Trichosporon austroamericanum

The species name austroamericanum derives from the Latin austro- ("southern") and americanum ("American"), referring to South America, where the first identified strain originated.^[1]

The first strain of T. austroamericanum was isolated in 2013 in Brazil from the urine of a 15-year-old renal transplant patient undergoing surgery for a urinary fistula.^[1] The isolate was initially identified as Trichosporon inkin due to strong phenotypic and molecular similarity between the two species.^[1]

In 2024, Francisco et al. formally described T. austroamericanum as a new species based on detailed phylogenetic analysis.^[1] The historical confusion with T. inkin is explained by their genetic proximity, which makes differentiation difficult using routine molecular tools.^[1]

In 2025, the first complete genome sequencing of T. austroamericanum (type strain CBS 17435) was performed using long-read Nanopore sequencing technology.^[3] Average Nucleotide Identity (ANI) between T. austroamericanum and T. inkin was 84.64%, well below the 95% threshold commonly used for species delimitation, confirming that they are distinct species.^[3] These findings were supported by comparative genomic analysis of three Japanese clinical isolates.^[4]

T. austroamericanum is an anamorphic (asexual) fungus that presents as a yeast. Like other species of Trichosporon, it produces arthroconidia through hyphal fragmentation.^[1] Its morphology is very similar to that of T. inkin, making differentiation difficult using conventional microscopic or macroscopic examination.^[1]

Differentiation relies mainly on molecular methods, including sequencing of the IGS1 (Intergenic Spacer 1) region and multilocus phylogenetic analysis. Phenotypic differences include thermotolerance (growth at 45 °C), absence of growth in media containing 50% glucose, and inability to utilize succinate or citrate.^[1]

The environmental reservoir of T. austroamericanum remains unknown.^[1] Like other Trichosporon species, it is part of the transient human microbiota and may colonize the skin and gastrointestinal tract without causing disease in immunocompetent individuals.^[1]

Strains of T. austroamericanum—initially misidentified as T. inkin—have been reported worldwide, suggesting a cosmopolitan distribution:^[1][2]

• Brazil (blood cultures)^[1]
• China (invasive infections)^[1]
• Thailand (urinary isolates)^[2]
• India (superficial mycoses)^[1]
• France and Argentina (various clinical cases)^[1]

A French study (2002–2022) found that T. austroamericanum accounted for 22.8% of Trichosporon isolates, making it the second most frequently identified species in the country.^[2]

Another study reidentified 17 isolates initially classified as T. inkin as T. austroamericanum using IGS1 sequencing.^[5]

Invasive infections mainly occur in immunocompromised patients or those undergoing major surgery.^[2] In a French cohort (21 cases):

• 86.4% were male
• 36.4% had recent surgery
• 36.4% were solid organ transplant recipients

Reported infection sites include:^[2]

• fungemia: 68.2%
• bone infections: 18.2%
• cutaneous infections: 4.5%

The 30-day mortality rate was 22.7% in the studied cohort.^[2]

A fatal case following heart transplantation has been reported, initially misidentified as T. inkin.^[5] Literature review highlights similar invasive infections after major thoracic surgeries in Europe.^[5]

Persistent fever in immunocompromised patients receiving echinocandin therapy may suggest infection with resistant Trichosporon species.^[5]

Identified virulence factors include:^[4]

• biofilm formation and protease production
• presence of a Zn(II)₂Cys₆ transcription factor gene (also found in Trichosporon asahii)
• high virulence in Galleria mellonella models, comparable to T. asahii