Spirochetes

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Spirochetes

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Spirochetes

  1. 1. SPIROCHETES Dr.T.V.Rao MD Dr.T.V.Rao MD 1
  2. 2. SpirochetesSpirochetes -are elongated motile,flexible bacteria twisted spirally along thelong axis are termed spirochetesContain – endoflegalla which are polarflagella wound along the helicalprotoplasmic cylinder and situatedbetween the outer membrane and cellwall Dr.T.V.Rao MD 2
  3. 3. TaxonomyOrder: Spirochaetales Family: Spirochaetaceae Genus: Trepanoma Borrelia Family: Leptospiraceae Genus: Leptospira Dr.T.V.Rao MD 3
  4. 4. Human pathogenA. Genera TrepanomaB. BorreiliaC. Leptospira Dr.T.V.Rao MD 4
  5. 5. How they appear Dr.T.V.Rao MD 5
  6. 6. What are TrepanomaTrepos – Turn Nema Meaning thread Relatively short and slender With fine spirals pointed and roundends May be pathogenic or commensals inthe mouth Dr.T.V.Rao MD 6
  7. 7. Spirochaetales Associated Human Diseases Genus Species DiseaseTreponema pallidum ssp. pallidum Syphilis pallidum ssp. endemicum Bejel pallidum ssp. pertenue Yaws carateum PintaBorrelia burgdorferi Lyme disease (borreliosis) recurrentis Epidemic relapsing fever Many species Endemic relapsing feverLeptospira interrogans Leptospirosis (Weil’s Disease) Dr.T.V.Rao MD 7
  8. 8. Venereal SyphilisVenereal Syphilis caused byT.pallidum Endemic syphilisT. pallidumYaws T.pertunePinta T.carateum Dr.T.V.Rao MD 8
  9. 9. Discovery “Everything” happened mostly in Germany from 1905 to 1910 ! With a short life of 35 years, Fritz Schaudinn (1871-1906) and Paul E. Hoffmann (1868-1959) discovered Treponema pallidum in serum in 1905. Paul Ehrlich, father of immunochemistry Fritz Dr.T.V.Rao MD 9and his assistent Hati. Schaudinn
  10. 10. SyphilisA. Named from poem published by the Italian physician and poet Girolamo Fracastoro – shepherd from Hispaniola named Syphilis who angered Apollo and was given the disease as punishment Dr.T.V.Rao MD 10
  11. 11. Syphilis"He who knows syphilis, knows medicine"Sir William Osler Dr.T.V.Rao MD 11
  12. 12. Treponema pallidum A. Described in 1905 by Schaudinn and Hoffman, Hamburg Dr.T.V.Rao MD 12
  13. 13. Trepanoma pallidumGreek words trepo “turning” & nema “head”A. Morphology 1. Motile, sluggish in viscous environments 2. Size: 5 to 20 μm in length & 0.09 to 0.5 μm in diameter, with tapered ends 3. Structure • Multilayer cytoplasmic membrane • Flagella-like fibrils • Cell wall • Outer sheath (outer cell envelope) • Capsule-like outer coat Dr.T.V.Rao MD 13
  14. 14. Treponema pallidum.A. Spiral spirochete that is mobile of spirals varies from 4 to 14 Length 5 to 20 microns and very thin 0.1 to o.5 microns. Can be seen on fresh primary or secondary lesions by dark field microscopy or fluorescent antibody techniques Dr.T.V.Rao MD 14
  15. 15. General Overview of SpirochaetalesA. Gram-negative spirochetesB. Spirochete from Greek for “coiled hair”C. Extremely thin and can be very longD. Tightly coiled helical cells with tapered endsE. Motile by Periplasmic flagella (a.k.a., axial fibrils or endoflegalla) Dr.T.V.Rao MD 15
  16. 16. General Overview of SpirochaetalesA. Outer sheath encloses axial fibrils wrapped around protoplasmic cylinderB. Axial fibrils originate from insertion pores at both poles of cellC. May overlap at centre of cell in Treponema and Borrelia, but not in LeptospiraD. Differing numbers of endoflegalla according to genus & species Dr.T.V.Rao MD 16
  17. 17. Trepanoma palladiumB. Physiology – Difficult to culture • Maintained in anaerobic medium with albumin, sodium bicarbonate, pyruvate, cysteine • Microaerophilic Dr.T.V.Rao MD 17
  18. 18. Cross-Section of Spirochete with Periplasmic Cross section ofBorrelia burgdorferi Flagella NOTE: a.k.a., endoflegalla, axial fibrils or axial filaments. (Outer sheath) Dr.T.V.Rao MD 18
  19. 19. Staining with special stainsStaining byGiemsaandFontana Dr.T.V.Rao MD 19
  20. 20. Antigenic structureA. The Antigens are complexB. Infection with Treponema will induce 3 types of AntigensC. Reagin Antibodies – STSD. Detected by Standard tests for SyphilisE. 1 Wasserman Test, 2 Kahn TestF. VDRL Test Dr.T.V.Rao MD 20
  21. 21. Beef Heart Extracts - AntigenLipid Hapten – CardiolipinChemically Dipphostidyl glycerolCardiolipin present in theTrenonems ?Or a product of tissue Damage ? Dr.T.V.Rao MD 21
  22. 22. Second Group Antigen T.pallidumA.Present in T.pallidum and Non pathogenic cultivable treponemesB.Reiters Trenonems Dr.T.V.Rao MD 22
  23. 23. Third AntigenPolysaccharidespecies specificPositive only insera of patientsinfected withpathogenicTreponema Dr.T.V.Rao MD 23
  24. 24. Dark field Microscopy Dr.T.V.Rao MD 24
  25. 25. Treponema cannot be cultivated in Culture MediaA. The inability to grow most pathogenic Treponema in vitro, coupled with the transitory nature of many of the lesions, makes diagnosis of Treponema infection impossible by routine bacteriological methods Dr.T.V.Rao MD 25
  26. 26. Cultivation of .. ?A. Although the Treponemes are distantly related to Gram-negative bacteria, they do not stain by Grams method, and modified staining procedures are used. Moreover, the pathogenic Treponemes cannot be cultivated in laboratory media and are maintained by subculture in susceptible animals. Dr.T.V.Rao MD 26
  27. 27. Trepanoma pallidumD. Clinical Infection: Syphilis 1. Transmission • Usually through sexual contact from an infected individual by invading intact mucous membranes or abraded skin 2. Pathogenesis • Disease of blood vessel & perivascular areas • Primary lesion due to inflammation at site of inoculation • Secondary lesion due to inflammation of ectodermal tissues • Tertiary lesion due to diffuse chronic inflammation to organ systems Dr.T.V.Rao MD 27
  28. 28. Trepanoma pallidumD. Clinical Infection: Syphilis 3. Clinical Manifestations i. Primary Disease • Chancre: single lesion, non-tender & firm with a clean surface, raised border & reddish color • Usually on the cervix, vaginal wall, anal canal • Draining lymph nodes enlarged & non- tender Dr.T.V.Rao MD 28
  29. 29. 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 Dr.T.V.Rao MD 29
  30. 30. Pathology Penetration: 1. T. pallidum enters the body via skin and mucous membranes through abrasions during sexual contact 2. Also transmitted transplacentallyA. Dissemination: 1. Travels via the lymphatic system to regional lymph nodes and then throughout the body via the blood stream 2. Invasion of the CNS can occur during any stage of syphilis Dr.T.V.Rao MD 30
  31. 31. PathologyA. The bacteria rapidly enter the lymphatics, are widely disseminated via the bloodstream and may lodge in any organ. The exact infectious dose for man is not known, but in experimental animals fewer than ten organisms are sufficient to initiate infection. Dr.T.V.Rao MD 31
  32. 32. PathologyThe bacteriamultiply at the initialentry site forming achancre, a lesioncharacteristic ofprimary syphilis,after an averageincubation period of3 weeks Dr.T.V.Rao MD 32
  33. 33. STAGES OF SYPHILIS1. Primary2. Secondary3. Latent i. Early latent ii. Late latent4. Late or tertiary i. May involve any organ, but main parts are: • Neurosyphilis • Cardiovascular syphilis • Late benign (gumma) Dr.T.V.Rao MD 33
  34. 34. Basic lesion of syphilisThe chancre ispainless and mostfrequently on theexternal genitalia,but it may occur onthe cervix, perianalarea, in the mouthor anal canal. Dr.T.V.Rao MD 34
  35. 35. Stages of syphilisA. Untreated syphilis may be a progressive disease with primary, secondary, latent and tertiary stages. T. pallidum enters tissues by penetration of intact mucosae or through abraded skin. Dr.T.V.Rao MD 35
  36. 36. Primary syphilisa) One or more painless chancres (indurated raise edges & clear bases) that erupt in the genitalia, anus, nipples, tonsils or eyelids.b) Starts as papule and then erodec) Disappear after three to six weeks even without treatment.d) Lymphadenopathy that is either unilateral or bilateral Dr.T.V.Rao MD 36
  37. 37. Trepanoma pallidumD. Clinical Infection: Syphilis 3. Clinical Manifestations iii. Latent disease a. Early latent (1st 4 years) • No signs & symptoms of active syphilis but remain seroactive b. Late latent (after 4 years) • If untreated, 60% continue to be asymptomatic while 40% progress to tertiaryDr.T.V.Rao MD stage 37
  38. 38. PathologyA. The chancre is painless and most frequently on the external genitalia, but it may occur on the cervix, peri-anal area, in the mouth or anal canal. Chancres usually occur singly, but in immunocompromised individuals, Dr.T.V.Rao MD 38
  39. 39. ChancreA. The chancre usually heals spontaneously within 3-6 weeks, and 2-12 weeks later the symptoms of secondary syphilis develop. These are highly variable and widespread but most commonly involve the skin where macular or pustular lesions develop, particularly on the trunk and extremities. The lesions of secondary syphilis are highly infectious. Dr.T.V.Rao MD 39
  40. 40. Progress of DiseaseA. Relapse of the lesions of secondary syphilis is common, and latent syphilis is classified as early (high likelihood of relapse) or late (recurrence unlikely). Individuals with late latent syphilis are not generally considered infectious, but may still transmit infection to the fetus during pregnancy and their blood may remain infectious. Dr.T.V.Rao MD 40
  41. 41. Trepanoma pallidumD. Clinical Infection: Syphilis 3. Clinical Manifestations i. Primary Disease • Chancre: single lesion, non-tender & firm with a clean surface, raised border & reddish color • Usually on the cervix, vaginal wall, anal canal • Draining lymph nodes enlarged & non- tender Dr.T.V.Rao MD 41
  42. 42. PRIMARY SYPHILIS (The Chancre)A. Incubation period 9-90 days, usually ~21 days.B. Develops at site of contact/inoculation.C. Classically: single, painless, clean-based, indurated ulcer, with firm, raised borders. Atypical presentations may occur.D. Mostly anogenital, but may occur at any site (tongue, pharynx, lips, fingers, nipples, etc...)E. Non-tender regional adenopathyF. Very infectious.G. May be darkfield positive but serologically negative.H. Untreated, heals in several weeks, leaving a faint scar. Dr.T.V.Rao MD 42
  43. 43. Primary Syphilis Dr.T.V.Rao MD 43
  44. 44. Clinical Manifestations Primary Syphilis- Penile Chancre Dr.T.V.Rao MD 44Source: CDC/ NCHSTP/ Division of STD Prevention, STD Clinical Slides
  45. 45. Primary Syphilis Dr.T.V.Rao MD 45
  46. 46. Primary Syphilis - Chancre Dr.T.V.Rao MD 46
  47. 47. Primary Syphilis - Chancre Dr.T.V.Rao MD 47
  48. 48. 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 Dr.T.V.Rao MD 48
  49. 49. Treponema pallidumD. Clinical Infection: Syphilis 3. Clinical Manifestations iv. Tertiary Disease a. Gummas (3-10 years after secondary disease) • Non-progressive, localized dermal lesions • Benign tertiary syphilis • Pronounced immunologic host reaction b. Neurosyphilis (>5 years after primary disease) • Paralytic dementia, tabes dorsalis, amyotropic lateral sclerosis, meningovascular syphilis, seizures, optic atrophy, gummatous changes Dr.T.V.Rao MD 49 of the cord
  50. 50. Secondary SyphilisA. Secondary syphilis at 6-8 weeks – diffuse symptoms: 1. Fever 2. Headache 3. Skin pustulesB. Usually disappears even without Dr.T.V.Rao MD 50 treatment
  51. 51. Treponema pallidumD. Clinical Infection: Syphilis 3. Clinical Manifestations v. Congenital Syphilis a. Transplacental infection of the developing fetus b. Abortion occurs during 2nd trimester of pregnancy c. Early symptoms: • Hepatosplenomegaly, jaundice, hemolytic anemia, pneumonia, multiple long bone involvement, snuffles, skin lesions, testicular masses Dr.T.V.Rao MD 51
  52. 52. Treponema pallidumD. Clinical Infection: Syphilis 3. Clinical Manifestations v. Congenital Syphilis d. Late symptoms: • Frontal bossae of Parrott, Short maxilla, high palatal arch, Hutchinson’s triad (Hutchinson’s teeth, Interstitial keratitis, eighth-nerve deafness), saddle nose, mulberry molars, Higoumenakis sign, relative protruberance of mandible, rhagades, saber shin, scaphoid scapulas, Clutton’s joint) Dr.T.V.Rao MD 52
  53. 53. Secondary Syphilis Dr.T.V.Rao MD 53
  54. 54. 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 Dr.T.V.Rao MD 54
  55. 55. Secondary Syphilis Dr.T.V.Rao MD 55
  56. 56. Secondary Syphilis Dr.T.V.Rao MD 56
  57. 57. Secondary syphilis Dr.T.V.Rao MD 57
  58. 58. Tertiary SyphilisA. Affects 2/3 of untreated cases 1. Gummata: rubbery tumors 2. Bone deformities 3. Blindness 4. Loss of coordination 5. Paralysis 6. Insanity Dr.T.V.Rao MD 58
  59. 59. 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 Dr.T.V.Rao MD 59
  60. 60. 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 Dr.T.V.Rao MD 60
  61. 61. NeurosyphilisA. Late Neurosyphilis develops in about 1/6 untreated cases, usually more than 5 years after initial infectionB. Central nervous system and spinal cord involvementC. Dementia, seizures, wasting, etc.D. Cardiovascular involvement appears 10-40 years after initial infection with resulting myocardial insufficiency and death Dr.T.V.Rao MD 61
  62. 62. Latent SyphilisA. Latent syphilis a) Reactive serologic test b) Asymptomatic until deathA. Late syphilisThree subtypes of Late syphilis 1. Late, benign syphilis *Develops between 1 to 10 years after the infection *Presence of gumma Dr.T.V.Rao MD 62
  63. 63. Dr.T.V.Rao MD 63
  64. 64. Mother to Child TransmissionInfection in uteromay have seriousconsequences forthe fetus. Rarely,syphilis has beenacquired bytransfusion ofinfected fresh humanblood. Dr.T.V.Rao MD 64
  65. 65. Pathogenesis of T. pallidum (cont.) Congenital SyphilisCongenital syphilis results from trans placental infection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 Dr.T.V.Rao MD 65
  66. 66. Treponema pallidum and ImmunityD. Clinical Infection: Syphilis 4. Immunity i. Syphilis has persistent infection for decades in spite vigorous host response due to: • Dense coat (with fibronectin, transferrin, cerruloplasmin) • Evasion from PMN detection • Inhibition of cell-mediated immunity ii. Relative but unreliable protection from reinfection in untreated patients iii. Minor protection from reinfection in treated patients Dr.T.V.Rao MD 66
  67. 67. Congenital SyphilisA. Passed from mother to fetus during pregnancy 1. Abnormally shaped teeth 2. Nasal septum collapses 3. Skeletal abnormalities Dr.T.V.Rao MD 67
  68. 68. DIAGNOSIS OF SYPHILISA. 1. History and clinical examination.B. 2. Dark-field microscopy: special technique use to demonstrate the spirochete as shiny motile spiral structures with a dark background.C. The specimen includes oozing from the lesion or sometimes L.N. aspirate. It is usually positive in the primary and secondary stages and it is most useful in the primary stage when the serological tests are still negative. Dr.T.V.Rao MD 68
  69. 69. Diagnosis of syphilisA. Direct detection of spirochetes : Darkfield microscopy (motile bugs + experience + prompt examination) Silver stainA. Culture : not usedB. Serology: non-specific and specific tests Dr.T.V.Rao MD 69
  70. 70. Serologic TestsA. Reveal patients immune status not whether they are currently infectedB. Use lipoidal antigens rather than T. pallidum or components of it; non- treponemal antigen testsC. RPR; rapid plasma reaginD. VDRL; Venereal Disease Research Laboratory Dr.T.V.Rao MD 70
  71. 71. Treponema pallidumF. Laboratory diagnosis 1. Serologic testing i. Nontreponemal Tests (uses Cardiolipin-lecithin as antigen) a. Complement-fixation tests (Wasserman & Kolmer test) b. Flocculation tests (Venereal Disease Research Laboratory, (VDRL), Dr.T.V.Rao MD & rapid reagin tests) Hinton 71
  72. 72. Serologic TestsA. Positive within 5 to 6 weeks after infectionB. Strongly positive in secondary phaseC. Strength of reaction is stated in dilutionsD. May become negative with treatment or over decades Dr.T.V.Rao MD 72
  73. 73. Treponema pallidumF. Laboratory diagnosis 1. Serologic testing ii. Treponemal Tests (uses syphilitic tissue as complement-fixing antigen) b. Reiter Protein Complement Fixation • Antigen is an extract from nonvirulent treponeme (Reiter strain) • Nonreactive in late stages of syphilis Dr.T.V.Rao MD 73
  74. 74. Non-treponemal testsA. Antigen: cardiolipin (beef heart) + lecithin + cholesterolB. Detect nonspecific antibody (Reagin): a mixture of IgM & IgG direct against some normal tissue antigensC. VDRL (Venereal Disease Research Laboratory) test for serum and CSF samples Dr.T.V.Rao MD 74
  75. 75. Venereal Disease Research Laboratory - VDRLA. Flocculation test, antigen consists of very fine particles that precipitate out in the presence of reagin.B. Utilizes an antigen which consists of cardiolipin, cholesterol and lecithin. 1. Antigen very technique dependent. 2. Must be made up fresh daily.C. Serum must be heated to 56 C for 30 minutes to remove anti-complementary activity which may cause false positive, if serum is not tested within 4 hours must be reheated for 10 minutes.D. Calibrated syringe utilized to dispense antigen must deliver 60 drops/mL +/- 2drops. Dr.T.V.Rao MD 75
  76. 76. VDRLA. Each preparation of antigen suspension should first be examined by testing with known positive or negative serum controls.B. The antigen particles appear as short rod forms at magnification of about 100x. Aggregation of these particles into large or small clumps is interpreted as degrees of positivityC. Reactive on left, non-reactive on right Dr.T.V.Rao MD 76
  77. 77. Rapid Plasma Reagin Test - RPRA. General screening test, can be adapted to automation.B. CANNOT be performed on CSF.C. Antigen 1. VDRL cardiolipin antigen is modified with choline chloride to make it more stable 2. attached to charcoal particles to allow macroscopic reading 3. antigen comes prepared and is very stable.D. Serum or plasma may be used for testing, serum is not heated. Dr.T.V.Rao MD 77
  78. 78. Treponema pallidumF. Laboratory diagnosis 1. Serologic testing ii. Treponemal Tests (uses syphilitic tissue as complement-fixing antigen) a. Treponema Pallidum Immobilzation (TPI) • Reaginic antibody & complement immobilize a suspension of living and motile treponemes maintained in rabbit testes & determined by darkfield microscopy • Difficult, expensive, requires living organisms • Positive for nonvenereal treponematoses, bejels, yaws & pinta Dr.T.V.Rao MD 78
  79. 79. Treponema pallidumF. Laboratory diagnosis 1. Serologic testing ii. Treponemal Tests (uses syphilitic tissue as complement-fixing antigen) b. Reiter Protein Complement Fixation • Antigen is an extract from nonvirulent treponeme (Reiter strain) • Nonreactive in late stages of syphilis Dr.T.V.Rao MD 79
  80. 80. Specific serological tests of syphilisA. A. Reiter protein complement fixation test.B. B. Fluorescent Treponemal antibody/absorption test, FTA/ABS. the most specific and most sensitive .C. C. Treponema pallidum haemagglutination test- TPHA- D. Treponema pallidum immobilization test- TPI Dr.T.V.Rao MD 80
  81. 81. Treponema pallidum haemagglutination (TPHA)A. Adapted to micro techniques (MHA- TP)B. Tanned sheep RBCs are coated with T. pallidum antigen from Nichol’s strain.C. Agglutination of the RBCs is a positive result. Dr.T.V.Rao MD 81
  82. 82. Specific serological tests of syphilisA. A. Reiter protein complement fixation test.B. B. Fluorescent Treponemal antibody/absorption test, FTA/ABS. the most specific and most sensitive .C. C. Treponema pallidum Haemagglutination test- TPHA- D. Treponema pallidum immobilization test- TPI Dr.T.V.Rao MD 82
  83. 83. Treponema pallidumF. Laboratory diagnosis 1. Serologic testing ii. Treponemal Tests (uses syphilitic tissue as complement-fixing antigen) c. Fluorescent Antibody Tests / Fluorescent Treponemal Antibody Absorption (FTA-ABS) Test • Uses lyophilized Nichols strain organisms as antigen  mixed with antitreponemal antibody (from test serum) in a slide  flourescein isothiocyanate-labeled antihuman Ig –> presence of antibody determined by darkfield microscopy • Used to diagnosed congenital syphilis & late stage syphilis, confirmation of nontreponemal tests Dr.T.V.Rao MD 83
  84. 84. Fluorescent Treponemal Antibody Absorption Test (FTA-ABS)A. Diluted, heat inactivated serum added to Reiter’s strain of T. pallidum to remove cross reactivity due to other Treponemes.B. Slides are coated with Nichol’s strain of T. pallidum and add absorbed patient serum.C. Slides are washed, and incubated with antibody bound to a fluorescent tag.D. After washing the slides are examined for fluorescence.E. Requires experienced personnel to read.F. Highly sensitive Dr.T.V.Rao MD and specific, but time 84 consuming to perform.
  85. 85. Positive FTA Test for Syphilis Viewed with a Fluorescent Microscope Dr.T.V.Rao MD 85
  86. 86. Serologic TestsA. To improve sensitivity and specificity tests using a specific treponemal antigen devisedB. MHA-TP: microhemagglutination assay for T. pallidumC. FTA-ABS: fluorescent treponemal antibody absorption testD. All positive nontreponemal test results should be confirmed with a specific treponemal test Dr.T.V.Rao MD 86
  87. 87. Treponema pallidumF. Laboratory diagnosis 1. Serologic testing ii. Treponemal Tests (uses syphilitic tissue as complement-fixing antigen) d. Haemagglutination Tests a. Microhemagglutination assay –T. pallidum (MHA-TP) Dr.T.V.Rao MD 87
  88. 88. Every Pregnant women Needs Screening Dr.T.V.Rao MD 88
  89. 89. Biologic False-Positive Test ResultsA. Positive STS in persons with no history or clinical evidence of syphilisB. Acute BFP: those that revert to negative in less than 6 monthsC. Chronic BFP: persist > 6 months Dr.T.V.Rao MD 89
  90. 90. BFP Test Results in SyphilisA. Acute BFP A. Chronic BFPB. Vaccinations B. Connective tissueC. Infections disease (SLE)D. pregnancy C. Liver disease D. Blood transfusions E. IVDA Dr.T.V.Rao MD 90
  91. 91. Advantage of VDRL:• cheap, easy to perform• quantitative, screen test• monitor disease course• trace theraputic effect, become “-” in 6-18 m after effective treatment. Dr.T.V.Rao MD 91
  92. 92. Treatment of Late SyphilisA. Late syphilis:B. benzathine penicillin 2.4 million units intramuscularly weekly for 3 weeks.C. procaine penicillin 1.2 million units intramuscularly daily for 21 daysD. Tetracycline or erythromycin 500 mg 4 times a day – or doxycycline 100 mg x2- by mouth for 30 daysE. Jarrisch-Herxheimer reactionF. Follow-up Dr.T.V.Rao MD 92
  93. 93. Prevention & Treatment of Syphilis Penicillin remains drug of choice • WHO monitors treatment recommendations • 7-10 days continuously for early stage • At least 21 days continuously beyond the early stage Prevention with barrier methods (e.g., condoms) Prophylactic treatment of contacts identified through epidemiological tracing Dr.T.V.Rao MD 93
  94. 94. Treponema pallidumG. Treatment & Prevention 1. Antibiotic treatment • DOC: Penicillin (complete recovery for stage I &II) • streptomycin, tetracycline, erythromycin (poor passage to fetal circulation) 2. Treatment of case contacts 3. Barrier methods (condom); “safe sex” Dr.T.V.Rao MD 94
  95. 95. Other Related to TreponemesA. Related Treponemes cause the non-venereal treponematoses bejel, or endemic syphilis (T. pallidum endemicum), yaws (T. pallidum pertenue), and pinta (T. carateum). Dr.T.V.Rao MD 95
  96. 96. Treponema pallidumG. Other treponemal diseases 1. Yaws (Frambesia) -Treponema pertenue • Resembles syphilis • Acquired in childhood other than sexual contact • Mother yaw (or framboise), a painless erythematous papule occurs a month after primary infection • Secondary lesion resemble primary lesion occurs 1-3 months after • Tertiary lesions involve the skin & bones, crab yaws • DOC: Penicillin Dr.T.V.Rao MD 96
  97. 97. Treponema pallidumG. Other treponemal diseases 2. Pinta - Treponema carateum • Acquired by person-to-person contact & rarely by sexual contact • Primary & secondary lesions are flat, erythematous & non-ulcerating; healing first becomes hyper pigmented and later depigmented scarring; occurs in hand, feet & scalp • Tertiary lesions are uncommon • DOC: Penicillin Dr.T.V.Rao MD 97
  98. 98. Treponema pallidumG. Other treponemal diseases 3. Bejel - Treponema pallidum variant • Endemic syphilis • Acquired by direct contact during childhood • Similar to syphilis • DOC: Penicillin Dr.T.V.Rao MD 98
  99. 99. Programme created byDr.T.V.Rao MD for Medical and Health Care Workers in the Developing World Email doctortvrao@gmail.com Dr.T.V.Rao MD 99

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