Leprosy

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  • Hello, Mr. Aniket, I did go through your presentation and it is a good piece of work. Although, I got little confused while reading about Nerve Damage. Could you please tell me what is "S, M, A, in the Nerve Damage portion for all such as Ulnar, Median, and Radial nerve damage. Please. Thank you.
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Leprosy

  1. 1. LEPROSY Dr. Sandeep Choudhary
  2. 2. LEPROSY OVERVIEW  LEPROSY      Introduction Epidemiology Bacteriology Classification Clinical features       Reactions Diagnosis Treatment Deformities Rehabilitation NLEP
  3. 3. INTRODUCTION     Chronic granulomatous infectious 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.
  4. 4. Historical aspect of leprosy   One of the Oldest and most dreaded disease known to Mankind. Earliest description from India in 600BC     Kustha Roga & attributed to punishment or curse of God Al-Bukhari’s Muslim Hadith (volume 1, 2.443) documented Prophet Mohammed’s apparent dread of leprosy in his statement: “Escape from the leprous the way you escape from a lion” Word leper comes from Greek word “scaling” M. leprae was discovered by Gerhard Henrik Armauer Hansen in 1873 in Norway. Hence referred to as Hansen’s disease.  Leprosy control started with the use of chaulmoogra oil and for the last three decades, MDT has been the main tool against leprosy.
  5. 5. Epidemiology WORLDWIDE AND INDIA
  6. 6. Distribution  Prevalence  Worldwide distribution but essentially a disease of developing countries.  The prevalence rate has dropped by 90 percent from 21.1cases/10000 in 1985 to <1/10000 in 2000.  Out of 122 countries, only 2 countries still have to reach the elimination goal : Brazil and East Timor  To date there has been no resistance to antileprosy medicines when used as MDT.
  7. 7. WORLDWIDE PREVALENCE AT THE TURN OF CENTURY
  8. 8. Leprosy Situation in India The goal of leprosy elimination at National level (i.e. PR of <1 case/10,000 population) as set by National Health Policy 2002 had been achieved in the month of December 2005.
  9. 9. Leprosy Situation in India 2012-13        A total of 1.35 lac new cases were detected during 2012-13 i.e, ANCDR of 10.78/lac population Prevalence was 0.92 lac cases as on 1st Apr’13 i.e, PR of 73/10000 population. Multibacillary cases were 49.92 percent Female cases were 37.72 percent, children 9.93 percent 3.45 percent cases were with visible deformity 33 states/UTs have already achieved the PR of <1 case/10000. Chhattisgarh(1.69), Dadra & Nagar Haveli(2.93) are yet to achieve the goal.
  10. 10. Leprosy Situation in India 2012-13   Three States viz. Bihar, Maharashtra and West Bengal which have achieved elimination earlier have shown slight increase in P.R. (1-1.2) in the current year due to the effect of SAP-2012. This brings the total number of persons affected by Leprosy cured of the disease in the country with MDT from the beginning till date to 12.80 million.
  11. 11. Bacteriology
  12. 12. Lepra bacilli  Gram positive Obligate intracellular bacillus - due to its large pool of non functional genes.  Acid fast stained with modified Fite stain or ZN stain  Short, thick, pink stained rods of Size: (5µ X 0.5 µ )  Occurs characteristically in clumps or bundles( “globi”)  Affinity for Schwann cells & cells of R-E system .  M. leprae grows best in cooler tissues (the skin, peripheral nerves, anterior chamber of the eye, upper respiratory tract, and testes), sparing warmer areas of the skin (the axilla, groin, scalp, and midline of the back).  Optimal temp. for growth is 30-33 centigrade
  13. 13.  M. leprae remains one 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)
  14. 14. The Leprosy Bacteria
  15. 15. Reservoir of infection  Main reservoir : Human being  Lepromatous case> Non lepromatous cases  Animal reservoirs  9-banded armadillos  Chimpanzees  Mangabey monkeys  Sphagnum moss
  16. 16. Portal of exit   Major portal of exit : Nasal Mucosa  LL cases harbour millions of M. leprae in their nasal mucosa discharged when they sneeze or blow nose. Ulcerated or broken skin of bacteriologically positive cases
  17. 17. 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 NB : Breast feeding and Transplacental infection do not occur.
  18. 18. Incubation period  Long incubation period   Ranged: 2 to 40 years or more Average: 3-5 years  Generation time : 12 days.  Infectivity : Leprosy is a highly infectious disease with low pathogenicity. Among household contacts of lepromatous cases about 5 to 12 percent is expected to show signs of leprosy within 5 yrs.
  19. 19. VIRULENCE FACTOR The bacterium's complex cell 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.
  20. 20. Host Factors  Leprosy affects all age groups but incidence generally rises to a peak between 10 to 20 years of age and then fall.  Higher incidence is seen in males, more marked among adults, more marked among lepromatous cases.  Cell Mediated Immunity is responsible for resistance to infection with M.leprae. In lepromatous leprosy there is complete breakdown of CMI.
  21. 21. Environmental factors  Humidity favors survival of M. leprae in environment  M. leprae remain viable in    Dried nasal secretions for 9 days Moist soil at room temperature for 46 days Overcrowding & lack of ventilation within households
  22. 22. Social factors    Often called a “social disease” In addition to the physical effects of the disease, patients have also suffered severe social stigma and ostracism from their families, communities, and even health professionals to such an extent that leprosy has been known since ancient times as “the death before death”. Social factors:   Poverty Poverty related circumstances    Overcrowding Poor housing Lack of personal hygiene
  23. 23. CLASSIFICATION OF LEPROSY
  24. 24. IMPORTANCE OF CLASSIFICATION     Identify the infectious cases – Epidemiological importance - Principal targets for treatment Identify the patients likely to develop the deformities and determine the prognosis Frame the line of treatment Helpful in planning and evaluation of leprosy control activities
  25. 25. Various Classifications     Indian Classification : clinicobacteriological Madrid Classification : clinicobacteriological Ridley Jopling classification : immunohistological Classification by WHO Study Group on Chemotherapy of Leprosy : clinicobacteriological.
  26. 26. Ridley- Jopling 1966 (Research purposes)       Most widely accepted  Divides Leprosy cases into five groups according to their position on an immunohistological scale.  It can be used only when full research facilities are available : Tuberculoid (TT) Borderline Tuberculoid (BT) Borderline Borderline (BB) Borderline Lepromatous (BL) Lepromatous (LL)
  27. 27. Indian classification      Indeterminate type Tuberculoid type Borderline type Lepromatous type Pure neuritic type
  28. 28. Immunity in leprosy LL - multibacillary state with multiple lesions due to low immune response (+) TT -paucibacillary state, few lesions due to high immune response (-) LLHD BLHD BBHD BTHD TTHD
  29. 29. Contd..  Borderline forms (BB, BT and BL) lie between these two poles and are immunologically unstable, tending to move towards one of the polar forms
  30. 30. (+++) Immunology & bacteriology in leprosy (spectrum) (+++) Bacilli (++) Bacilli Immunity (++) Immunity (+) (+) (-) (-) LLHD
  31. 31. WHO Classification(1981,87,93) Clinical Feature on Skin Lesion Including macular flat lesion, papules & nodules Paucibacillary Leprosy PB 1 to 5 lesion Asymmetrical distribution Definite loss of sensation  BI <2 at all sites in the initial skin smear Multi Bacillary Leprosy MB More than 5 lesion Symmetrical distribution Loss of sensation may or may not be present  BI >= 2 at any site in the initial skin smear
  32. 32. W H O classification (For chemotherapy – M. leprae) Paucibacillary  Indeterminate - I  Tuberculoid – TT  Borderline Tuberculoid – BT  If any of these have positive bacterial index they should be classified as multibacillary for multidrug therapy Multibacillary  Mid borderline – BB  Borderline Lepromatous – BL  Lepromatous – LL  All smear positive cases
  33. 33. Clinical Feature
  34. 34. Indeterminate Leprosy  Earliest & transitory stage  One or two vague hypopigmented macule with definite sensory impairment.
  35. 35. Indeterminate Leprosy  If untreated may progress towards tuberculoid, borderline or lepromatous leprosy  Spontaneous regression may occur  Bacteriologically Negative
  36. 36. TUBERCULOID LEPROSY  Single or a few lesions  Asymmetrically distributed on trunk and limbs  Sharply defined, dry, flat or raised, erythematous or hypopigmented, and are anesthetic.  One or two nerves may be enlarged near the skin lesion  SS for AFB: Negative  Lepromin test may be strongly positive
  37. 37. Tuberculoid Leprosy
  38. 38. Borderline Tuberculoid  Four or more lesions, asymmetrically distributed  Macules or plaques of variable sizes with well or illdefined margins & satellite lesions   Peripheral nerves enlarged asymmetrically Sensation: hypoesthesia  SS for AFB: may or may not be positive.  Lepromin test may be weakly positive
  39. 39. Borderline Tuberculoid
  40. 40. Borderline Borderline  Multiple erythematous macules & plaques  Various sizes and shapes with punched out center and ill defined slopping outer margin  Tend to be symmetrical  Nerves may be asymmetrically enlarged  Sensation:+/-  SS for AFB: seen +/-  Lepromin test-usually negative, may be doubtful
  41. 41. Borderline Borderline
  42. 42. Borderline Lepromatous  Numerous, symmetrically distributed lesions  Hypopigmented or erythematous irregularly shaped maculopapular, infiltrative nodules, or plaques, with smooth surfaces & ill defined borders, sloping outwards  Nerves may be symmetrically or asymmetrically enlarged  Sensation:+/-  SS for AFB: numerous seen  Lepromin test -negative
  43. 43. Borderline Lepromatous
  44. 44. Lepromatous Leprosy  Numerous macules, plaques, nodules or diffusely infiltrated lesions, shiny, smooth, symmetrically distributed on face, trunk and extremities with illdefined margin which may be slightly hypopigmented or erythematous  Symmetrical nerve enlargement is seen  Sensation: normal  SS for AFB: numerous seen  Lepromin test - negative
  45. 45. Lepromatous Leprosy
  46. 46. Ear lobes involvement
  47. 47.    Diffuse thickening of the skin, with loss of hair (eyebrows and eyelashes) : madarosis. Saddle nose deformity Leonine facies
  48. 48. Clinical, Bacteriologic, Pathologic, and Immunologic Spectrum of Leprosy Feature Tuberculoid (TT, BT) Leprosy Borderline (BB, BL) Leprosy Lepromatous (LL) Leprosy Skin lesion One or a few sharply defined annular asymmetric macules or plaques with a tendency toward central clearing, elevated borders Intermediate between BT- and LL-type lesions; ill-defined plaques with an occasional sharp margin; few or many in number Symmetric, poorly marginated, multiple infiltrated nodules and plaques or diffuse infiltration; xanthoma-like or dermatofibroma papules; leonine facies and eyebrow alopecia Nerve lesion Skin lesions anesthetic early; nerve near lesions sometimes enlarged; nerve abscesses most common in BT Hypoesthetic or anesthetic skin lesions; nerve trunk palsies, at times symmetric Hypoesthesia a late sign; nerve palsies variable; acral, distal, symmetric anesthesia common BI(Bacteriological index) 0-1+ 3-5+ 4-6+ lymphocytes 2+ 1+ 0-1+ Macrophage differentiation Epitheloid Epitheloid in BB,usually undiff but may have foamy changes in BL Foamy change is the rule,may be undifferentiated in early lesions Langhans giant cells 1-3+ - - Lepromin skin test +++ - - Lymphocyte transformation test Generally positive 1 to 10 1 to 2 CD4 : CD8 ratio 1.2 BB(NT),BL:0.48 0.50 PGL1 antibodies 60 85 95
  49. 49. Other Variants of Leprosy    HISTOID LEPROSY : variant of LL with better CMI. Usually seen in patients with incomplete chemotherapy or acquired drug resistance. Characterized by presence of spindle shaped histiocytes in tissue section. LUCIO LEPROSY : mimics myxedema, diffuse nonnodular type of leprosy ch. by melancholy look, thick shiny skin, widespread sensory loss, hoarseness of voice and ulceration of nasal mucosa. LAZARINE LEPROSY : seen in association with HIV.
  50. 50. General Findings  Eye : The anterior chamber can be invaded in LL with resultant glaucoma and cataract formation. Iritis/Iridocyclitis  Testes : May be involved in LL with resultant hypogonadism.  Systemic involvement – Respiratory, Bones, Kidneys, Lymph glands, etc.
  51. 51. Nerve involvement in Leprosy
  52. 52. M. Leprae : superficial nerve involvement W Britton
  53. 53. Nerve Involvement      Neural involvement leads to muscle weakness, muscle atrophy, severe neuritic pain, and contractures of the hands and feet. Ulnar nerve is most commonly involved , least common is radial. Most common cranial nerve involved is Trigeminal. >30 percent neural loss required for loss of sensation. First sensation to go is thermal (cold>fine touch). Proprioception is usually preserved.
  54. 54. Face Facial Nerve  Lagophthalmos  Facial droop Trigeminal Nerve  Corneal anesthesia
  55. 55. NERVE DAMAGE UPPER LIMB
  56. 56. Ulnar S  Anesthesia medial 1/3 palm M Claw ring and little fingers A  Dryness medial 1/3 palm
  57. 57. Median S Anesthesia lateral 2/3 palm M Claw mid + index + loss Opposition A Dryness lateral 2/3 palm
  58. 58. Radial S Anesthesia dorsum hand M Wrist drop
  59. 59. NERVE DAMAGE LOWER LIMB
  60. 60. Lateral (common) Popliteal  Foot drop
  61. 61. Posterior Tibial S Sole anesthesia M Claw Toes A Dryness in sole
  62. 62. CASE DEFINITION  Leprosy is clinically defined by one or more of the following cardinal features : Hypopigmented patches II. Partial or total loss of cutaneous sensation in affected area. III. Presence of thickened nerves and I. IV. Presence of AFB in the skin or nasal smears It also includes : patients who started MDT but did not receive for 12 consecutive months and subsequently presents with signs of active disease as well as patient who relapse after completing a full course of treatment.
  63. 63. DIAGNOSIS        HISTORY CLINICAL EXAMINATION BACTERIOLOGICAL EXAMINATIONS FOOT-PAD CULTURE HISTAMINE TEST BIOPSY IMMUNOLOGICAL TEST
  64. 64. DIAGNOSIS HISTORY History should include the following points : Patients Bio data : name, age, sex, address Presenting complaints Family history of leprosy Contact with leprosy cases Previous history of treatment for leprosy, if any
  65. 65. DIAGNOSIS CLINICAL EXAMINATION Physical examination should include : A thorough inspection of the body surface(skin). Palpation of commonly involved superficial nerves: 1.Ulnar N. near the medial epicondyle. 2.Greater Auricular N as it turns over SCM muscle. 3.Lateral Popliteal N. 4.Dorsal branch of Radial N. Testing for : 1.Loss of sensation : heat, cold, pain, touch . 2.Paresis or paralysis of muscles of hands and feet.
  66. 66. Nerve palpation
  67. 67. DIAGNOSIS BACTERIOLOGICAL EXAMINATION This includes : Skin Smears : Nasal Smears or blows : Nasal Scrapings :
  68. 68. DIAGNOSIS BACTERIAL INDEX    Bacterial index is the only objective way of monitoring benefit of treatment. According To Ridley’ Logarithmic Scale It Ranges From 0 To 6+ and is based on the no. of bacilli seen in an average microscopic field. B 0 stands for no bacilli in any of 100 oil immersion field.
  69. 69. DIAGNOSIS BACTERIAL INDEX
  70. 70. DIAGNOSIS BACTERIAL INDEX
  71. 71. DIAGNOSIS BACTERIAL INDEX
  72. 72. DIAGNOSIS MORPHOLOGICAL INDEX     The MI is calculated after examining 200 pink-stained free standing bacilli. The percentage of solid staining bacilli in a stained smear is referred to as MI. It is a valuable indicator of the patient’s response to treatment during the first few months and helps to signal drug resistance. SOLID FRAGMENTED GRANULAR(SFG) PERCENTAGE : similar to MI but a more sensitive indicator of the patient’s response to treatment.
  73. 73. DIAGNOSIS FOOT-PAD CULTURE     1. 2. 3.  Only certain way of identifying M. Leprae. 10 times more sensitive at detecting the bacilli than slit skin smear. Time consuming : requires 6 to 9 months. Used for : Detecting drug resistance. Evaluating the potency of anti-leprosy drugs. Detecting the viability of bacilli during treatment. Newer in vitro macrophage culture which takes only 3 – 4 weeks.
  74. 74. DIAGNOSIS HISTAMINE TEST     Reliable test for detecting at an early stage peripheral nerve damage due to leprosy. Method : carried out by injecting 0.1ml of a 1:1000 solution of histamine phosphate into hypopigmented patches or in areas of anesthesia. Result : in normal person it gives rise to a wheal surrounded by erythematous flare(Lewis triple response). In case of leprosy where the nerve supply is destroyed, flare response is lost. Particularly useful in cases of indeterminate leprosy.
  75. 75. DIAGNOSIS BIOPSY  Usually resorted to when there is high clinical suspicion but the other test are unyielding. It also gives information about the bacterial content of skin.
  76. 76. DIAGNOSIS IMMUNOLOGICAL TESTS   Tests for cell mediated immunity(CMI) LEPROMIN TEST  Tests for humoral antibodies(serological tests)  FLA-ABS test : used for detecting subclinical infections. 92.3 percent sensitive and 100 percent specific in detecting specific antibodies in all types leprosy irrespective of type and duration of disease. Monoclonal antibodies Others : RIA, ELISA.  
  77. 77. DIAGNOSIS LEPROMIN TEST Method : it is performed by injecting 0.1ml of lepromin into inner aspect of the forearm. The reaction is read at 48 hours and 21 days. Two types of reaction have been described : EARLY REACTION(FERNANDEZ REACTION) : an inflammatory reaction develops within 24 to 48 hours and this tends to disappear in 3 to 4 days. If the diameter of the red area is more than 10mm the test is considered positive. It is a delayed type hypersensitivity reaction to soluble constituents of lepra bacilli and indicates whether or not a person has been sensitized by exposure to and infection by lepra bacilli.
  78. 78. DIAGNOSIS LEPROMIN TEST LATE REACTION(MITSUDA REACTION) : It is characterized by the appearance of a nodule which becomes apparent in 7 to 10 days and reaches its maximum in 3 to 4 weeks. The test is read at 21 days. If the nodule is more than 5 mm it is considered positive. It is induced by the bacillary component and indicates cell mediated immunity. In the first six months of life most children are lepromin negative BCG vaccination is capable of converting lepra reaction from negative to positive.
  79. 79. DIAGNOSIS LEPROMIN TEST VALUE OF LEPROMIN TEST : Useful tool for evaluating the immune status of leprosy patients. Aid to classify the type of disease. Estimating the prognosis Strongly positive in a typical tuberculoid case and getting weaker towards the lepromatous end, the typical lepromatous case being lepromin negative indicating failure of CMI. The greatest drawback being high false positive and false negative cases hence not used as a diagnostic test. OTHER TESTS FOR CMI :   Lymphocyte transformation test(LTT) Leucocyte migration inhibition test(LMIT)
  80. 80. TREATMENT MULTIDRUG CHEMOTHERAPY In the absence of effective of primary prevention by a leprosy vaccine leprosy control is based on effective multidrug chemotherapy(secondary prevention). OBJECTIVES : To interrupt transmission of infection Early detection and treatment of cases to prevent deformities To prevent drug resistance
  81. 81. TREATMENT MULTIDRUG CHEMOTHERAPY In multidrug regimens only bactericidal drugs are used : First line drugs : rifampicin, dapsone, clofazimine, ethionamide and prothionamide. Second line drugs : quinolones, minocycline, clarithromycin.
  82. 82. TREATMENT MULTIDRUG CHEMOTHERAPY WHO RECOMMENDED REGIMENS OF CHEMOTHERAPY : MULTIBACILLARY LEPROSY Rifampicin : 600mg once monthly under supervision Dapsone : 100mg daily self administered clofazimine : 300mg once monthly under supervision 50mg daily self-administered Where clofazimine is unacceptable due skin coloration it may be substituted by 250 to 375mg daily dose of ethionamide or prothionamide. The above regimen needs to taken for 12 months within 18 months
  83. 83. TREATMENT MULTIDRUG CHEMOTHERAPY WHO RECOMMENDED REGIMENS OF CHEMOTHERAPY : PAUCIBACILLARY LEPROSY : The above regimen needs to be taken for 6months within 9 months
  84. 84. TREATMENT MULTIDRUG CHEMOTHERAPY Treatment regimen for children 10-14 years : MULTIBACILLARY LEPROSY Rifampicin Dapsone clofazimine : 450mg once monthly under supervision : 50mg daily self administered : 150mg once monthly under supervision 50mg every other day self-administered PAUCIBACILLARY LEPROSY Rifampicin Dapsone : 450mg once a month under supervision : 50mg daily self administered.
  85. 85. TREATMENT MULTIDRUG CHEMOTHERAPY
  86. 86. TREATMENT MULTIDRUG CHEMOTHERAPY Important points : MDT is not contraindicated in patients with HIV infection. MDT is safe during pregnancy. Drugs are excreted in breast milk but no reports of adverse reaction except for mild discoloration of infants skin by clofazimine Leprosy is exacerbated during pregnancy, it is important that MDT is continued
  87. 87. TREATMENT MULTIDRUG CHEMOTHERAPY Drugs Rifampicin : highly bactericidal, a single 1500mg dose kills 99 percent of viable organisms Toxic effects includes anorexia, nausea, vomiting, abdominal discomfort and orange discoloration of body secretions. It is hepatotoxic Dapsone : weakly bactericidal. Adverse effects include hemolytic anemia, methemoglobinemia, agranulocytosis, hepatitis, neuropathy, psychosis and rarely…
  88. 88. TREATMENT MULTIDRUG CHEMOTHERAPY DDS syndrome ch. by fever, maculopapular rash, enlarged lymph nodes, hepatitis and exfoliative dermatitis. Clofazimine : was originally synthesized for TB. Less effective than dapsone but has added advantage of preventing lepra reaction. More expensive but less toxic which includes dark red discoloration of skin, mucus membranes, sweat and urine.
  89. 89. TREATMENT MULTIDRUG CHEMOTHERAPY Ethionamide and Prothionamide : highly bactericidal killing 98 percent of viable bacilli in 3 to 4 days. Relatively more expensive and more toxic.
  90. 90. LEPRA REACTIONS During the course of leprosy, immunological mediated episodes of acute or subacute inflammation known as reaction may occur.  There are two types of reactions :  Type 1 or Reversal reaction  Type 2 or erythema nodosum leprosum Both types can occur before the start of MDT, during treatment or after completion of treatment. 
  91. 91. LEPRA REACTIONS REVERSAL REACTION       In reversal reaction the leprosy skin lesions themselves become inflamed red, swollen and painful. It is type of delayed type of hypersensitivity. Occurs in both PB and MB Nerves may be enlarged, tender and painful with loss of function. General symptoms are uncommon Do not affect other organs.
  92. 92. LEPRA REACTIONS ERYTHEMA NODOSUM LEPROSUM       In ENL new inflamed, red nodules appear under the skin, while the original lesions remain same. Commonly on face, arm and legs & bilaterally symmetrical. They appear in crops and subside within few days even without treatment It is antigen antibody reaction. Seen in MB cases only. Nerves may be affected but is uncommon Other organs like testis, eye, kidney may be affected General symptoms of fever, joint pain, red eyes and watering may be associated.
  93. 93. LEPRA REACTIONS TREATMENT     Because of high risk of permanent nerve damage reversal reaction needs to be promptly diagnosed and treated adequately Standard 12 wk. regimen of prednisolone is the treatment of choice. ENL varies in severity, duration and organ involvement, and can be treated with prednisolone as reversal reaction. Treatment includes bed rest, splinting of affected nerves, analgesics and prednisolone.
  94. 94. LEPRA REACTIONS TREATMENT Prednisolone regimen Add clofazimine in ENL 40mg daily for first 2 weeks 30mg daily or week 3 and 4 100mg tds x 4 weeks 20mg daily for week 5 and 6 15mg daily for week 7 and 8 100mg bd x 4weeks 10mg daily for week 9 and 10 5mg daily for week 11 and 12 100mg od x 4 weeks For neuritis, treatment with prednisolone 20mg onwards Should be prolonged to four weeks from
  95. 95. LEPRA REACTIONS TREATMENT    For pregnant women prednisolone should be started at 30mg dose instead of 40mg and limit the course for 10weeks in PB cases and 20 weeks for MB cases. For children dose should be started at 1mg/kg of body wt. per day. Thalidomide : was reintroduced for the treatment of ENL, mainly because of its antipyretic action. WHO does not recommend the use of thalidomide in leprosy. Prednisolone is more effective in controlling ENL and associated neuritis, clofazimine is the drug of choice for the management of chronic, recurrent ENL reactions. Another drug claimed to be useful in ENL is pentoxyfylline.
  96. 96. IMMUNOPROPHYLAXIS   Till date there is no effective vaccine against leprosy The vaccine undergoing trials are :     BCG –34.1% PROTECTION BCG+KILLED M.LEPRAE – 64.0% M.W – 25.7% ICRC – 65.5%
  97. 97. CHEMOPROPHYLAXIS  Chemoprophylaxis as a public health measure is not recommended on account of lack of consistent results from various studies.
  98. 98. DEFORMITIES    As a single disease entity leprosy is the foremost cause of deformities and crippling. Approx. 25 percent of cases who are not properly treated at an early stage develop deformities of hands and feet. Deformities may results from the disease process, or from muscle paralysis due nerve damage, or due to injuries or infections.
  99. 99. DEFORMITIES Face Masked face, facies leonina, sagging face, lagopthalmos, madarosis(eyebrows, cilliary) corneal ulcers and opacities, perforated nose, depressed nose, nodules on ears and elongated lobules Hands Claw hand, wrist drop, ulcers, absorption of digits, thumb web contracture, hollowing of interosseus space, swollen hand Feet Plantar ulcers, foot drop, inversion of foot, clawing of toes, absorption of toes, collapsed foot, swollen foot and callosities Others Gynaecomastia and perforation of palate.
  100. 100. DEFORMITIES PREVENTION       Measures include care of dry and denervated skin of palms and soles. Treating wounds, ulcers, and cracks in palms & soles Use of protective gloves and footwear Prevent joint stiffness in case of paralysis Protection of eyes Periodic check up for progression of disease.
  101. 101. DEFORMITIES IMPROVEMENT  Improvement of disabilities is achieved through the use of prostheses and orthopaedic devices, including corrective splints as well as by corrective surgery.
  102. 102. REHABILITATION   Rehabilitation includes all the measures used for reducing the impact of disability for an individual, enabling him/her to achieve independence, social integration, a better quality of life and self actualization. Community Based Rehabilitation (CBR) is a strategy within community development for the rehabilitation, equalization of opportunities, poverty alleviation and social inclusion of all the people with disabilities. It is implemented with combined efforts of people with disability, their families, community, social and government organisation..
  103. 103. REHABILITATION Basic principles of CBR includes : Participation Empowerment Raising awareness Self–advocacy Gender sensitivity and special needs Partnerships Sustainability
  104. 104. NATIONAL LEPROSY ERADICATION PROGRAMME      The history of anti leprosy work in India goes back to 1874 when the mission to lepers(leprosy mission) was founded by Bailey at Chamba, HP The NLCP was launched in 1954 later converted to NLEP in 1983 The prevalence rate was 57cases/10000 population in 1981 which declined to 5.7/10000 in 2000 In Dec 2005 India achieved the target of leprosy elimination envisaged in NHP 2002, when PR was brought down to <1/10000. Chhattisgarh and Dadra & Nagar haveli are yet to reach the target.
  105. 105. Thank You

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