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LEPROSY By Sriloy Mohanty B.N.Y.S

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Contents… introduction

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INTRODUCTION Chronic infectious disease Surface infection Caused by M leprae Affects mainly the peripheral nerves

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Cardinal features Hypo-pigmented patches Loss of cutaneous sensations Thickened nerves Presence of acid-fast bacilli in the skin or nasal smearSigns 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

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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

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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)

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 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

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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

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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

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 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

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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

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 Genetic factors  Human lymphocyte antigen (HLA) linked genes influence the type of immune response that develops

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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

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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

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Incubation period 3 to 5 years or more

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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

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 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

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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

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 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

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 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

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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

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 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

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Estimation of problem Disease load on the community has to be estimated by surveys Prevalence can be determined by examining school – age children

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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

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 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

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Biopsy When the examination do not yield diagnosis histo- pathological examination may be necessary It gives an accurate classification of the disease

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Immunological tests Two types of tests  Test for detecting cell mediated immunity  Test for detecting humoral antibodies

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Test for CMI Lepromin test Injecting 0.1ml of lepromin intradermally 2 types of reaction is seen  Early reaction  Late reaction

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 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

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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

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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

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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

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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

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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 feets Paralysis may occur to some muscle

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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

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Social support Chemotherapy alone is not likely to solve this problem It needs social support also Economic and social problems should be identified

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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)

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Thank you…