Treponema pallidum - Pathogenesis, Transmission, Host Immunity, Virulence factors

Last Modified: July 20, 2022

Contents

Pathogenesis of Treponema pallidum

causes disease by invasion and multiplication at the site of infection
it then spreads via host blood circulation, resulting in disseminated disease.
host immune response, in turn, causes primary tissue damage and pathogenic lesions- a hallmark of syphilis in patients.
during sexual intercourse, Treponema pallidum transmission from the infected to another partner occurs through intact mucous membrane or minor skin abrasions.
at the site of infection, organisms invade the skin, multiply, and chancre (a primary lesion) develops at the site
via blood, the infection spreads and produces disseminated lesions- papular skin rashes, mucous patches in the oro-pharynx, etc.
as syphilis progresses to its late stages, all tissues are possibly affected by Treponema pallidum
localized multiplication and tissue destruction are also observed.

transmission of Treponema pallidum is primarily through sexual contact by inoculation of the spirochetes through mucosal surfaces and abrasions on the epithelial surfaces
vertical transmission transplacentally
transfusion of Treponema pallidum-contaminated blood

specific treponemal antibodies and non-specific reaginic antibodies are produced.
cell-mediated immunity is also induced
immunity is incomplete: both humoral and CMI prevent the formation of the chancre, and reinfection with Treponema pallidum. But the host immunity cannot clear organisms from the site of infection.
Failure to kill Treponema pallidum is due to:
- presence of an outer layer of Treponema which lacks immunologic molecules
- it may be due to the downregulation of T_H cells.