Experimental disseminated trichosporonosis in mice: tissue distribution and therapy with antifungal agents

K Yamamoto1, K Makimura, T Sudo

  • 1Teikyo University Institute of Medical Mycology, Tokyo, Japan. masa@kiwi.co.jp

Insights

This study shows that Trichosporon asahii infection in mice leads to fungal growth in multiple organs. Antifungal treatments like fluconazole improved survival and reduced fungal load, with fluconazole being more effective.

Area of Science:

  • Mycology
  • Infectious Diseases
  • Pharmacology

Background:

  • Trichosporon asahii is an emerging fungal pathogen causing invasive infections.
  • Cyclophosphamide-induced immunosuppression is a common model for studying opportunistic fungal infections.

Purpose of the Study:

  • To investigate the pathogenicity of Trichosporon asahii in an immunocompromised murine model.
  • To evaluate the efficacy of fluconazole and amphotericin B in treating Trichosporon asahii infections.

Main Methods:

  • Intravenous infection of cyclophosphamide-treated mice with Trichosporon asahii.
  • Monitoring mortality, survival time, and fungal burden (CFU) in various organs.
  • Assessing serum (1-->3)-beta-D-glucan levels as a biomarker.

Main Results:

  • Mortality and survival time were dose-dependent on the fungal inoculum.
  • Fungal growth was observed in the lung, heart, liver, spleen, kidney, and brain.
  • Both fluconazole and amphotericin B prolonged survival and reduced kidney fungal burden, with fluconazole demonstrating superior efficacy.
  • Serum (1-->3)-beta-D-glucan levels decreased with antifungal therapy and correlated with kidney fungal burden.

Conclusions:

  • Trichosporon asahii can cause disseminated infections in immunocompromised hosts.
  • Fluconazole is an effective treatment for Trichosporon asahii infections, outperforming amphotericin B.
  • Serum (1-->3)-beta-D-glucan may serve as a useful biomarker for treatment response in kidney infections.

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