This project examines mechanisms of pathogenesis of obligately intracellular bacteria. Primary emphasis is on the identification of surface structures which may function in host-parasite interactions, such as attachment or penetration, or otherwise act as determinants of virulence. Two obligately intracellular parasites with quite different modes of intracellular survival are presently being studied. Chlamydia trachomatis, the leading cause of preventable blindness worldwide and of sexually transmitted disease in this country, is being examined with a goal of identifying components which may function in the initial, adsorptive step of chlamydia-host interaction. Two surface proteins have been identified which display a number of properties that, collectively, suggest a role as adhesins. These proteins are present only on the infectious stage of the life cycle, display affinity for eucryotic cell surface components, and vary among serotypes of C. trachomatis in correlation with the type of disease associated with a particular serotype. Studies of Coxiella burnetii, the etiological agent of Q fever, have focused on the lipopolysaccharides (LPS) since this component seems to be the predominant surface structure that varies in virulent to avirulent transitions. To explore the role of LPS in chronic human infections, we examined the LPS type from a number of C. burnetii strains. Three LPS groups, based either on SDS-PAGE profile or antigenic analysis, were identified. Two of these groups were comprised almost exclusively of isolates from Q fever endocarditis patients. This is the first demonstration of variation in the phase I antigen (LPS) of C. burnetii.
