Pathology of Leprosy.pptx

1,046 views 24 slides Jun 21, 2023
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About This Presentation

Pathophysiology of Leprosy


Slide Content

Leprosy

Leprosy Hansen disease Slowly progressive infection caused by Mycobacterium leprae Mainly affects the skin and peripheral nerves Gerhard Armer Hansen

Mode of Transmission Still not known Human respiratory secretions or soil are likely origins Droplet infection: through aerosols from person to person Long incubation period : 2-7 years upto 20 years Low transmission rates Due to the slow-growing nature of the bacteria and the long time it takes to develop signs of the disease, it is often very difficult to find the source of infection.

Pathogenesis M. leprae is taken up by alveolar macrophages and disseminates in the blood replicates primarily in relatively cool tissues of the skin, extremities, peripheral nerves, eyes etc It proliferates best at 32° to 34°C, the temperature of the human skin

Classification Indian classification Madrid WHO Ridley Jopling

Pathogenesis M. leprae causes two strikingly different patterns of disease Tuberculoid Lepromatous Determined by the helper T-lymphocyte response to M. leprae

Ridley Jopling Classification Immune response Strong cell mediated Weak cell mediated Clinical Presentation Pure Tuberculoid Pure Lepromatous Variable cell mediated Borderline TT BB BT BL LL Paucibacillary Multibacillary

Tuberculoid leprosy Strong Th1 response Associated with production of IL-2 and IFN-γ as well as a Th17 response. IFN-γ functions to elicit an effective host macrophage response, and hence the microbial burden is low. Antibody production is low.

Lepromatous Leprosy Associated with a weak Th1 response Result is weak cell-mediated immunity → inability to control the bacteria→ can be readily visualized in tissue sections. Occasionally, antibodies are produced against M. leprae antigens. These antibodies are usually not protective, but they may form immune complexes with free antigens → that can lead to erythema nodosum, vasculitis, and glomerulonephritis.

Case 1 35/M with 2 hypopigmented lesions on the forearm On examination the lesions were anaesthetic

Slit Skin smear Air dry and stain Modified ZN stain (decolorize with 5% sulphuric acid) NO AFB SEEN

Biopsy

Biopsy Multiple granulomas Tuberculoid leprosy

Case 2 40 year old male with progressive loss of eyebrows, patchy hypopigmentation and multiple nodules on face and arms On examination, coarse facial features, firm subcutaneous nodules and anaesthetic patches

Slit skin smear was made

Biopsy Diffuse sheets of histiocytes Definite Grenz zone No granulomas

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