Evaluation of an isogenic hemolysin-deficient mutant in the human model of Haemophilus ducreyi infection

K. L. Palmer, A. C. Thornton, K. R. Fortney, A. F. Hood, R. S. Munson, S. M. Spinola

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

Haemophilus ducreyi causes the genital ulcerative disease chancroid. One putative virulence factor of H. ducreyi is a pore-forming hemolysin that displays toxicity against human fibroblasts and keratinocytes. In order to test the role of the hemolysin in pathogenesis, an isogenic hemolysin- deficient mutant was constructed, designated 35000HP-RSM1. The lipooligosaccharide, outer membrane protein patterns, and growth attributes of 35000HP-RSM1 were identical to its parent, 35000HP. Human subjects were challenged on the upper arm with the isogenic isolates in a double-blinded, randomized, escalating dose-response study. Pustules developed at a similar rate at sites inoculated with the mutant or parent. The cellular infiltrate and bacterial load in lesions were also similar. These results indicate the hemolysin does not play a role in pustule formation. Due to the limitations of this model, the role of the hemolysin at later stages of infection could not be determined.

Original languageEnglish (US)
Pages (from-to)191-199
Number of pages9
JournalJournal of Infectious Diseases
Volume178
Issue number1
DOIs
StatePublished - Jan 1 1998

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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