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Staphylococcus aureus isolates from patients with Kawasaki disease express high levels of protein A

E R Wann1, A P Fehringer, Y V Ezepchuk

  • 1Albert A. Alkek Institute of Biosciences and Technology, Texas A & M University Health Science Center, Houston, Texas 77030-3303, USA.

Infection and Immunity
|August 24, 1999
PubMed

Insights

Kawasaki disease (KD) isolates exhibit an agr-defective phenotype, showing increased staphylococcal protein A (SpA) but normal toxic shock syndrome toxin 1 (TSST-1) production. This suggests a complex regulatory mechanism in KD pathogenesis, not a simple agr defect.

Area of Science:

  • Microbiology
  • Immunology
  • Pediatric Infectious Diseases

Background:

  • Kawasaki disease (KD) is an acute childhood vasculitis potentially linked to superantigen involvement.
  • Staphylococcus aureus strains from KD patients secrete toxic shock syndrome toxin 1 (TSST-1).
  • Previous studies suggested KD isolates might have defects in the accessory gene regulator (agr) locus.

Purpose of the Study:

  • To investigate the agr regulatory system's role in Staphylococcus aureus isolates from Kawasaki disease patients.
  • To characterize the expression of staphylococcal protein A (SpA) and TSST-1 in KD isolates compared to toxic shock syndrome (TSS) isolates.
  • To determine if KD isolates exhibit an agr-defective phenotype.

Main Methods:

  • Analysis of exoprotein production, specifically TSST-1 and SpA, in KD and TSS isolates.
  • Quantification of spa mRNA levels in KD and TSS isolates.
  • Assessment of RNAIII transcript levels and nucleotide sequence analysis of the RNAIII-coding region.
  • Evaluation of RNAIII's effect on spa mRNA transcription in KD isolates.

Main Results:

  • KD isolates exhibited higher levels of staphylococcal protein A (SpA) and spa mRNA compared to TSS isolates, indicative of an agr-defective phenotype.
  • Both KD and TSS isolates produced comparable levels of toxic shock syndrome toxin 1 (TSST-1).
  • KD isolates were not found to be defective in RNAIII, the effector molecule of the agr system, though RNAIII induction did not significantly decrease spa mRNA levels.

Conclusions:

  • Kawasaki disease-associated Staphylococcus aureus isolates display characteristics of an agr-defective phenotype, notably elevated SpA production.
  • The findings suggest a nuanced regulatory mechanism in KD isolates, where the agr system may not be globally defective.
  • Further research is needed to elucidate the precise role of superantigens and bacterial regulatory pathways in Kawasaki disease pathogenesis.

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