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Strain-specific iron-dependent virulence in Escherichia coli

S Telang1, E Vimr, J R Mahoney

  • 1Department of Pediatrics, Baylor College of Medicine, Houston, Texas, USA.

The Journal of Infectious Diseases
|June 26, 2001
PubMed

Insights

Certain virulent Escherichia coli strains exhibit iron-dependent virulence. This virulence is linked to polysialic acid capsules that slow clearance, allowing bacteria to thrive with iron.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Bacterial Virulence

Background:

  • Certain strains of Escherichia coli (E. coli) demonstrate increased virulence when exposed to iron sources like hemoglobin.
  • The mechanisms underlying this iron-dependent virulence are not fully understood.

Purpose of the Study:

  • To investigate the role of polysialic acid capsules in the iron-dependent virulence of E. coli.
  • To elucidate the relationship between bacterial clearance, capsule formation, and iron availability in vivo.

Main Methods:

  • Comparison of in vitro growth and in vivo clearance of virulent and nonvirulent E. coli strains with and without hemoglobin.
  • Analysis of polysialic acid capsule presence in virulent and nonvirulent strains.
  • Assessment of clearance rates for E. coli grown under conditions that inhibit polysialylation.
  • Evaluation of virulence in a knockout mutant lacking polysialyltransferase.

Main Results:

  • Virulent E. coli strains possess a polysialic acid capsule, absent in nonvirulent strains.
  • Polysialylation significantly slows the in vivo clearance of E. coli, even without supplemental iron.
  • Inhibition of polysialylation restores rapid clearance of virulent E. coli.
  • Deletion of polysialyltransferase in a virulent strain accelerates clearance and reduces iron-dependent virulence.

Conclusions:

  • Iron-dependent virulence in E. coli is a multifactorial phenomenon.
  • Outer membrane polysialylation contributes to virulence by impeding host clearance.
  • Combined effects of slow in vivo clearance due to polysialylation and iron-enhanced growth contribute to E. coli pathogenesis.

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