text: R. rickettsii also has an outer layer or a "microcapsule", which acts similarly to the S-layer or slime layer of other bacteria.  This slime layer consists mostly of polysaccharides, and the "microcapsule" contributes to mechanisms involving anti-phagocytosis and attachment to host cells.
  Pathophysiology
  While humans are hosts for R. rickettsii, they do not contribute to rickettsial transmission. Rather, the pathogen is maintained through its vector: ticks. R. rickettsii invades the endothelial cells that line the blood vessels in the host's body. Increased permeability of vessels, microvascular hemorrhages, and necrosis can result from damage to the cells. The pathogen causes changes in the host cell cytoskeleton that induces phagocytosis, and R. rickettsii replicates further and infects other cells in the host's body. R. rickettsii's survival in immune system cells increases the pathogen's virulence in mammalian hosts.
  Actin-Based Motility (ABM) is a virulence factor that allows for the pathogen to evade the host's immune cells and spread to neighboring cells. It is suggested that the Sca2 gene, which is an actin-polymerizing determinant, is a distinguishing factor for the Rickettsia family, as R. rickettsii mutants with a Sca2 transposon the bacteria can avoid autophagic processes by host phagocytic cells. This leads to an increase in disease manifestation for the host.