Rickettsial infections continue to pose a significant health threat to humans of all ages across the globe. Rickettsiae are obligate intracellular, Gram-negative bacteria with tropism for microvascular endothelium in humans during natural transmission from arthropod vectors and in experimental mouse models of infection. Consequently, pathogenesis of rickettsioses primarily involves endothelial activation, inflammation, dysfunction, and compromised barrier integrity, collectively referred to as "rickettsial vasculitis." A procoagulative phenotype may develop in rickettsial infection, resulting in the formation of hemostatic plugs at the sites of severe vascular damage, but only rare occurrence of disseminated intravascular coagulation. This chapter summarizes unique features of pathogenic Rickettsia species, the spectrum of rickettsial diseases, and recent advancements in cellular and molecular mechanisms of pathogenesis with primary focus on endothelial cell responses to infection. Comprehensive understanding of interactions between this unique group of cytoplasmic pathogens and the host vasculature should facilitate the development of new therapeutics to prevent or reverse endothelial dysfunction and vascular leakage associated with rickettsial infections.
|Original language||English (US)|
|Title of host publication||Vascular Responses to Pathogens|
|Number of pages||12|
|State||Published - Jan 1 2016|
- Host response
ASJC Scopus subject areas