This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by LaFond, R. E. Articles by Lukehart, S. A. Search for Related Content PubMed PubMed Citation Articles by LaFond, R. E. Articles by Lukehart, S. A.

 Previous Article  |  Next Article 

Clinical Microbiology Reviews, January 2006, p. 29-49, Vol. 19, No. 1
0893-8512/06/$08.00+0     doi:10.1128/CMR.19.1.29-49.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Biological Basis for Syphilis

Departments of Pathobiology,¹ Medicine, University of Washington, Seattle, Washington²

Syphilis is a chronic sexually transmitted disease caused by Treponema pallidum subsp. pallidum. Clinical manifestations separate the disease into stages; late stages of disease are now uncommon compared to the preantibiotic era. T. pallidum has an unusually small genome and lacks genes that encode many metabolic functions and classical virulence factors. The organism is extremely sensitive to environmental conditions and has not been continuously cultivated in vitro. Nonetheless, T. pallidum is highly infectious and survives for decades in the untreated host. Early syphilis lesions result from the host's immune response to the treponemes. Bacterial clearance and resolution of early lesions results from a delayed hypersensitivity response, although some organisms escape to cause persistent infection. One factor contributing to T. pallidum's chronicity is the paucity of integral outer membrane proteins, rendering intact organisms virtually invisible to the immune system. Antigenic variation of TprK, a putative surface-exposed protein, is likely to contribute to immune evasion. T. pallidum remains exquisitely sensitive to penicillin, but macrolide resistance has recently been identified in a number of geographic regions. The development of a syphilis vaccine, thus far elusive, would have a significant positive impact on global health.

This article has been cited by other articles:

• Kastenmuller, G., Gasteiger, J., Mewes, H.-W. (2008). An environmental perspective on large-scale genome clustering based on metabolic capabilities. Bioinformatics 24: i56-i62 [Abstract]  
• Cruz, A. R., Moore, M. W., La Vake, C. J., Eggers, C. H., Salazar, J. C., Radolf, J. D. (2008). Phagocytosis of Borrelia burgdorferi, the Lyme Disease Spirochete, Potentiates Innate Immune Activation and Induces Apoptosis in Human Monocytes. Infect. Immun. 76: 56-70 [Abstract] [Full Text]  
• Salazar, J. C., Rathi, A., Michael, N. L., Radolf, J. D., Jagodzinski, L. L. (2007). Assessment of the Kinetics of Treponema pallidum Dissemination into Blood and Tissues in Experimental Syphilis by Real-Time Quantitative PCR. Infect. Immun. 75: 2954-2958 [Abstract] [Full Text]  
• Deka, R. K., Brautigam, C. A., Tomson, F. L., Lumpkins, S. B., Tomchick, D. R., Machius, M., Norgard, M. V. (2007). Crystal Structure of the Tp34 (TP0971) Lipoprotein of Treponema pallidum: IMPLICATIONS OF ITS METAL-BOUND STATE AND AFFINITY FOR HUMAN LACTOFERRIN. J. Biol. Chem. 282: 5944-5958 [Abstract] [Full Text]  
• Lazarus, J. J., Meadows, M. J., Lintner, R. E., Wooten, R. M. (2006). IL-10 Deficiency Promotes Increased Borrelia burgdorferi Clearance Predominantly through Enhanced Innate Immune Responses. J. Immunol. 177: 7076-7085 [Abstract] [Full Text]