Review of Treponema pallidum
ssp. pallidum
General Characteristics of
Treponema pallidum
Too thin to be seen with light microscopy in specimens stained with Gram stain or Giemsa stain
•Motile spirochetes can be seen with darkfield micoscopy
•Staining with anti-treponemal antibodies labeled with fluorescent dyes
Intracellular pathogen
Cannot be grown in cell-free cultures in vitro
• Koch’s Postulates have not been met
Do not survive well outside of host
• Care must be taken with clinical specimens for |
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laboratory culture or testing |
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Epidemiology of T. pallidum
Transmitted from direct sexual contact or from mother to fetus
Not highly contagious (~30% chance of acquiring disease after single exposure to infected partner) but transmission rate dependent upon stage of disease
Long incubation period during which time host is non-infectious
•Useful epidemiologically for contact tracing and administration of preventative therapy
Prostitution for drugs or for money to purchase drugs remains central epidemiologic aspect of transmission
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Pathogenesis of T. pallidum
Tissue destruction and lesions are primarily a consequence of patient’s immune response
Syphilis is a disease of blood vessels and of the perivascular areas
In spite of a vigorous host immune response the organisms are capable of persisting for decades
•Infection is neither fully controlled nor eradicated
•In early stages, there is an inhibition of cell-mediated immunity
•Inhibition of CMI abates in late stages of disease, hence late lesions tend to be localized
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Virulence Factors of T. pallidum
Outer membrane proteins promote adherence
Hyaluronidase may facilitate perivascular infiltration
Antiphagocytic coating of fibronectin
Tissue destruction and lesions are primarily result of host’s immune response (immunopathology)
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Pathogenesis of T. pallidum (cont.)
Primary Syphilis
Primary disease process involves invasion of mucus membranes, rapid multiplication & wide dissemination through perivascular lymphatics and systemic circulation
Occurs prior to development of the primary lesion
10-90 days (usually 3-4 weeks) after initial contact the host mounts an inflammatory response at the site of inoculation resulting in the hallmark syphilitic lesion, called the chancre (usually painless)
•Chancre changes from hard to ulcerative with profuse shedding of spirochetes
•Swelling of capillary walls & regional lymph nodes w/ draining
•Primary lesion heals spontaneously by fibrotic walling-off
within two months, leading to false sense of relief
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Pathogenesis of T. pallidum (cont.) Secondary Syphilis
Secondary disease 2-10 weeks after primary lesion
Widely disseminated mucocutaneous rash
Secondary lesions of the skin and mucus membranes are highly contagious
Generalized immunological response
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Pathogenesis of T. pallidum (cont.) Latent Stage Syphilis
Following secondary disease, host enters latent period
•First 4 years = early latent
•Subsequent period = late latent
About 40% of late latent patients progress to late tertiary syphilitic disease
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Pathogenesis of T. pallidum (cont.) Tertiary Syphilis
Tertiary syphilis characterized by localized granulomatous dermal lesions (gummas) in which few organisms are present
•Granulomas reflect containment by the immunologic reaction of the host to chronic infection
Late neurosyphilis develops in about 1/6 untreated cases, usually more than 5 years after initial infection
•Central nervous system and spinal cord involvement
•Dementia, seizures, wasting, etc.
Cardiovascular involvement appears 10-40 years after initial infection with resulting myocardial
insufficiency and death
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Diagram of a
Granuloma
(a.k.a. gumma in skin or soft tissue)
NOTE: ultimately a fibrin layer develops around granuloma, further “walling off” the lesion
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