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Leprosy . Dr. Abhinav Golla , Associate Professor , Lab Director & Consultant Pathologist . Aadhya Medicure Pathlabs .
- 1. Dr.Abhinav Golla MBBS,MD Pathology AssistantProffesor AIMS. Medicure Diagnostics & research center , Vijayanagar colony , Hyderabad,Telangana.
- 2. INTRODUCTION • Chronic granulomatousinfectious disease. • Caused by Mycobacterium leprae • Mainly involves the peripheral nerves and skin • Other organs may involve: Mucosa of mouth Upper respiratory tract Eyes Bones & Muscles. Testes etc. • Commonly involves every organ except : CNS, Ovary and Lungs.
- 3. • Oldest andmost dreaded disease known to Mankind. India in 600BC Kustha Roga & attributed to punishment or curse of God M. leprae was discovered by Gerhard Henrik Armauer Hansen in 1873 in Norway. Hence referred to as Hansen’s disease.
- 4. Lepra bacilli • Grampositive Obligate intracellular bacillus . • Acid fast stained with modified Fite stain or ZN stain. • M. leprae grows best in cooler tissues (the skin, peripheral nerves, anterior chamber of the eye, upper respiratory tract, and testes), • Optimal temp. for growth is 30-33 centigrade
- 5. M. leprae remainsone of the few bacterial species that still has not been cultivated on artificial medium or tissue culture and produces no known toxins, but can grow in Nude mouse Nine banded armadillos(best)
- 6. Mode of transmission •Transmission by inhalation • Droplet infection(most common) Transmission by contact • Skin to skin contact with infectious cases • Contact with soil or fomites . • Other Routes . • Insect Vectors e.g.. Mosquito, Bedbugs • Tattooing needles • Breast feeding and Transplacental infection do not occur.
- 7. Incubation period • Longincubation period • Ranged: 2 to 40 years or more Average: 3-5 years • Generation time : 12 days.
- 8. VIRULENCE FACTOR • Thecell wall contains large amounts of an M. leprae– specific phenolic glycolipid (PGL-1), which is detected in serologic tests. • The unique trisaccharide of M. leprae binds to the basal lamina of Schwann cells; this interaction is probably relevant to the fact that M. leprae is the only bacterium to invade peripheral nerves.
- 10. • Ridley- Jopling1966 (Research purposes) • Most widely accepted Divides Leprosy cases into five groups according to their position on an immunohistological scale. • Tuberculoid (TT) • Borderline Tuberculoid (BT) • Borderline Borderline (BB) • Borderline Lepromatous (BL) • Lepromatous (LL)
- 12. What are thetypes of leprosy?• • Lepromatous: damages respiration, eyes, and skin (Multibacillary Leprosy(MB) • Tuberculoid: affects nerves in fingers and toes, and surrounding skin Paucibacillary Leprosy (PB) • Borderline: (BL) has effects of both types
- 13. 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.
- 14. Tuberculoid leprosy • Atypical 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.
- 16. MICROSCOPY Histologically TT resemble tuberculosis. Characterizedby 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.
- 17. 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.
- 18. • 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. • Lepromatous Leprosy: Leonine Face
- 19. • Lepromatous lesionscontain 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.
- 20. MICROSCOPY • Characterized bydiffuse infiltration of foamy macrophages in the dermis. • Lymphocytes are scanty and giant cells typically absent. • Lepromatous leprosy. Acid- fast bacilli (“red snappers”) within macrophages Lepromatous leprosy- the dermis shows clear space.
- 21. BODERLINE TUBERCULOID • Fouror 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
- 22. Diagnosis 1-Clinical symptoms diagnosis: (anesthesia, nerveenlargement, and characteristic skin lesions). 2-Slit-skin smears: Ziehl Neelson staining of skin smear. 3-Skin biopsy. 4-Nerve biopsy. 5-Lepromin test.
- 23. Skin Smear Tests •Ziehl Neelsen Carbol Fuchsin Stain (ZNCF) • Absence of bacteria in smear: Paucibacillary • Presence of bacteria in smear: Multibacillary
- 25. Procedure to LeprominSkin 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) • After 21 days(late reaction- Mitsuda reaction:- nodule>5mm).
- 26. WORLDS LEPROSY DAY January 30 •Date was chosen by French humanitarian Raoul Follereau as a tribute to the life of the Mahatma Gandhi who had compassion for people afflicted with leprosy.