Pathogenesis of Syphilis
Justin D. Radolf, Karsten R. O. Hazlett, and Sheila A. Lukehart
from: Pathogenic Treponema: Molecular and Cellular Biology (Edited by: Justin D. Radolf and Sheila A. Lukehart). Caister Academic Press, U.K. (2006)
Abstract
Venereal syphilis is caused by Treponema pallidum, a noncultivatable, microaerophilic spirochete and obligate human pathogen. T. pallidum utilizes glycolysis for energy production, has extremely limited biosynthetic capacity, and possesses limited tolerance for environmental stress. Transmission of T. pallidum occurs in a high percentage of individuals exposed to primary or secondary syphilitic lesions. T. pallidum is extremely invasive. Invasion at the local site occurs shortly after inoculation, while hematogenous dissemination occurs well before the appearance of the primary lesion (chancre). Penetration of the blood-brain barrier by T. pallidum, a distinctive aspect of human disease, is common during early syphilis and, in untreated individuals, sets the stage for the subsequent development of neurological complications (neurosyphilis). Clinical manifestations result from the inflammatory responses elicited by spirochetes and spirochetal constituent (e.g., lipoproteins) locally and systemically. Clearance of spirochetes from sites of infection is accomplished by activated macrophages most likely in concert with opsonic antibodies. The limited surface antigenicity of T. pallidum is thought to be a major factor in the spirochete's ability to establish persistent infection; selection of tprK sequence variants also may contribute to immune evasion. As with other spirochetal pathogens, motility is thought to be critical for treponemal invasiveness. The lack of orthologs for well characterized virulence determinants in the T. pallidum genome emphasizes the uniqueness of the bacterium's parasitic strategies. Genetic approaches for identifying treponemal virulence determinants are beginning to emerge read more ...
