Pathogenesis of rickettsial infections emphasis on Q fever

Abstract

The underlying mechanisms at the organismic, cellular and molecular levels that account for rickettsial pathogenesis are beginning to be revealed. In the case of Coxiella burnetii infection, relatively recent genetic and biochemical data, as well as drug susceptibility studies, indicate a correlation between isolate type and clinical disease--chronic or short-term acute. The use of cultured cells as model host systems has revealed that, indeed, different isolates from the major classified strains of C. burnetii cause different host cell responses. Use of this and other models (guinea pigs, mice) have revealed other characteristics and properties of the rickettsiae and the infected hosts and host cells that may account, in part, for acute disease and persistent infection culminating in chronic disease. The virulence factors involved apparently include the agent's surface lipopolysaccharide; other unidentified factors have not been excluded. Molecular cloning will play a major role in elucidating the roles of these factors and in identifying other virulence determinants.