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Leprosy
This document provides an overview of leprosy (Hansen's disease), including: - It is caused by Mycobacterium leprae bacteria and primarily affects nerves and skin. - Signs include pale skin lesions with reduced sensation. Advanced cases show disfigurements like clawing of hands/feet. - Leprosy has affected humans for thousands of years and treatments now cure most cases. - It is classified and treated differently depending on bacterial load and symptoms. Multi-drug regimens including rifampin are usually effective. - Prevention relies on early detection, treatment, health education, and social support for those affected. While rates have declined greatly, ongoing efforts are needed for full control
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Leprosy
- 1. LEPROSY By Sriloy Mohanty B.N.Y.S
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- 3. INTRODUCTION Chronic infectiousdisease Surface infection Caused by M leprae Affects mainly the peripheral nerves
- 4. Cardinal features Hypo-pigmentedpatches 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. History Oldest diseaseknown 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. 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. Main elementsof 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. India Leprosy waswidely 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. 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. Portal ofexit 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. 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. Genetic factors Human lymphocyte antigen (HLA) linked genes influence the type of immune response that develops
- 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. 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. Incubation period 3to 5 years or more
- 16. Classification Three typesof classification Ridly and jopling classification Madrid classification Indian Classification Indian classification Indeterminate type Tuberculoid type Borderline type Lepromatus type Pure neuritic type
- 17. Ridly andjopling classification Indeterminate type Tuberculoid type Borderline type Lepromatus type Pure neuritic type Madrid classification Indeterminate type Tuberculoid type Borderline type Lepromatus type
- 18. Drugs Only bactericidaldrugs 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. 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. 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. WHO Recommeneded Foradults 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. For children10-14years 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. Estimation of problem Disease load on the community has to be estimated by surveys Prevalence can be determined by examining school – age children
- 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. 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. Biopsy When theexamination do not yield diagnosis histo- pathological examination may be necessary It gives an accurate classification of the disease
- 27. Immunological tests Twotypes of tests Test for detecting cell mediated immunity Test for detecting humoral antibodies
- 28. Test for CMI Lepromin test Injecting 0.1ml of lepromin intradermally 2 types of reaction is seen Early reaction Late reaction
- 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. 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. Test for humoralresponse 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. Surveillance Paucibacillary leprosy-recomendedto 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. immunoprophylaxis BCG canprovide some protection against leprosy Several alternative vaccines are under development Called as candidate vaccines None of them attained “vaccine hood” yet
- 34. deformities If leprosynot 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. Health Education Anti-leprosycampaign 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. Social support Chemotherapyalone is not likely to solve this problem It needs social support also Economic and social problems should be identified
- 37. Anti-leprosy activates inIndia 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)
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