logging in or signing up leprocy d_talreja Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 198 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: January 20, 2010 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... By: drvivekshimla (19 month(s) ago) Hello Doctor, Nice presentation indeed!. Can I download? Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript LEPROSY : By. Dr. Deepak Kumar Talreja LEPROSY DEFINITION : DEFINITION A chronic granulomatous disease Caused by Mycobacterium leprae Affecting peripheral nerves and skin. BACKGROUND : BACKGROUND Armauer Hansen Discovered M leprae in Norway in 1873 First bacillus to be Associated with human disease Humans Primary reservoir Animal reservoirs 9-banded armadillos Chimpanzees Mangabey monkeys Every year January 27 is World Leprosy Day GEOGRAPHICAL DISTRIBUTION : GEOGRAPHICAL DISTRIBUTION Endemic in Asia Africa Latin America India 70% of the world’s leprosy cases EPIDEMIOLOGY : EPIDEMIOLOGY Incidence Around 800 000 Prevalence 4 million people Age 10-14 years 35-44 years Sex In adults (lepromatous type) Male-to-female ratio of 2:1 In children (tuberculoid form) PATHOGENESIS : PATHOGENESIS M leprae Intracellular Acid-fast Gram-positive Bacillus Transmission Aerosol Spread Abraded Skin Incubation Time Tuberculoid Cases 2–5 Years Lepromatous Cases 8–12 Years PATHOGENESIS : PATHOGENESIS (HLA) associations Tuberculoid HLA-DR2 and HLADR3 Lepromatous HLA-DQ1 Susceptible loci on chromosome10p13 and chromosome 6 Prefer cool parts Superficial peripheral nerves Skin Mucous membranes of U.R.T Anterior chamber of the eyes Testes PATHOGENESIS : PATHOGENESIS PATHOGENESIS : PATHOGENESIS 4 principle causes of tissue damage The degree to which CMI is expressed The extent of bacillary spread & multiplication Lepra reactions The nerve damage & its complications PATHOGENESIS : PATHOGENESIS CLINICAL SPECTRUM : CLINICAL SPECTRUM HISTOLOGY TUBERCULOID LEPROSY (TT) : HISTOLOGY TUBERCULOID LEPROSY (TT) Granulomas Surround N.V. elements in foci Papillary zone may be invaded Bacilli not visible Cutaneous nerves swollen HISTOLOGY TUBERCULOID LEPROSY (TT) : HISTOLOGY TUBERCULOID LEPROSY (TT) HISTOLOGY TUBERCULOID LEPROSY (TT) : HISTOLOGY TUBERCULOID LEPROSY (TT) HISTOLOGY TUBERCULOID LEPROSY (TT) : HISTOLOGY TUBERCULOID LEPROSY (TT) HISTOLOGY BORDERLINE LEPROSY : HISTOLOGY BORDERLINE LEPROSY In BT Granuloma is more diffuse Fine but narrow papillary zone FB giant cells Dermal nerves moderately swollen AFB’s absent or scanty In mid BB Lymphocytes scanty No giant cells Nerves slightly swollen AFB’s in moderate number HISTOLOGY BORDERLINE LEPROSY : HISTOLOGY BORDERLINE LEPROSY In BL Macrophages slightly foamy Occasional epitheloid cells Scanty cellular infiltrate Clear papillary zone Leprosy bacilli plentiful, Singly or in clumps HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) Epidermis thin Rete ridges flattened Papillary layer appear as a clear band Typical diffuse leproma Lymphocytes & plasma cells few Enormous no. of AFB’s Singly In clumps Globi HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) HISTOLOGY INDETERMINATE LEPROSY : HISTOLOGY INDETERMINATE LEPROSY Scattered infiltrate Histiocytic lymphocytic Rarely single bacillus In a dermal nerve CLINICAL FEATURES : CLINICAL FEATURES Early lesions Classic lesion is that of IL Macules (character) One or more Few cms. in diameter Margins poorly defined Sites Face Extensor surface (limbs) Alternatively, features of One of est. forms CLINICAL FEATURESTUBERCULOID LEPROSY (TT) : CLINICAL FEATURESTUBERCULOID LEPROSY (TT) Few lesions often solitary Typically a plaque Copper coloured or purple Edges raised, slope towards centre Surface Dry Hairless Insensitive Sometimes purely neural Pain & swelling of the affected nerve Anaesthesia &/or muscle weakness & wasting CLINICAL FEATURES TUBERCULOID LEPROSY (TT) : CLINICAL FEATURES TUBERCULOID LEPROSY (TT) CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) : CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) Early symptoms Dermal Macules, Diffuse papules Nodules Or all three Nasal Stuffiness Discharge Epistaxis Oedema of legs CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) : CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) Skin lesions Multiple Bilaterally symmetrical Sites Face Arms Legs Spared areas Scalp Axillae Groins Perineum CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) : CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) Oral lesions Papules on lips Nodules on Palate Uvula Tongue Gums CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY Untreated advanced disease Thickened facial skin “Leonine facies” Thickened ear lobes Collapsed nose Loss of eye brows Hoarseness Fall of upper incisor teeth Nerve involvement Icthyosis CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY Nerve involvement Skin manifestations antedate nerve damage Thickening of nerves Sensory or motor dysfunction Blistering of anaesthetic skin CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY Eye changes 2 means Leprous deposits Keratitis Iridocyclitis (uveitis) Iris atrophy Lagophthalmos Exposure keratitis Blindness CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY Bone changes Osteoporosis in the phalanges Small osteolytic cysts Compression fractures Crooked or short fingers Nails Thin & brittle Testicular atrophy CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY LUCIO LEPROSY A pure diffuse type of LL Described in 1852 (Mexico) Initial symptoms Sensory impairment Hands and feet Gradual loss of Eyebrows Eyelashes Body hair. Diffuse scleroderma like skin Absent nodules & plaques CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY HISTOID LESIONS Distinct cutaneous nodules Characteristic of relapse after treatment CLINICAL FEATURES BORDER LINE LEPROSY : CLINICAL FEATURES BORDER LINE LEPROSY Commonest type Lesions Macules Plaques Annular Bizarre-shaped bands Intermediate in number Asymmetrical distribution In the middle of the spectrum Characteristic plaques with a “punched out” appearance CLINICAL FEATURES BORDER LINE LEPROSY : CLINICAL FEATURES BORDER LINE LEPROSY DIMORPHIC CLINICAL FEATURES BORDER LINE LEPROSY : CLINICAL FEATURES BORDER LINE LEPROSY Tuberculoid end of the spectrum Lesions few and dry More hair loss & anhidrosis Fewer bacilli in smears & biopsies And vice versa towards the lepromatous pole One or more nerves thickened Border line disease is unstable CLINICAL FEATURES BORDERLINE TUBERCULOID : CLINICAL FEATURES BORDERLINE TUBERCULOID Tuberculoid leprosy CLINICAL FEATURES BORDERLINE LEPROMATOUS : CLINICAL FEATURES BORDERLINE LEPROMATOUS Borderline tuberculoid CLINICAL FEATURES PURE NEURITIC LEPROSY : CLINICAL FEATURES PURE NEURITIC LEPROSY Accounts for 5-10% of patients Seen in India & Nepal Peripheral nerve lesions Asymmetrical No visible skin lesions REACTIONS : REACTIONS Type I reactions Occur in border line disease Seen after starting treatment Cell mediated Presents with Acute neuritis Acutely inflamed skin lesions Nerves Tender Loss of function Sensory & motor New lesions may appear Can occur spontaneously REACTIONS : REACTIONS Type II ENL reactions A systemic disorder Antibody mediated Occur in MB disease (LL & BL) Spontaneous On treatment No change in existing lesions Presents Fever Painful red nodules Face & limbs Superficial or deep Ulceration LUCIO REACTIONS : LUCIO REACTIONS Occurs only in lucio leprosy Untreated pts presents Severe systemic upset Can be fatal Erythematous patches Bullae & necrosis Deep painful ulcers PROGNOSIS : PROGNOSIS Nerve damage Cannot be reversed Severe disability Esp. When all 4 limbs & both eyes are affected Anti-bacterial treatment Highly effective Low relapse rates DIAGNOSIS : DIAGNOSIS Usually clinical (on the basis of 2 out of 3) Anaesthesia of a skin lesion Thickened nerves Typical skin lesions Slit skin smears Bacteriological index Morphological index Skin biopsy Nerve biopsy BACTERIOLOGICAL INDEX (BI) : BACTERIOLOGICAL INDEX (BI) MORPHOLOGICAL INDEX : MORPHOLOGICAL INDEX Percentage of solid staining bacteria DIAGNOSIS : DIAGNOSIS Lepromin skin test Analogous to the Tuberculin test Positive at 48 hours = Fernandez reaction Delayed hypersensitivity Positive again at 3 - 4 weeks = Mitsuda reaction Granulomatous response Strongly positive in TT Weakly positive in BT Negative in BB, BL and LL Unpredictable in indeterminate leprosy DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Macular lesions Birth marks Vitiligo Pityriasis Alba Pityriasis Versicolor Tinea Corporis Post inflammatory hypochromia DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Birthmark Single or few in number Present from birth Unchanging Normal sweating and sensation DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Post-inflammatory hypochromia Hypochromia at site of inflamation Take a history examine for loss of sensation DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Tinea versicolor Well-defined, scaly lesions Over the trunk, neck and limbs Sensation and sweating normal Fungal elements seen under microscope DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Tinea corporis Prominent, scaly lesion Respond to antifungal Sensation and sweating normal DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Vitiligo White lesions (de-pigmentation) Sensation, sweating are normal DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Plaques & annular lesions Ring worm Granuloma Multiforme Sarcoidosis Cutaneous TB Granuloma annulare DIFFERENTIAL DIAGNOSES Plaques & annular : DIFFERENTIAL DIAGNOSES Plaques & annular Granuloma annulare Affects mainly children and young adults Papules or nodules in a annular pattern Symptomless No enlarged peripheral nerves Sensation and sweating are normal DIFFERENTIAL DIAGNOSES Plaques & annular : DIFFERENTIAL DIAGNOSES Plaques & annular Granuloma multiforme Occurs mainly in nigeria Variant of granuloma annulare Initialy itching Disappear spontaneously Sensation, sweating and peripheral nerves –all normal DIFFERENTIAL DIAGNOSES Plaques & annular : DIFFERENTIAL DIAGNOSES Plaques & annular Sarcoidosis Sensation normal No enlargement of Nerves DIFFERENTIAL DIAGNOSES Plaques & annular : DIFFERENTIAL DIAGNOSES Plaques & annular Lupus Vulgaris Tendency to ulceration and scar formation Nerves are not involved Sensation is normal DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Nodules Cutaneous Leishmaniasis Post-kala-azar dermal leishmaniasis (PKDL) DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Nerves Hereditary sensory motor neuropathy type III Amyloidosis Peroneal muscular atrophy (CMTD) Causes of other polyneuropathies AIDS DM Alcoholism Heavy metal poisoning DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Eye disease Trachoma Onchocerciasis which causes uveitis TREATMENT : TREATMENT 5 main principles of treatment Stop the infection with chemotherapy Treat reactions & reduce risk of N. damage Educate the pt. to cope with existing N. dam. Treat the complications of N. damage Rehabilitation Social Psychological TREATMENT : TREATMENT WHO multidrug therapy regimen TREATMENT : TREATMENT Relapse Low relapse rates Relapsed MB pts. treated with triple therapy REACTION & NEURITIS : REACTION & NEURITIS Peak time for reversal reactions First 6 months Patient warning important Treatment aim Controlling acute inflammation Easing pain Reversing nerve & eye damage Reassuring the patient MDR continued TREATMENT : TREATMENT Lepra Type 1 Reactions Prednisolone 40-60 mg/d Taper in 2- to 3-month period Indications for prednisone Neuritis Lesions appearing at face Ulcerating lesions TREATMENT : TREATMENT Lepra Type 2 Reactions ENL High dose steroids 80 mg/d, Rapid tapering Recurrent ENL Thalidomide 400 mg daily Clofazimine 300 mg daily Acute Iridocyclitis Hydrocortisone 1% eye drops, 4 hrly Atropine 1% eye drops, 12 hrly COMPLICATIONS OF NERVE DAMAGE : COMPLICATIONS OF NERVE DAMAGE Preventable Early diagnosis Self awareness of the patient Appropriate shoe protection Special shoe for deformities Rest in case of plantar ulceration Weakness & Paralysis Physiotherapy VACCINES AGAINST LEPROSY : VACCINES AGAINST LEPROSY Cross-reactivity b/w BCG & M. Leprae BCG agianst leprosy Statistically significant but variable protection THANK YOU : THANK YOU You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
leprocy d_talreja Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 198 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: January 20, 2010 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... By: drvivekshimla (19 month(s) ago) Hello Doctor, Nice presentation indeed!. Can I download? Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript LEPROSY : By. Dr. Deepak Kumar Talreja LEPROSY DEFINITION : DEFINITION A chronic granulomatous disease Caused by Mycobacterium leprae Affecting peripheral nerves and skin. BACKGROUND : BACKGROUND Armauer Hansen Discovered M leprae in Norway in 1873 First bacillus to be Associated with human disease Humans Primary reservoir Animal reservoirs 9-banded armadillos Chimpanzees Mangabey monkeys Every year January 27 is World Leprosy Day GEOGRAPHICAL DISTRIBUTION : GEOGRAPHICAL DISTRIBUTION Endemic in Asia Africa Latin America India 70% of the world’s leprosy cases EPIDEMIOLOGY : EPIDEMIOLOGY Incidence Around 800 000 Prevalence 4 million people Age 10-14 years 35-44 years Sex In adults (lepromatous type) Male-to-female ratio of 2:1 In children (tuberculoid form) PATHOGENESIS : PATHOGENESIS M leprae Intracellular Acid-fast Gram-positive Bacillus Transmission Aerosol Spread Abraded Skin Incubation Time Tuberculoid Cases 2–5 Years Lepromatous Cases 8–12 Years PATHOGENESIS : PATHOGENESIS (HLA) associations Tuberculoid HLA-DR2 and HLADR3 Lepromatous HLA-DQ1 Susceptible loci on chromosome10p13 and chromosome 6 Prefer cool parts Superficial peripheral nerves Skin Mucous membranes of U.R.T Anterior chamber of the eyes Testes PATHOGENESIS : PATHOGENESIS PATHOGENESIS : PATHOGENESIS 4 principle causes of tissue damage The degree to which CMI is expressed The extent of bacillary spread & multiplication Lepra reactions The nerve damage & its complications PATHOGENESIS : PATHOGENESIS CLINICAL SPECTRUM : CLINICAL SPECTRUM HISTOLOGY TUBERCULOID LEPROSY (TT) : HISTOLOGY TUBERCULOID LEPROSY (TT) Granulomas Surround N.V. elements in foci Papillary zone may be invaded Bacilli not visible Cutaneous nerves swollen HISTOLOGY TUBERCULOID LEPROSY (TT) : HISTOLOGY TUBERCULOID LEPROSY (TT) HISTOLOGY TUBERCULOID LEPROSY (TT) : HISTOLOGY TUBERCULOID LEPROSY (TT) HISTOLOGY TUBERCULOID LEPROSY (TT) : HISTOLOGY TUBERCULOID LEPROSY (TT) HISTOLOGY BORDERLINE LEPROSY : HISTOLOGY BORDERLINE LEPROSY In BT Granuloma is more diffuse Fine but narrow papillary zone FB giant cells Dermal nerves moderately swollen AFB’s absent or scanty In mid BB Lymphocytes scanty No giant cells Nerves slightly swollen AFB’s in moderate number HISTOLOGY BORDERLINE LEPROSY : HISTOLOGY BORDERLINE LEPROSY In BL Macrophages slightly foamy Occasional epitheloid cells Scanty cellular infiltrate Clear papillary zone Leprosy bacilli plentiful, Singly or in clumps HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) Epidermis thin Rete ridges flattened Papillary layer appear as a clear band Typical diffuse leproma Lymphocytes & plasma cells few Enormous no. of AFB’s Singly In clumps Globi HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) HISTOLOGY LEPROMATOUS LEPROSY (LL) : HISTOLOGY LEPROMATOUS LEPROSY (LL) HISTOLOGY INDETERMINATE LEPROSY : HISTOLOGY INDETERMINATE LEPROSY Scattered infiltrate Histiocytic lymphocytic Rarely single bacillus In a dermal nerve CLINICAL FEATURES : CLINICAL FEATURES Early lesions Classic lesion is that of IL Macules (character) One or more Few cms. in diameter Margins poorly defined Sites Face Extensor surface (limbs) Alternatively, features of One of est. forms CLINICAL FEATURESTUBERCULOID LEPROSY (TT) : CLINICAL FEATURESTUBERCULOID LEPROSY (TT) Few lesions often solitary Typically a plaque Copper coloured or purple Edges raised, slope towards centre Surface Dry Hairless Insensitive Sometimes purely neural Pain & swelling of the affected nerve Anaesthesia &/or muscle weakness & wasting CLINICAL FEATURES TUBERCULOID LEPROSY (TT) : CLINICAL FEATURES TUBERCULOID LEPROSY (TT) CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) : CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) Early symptoms Dermal Macules, Diffuse papules Nodules Or all three Nasal Stuffiness Discharge Epistaxis Oedema of legs CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) : CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) Skin lesions Multiple Bilaterally symmetrical Sites Face Arms Legs Spared areas Scalp Axillae Groins Perineum CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) : CLINICAL FEATURESLEPROMATOUS LEPROSY (LL) Oral lesions Papules on lips Nodules on Palate Uvula Tongue Gums CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY Untreated advanced disease Thickened facial skin “Leonine facies” Thickened ear lobes Collapsed nose Loss of eye brows Hoarseness Fall of upper incisor teeth Nerve involvement Icthyosis CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY Nerve involvement Skin manifestations antedate nerve damage Thickening of nerves Sensory or motor dysfunction Blistering of anaesthetic skin CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY Eye changes 2 means Leprous deposits Keratitis Iridocyclitis (uveitis) Iris atrophy Lagophthalmos Exposure keratitis Blindness CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY Bone changes Osteoporosis in the phalanges Small osteolytic cysts Compression fractures Crooked or short fingers Nails Thin & brittle Testicular atrophy CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY LUCIO LEPROSY A pure diffuse type of LL Described in 1852 (Mexico) Initial symptoms Sensory impairment Hands and feet Gradual loss of Eyebrows Eyelashes Body hair. Diffuse scleroderma like skin Absent nodules & plaques CLINICAL FEATURES LEPROMATOUS LEPROSY : CLINICAL FEATURES LEPROMATOUS LEPROSY HISTOID LESIONS Distinct cutaneous nodules Characteristic of relapse after treatment CLINICAL FEATURES BORDER LINE LEPROSY : CLINICAL FEATURES BORDER LINE LEPROSY Commonest type Lesions Macules Plaques Annular Bizarre-shaped bands Intermediate in number Asymmetrical distribution In the middle of the spectrum Characteristic plaques with a “punched out” appearance CLINICAL FEATURES BORDER LINE LEPROSY : CLINICAL FEATURES BORDER LINE LEPROSY DIMORPHIC CLINICAL FEATURES BORDER LINE LEPROSY : CLINICAL FEATURES BORDER LINE LEPROSY Tuberculoid end of the spectrum Lesions few and dry More hair loss & anhidrosis Fewer bacilli in smears & biopsies And vice versa towards the lepromatous pole One or more nerves thickened Border line disease is unstable CLINICAL FEATURES BORDERLINE TUBERCULOID : CLINICAL FEATURES BORDERLINE TUBERCULOID Tuberculoid leprosy CLINICAL FEATURES BORDERLINE LEPROMATOUS : CLINICAL FEATURES BORDERLINE LEPROMATOUS Borderline tuberculoid CLINICAL FEATURES PURE NEURITIC LEPROSY : CLINICAL FEATURES PURE NEURITIC LEPROSY Accounts for 5-10% of patients Seen in India & Nepal Peripheral nerve lesions Asymmetrical No visible skin lesions REACTIONS : REACTIONS Type I reactions Occur in border line disease Seen after starting treatment Cell mediated Presents with Acute neuritis Acutely inflamed skin lesions Nerves Tender Loss of function Sensory & motor New lesions may appear Can occur spontaneously REACTIONS : REACTIONS Type II ENL reactions A systemic disorder Antibody mediated Occur in MB disease (LL & BL) Spontaneous On treatment No change in existing lesions Presents Fever Painful red nodules Face & limbs Superficial or deep Ulceration LUCIO REACTIONS : LUCIO REACTIONS Occurs only in lucio leprosy Untreated pts presents Severe systemic upset Can be fatal Erythematous patches Bullae & necrosis Deep painful ulcers PROGNOSIS : PROGNOSIS Nerve damage Cannot be reversed Severe disability Esp. When all 4 limbs & both eyes are affected Anti-bacterial treatment Highly effective Low relapse rates DIAGNOSIS : DIAGNOSIS Usually clinical (on the basis of 2 out of 3) Anaesthesia of a skin lesion Thickened nerves Typical skin lesions Slit skin smears Bacteriological index Morphological index Skin biopsy Nerve biopsy BACTERIOLOGICAL INDEX (BI) : BACTERIOLOGICAL INDEX (BI) MORPHOLOGICAL INDEX : MORPHOLOGICAL INDEX Percentage of solid staining bacteria DIAGNOSIS : DIAGNOSIS Lepromin skin test Analogous to the Tuberculin test Positive at 48 hours = Fernandez reaction Delayed hypersensitivity Positive again at 3 - 4 weeks = Mitsuda reaction Granulomatous response Strongly positive in TT Weakly positive in BT Negative in BB, BL and LL Unpredictable in indeterminate leprosy DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Macular lesions Birth marks Vitiligo Pityriasis Alba Pityriasis Versicolor Tinea Corporis Post inflammatory hypochromia DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Birthmark Single or few in number Present from birth Unchanging Normal sweating and sensation DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Post-inflammatory hypochromia Hypochromia at site of inflamation Take a history examine for loss of sensation DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Tinea versicolor Well-defined, scaly lesions Over the trunk, neck and limbs Sensation and sweating normal Fungal elements seen under microscope DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Tinea corporis Prominent, scaly lesion Respond to antifungal Sensation and sweating normal DIFFERENTIAL DIAGNOSESMacular lesions : DIFFERENTIAL DIAGNOSESMacular lesions Vitiligo White lesions (de-pigmentation) Sensation, sweating are normal DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Plaques & annular lesions Ring worm Granuloma Multiforme Sarcoidosis Cutaneous TB Granuloma annulare DIFFERENTIAL DIAGNOSES Plaques & annular : DIFFERENTIAL DIAGNOSES Plaques & annular Granuloma annulare Affects mainly children and young adults Papules or nodules in a annular pattern Symptomless No enlarged peripheral nerves Sensation and sweating are normal DIFFERENTIAL DIAGNOSES Plaques & annular : DIFFERENTIAL DIAGNOSES Plaques & annular Granuloma multiforme Occurs mainly in nigeria Variant of granuloma annulare Initialy itching Disappear spontaneously Sensation, sweating and peripheral nerves –all normal DIFFERENTIAL DIAGNOSES Plaques & annular : DIFFERENTIAL DIAGNOSES Plaques & annular Sarcoidosis Sensation normal No enlargement of Nerves DIFFERENTIAL DIAGNOSES Plaques & annular : DIFFERENTIAL DIAGNOSES Plaques & annular Lupus Vulgaris Tendency to ulceration and scar formation Nerves are not involved Sensation is normal DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Nodules Cutaneous Leishmaniasis Post-kala-azar dermal leishmaniasis (PKDL) DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Nerves Hereditary sensory motor neuropathy type III Amyloidosis Peroneal muscular atrophy (CMTD) Causes of other polyneuropathies AIDS DM Alcoholism Heavy metal poisoning DIFFERENTIAL DIAGNOSES : DIFFERENTIAL DIAGNOSES Eye disease Trachoma Onchocerciasis which causes uveitis TREATMENT : TREATMENT 5 main principles of treatment Stop the infection with chemotherapy Treat reactions & reduce risk of N. damage Educate the pt. to cope with existing N. dam. Treat the complications of N. damage Rehabilitation Social Psychological TREATMENT : TREATMENT WHO multidrug therapy regimen TREATMENT : TREATMENT Relapse Low relapse rates Relapsed MB pts. treated with triple therapy REACTION & NEURITIS : REACTION & NEURITIS Peak time for reversal reactions First 6 months Patient warning important Treatment aim Controlling acute inflammation Easing pain Reversing nerve & eye damage Reassuring the patient MDR continued TREATMENT : TREATMENT Lepra Type 1 Reactions Prednisolone 40-60 mg/d Taper in 2- to 3-month period Indications for prednisone Neuritis Lesions appearing at face Ulcerating lesions TREATMENT : TREATMENT Lepra Type 2 Reactions ENL High dose steroids 80 mg/d, Rapid tapering Recurrent ENL Thalidomide 400 mg daily Clofazimine 300 mg daily Acute Iridocyclitis Hydrocortisone 1% eye drops, 4 hrly Atropine 1% eye drops, 12 hrly COMPLICATIONS OF NERVE DAMAGE : COMPLICATIONS OF NERVE DAMAGE Preventable Early diagnosis Self awareness of the patient Appropriate shoe protection Special shoe for deformities Rest in case of plantar ulceration Weakness & Paralysis Physiotherapy VACCINES AGAINST LEPROSY : VACCINES AGAINST LEPROSY Cross-reactivity b/w BCG & M. Leprae BCG agianst leprosy Statistically significant but variable protection THANK YOU : THANK YOU