Haemophilus ducreyi requires an intact flp gene cluster for virulence in humans

Stanley M Spinola1, Kate R Fortney, Barry P Katz

  • 1Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA. sspinola@iupui.edu

Infection and Immunity
|November 26, 2003
PubMed

Insights

The Haemophilus ducreyi flp operon is vital for microcolony formation. A tadA mutant showed reduced pustule formation in humans, indicating flp locus proteins are key for H. ducreyi virulence in people.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Infectious Diseases

Background:

  • Haemophilus ducreyi causes chancroid, a sexually transmitted infection.
  • The flp operon and its gene tadA are implicated in bacterial virulence and secretion systems.

Purpose of the Study:

  • To investigate the role of the tadA gene within the H. ducreyi flp operon in virulence.
  • To compare the virulence of a tadA mutant and wild-type H. ducreyi in human and animal models.

Main Methods:

  • Experimental infection of human volunteers with wild-type H. ducreyi and a tadA mutant.
  • Assessment of lesion development (papules and pustules) in human participants.
  • Evaluation of lesion scores in a temperature-dependent rabbit model of chancroid.

Main Results:

  • Papule formation rates were similar between the mutant and wild-type strains in humans.
  • Pustule formation was significantly reduced in human sites inoculated with the tadA mutant (0%) compared to the wild-type (36.4%).
  • The tadA mutant showed a modest but significant reduction in lesion scores in the rabbit model.

Conclusions:

  • Proteins secreted by the flp locus are essential for full H. ducreyi virulence in humans, particularly for pustule development.
  • The flp locus plays a less significant role in virulence in the rabbit model of chancroid compared to human infections.

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