leprosysyphilis - LEPROSY & SYPHILIS.pptx

LEPROSY & SYPHILIS

It is a chronic infectious disease
characterized by lesions of the peripheral nerve, skin, and mucus
membrane of the URT(nasal mucosa).
World's oldest recorded disease

1. LEPROSY & SYPHILIS Department of Pathology 1

2. LEPROSY

3. What is leprosy? It is a chronic infectious disease characterized by lesions of the peripheral nerve, skin, and mucus membrane of the URT(nasal mucosa). World's oldest recorded disease 3 Every year January 27 is World Leprosy Day

4. What causes leprosy ? Mycobacterium leprae Rod Shaped First bacterium disease in humans 4

5. M. leprae is discovered by Hansen from Norway in 1873 5

6. Leprosy develops slowly from 6 months up to 40 yrs Results in skin lesions and deformities, most often affecting the cooler places on the body ( for example: eyes, nose, earlobes, hands, feet, and testicles) that can be very disfiguring. 6

7. Mode of infection Although human-to-human transmission is the primary source of infection, two other species can carry and (rarely) transfer M. leprae to humans: chimpanzees and nine-banded armadillos. 7

8. Mode of transmission The exact route of transmission is not fully known . The spread of leprosy is believed to be via nasal discharge (Droplet infection). Every 1 cc of nasal secretion contains 1- 2millions lepra bacilli

9. Predisposing or risk factors Residence in an endemic area . Poverty (malnutrition). Contact with affected armadillo. Immunity 9

10. The incubation period range from 3 -5 years. Males appear to be twice common than females. Bimodal age (10-14 years & 35-44 years). Children are more susceptible to disease. 10

11. 11 RIDLEY- JOPLING CLASSIFICATION INDETERMINATE TUBERCULOID (TT) BORDERLINE (BL) LEPROMATOUS (LL) BORDERLINE TUBERCULOID (BT) MID BORDERLINE (BB) BORDERLINE LEPROMATOUS (BL) BASED ON CELL MEDIATED IMMUNITY It is used globally and forms the basis of clinical studies of leprosy

12. INDETERMINATE LEPROSY Earliest & transitory phase. One or two vague hypopigmented macule with definite sensory impairment. If untreated may progress towards tuberculoid , borderline or lepromatous leprosy. Spontaneous regression may occur.

13. TUBERCULOID LEPROSY A typical lesion shows asymmetrical hypopigmented , sharply demarcated macules or reddish plaques, which spreads at the periphery and heals in the centre. Lepromin Skin Test is positive. 13

14. Tuberculoid Leprosy: Annular, erythematous, anaesthetic patch with well defined and raised borders. 14

15. TUBERCULOID LEPROSY

16. TUBERCULOID LEPROSY M/E: Histologically TT resemble tuberculosis. Characterized by tuberculoid granuloma , made up of epitheloid cell in the center surrounded by Langhans giant cells, lymphocytes and foci of non-caseating necrosis. Weak acid-fast bacilli. 16

17. LEPROMATOUS LEPROSY Lepromatous leprosy involves: the skin, peripheral nerves, anterior chamber of the eye, upper airways (down to the larynx), testes, hands and feet. The vital organs and CNS are rarely affected, presumably because the core temperature is too high for growth of M. leprae . 17

18. LEPROMATOUS LEPROSY Lepromatous lesions contain large aggregates of lipid-laden macrophages ( lepra cells), often filled with masses (“ globi ”) of acid-fast bacilli. Because of the abundant bacteria, lepromatous leprosy is referred to as “ multibacillary ”. Lepromin skin test is negative. 18

19. Macular, papular , or nodular lesions form on the face, ears, wrists, elbows, and knees. With progression, the nodular lesions coalesce to yield a distinctive leonine facies . Skin smear shows high bacterial count. 19 Lepromatous Leprosy: Leonine Face

20. LEPROMATOUS LEPROSY

21. LEPROMATOUS LEPROSY

22. M/E: Characterized by diffuse infiltration of foamy macrophages in the dermis. Lymphocytes are scanty and giant cells typically absent. 22 Lepromatous leprosy. Acid-fast bacilli (“red snappers”) within macrophages Lepromatous leprosy- the dermis shows clear space.

23. 23 Leprosy. A, Peripheral nerve. Note the inflammatory cell infiltrates in the endoneural and epineural compartments. B, Cells within the endoneurium contain acid-fast positive lepra bacilli

24. BORDERLINE TUBERCULOID (BT) Four or more lesions, asymmentrically distributed. Macules or plaques of variable sizes with well or ill-defined margins & satellite lesions. Peripheral nerves enlarged asymmentrically . Senstaion : hypoesthesia. Lepromin test may be weakly positive.

25. MID BORDERLINE (bb) Tends to be unstable. With time, an evolution to BT or BL may be seen. The lesions are many and may be extensive, annular with some tendency towards symmetrical distribution. 25

26. BORDERLINE LEPROMATOUS LEPROSY (BL) Numerous moderately well defined, usually large & small plaques, dome shaped lesions / nodules. Sometimes with a slightly hypopigmented halo & a tendency towards symmetrical distribution. Skin smears strongly positive. 26

27. Lepromin Skin Test Procedure to Lepromin Skin Test A tiny sample of leprosy antigen is injected under the skin, usually in the forearm. The skin gets pushed up, forming a small bump. This is an indication that the antigen has been injected to the correct depth. The site of the injection is marked, and is examined for reaction, first after 3 days(early reaction-Fernandez reaction:-redness and induration ) and then again after 21 days(late reaction- Mitsuda reaction:-nodule>5mm).

28. It is a sudden change in the clinical picture of the disease because of conflict between the bacilli and the immune system of the host. The precipitating factors - Effective treatment. Intercurrent infection. Physical stress. Surgical operation. Pregnancy. Sometimes spontaneously. LEPROSY REACTION

29. TYPES OF LEPRA REACTIONS Type I Change in host CMI Seen in borderlines Skin and nerve lesions Type II Antigen antibody Seen in LL & BL leprosy Skin, nerve & systemic involvement

30. Type I Lepra Reaction (Reversal Reaction) Seen in BT, BB & BL. Sudden onset. Eythematous & oedematous changes in old lesions. Appearing of new lesions. Tenderness & swelling of peripheral nerves.

31. Type II Lepra Reaction- Erythema Nodosum Leprosum (ENL) Appearance of Erythema nodosum leprosum (ENL)-like skin lesions- Erythematous Tender Subcutaneous Resolve in 7 to 10 days Appear in crops Occur any where Associated with fever & joint pains May be vesicular, pustular & may ulcerate

32. DIAGNOSIS Skin Scrapings Samples from the skin are obtained from the edge of the lesion, which is smeared on the slide and stained with Fite - Faraco technique to demonstrate the bacilli. Biopsy Useful in classification & definitive diagnosis 32

33. COMPLICATIONS Contractures, paralyses, and autoamputation of fingers or toes may ensue. Facial nerve involvement can lead to paralysis of the eyelids, with keratitis and corneal ulcerations. 33

34. SYPHILIS

35. SYPHILIS Sexually acquired infection Etiologic agent: Treponema pallidum Disease progresses in stages May become chronic without treatment 35

36. ETIOLOGY Etiologic agent: Treponema pallidum Corkscrew-shaped, motile microaerophilic bacterium Cannot be cultured in vitro Cannot be viewed by normal light microscopy 36 Treponema pallidum on darkfield microscopy Electron photomicrograph, 36,000 x.

37. PATHOLOGY Penetration: T. pallidum enters the body via skin and mucous membranes through abrasions during sexual contact Also transmitted transplacentally Dissemination: Travels via the lymphatic system to regional lymph nodes and then throughout the body via the blood stream Invasion of the CNS can occur during any stage of syphilis 37 Pathogenesis

38. Primary Syphilis Primary lesion or "chancre" develops at the site of inoculation Chancre: Typically painless, relatively avascular , circumscribed, indurated , superficially ulcerated lesion and has a clean base Progresses from macule to papule to ulcer Highly infectious Heals spontaneously within 1 to 6 weeks 25% present with multiple lesions Regional lymphadenopathy : classically rubbery, painless, bilateral Serologic tests for syphilis may not be positive during early primary syphilis. 39 Clinical Manifestations

39. Primary Syphilis On histologic examination, Treponemes are visible at the surface of the ulcer with silver stains (e.g., Warthin -Starry stain) or immunofluorescence techniques. Chancre contains an intense infiltrate of plasma cells, with scattered macrophages and lymphocytes and a proliferative endarteritis. 40

40. Secondary Syphilis Secondary lesions occur 3 to 6 weeks after the primary chancre appears; may persist for weeks to months. Primary and secondary stages may overlap. Mucocutaneous lesions - most common. Manifestations: Rash (75%-100%) Lymphadenopathy (50%-86%) Malaise Mucous patches (6%-30%) Condylomata lata (10%-20%) Alopecia (5%) Serologic tests are usually highest in titre during this stage 41 Clinical Manifestations

41. Secondary Syphilis Mucosal lesions (highly infectious): 30% develop mucous patch (slightly raised, oval area covered by a gray white membrane, a pink base that does not bleed. Skin rash: Diffuse, papulosquamous lesions, may leave residual pigmentation or depigmentation . Red lesions in the mouth or vagina contain the most organisms and are the most infectious. 42 Clinical Manifestations

42. Tertiary Syphilis Most frequently involves the aorta; the CNS; and the liver, bones, and testes. The aortitis is caused by endarteritis of the vasa vasorum of the proximal aorta. Occlusion of the vasa vasorum results in scarring of the media of the proximal aortic wall, causing a loss of elasticity, followed by aneurysm, giving a tree bark appearance. There may be narrowing of the coronary artery ostia caused by subintimal scarring with resulting myocardial ischemia. 43 Clinical Manifestations

43. Syphilitic aortitis , gross, showing tree-barking  

44. Syphilitic aortic aneurysm with erosion into spine, gross, L.P.  

45.   Syphilitic aortic aneurysm with erosion into spine, gross, H.P.

46. Tertiary Syphilis - GUMMAS Syphilitic gummas are white-gray and rubbery, occur singly or multiply, and vary in size from microscopic lesions resembling tubercles to large tumor -like masses. They occur in most organs but particularly in skin, subcutaneous tissue, bone, and joints. 47 Clinical Manifestations

47. Tertiary Syphilis On histologic examination, Gummas have centers of coagulated, necrotic material and margins composed of plump, palisading macrophages and fibroblasts surrounded by large numbers of mononuclear leukocytes, chiefly plasma cells. Treponemes are scant in gummas and are difficult to demonstrate. 48 Trichrome stain of liver shows a gumma (scar), stained blue, caused by tertiary syphilis (the hepatic lesion is also known as hepar lobatum

48. Neurosyphilis Occurs when T. pallidum invades the CNS. May occur at any stage of syphilis Can be asymptomatic Early neurosyphilis occurs a few months to a few years after infection Clinical manifestations include acute syphilitic meningitis, meningovascular syphilis, ocular involvement Late neurosyphilis occurs decades after infection and is rarely seen Clinical manifestations include general paresis, tabes dorsalis , ocular involvement 49

49. Congenital Syphilis Occurs when T. pallidum is transmitted from a pregnant woman with syphilis to her fetus May lead to stillbirth, neonatal death, and infant disorders such as deafness, neurologic impairment, and bone deformities Transmission to the fetus in pregnancy can occur during any stage of syphilis; risk is much higher during primary and secondary syphilis Wide spectrum of severity exists; only severe cases are clinically apparent at birth Early lesions (most common): Infants <2 years old; usually inflammatory Late lesions: Children >2 years old; tend to be immunologic and destructive 50

50. 51 Manifestations of syphilis

51. Non treponemal 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 Non treponemal tests include VDRL, Rapid Plasma Reagin test 52 Diagnosis

52. Treponemal Serologic Tests Principles Measure antibody directed against T. pallidum antigens Qualitative Usually reactive for life Treponemal tests include TP- hemaglutination assay, Flourescent treponemal Ab test, Enzyme Immuno Assay 53 Diagnosis

53. 54