Treponema Summary


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Treponema pallidum ssp. pallidum:

  Motile, Gram-negative, microaerophilic spirochaete (with tapered end)
(see WebLinked image)

  Cause of venereal syphilis

  Outer sheath encloses axial fibrils wrapped around protoplasmic cylinder

  Axial fibrils originate at both poles and may overlap at center of cell in Treponema and Borrelia, but not in Leptospira

  Obligate intracellular pathogen
(see WebLinked image)

  Cannot be grown in vitro

  Do not survive well outside of host

  Transmitted from direct sexual contact or from mother to fetus

  Not highly contagious (about 1 chance in 10 of acquiring disease from infected partner

  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

  Capacity to invade intact mucus membranes or skin with abrasions

  Most common sites of inoculation are the cervix or vagina in the female and the penis in the male

  Syphilis is a disease of blood vessels and of the perivascular areas

  Primary disease process involves invasion of mucus membranes, rapid multiplication, wide dissemination through perivascular lymphatics and systemic circulation 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 (changes from hard to ulcerative), with profuse shedding of spirochetes; swelling of capillary walls and regional lymph nodes with draining

  Prmary lesion is resolved by fibrotic walling-off

  Secondary disease appears 2-10 weeks after primary lesion

  Secondary lesions of the skin and mucus membranes are highly contagious

  Generalized immunological response

  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

  Tertiary syphilis characterized by localized dermal lesions (gummas) in which few organisms are present and reflects the immunologic reaction of the host

  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 intial infection with resulting myocardial insufficiency and death

  Congenital syphilis results from transplacental infection with T. pallidum

  Septicemia in the developing fetus and widespread dissemination

  Abortion, neonatal mortality, and late mental or physical problems resulting from scars from the active disease and progression of the active disease state

  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 that abate in late stages of disease, hence late lesions tend to be localized

  Penicillin remains drug of choice but WHO monitors treatment recommendations

  7-10 days continuous for early stage and at least 21 days continuous beyond the early stage

  Prevention with barrier methods and prophylactic treatment of contacts identified through epidemiological tracing

  Other nonvenereal treponemal diseases include yaws (T. pallidum ssp. pertenue), pinta (T. carateum), and bejel (T. pallidum ssp. endemicum)

  Diagnostic serological test = Wassermann test

   Return to Pathogen List



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