Haemophilus ducreyi, the causative agent of the sexually transmitted infection chancroid, is primarily a pathogen of human skin. During infection, H. ducreyi thrives extracellularly in a milieu of professional phagocytes and other antibacterial components of the innate and adaptive immune responses. This review summarizes our understanding of the interplay between this pathogen and its host that leads to development and persistence of disease.
H. ducreyi expresses key virulence mechanisms to resist host defenses. The secreted LspA proteins are tyrosine-phosphorylated by host kinases, which may contribute to their antiphagocytic effector function. The serum resistance and adherence functions of DsrA map to separate domains of this multifunctional virulence factor. An influx transporter protects H. ducreyi from killing by the antimicrobial peptide LL37. Regulatory genes have been identified that may coordinate virulence factor expression during disease. Dendritic cells and natural killer cells respond to H. ducreyi and may be involved in determining the differential outcomes of infection observed in humans.
A human model of H. ducreyi infection has provided insights into virulence mechanisms that allow this human-specific pathogen to survive immune pressures. Components of the human innate immune system may also determine the ultimate fate of H. ducreyi infection by driving either clearance of the organism or an ineffective response that allows disease progression.
aDepartment of Medicine, USA
bDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA
* Diane M. Janowicz and Wei Li contributed equally to this article.
Correspondence to Margaret E. Bauer, PhD, Department of Microbiology and Immunology, Indiana University School of Medicine, 635 Barnhill Drive, Room MS 420, Indianapolis, IN 46202-5124, USA Tel: +1 317 274 8143; fax: +1 317 274 4090; e-mail: email@example.com