Phenotypic profiling of Scedosporium aurantiacum, an opportunistic pathogen colonizing human lungs

Jashanpreet Kaur1, Shu Yao Duan2, Lea A I Vaas3

  • 1Department of Chemistry and Biomolecular Sciences, Macquarie University, Sydney, Australia; Biomolecular Frontiers Research Centre, Macquarie University, Sydney, Australia.

Plos One
|March 27, 2015
PubMed

Insights

Scedosporium aurantiacum, prevalent in Australia and infecting cystic fibrosis patients, shows varied metabolic capabilities. Virulent strains utilize different carbon sources and adapt better to temperature changes, differentiating them from less virulent ones.

Area of Science:

  • Medical Mycology
  • Fungal Pathogenesis
  • Genomics and Metabolomics

Background:

  • Scedosporium aurantiacum is a prevalent fungal species in Australia.
  • This fungus colonizes the respiratory tracts of cystic fibrosis (CF) patients.
  • Understanding S. aurantiacum's metabolic differences is crucial for predicting virulence.

Purpose of the Study:

  • To investigate the metabolic substrate utilization patterns of S. aurantiacum isolates.
  • To correlate metabolic profiles with fungal virulence in a Galleria mellonella model.
  • To integrate metabolomic and genomic data for pathway reconstruction.

Main Methods:

  • Phenotype Microarray (PM) analysis of 94 substrates.
  • Galleria mellonella infection model to assess isolate virulence.
  • Whole-genome sequencing for pathway analysis.

Main Results:

  • Significant differences in substrate utilization were observed between low and high virulence S. aurantiacum strains.
  • Low virulence strains utilized sucrose, while high virulence strains utilized D-turanose.
  • Highly virulent strains demonstrated greater metabolic adaptability at 28°C and 37°C.

Conclusions:

  • Metabolic profiling can distinguish S. aurantiacum strains with different virulence levels.
  • Specific substrate utilization patterns are linked to S. aurantiacum virulence.
  • Integrated omics data provide insights into S. aurantiacum's metabolic pathways and virulence factors.

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