LEPROSY (Hansen’s Disease)
Causative Organism- Mycobacterium leprae Affects mainly cooler parts of the body Skin, mouth, Respiratory Tract, eyes, Peripheral nerves, Testis, etc Earliest --------Skin & Nerves
PATHOGENESIS Acid fast, obligate intracellular organism Poor growth in culture, but grows in armadillo, foot pad of mice Virulence– cell wall properties Cell mediated immunity– Lepromin Test
DIAGNOSIS Split skin smears & nasal smears AFB ( Ziehl – Neelson) stain Fite Faraco Stain Silver stain
Bacteriological Index Morphological Index Solid staining – Live Fragmented / Beaded - Dead Paucibacillary – No Bacilli Multibacillary – Some or many Bacilli
TRANSMISSION ? Inhalation Direct Contact Maternofetal transmission
Classification 2 Main types ( polar forms); Lepromatous – Low Immunity Tuberculoid – High Immunity
Modified Ridley Jopling’s Classification Indeterminate TT – Tuberculoid BT – Borderline Tuberculoid BB – Mid Borderline BL – Borderline Lepromatous LL -- Lepromatous
FEATURES TT LL Skin Lesions Asymmetrical Symmetrical (Leonine Facies) Nerve Involvement +, Sensory disturbance ++ Sensory disturbance Foam Cells, ‘Grenz Zone’ + Microscopy Tubercle, ‘Grenz Zone’ -ve Bacilli load ‘Globi’ / cigarette pack Few are seen Immunity High Low Lepromin Test + -
Tuberculoid Leprosy
Tuberculoid Leprosy: Skin lesions Nerve lesionsAnaesthesia, Skin & muscle atrophy, Trophic ulcers, Contractures,etc MC – Ulnar, Radial, Common peroneal VII Cranial nerve Keratitis, Corneal ulcer
Lepromatous Leprosy: Widespread invasion of shwann cells, neural macrophages GlobiAggregates of foam cells filled with masses of AFB Macules, Papules,Nodules Leonine Facies Testes- Extensive destructionSterility
REACTIONS IN LEPROSY Type I ( Reversal Reaction) Upgrading Reaction Downgrading Reaction Type II ( Erythema Nodosum Leprosum) Usually after chemotherapy Occurs in LL Tender nodules, Iridocyclitis, Lymph node involvement Infiltration of neutrophils, Vasculitis Responds to Treatment
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