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  1. 1. Treponema pallidum *
  2. 2.  Extremely thin and can be very long  Tightly coiled helical cells with tapered ends  Motile by periplasmic flagella (also known as axial fibrils or endoflagella)  Outer sheath encloses axial fibrils wrapped around protoplasmic cylinder General overview of Spirochaetales • Axial fibrils originate from insertion pores at both poles of cell • May overlap at center of cell in Treponema and Borrelia, but not in Leptospira • Differering numbers of endoflagella present according to genus & species Figure: Periplasmic flagella diagram Figure: Treponema pallidum
  3. 3. Genus Species Disease Treponema pallidum ssp. pallidum pallidum ssp. endemicum pallidum ssp. pertenue carateum Syphilis Bejel Yaws Pinta Borrelia burgdorferi recurrentis Many species Lyme disease (borreliosis) Epidemic relapsing fever Endemic relapsing fever Leptospira interrogans Leptospirosis (Weil’s Disease) Spirochaetales Associated Human Diseases
  4. 4. Bejel (also known as endemic syphilis) • Caused by Treponema pallidum subsp. endemicum • Initial lesions: nondescript oral lesions • Secondary lesions: oral papules and mucosal patches • Late: gummas (granulomas) of skin, bones & nasopharynx • Transmitted person-to-person by contaminated eating utensils Yaws: granulomatous disease • Caused by Treponema pallidum ssp. pertenue • Early: skin lesions Late: destructive lesions of skin, lymph nodes & bones • Transmitted by direct contact with lesions containing abundant spirochetes Figure: Papillomatous Lesions of Yaws (painless nodules widely distributed over body with abundant contagious spirochetes)
  5. 5. Pinta: (primarily restricted to skin) • Caused by Treponema carateum •1-3 week incubation period • Initial lesions: small pruritic papules • Secondary: enlarged plaques persist for months to years • Late: disseminated, recurrent hypopigmentation or depigmentation of skin lesions; scarring & disfigurement Transmitted by direct contact with skin lesions Figure: Hypopigmented Skin Lesions of Pinta Syphilis: (Venereal Treponemal Disease) • Primarily sexually transmitted disease (STD) caused by T. pallidum subsp. pallidum • May be transmitted congenitally (from mother to fetus)
  6. 6.  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 laboratory culture or testing General Characteristics of Treponema pallidum
  7. 7. 1. Primary 2. Secondary 3. Latent 4. Late or tertiary * May involve any organ, but main parts are: * Neurosyphilis * Cardiovascular syphilis * Late benign (gumma) Stages of Acquired veneral Syphilis
  8. 8. * Primary disease process involves invasion of mucus membranes, rapid multiplication & wide dissemination through perivascular lymphatics and systemic circulation * Develops at site of contact/inoculation and incubation period ranges from 9-90 days, usually ~21 days. * Classically: single, painless, clean-based, indurated ulcer, with firm, raised borders. Atypical presentations may occur. * Mostly anogenital, but may occur at any site (tongue, pharynx, lips, fingers, nipples, etc...) * Non-tender regional adenopathy, Very infectious. * May be darkfield positive but serologically negative. * Untreated, heals in several weeks, leaving a faint scar. Primary Syphilis
  9. 9. * Secondary syphilis usually starts to manifest itself 3 to 8 weeks after healing of primary chancre. Secondary lesions results from the widespread multiplication of the treponemes and their dissemination through the blood. * Clinical signs include low fever, malaise, lymphadenopathy and alopecia areata. * On skin, the rash is most often maculopapular and is found on the palms and soles. * On mucous membranes, the rash appears in the form of discolored patches. Condylomata lata (flat plaques) are characteristic and found on the anal mucosa. * In most patients, the disease is cured spontaneously due to sufficient build up of immune response. About 13-15 % of the untreated cases will progress to a letent stage and finally to the tertiary stage. Secondary Syphilis
  10. 10. *Condylomata lata *Condylomata lata
  11. 11. Alopecia areata
  12. 12. * In latent stage, the infection remains dormant (latent) for variable period ( usually up to 2 years) without any clinical signs and symptoms but serological tests are positive during latent stage. Latent Syphilis Tertiary or late stage Syphilis Tertiary syphilis is 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 May also involve deep visceral organs, particularly the respiratory tract, gastrointestinal tract, bones, larynx, lung, liver,
  13. 13. Neurosyphilis - spirochetes in neural tissue Neurosyphilis - spirochetes in neural tissue Late syphilis - ulcerating gumma Tertiary or late stage Syphilis Late syphilis - serpiginous gummata of forearm
  14. 14. *Congenital syphilis is transmitted in utero after the first 16 weeks of pregnancy, therefore it is usually not a cause of abortion during the first trimester. *The infected child born later in a family usually has less severe syphilis. *Again, it has been divided according to the arbitrary dividing line of two years into early and late types. *Early Congenital *The features are similar to secondary syphilis. Usually it occurs 2-8 weeks after birth, presenting with failure to thrive, muco-cutaneous lesions (condylomata lata), generalized lymphadenopathy, nasal snuffles and skin rash. *Late Congenital *The onset usually occurs at or near puberty. Well-known stigmata include nerve deafness, interstitial keratitis, Hutchison's teeth (Hutchison's triad), rhagades around mouth, clutton's joint, osteitis & chondritis (saddle nose, frontal bossing, sabre tibia) and perforated palate. Congenital syphilis
  15. 15. Congenital syphilis - perforation of palate
  16. 16. Diagnostic Tests for Syphilis NOTE: Treponemal antigen tests indicate experience with a treponemal infection, but cross-react with antigens other than T. pallidum ssp. pallidum. (Original Wasserman Test)
  17. 17. Laboratory diagnosis • Since T. pallidum cannot be cultured in clinical laboratory, the diagnosis of syphilis consist of direct demonstration of the treponema and serological tests for detection of antibodies . A. Direct demonstration of treponema by dark-ground microscopy: Under dark-ground illumination, T. pallidum appears as a slender, spiral organism exhibiting rotational as well as flexion and extension movements B. Stained preparation: for direct demonstration of T. pallidum , acetone fixed smears are made from exudate and stained either by silver impregnation method (Fontana’s stain) or by fluorescein labelled anti-treponemal antibody (fluorescein labelled antibody test). In positive cases, treponemes fluoresce displaying typical morphology when viewed under fluorescent microscope.
  18. 18. C. Tissue Biopsy: Treponemes can be demonstrated in tissues (skin, visceral lesion) by silver impregnation method of staining or by Warthin-Starry stain or by immunofluorescence in tertiary syphilis. Serological Tests: In addition to blood, CSF is also examined in relevant cases. I. Non-treponemal tests: In the standard tests for syphilis (STS), reagin antibodies in patient serum is detected by cardiolipin antigen. Before performing the test, the patient’s serum is inactivated by heating in a waterbath at 560C for 30 minutes to destroy the complement. The STS includes flocullation tests (VDRL, RPR, TRUST, KT) and complement fixation test a. Flocculation test: VDRL (Venereal Disease Research laboratory) test It is the most widely used simple and rapid test. The VDRL antigen must be prepared freshly. In a specially prepared slide with depression of 14 mmdiameter each, 0.05 ml decomplemented serum is taken to which one drop of freshly prepared cardiolipin antigen is added by a syringe delivering 60 drops in one ml. the slide is then rotated at 180 revolutions per minute for four minutes either by VDRL rotator or manually. The antigen-antibody reaction is then studied under low power objective of microscope. Uniformly distributed crystals indicate negative test while presence of clumps signifies positive reaction. Quantitative tests with serial dilutions (1:4, 1:8 and so on ) of positive serum are performed.
  19. 19. b. Rapid plasma reagin (RPR) test: It is almost similar to VDRL test where finely divided carbon (charcoal) particles and choline are added to stabilized VDRL antigen. The addition of finely divided carbon particles enable the result to be read visually instead of microscopically. C. Toludine red unheated serum test (TRUST): It is a modification of RPR card test. The antigen is more stable then RPR antigen and can be stored at room temperature.  Commonly used specific tests for syphilis are the treponemal antibody test, FTA-ABS test and the MHA-TP: These tests use recombinant proteins or treoponemal antigens extracted from T. pallidum. Tests in common use include: • Enzyme-linked immunosorbent assays which detect IgM and IgG. • The Fluorescent treponemal antibody absorption (FTA-ABS) test in which the patient’s serum is first absorbed with non-pathogenic treponemes to remove cross-reacting antibodies before reaction with T. pallidum antigens; • The micro-hemagglutination assay for T. pallidum (MHA-TP)