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Leprosy

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Leprosy

  1. 1. LEPROSY By Sriloy Mohanty B.N.Y.S
  2. 2. Contents…  introduction
  3. 3. INTRODUCTION  Chronic infectious disease  Surface infection  Caused by M leprae  Affects mainly the peripheral nerves
  4. 4. Cardinal features  Hypo-pigmented patches  Loss of cutaneous sensations  Thickened nerves  Presence of acid-fast bacilli in the skin or nasal smear Signs of advanced disease are:  Lumps in the skin of the face and ears  Plantar ulcers  Loss of fingers or toes  Nasal depression  Foot drop and claw toes
  5. 5. History  Oldest disease known to mankind  Leper - Greek word – scaly  Confused with psoriasis, elephantitis and pellagra  Known as kushta roga  1873 – Hansen of Norway discovered M. leprae  1943 – sulphone drugs used in the treatment
  6. 6. Problem Statement  1991 – WHO Member State resolved to decrease the level of leprosy by over 90%  Fall in prevalence rate largely is due to  Improvement in management of cases  Low rates of relapse  High cure rate  Absence of drug resistance  Short duration treatment  WHO global strategy for further reducing the leprosy burden and sustaining leprosy control activities(2006-10)
  7. 7.  Main elements of the strategy are  Sustain leprosy control activities in all endemic countries  Use case detection as the main indicator to monitor progress  Ensure high-quality diagnosis, case management, recording and reporting and reporting in all endemic communities  Strengthen routine and referral services  Discontinue the campaign approach  Develop tools and procedures that are home/community based, integrated and locally appropriate for the prevention of disabilities/impairments and for provision of rehabilitation services  Promote operational research in order to improve implementation of a sustainable strategy  Encourage supportive walking arrangements with partners at all levels
  8. 8. India  Leprosy was widely prevalent in India  Now out of 611 districts,487 are free from leprosy  A total of 0.87 lakh cases are recorded on 1st April 2008  Prevalence rate is 0.74 leprosy cases/10,000 population
  9. 9. Epidemiological determinants  Agent :  Caused by M. leprae  They have affinity for Schwann cells and cells of the reticulo-endocrine system  The bacterial load is the highest in the lepromatous cases (2 to 7 billion were estimated in one gram of leproma)  Phenolic glycolipid (PGL) is the specific M. leprae  Source of infection  Multibacillary cases imp source of infection  All patients with “active leprosy” must be considered infectious  Man is the only source and host
  10. 10.  Portal of exit  Nose is a major portal of exit  M. leprae are discharged in the nasal mucosa  Can also exit through ulcerated or broken skin  Infectivity  Highly infectious but of low pathogenicity  Can be rendered non – infectious by treatment of 3 weeks  Local application of rifampicin can destroy bacilli within 8 days  Attack Rate  In households 4.4% to 12% is expected to show signs of leprosy within 5 years
  11. 11. Host factors  Age  Infection can take place at any time depending upon the opportunity for exposure  Incidence rates peak between 10 and 20 years of age and then fall  A high prevalence of infection among children means that the disease is active and spreading  Sex  Incidence and prevalence higher in males than in females  Migration  Mostly a rural problem  Due to migration it is causing a problem in urban areas also
  12. 12.  Genetic factors  Human lymphocyte antigen (HLA) linked genes influence the type of immune response that develops
  13. 13. Environmental Factors  Humidity favors survival of M.leprae  Can remain viable in dried nasal secretion at least 9 days  In moist soil at room temp. for 46 days
  14. 14. Modes of transmission  Droplet infection  Aerosols containing M. leprae  Contact transmission  Person to person by close contact (direct or indirect)  Other routes  Insect vectors  Tattooing needles
  15. 15. Incubation period  3 to 5 years or more
  16. 16. Classification  Three types of classification  Ridly and jopling classification  Madrid classification  Indian Classification  Indian classification  Indeterminate type  Tuberculoid type  Borderline type  Lepromatus type  Pure neuritic type
  17. 17.  Ridly and jopling classification  Indeterminate type  Tuberculoid type  Borderline type  Lepromatus type  Pure neuritic type  Madrid classification  Indeterminate type  Tuberculoid type  Borderline type  Lepromatus type
  18. 18. Drugs  Only bactericidal drugs are used  Rifampicin  High bactericidal against M.leprae  Single dose of 1500mg  3-4 consecutive daily doses of 600mg  Side-effects are nausea,abdominal pain,vomiting  Dapsone  Used all over the world for 30years  1-2mg/kg of body weight  Weakly bactericidal effect
  19. 19.  Clofazimine  Synthesized for treatment of TB  Found to have greater value against M.leprae  May give darkish coloration to the skin,urine,sweat  Ethionamide and protionamide  Bactericidal drugs killing 98% of M.leprae in 4-5 days  More expensive and toxic  Used as the 3rd durgs in multibacillary leprosy
  20. 20.  Quinolones  Inhibiting DNA synthesis during bacterial replication  Ofloxacin is most preferable drug in this group  22 doses of Ofloxacin kill 99.9% of viable M.laprae
  21. 21. WHO Recommeneded  For adults  Multibacillary leprosy  Rifampicin-600mg once monthly  Dapsone-100mg daily  Clofazimine-300mg once monthly 50 mg daily  Paucibacillary leprosy  Rifampicin-600mg once monthly  Dapsone-100mg daily for 6 months
  22. 22.  For children 10-14years  Multibacillary leprosy  Rifampicin-450mg once monthly  Dapsone-50mg daily  Clofazimine-150mg once monthly 50 mg daily  Paucibacillary leprosy  Rifampicin-400mg once a day  Dapsone-50mg daily
  23. 23. Estimation of problem  Disease load on the community has to be estimated by surveys  Prevalence can be determined by examining school – age children
  24. 24. Diagnosis  Clinical examination  Integration  Collection of bio data  Family history  History of contact with leprosy case  Previous history of treatment  Present complaint  Physical examination  Inspection of skin  Palpation of commonly involved peripheral and cutaneous nerve  Presence of thickening of nerves  Testing for loss of sensation for heat, cold, pain and touch in skin patches
  25. 25.  Bacteriological examination  Skin smears  Material from the skin obtained from an active lesion and also from both ear lobes  Nasal smears  Best preparation from early morning mucous material  Nasal scraping  Nasal mucosal scrapper is used
  26. 26. Biopsy  When the examination do not yield diagnosis histo- pathological examination may be necessary  It gives an accurate classification of the disease
  27. 27. Immunological tests  Two types of tests  Test for detecting cell mediated immunity  Test for detecting humoral antibodies
  28. 28. Test for CMI  Lepromin test  Injecting 0.1ml of lepromin intradermally  2 types of reaction is seen  Early reaction  Late reaction
  29. 29.  Early reaction  Known as fernandez reaction  Inflamatory reaction seen in 24-48hrs  Tends to disappear in 3-4 days  If the redness is more then 10mm at the end of 48hrs then the test is considered to be positive  Indicates previous sensitisation  Late reaction  Reaction becomes apperent in 7-8 days  Maximum in 3-4weeks  If there is a nodule more then 5mm in diameter then test is positive
  30. 30. LTT & LMIT  Newer in in vitro tests such as lymphocyte transformation test and leucocyte migration inhibition test has been developed  They give a measure of CMI  Used to detect sub clinical infection
  31. 31. Test for humoral response  FLA-ABS test (Fluorescent Leprosy Antibody Absorption Test)  Used to identify sub clinical infections  It is 92% sensitive and 100% specific in detecting M.leprae  Monoclonal antibodies  These against M. leprae antigens have been produced  If antibodies against specific antigens are found, they will become reagent of choice for identifying M. leprae  ELISA test  Based on a phenolic glycolipid (PGL) antigen
  32. 32. Surveillance  Paucibacillary leprosy-recomended to be examined clinically atleast once a year for minimum 2 years  Multibaccilary leprosy-leprosy-recommended to be examined clinically at least once a year for minimum 5 years
  33. 33. immunoprophylaxis  BCG can provide some protection against leprosy  Several alternative vaccines are under development  Called as candidate vaccines  None of them attained “vaccine hood” yet
  34. 34. deformities  If leprosy not treated at an early stage develops deformities  It is due to damage of peripheral nerve trunks or injury from infection to hand and feet's  Paralysis may occur to some muscle
  35. 35. Health Education  Anti-leprosy campaign is incomplete without education  Health education aims at helping people to avoid this type of diseases  It should be direct towards the patient and his/her family  It should educate people on the true facts about leprosy and removes superstation and wrong beliefs and the social stigma associated with leprosy
  36. 36. Social support  Chemotherapy alone is not likely to solve this problem  It needs social support also  Economic and social problems should be identified
  37. 37. Anti-leprosy activates in India  1874-Mission To Leprosy was found by Baily at Chamba in the Himachal Pradesh  After that a lot of organizations are established  Hindu Kusth Nivaran Sangha  Gandhi Memorial Leprosy Foundation  National Leprosy organization(1965)  German Leprosy Relief Association  Damien Foundation  Danish save the child foundation  National Leprosy Control Program(1954) was converted in to Eradication Programme(1983)
  38. 38. Thank you…

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