Walsh & Hoyt: Pathology and Pathogenesis

Vasculitis is the pathologic common denominator of all infections caused by rickettsiae. The organisms are introduced into the blood directly by various feeding arthropods or by inoculation of infected arthropod feces by scratching. Once in the bloodstream, the rickettsiae enter host cells, particularly the endothelial and smooth muscle cells of the blood vessels, and proliferate. After entry by induced phagocytosis, some species of rickettsiae multiply within the endocytic vacuoles, but most escape from the phagosome and proliferate in the cytoplasm, the nucleus, or both, depending on the particular rickettsiae involved. Regardless of the site or sites of proliferation, however, the multiplying rickettsiae divert cellular nutrients and energy for their own use, and this eventually causes destruction of the cell. Death of endothelial and smooth muscle cells in turn causes increased vascular permeability, formation of microthrombi, recruitment of mononuclear inflammatory cells, and secondary thrombosis with microinfarction of the tissue normally supplied by the affected vessels. In addition, the increased vascular permeability results in edema, hypovolemia, hypotension, and hypoalbuminemia. Hyponatremia may occur from secretion of antidiuretic hormone in response to hypovolemia.