BSCI 424 — PATHOGENIC MICROBIOLOGY — Fall 2000

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
 
 

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Copyright © 2000, D.M. Rollins and S.W. Joseph
Revised: August 2000
URL: http://life.umd.edu/classroom/bsci424