Metabolic and phenotypic plasticity may contribute for the higher virulence of Trichosporon asahii over other Trichosporonaceae members.

Abstract

The Trichosporonaceae family comprises a large number of basidiomycetes widely distributed in nature. Some of its members, especially Trichosporon asahii, have the ability to cause human infections. This ability is related to a series of virulence factors, which include lytic enzymes production, biofilm formation, resistance to oxidising agents, melanin and glucuronoxylomannan in the cell wall, metabolic plasticity and phenotypic switching. The last two are poorly addressed within human pathogenic Trichosporonaceae. These factors were herein studied to contribute with the knowledge of these emerging pathogens and to uncover mechanisms that would explain the higher frequency of T.asahii in human infections. We included 79 clinical isolates phenotypically identified as Trichosporon spp. and performed their molecular identification. Lactate and N-acetyl glucosamine were the carbon sources of metabolic plasticity studies. Morphologically altered colonies after subcultures and incubation at 37°C indicated phenotypic switching. The predominant species was T.asahii (n=65), followed by Trichosporon inkin (n=4), Apiotrichum montevideense (n=3), Trichosporon japonicum (n=2), Trichosporon faecale (n=2), Cutaneotrichosporon debeurmannianum (n=1), Trichosporon ovoides (n=1) and Cutaneotrichosporon arboriforme (n=1). T.asahii isolates had statistically higher growth on lactate and N-acetylglucosamine and on glucose during the first 72h of culture. T.asahii, T.inkin and T.japonicum isolates were able to perform phenotypic switching. These results expand the virulence knowledge of Trichosporonaceae members and point for a role for metabolic plasticity and phenotypic switching on the trichosporonosis pathogenesis.