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O06.1 Investigating the interaction of the stealth pathogen and causative agent of syphilis, treponema pallidum, with human platelets
  1. Brigette Church1,
  2. John R Webb2,
  3. Caroline E Cameron1
  1. 1University of Victoria, Victoria, Canada
  2. 2BC Cancer Agency, Victoria, Canada

Abstract

Introduction Treponema pallidum ssp. pallidum, the causative agent of syphilis, is a highly invasive pathogen that interacts with a diverse repertoire of host cells during infection. The pathogen invades immunologically privileged sites and crosses the placental, blood-brain, endothelial and blood-retina barriers to establish widespread infection. Treponema pallidum disseminates via the circulatory and lymphatic systems, avoiding the prevalent inflammatory reactions raised against other blood-borne pathogens. In this study we investigate if T. pallidum uses an interaction with human platelets, key mediators of homeostasis and immune surveillance, to facilitate host persistence. We demonstrate that T. pallidum adheres to human platelets enabling survival for an extended period, and we discuss how this interaction may aid T. pallidum pathogenesis.

Methods Platelet rich plasma prepared from donor blood was incubated under host-mimicking microaerophilic conditions with viable T. pallidum, followed by examination for T. pallidum-platelet interactions via darkfield microscopy and flow cytometry analyses. Viability was confirmed using microscopic and fluorescent staining methodologies.

Results Treponema pallidum binds both the rounded and spread morphologies of activated platelets via a polar tip structure, maintaining a firm tether under fluidic conditions. A lack of interaction between heat-killed T. pallidum and platelets confirmed specificity and identified heat-labile T. pallidum surface components as mediators of this interaction. Viability assays illustrated T. pallidum retained viability in platelet rich plasma for >3 days under these conditions.

Conclusion The demonstration in this study of (1) prolonged T. pallidum survival within human platelet rich plasma and (2) T. pallidum-platelet interactions indicates that platelets do not exhibit a direct antimicrobial effect on T. pallidum and that T. pallidum mediates a strong and specific interaction with human platelets. These findings may reveal a novel mechanism of host survival employed by this elusive pathogen.

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