Rickettsia parkeri are obligate intracellular, arthropod-borne pathogens that are classified within the spotted fever group (SFG) of Rickettsia species. R. parkeri are capable of causing eschar-associated spotted fever rickettsiosis in humans. SFG Rickettsia infection of humans occurs when a human is bitten by an infected tick. In the human host, Rickettsia invade host cells, escape from vacuoles, and undergo two modes of actin-based motility mediated by either the effectors, RickA or Sca2. RickA-motility occurs during early timepoints of infection (<2 hrs) and involves the activation of host Arp2/3 complexes to polymerize branched actin filaments against the bacterial surface. Sca2-motility occurs at later timepoints of infection (>5 hrs) and alone, is sufficient to polymerize bundled actin filaments against the bacterial surface. The forces generated by actin polymerization against the bacterial surface propels bacteria in the host cytosol. Sca2-motility has been implicated in cell-to-cell spread, a process that allows bacteria to infect nearby cells without being exposed to the extracellular environment via short protrusions of the host plasma membranes. The role of RickA-motility has been unclear. Using live-cell imaging of sca2::Tn mutant R. parkeri, which only undergo RickA-motility, we discovered a role for RickA-motility in cell-to-cell spread. Indeed, bacteria undergoing RickA-motility were observed to collide against host plasma membranes to form long protrusions that extended into and were engulfed by neighboring recipient cells. We compared the dynamics of RickA-spread to Sca2-spread and discovered that RickA-spread involves longer protrusions, longer time, and larger fluctuations in length during periods of oscillation, suggesting that RickA-motility and Sca2-motility contribute to two mechanistically different forms of cell-to-cell spread. We lastly assessed the role of RickA and Sca2 in pathogenesis during infection of Ifnar1-/-; Ifngr1-/- double knock out (DKO) mice, which can succumb to infection with wild-type R. parkeri and form eschars following intradermal inoculation. We discovered that RickA is involved in eschar formation while Sca2 contributes to larger foci of infection in skin, as well as dissemination from the skin into the internal organs. Overall, our results suggest that Rickettsia undergo two different forms of cell-to-cell spread during their infectious lifecycle and that these forms of spread contribute to different processes in pathogenesis. Further investigations on the molecular mechanisms of RickA-spread and Sca2-spread will improve our understanding of how bacteria can highjack host processes to support their infectious lifecycle; and continued studies of R. parkeri using the Ifnar1-/-; Ifngr1-/- DKO mice will expand our knowledge of rickettsial pathobiology.