Treponema pallidum

T. pallidum is the etiological agent of syphilis. It is a long spiral-shaped rod cncased in a protoplasmic cylinder. It has a peptidoglycan layer and is motile by means of an axial filament. The fact that this bacteria

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Gonococci

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Figure 1 Immunobiology of gonococcal infection of the human fallopian tube mucosa. Gonococci attach to the microvilli on noncih-ated epithelial cells and are internalized by a phagocytic mechanism that results in a membrane-bound vesicle. This process takes approximately 24 h. At the same time, the gonococci liberate from their surface two molecules (lipo-oligosaccharide and peptidoglycan) that are toxic to the ciliated epithelial cells and they slough as a result of this action. Gonococci continue to migrate through the epithelial cell and by 72 h after infection they have begun an orderly exocytosis from the epithelial cell. At this point in the infection, the gonococci are present in the lamina propria where they can encounter a variety of immunocompetent cells to initiate both B and T cell responses as well as the increased production of cytokines (e.g. TNFa). (Reproduced from Cooper and Moticka (1996) by copyright permission of Blackwell Science.)

cannot be cultured on artifical media has hampered studies to characterize the organism and study the immune response to the infection. No toxin production has been documented.

After infection with T. pallidum, polymorphonuclear leukocytes are attracted to the site where tre-ponemas are killed. Activated macrophages also phagocytose and kill T. pallidum. Specific responses to treponemal infection involve both T and B cells. The initial humoral response is the production of antibodies which are nonspecific for T. pallidum. These are detected by serological tests such as the Venereal Disease Research Laboratory (VDRL) or the RPR (rapid plasma reagin) tests which are used to screen for syphilis.

By the time of the primary infection (chancre), specific humoral and cell-mediated immune mechanisms have been activated. Treponema-sensitized lymphocytes and activated macrophages are present in the lesions and antitreponemal antibody is detectable in serum. This leads to a decrease but not elimination of the treponemas. In the absence of treatment incompletely understood events occur and a generalized infection called secondary syphilis occurs. The time and appearance of disseminated lesions suggest that there is a hematogenous spread throughout the body. The development of systemic immunity modulates the appearance and severity of the lesions. The infected individual has high nonspecific as well as specific antibody titers. However, delayed-type hypersensitivity (DTH) is usually absent.

Eventually the host suppresses the infectious process sufficiently and lesions are no longer apparent. This leads to a period of clinical latency. By this point, cell-mediated immunity is now present. Immobilizing treponemal antibody is present but it is difficult to demonstrate a protective humoral immune response. Even during latency, T. pallidum can be isolated from both human and experimentally infected animals. The spirochetes may be sequestered in an immunologically privileged site, e.g. the central nervous system. The infection may remain latent for the remaining natural course of the disease or manifest itself as tertiary syphilis.

Figure 2 Immunobiology of chlamydial infection of the human fallopian tube mucosa. Elementary bodies (EBs) attach to the microvilli of epithelial cells prior to invasion of the epithelium. In some cases, where EB aggregates are large, a local cytotoxicity is seen. The chlamydia have a normal developmental cycle in the epithelial cells but do not usually penetrate the basolateral portion of the cell. The EBs cause a lesion in the luminal surface of the infected epithelial cells and are released where they are capable of infecting other cells. (Reproduced from Cooper and Moticka (1996) by copyright permission of Blackwell Science.)

Figure 2 Immunobiology of chlamydial infection of the human fallopian tube mucosa. Elementary bodies (EBs) attach to the microvilli of epithelial cells prior to invasion of the epithelium. In some cases, where EB aggregates are large, a local cytotoxicity is seen. The chlamydia have a normal developmental cycle in the epithelial cells but do not usually penetrate the basolateral portion of the cell. The EBs cause a lesion in the luminal surface of the infected epithelial cells and are released where they are capable of infecting other cells. (Reproduced from Cooper and Moticka (1996) by copyright permission of Blackwell Science.)

Since the natural history of the disease is unique and much remains to be understood about the biology of the spirochete, discussions regarding the development of a vaccine are premature.

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