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 lesionsAnaesthesia, 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 GlobiAggregates of foam cells filled with masses of AFB Macules, Papules,Nodules Leonine Facies Testes- Extensive destructionSterility

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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