trichosporonosis due to T. asahii is life threatening with a high mortality rate and a very poor prognosis (10,16,29,31). In addition, T. asahii is relatively resistant to amphotericin B (21, 30), and the number of reports of deep-seated trichosporonosis in immunocompromised hosts caused by T. asahii has been increasing. Despite the increased frequency and poor prognosis, few of the virulence factors of this organism have been elucidated. Only human host defenses against this microorganism have been investigated (14,15). Several known virulence factors contribute to the pathogenicity of Candida albicans: the production of extracellular enzymes such as secreted aspartyl proteinase and phospholipase, phenotypic switching, and dimorphism (3,5,13,25