EVALUATION OF AN DLTA MUTANT IN EXPERIMENTAL HUMAN INFECTION WITH HAEMOPHILUS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Haemophilus ducreyi is the etiologic agent of the genital ulcer disease chancroid. Recently, the gene encoding a novel surface lipoprotein called DltA for Ducreyi Lectin A was described by Elkins and colleagues. A dltA mutant, called FX533, was susceptible to killing by 50% normal human serum. In the human challenge model of H. ducreyi infection, bacteria are introduced into the skin via puncture wounds, and serum transudates into the wounds. Serum resistance is an important virulence determinant in the human challenge model. The purpose of this study is to test the hypothesis that a DltA mutant is impaired in its ability to infect human skin when compared to its isogenic parent. To test this hypothesis, we will compare the ability of the parent and the mutant to cause experimental infection in human subjects. These studies will establish whether expression of DltA is required for H. ducreyi to cause pustules, and may provide a rationale to develop a vaccine against H. ducreyi.