Ticks are hematophagous ectoparasites capable of transmitting multiple human pathogens. Environmental changes have supported the expansion of ticks into new geographical areas that have become the epicenters of tick-borne diseases (TBDs). The spotted fever group (SFG) of Rickettsia frequently infects ticks and causes tick-transmitted rickettsioses in areas of endemicity where ixodid ticks support host transmission during blood feeding. Ticks also serve as a reservoir for SFG Rickettsia. Among the members of SFG Rickettsia, R. rickettsii causes Rocky Mountain spotted fever (RMSF), the most lethal TBD in the United States. Cases of RMSF have been reported for over a century in association with several species of ticks in the United States. However, the isolation of R. rickettsii from ticks has decreased, and recent serological and epidemiological studies suggest that novel species of SFG Rickettsia are responsible for the increased number of cases of RMSF-like rickettsioses in the United States. Recent analyses of rickettsial genomes and advances in genetic and molecular studies of Rickettsia provided insights into the biology of Rickettsia with the identification of conserved and unique putative virulence genes involved in the rickettsial life cycle. Thus, understanding Rickettsia-host-tick interactions mediating successful disease transmission and pathogenesis for SFG rickettsiae remains an active area of research. This review summarizes recent advances in understanding how SFG Rickettsia species coopt and manipulate ticks and mammalian hosts to cause rickettsioses, with a particular emphasis on newly described or emerging SFG Rickettsia species.
Keywords: Rickettsia; endothelial cell; macrophages; pathogenesis; rickettsiosis; spotted fever; tick.