Examining Trichophyton tonsurans genotype and biochemical phenotype as determinants of disease severity in tinea

Susan M Abdel-Rahman1, Nasreen Talib, Ada Solidar

  • 1Division of Pediatric Clinical Pharmacology, The Children's Mercy Hospitals and Clinics, and Department of Pediatrics, University of Missouri-Kansas City, School of Medicine, Kansas City, MO 64108, USA. srahman@cmh.edu

Medical Mycology
|April 12, 2008
PubMed

Insights

Fungal genotype significantly influences Trichophyton tonsurans infection severity in children. Ancestral strains are linked to more severe tinea capitis, highlighting fungal factors in disease presentation.

Area of Science:

  • Mycology
  • Dermatology
  • Genetics

Background:

  • Trichophyton tonsurans causes tinea capitis with variable inflammation.
  • Understanding fungal factors influencing disease severity is crucial.

Purpose of the Study:

  • To investigate if fungal factors, specifically genotype and protease activity, correlate with the clinical severity of tinea capitis in children.
  • To determine the relationship between Trichophyton tonsurans strain type and disease presentation.

Main Methods:

  • Genotyping of Trichophyton tonsurans strains from 54 infected children using rDNA and ALP1 loci.
  • Quantification of secreted protease activity (keratinase, collagenase, elastase).
  • Correlation analysis between fungal genotype, protease activity, and clinical severity score (CSS).

Main Results:

  • Seventeen unique genotypes were identified among the T. tonsurans strains.
  • Significant variation in keratinase, collagenase, and elastase activity was observed.
  • A strong association between fungal genotype and disease severity was found, with rDNA variations explaining over 50% of CSS variation (r2=0.539; P<0.001).

Conclusions:

  • Fungal genotype is a significant determinant of tinea capitis severity in children.
  • Phylogenetic analysis suggests ancestral T. tonsurans strains are associated with more severe disease.
  • These findings support the hypothesis that evolving anthropophilic strains may lead to less inflammatory infections.

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