Pathophysiological concept of Haemophilus ducreyi infection (chancroid)

Our knowledge concerning the pathogenesis of infection due to Haemophilus ducreyi is incomplete. In order to produce disease, H. ducreyi must presumably penetrate the skin of the external genitalia, colonize subcutaneous tissues, then produce tissue damage which results in ulcer formation. Penetration of the normal skin most likely occurs via minor abrasions. Adherence of H. ducreyi to different cell lines in vitro has been described, and might be mediated by adhesions such as pili or haemagglutinins. In addition, binding to extracellular matrix proteins has also been reported. Extracellular tissue-degrading enzymes were absent from broth culture supernatants of H. ducreyi. Such supernatants also failed to produce cytopathic effects with established or primary cell lines. Both live and heat-killed H. ducreyi organisms were able to produce lesions in a rabbit or a mouse model, although ulcer formation was dependent on viable H. ducreyi organisms in a recently introduced temperature-dependent rabbit model. With an excessive supply of iron, a more prolonged localized inflammatory disease effect was observed. Results derived from a subcutaneous chamber model demonstrated considerable changes in the expression of outer membrane proteins combined with antibody modulation during in vivo growth of H. ducreyi. These might be important factors for maintenance of infection in the human host particularly as these changes also occur in humans. Despite an increased knowledge of the pathogenesis of chancroid, important questions such as growth requirements, bubo-formation, role of cell-mediated immunity and ulcer formation are still unanswered. The application of molecular biological techniques in order to study these problems will be helpful.