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Syphilis
- 1. "He who knows syphilis, knows medicine" Sir William Osler SYPHILIS NIBIN M MBBS Student Calicut Medical College
- 2. INTRODUCTION Syphilis is a chronic sexually transmitted disease with varied clinical and pathological manifestations Causative org: Treponema pallidum Transmission: Sexual and vertical
- 3. SPIROCHETES Long, slender, helically tightly coiled bacteria Gram-negative Corkscrew motility Can be free living or parasitic Best-known are those which cause disease: Syphilis and Lyme’s disease
- 4. TRYPONEMA PALLIDUM Microaerophilic spirochete Not seen in gram stain By silver stains and immunofluorescence or dark- field microscopy
- 5. PATHOGENESIS Penetration • Via skin and mucuos membrane through abrasions during sexual contact •Also transplacentally Dissemination • Lymphatic and haematological
- 6. PATHOLOGY Proliferative endarteritis Ischaemia produced by vascular lesions Immune response Chancres and rashes – T-cells, plasma cells and macrophages TprK – structural diversity by gene recombination
- 8. PRIMARY SYPHILIS 3 weeks after infection CHANCRE : Single firm non-tender, raised, red lesion •Progresses from macule to papule to ulcer • Plasma cells , scattered macrophages, lymphocytes • Proliferative endarteritis • Endothelial cell activation to proliferation to fibrosis Regional lymphadenopathy: classically rubbery, painless, bilateral Serologic tests for syphilis may not be positive during early primary syphilis
- 10. SECONDARY SYPHILIS 2-10 Weeks after primary chancre Painless mucocutaneous lesions Skin lesions on palms and soles Same plasma cell infiltrate as primary chancre
- 11. SECONDARY SYPHILIS Condylomata lata – broad based elevated plaques - in moist areas of skin
- 12. Other manifestations of secondary syphilis - lymphadenopathy,Rashes, -Malaise, fever,weight loss - Alopecia - Neurosyphilis Serological tests – highest especially in red lesions in vagina or mouth
- 13. Latent Syphilis Host suppresses the infection enough so that no lesions are clinically apparent Only evidence is positive serologic test for syphilis May occur between primary and secondary stages, between secondary relapses, and after secondary stage Categories: Early latent: <1 year duration Late latent: 1 year duration
- 14. TERTIARY SYPHILIS CARDIOVASCULAR SYPHILIS NEUROSYPHILIS BENIGN TERTIARY SYPHILIS
- 15. CARDIOVASCULAR SYPHILIS Syphilitic aortitis Immune response Aortitis dilation valve incompetence aneurysm
- 16. CARDIOVASCULAR SYPHILIS – MORPHOLOGIC CHANGES Aortitis – endarteritis of vaso vasorum of proximal aorta Occlusion of vaso vasorum- scaring of media of proximal aortic wall - loss of elasticity Narrowing of coronary artery ostia – subintimal scarring
- 17. NEUROSYPHILIS SYMPTOMATIC • 10% untreated individuals •Meningovascular, paretic, tabes dorsalis •Taboparesis •AIDS patients - meningovascular
- 18. Meningovascular neurosyphilis • Chronic meningitis • obliterative endarteritis Paretic neurosyphilis • progressive mental deficits leading to dementia • parenchymal damage in cerebral cortex Tabes dorsalis • Damage to sensory nerves – loss of position&pain sense • loss of axons and myelin in dorsal roots
- 19. ASYMPTOMATIC NEUROSYPHILIS • One third of neurosyphilic cases CSF shows: •Lymphocytic pleocytosis •Elevated protein and usually normal glucose concentrations •VDRL test is usually reactive. • It can mimic tuberculous or fungal meningitis or aseptic meningitis of various causes. • Often involves the base of the brain and may result in unilateral or bilateral cranial nerve palsies. • Without treatment, syphilitic meningitis usually resolves, like the other manifestations
- 20. BENIGN TERTIARY SYPHILIS Gummas in bone, skin , and mucous membrane Gummas – nodular lesions - delayed hypersensitivity Bone – pain, tenderness, swelling, pathologic fractures Skin & mucuos membrane – Nodular lesions - ulcerative lesions
- 22. Syphilitic gummas White, gray, and rubbery single or multiple, vary in size In liver – scarring causes hepar lobatum Histologically, centre- coagulated necrotic material margins - macrophages, fibroblasts, - large no. of MNL • Treponemes are scanty
- 24. Aspects of Syphilis Diagnosis 1. Clinical history 2. Physical examination 3. Laboratory diagnosis
- 25. Clinical History Assess: History of syphilis Known contact to an early case of syphilis Typical signs or symptoms of syphilis in the past 12 months Most recent serologic test for syphilis
- 26. Physical Examination Oral cavity Lymph nodes Skin Palms and soles Genitalia and perianal area Neurologic examination
- 27. Laboratory Diagnosis Identification of Treponema pallidum in lesions Darkfield microscopy Direct fluorescent antibody - T. pallidum (DFA-TP) Serologic tests Nontreponemal tests Treponemal tests
- 28. Nontreponemal Serologic Tests Principles Measure antibody directed against a cardiolipin-lecithin- cholesterol antigen Not specific for T. pallidum Titers usually correlate with disease activity and results are reported quantitatively May be reactive for life Nontreponemal tests include VDRL, RPR Diagnosis
- 29. Treponemal Serologic Tests Principles Measure antibody directed against T. pallidum antigens Qualitative Usually reactive for life Treponemal tests include , FTA-ABS, EIA
- 30. Usefullness Primary syphilis – both moderatively sensitive secondary – very sensitive Tertiary and latent – Treponemal sensitive - non treponemal less To monitor therapy – non –treponemal Good for screening ,confirmatory test req False positive results – Pregnancy, autoimmune diseases, infections
- 31. TREATMENT PENICILLIN Intramuscularly or intravenously Treatment at any stage
- 32. PREVENTION Abstinance is the most effective way to prevent the contraction of the disease practice safe sex be tested regularly for syphilis if married or sexually active avoid direct contact with blood, sores or bodily fluid learn about safe sex and injection practices get tested for syphilis if pregnant