logging in or signing up EPIDEMIOLOGY OF LEPROSY drmhmomin Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 1394 Category: Science & Tech.. License: All Rights Reserved Like it (4) Dislike it (0) Added: June 25, 2011 This Presentation is Public Favorites: 4 Presentation Description No description available. Comments Posting comment... By: psjain07 (21 month(s) ago) very nice Saving..... Post Reply Close Saving..... Edit Comment Close By: gauranggups (31 month(s) ago) hey i neeed this presentation ..pls alow me download ...next to tomarow i have to present it Saving..... Post Reply Close By: drmhmomin (31 month(s) ago) Please send me your e mail address. so that i can send u ppt Saving..... Edit Comment Close By: gaurarohi (31 month(s) ago) very good presentation sir, i have get very good information from that Saving..... Post Reply Close By: gaurarohi (31 month(s) ago) thank u sir for reply, i m Dr. Gaurav Desai, 2nd year resident, community medicine department, SBKS MI & RC, Piparia, Vadodara. i also request u sir to send me your presentation... my email id- email@example.com By: drmhmomin (31 month(s) ago) Thanks please give your introduction Saving..... Edit Comment Close By: john4william (31 month(s) ago) good one Saving..... Post Reply Close By: drmhmomin (31 month(s) ago) Thanks if u will give your intro it will be better Saving..... Edit Comment Close By: pbansalpsm (34 month(s) ago) excellent presentation. i want to teach the same to MBBS students. Saving..... Post Reply Close By: drmhmomin (34 month(s) ago) Thanks if u will give your intro it will be better Saving..... Edit Comment Close Premium member Presentation Transcript Leprosy Anti Leprosy day 30th January: Leprosy Anti Leprosy day 30th January DrMuhammedirfan H. Momin Assistant Professor Community Medicine Department Government Medical College Surat.Slide 3: Leprosy Leprosy is a chronic, infectious, slow-developing disease. Affecting mainly the peripheral nerves and the skin. Caused by bacteria , known as Mycobacterium leprae .Slide 4: Though it is highly infectious disease , but we are not getting too many cases in the society , because these bacilli are having very Low Pathogenicity (Capacity to produce clinical form of disease )Slide 5: History :History Appears in an Egyptian Papyrus document written around 1550 B.C. Around 600 B.C. In Europe, leprosy first appeared in the records of ancient Greece after the army of Alexander the Great. For a long time leprosy was thought to be a hereditary disease, a curse, or a punishment from God 1873: :1873: Dr.Armauer Hansen of Norway was the first person to identify the germ that causes leprosy under a microscope. early 20th century: :early 20th century: Until the late 1940s, leprosy doctors all over the world treated patients by injecting them with oil from the chaulmoogra nut. 1941: :1941: Promin, a sulfone drug, was introduced as a treatment for leprosy.Slide 6: Leprosy is most important disease because: It has potential to cause permanent and progressive physical disability . The disease & its visible disabilities , contribute to social discrimination of patients. Why Leprosy is an important disease ?Slide 7: With long incubation period between 9 months to 20 years, after infection leprosy can affect all age groups. The signs and symptoms may vary between PB to MB depending upon the degree of patient’s immunity to M. leprae , the causative agent.Slide 8: The early detection and prompt treatment of Leprosy with prescribed MDT not only cures Leprosy but also interrupts its transmission to others.Slide 9: Leprosy is caused by Mycobacterium leprae , which was discovered in 1873 by G.H.Armauer Hansen at Bergen in Norway. These Mycobacterium leprae are pleomorphic , straight or slightly curved, rod – shaped gram positive micro - organisms. They may appear like solid rods, fragmented or granular.Slide 10: The presence of the bacilli can be demonstrated by taking skin smears , and after staining with Zeihl Neilson stain , these bacilli can be seen under microscope. As per GOI and WHO guidelines , skin smear examination has now been stopped . Leprosy Patients Skin Smear Positive Skin Smear Negative Infective Non InfectiveHost Factors.: Host Factors . 95% population naturally immune to leprosy in India Age Distribution: 10 -20 years ,acquired infection commonly during childhood but can occur at any Age. (Any Age) Gender wise distribution: Male > Female Migration :- mostly a rural problem because of migration problem in urban area also.Host Factors.: Host Factors . Distribution by ethnic factors Europeans, Chinese and Burmese belong to a ‘highly susceptible' group as compared with Africans, Indians and Malaysians. Mortality Leprosy is rarely an immediate and direct cause of death.Environmental Factors: Environmental Factors Socio-Economic Factor: Poverty Related Factors: Overcrowding, Lack of hygiene, Lack of ventilation Improved socio-economic conditions Migration: Affecting elimination & Major cause of spread of leprosy Fear of Stigma & discriminationSlide 14: 1943 - Dapsone introduced in treatment of leprosy. 1955- GOI, Started NLCP based on Dapsone domiciliary treatment 1983- MDT introduced in the programme NLEP launched 1991- World Health Assembly resolved to eliminate Leprosy as public Health problem by the year 2000 2001 – Process of Integration of NLEP into GHCS started 2005 (Dec) - India achieved elimination at National level Milestones in NLEP in IndiaSlide 15: Elimination was defined as achieving a prevalence rate of less than one per 10,000 population, clearly an ambitious target. Global Leprosy Situation: Global Leprosy Situation LEPROSY HAS BEEN ELIMINATED FROM THE WORLDLeprosy: 6 top countries: Leprosy: 6 top countries 6 top endemic countries: India, Brazil, Myanmar, Madgascar , Mozambique, Nepal contribute 85% of global case load: (69% from India) • 91% of global case new cases (81% from India)Slide 18: Current Status India (March 31, 2008) New cases detected- 1.38 lakh (2007-08) ANCDR - 11.70/ lakh pop Cases: 31 st Mar 08 -0.87 lakh PR: 0.74/10,000 pop MB 47.2%, Female 34.5 %, Child 9.4%, GII disability 2.5 %Slide 19: Trend of Leprosy Prevalence & Annual New Case Detection (ANCDR) RatesSlide 20: As on 1 st April 2008 the Five endemic states are as follows: 1. Bihar (1.81), 2. Chattisgarh (1.6), 3. Jharkhand (1.68), 4. Chandigarh (1.14), 5. West Bengal (1.82)State wise Contribution New Leprosy Cases - year 2007-08: State wise Contribution New Leprosy Cases - year 2007-08 Contribution by six states 20.8% pop & 34.5% new casesSlide 22: Navsari Valsad – 2. 18 Dang – 4.26 Surat - 1. 39 Narmada - 1.26 Bharuch Vadodara – 1.10 PM 2.22 Dahod- 2.25 P.R.- 0.87 2.77 2. 04 Endemicity of Leprosy – March.09 > 5 2 - 3 1 - 2 < 1 P.R. 3 - 5 Gujarat achieved elimination as on Oct-04Slide 23: India Gujarat (2005-06) (2007-08) State Population 1131431383 58239804 No. of Districts 596 25 Prevalence Rate of Leprosy per 10,000 Populations 0.84 0.82 Districts with PR < 1 439 16(64%) Districts with PR > 1 157 9 (36%) New Cases Detected 161457 7228 New Case Detection Rate 1.43 1.24Situation in Surat:: Situation in Surat: The prevalence rate 1.44 by 2006 . The new case detection rate 2.57 in the year 2006. Male:female ratio as 58:42 (2006). Child cases among new cases of leprosy 12.8% (2006). Multibacillary cases among new cases 50.1%, 2006. Grade II disability 1.38% (2006).Slide 26: Source of Infection : Man is the only known source for M.leprae. Among human beings it is the untreated MB leprosy patient who acts as a source of infection. Spread of LeprosySlide 27: The occurrence or the non – occurrence of the disease is closely associated with the cell – mediated immune response of the host , to the challenge by the Leprosy bacillus.Slide 28: Transmission of Leprosy : Leprosy is transmitted from one untreated Multibacillary patient to another person via mainly the respiratory tract or skin. Portal of Exit : The major sites from which bacilli escape from the body of an infectious patient are the nose.Slide 29: Lepromatous patients in their nasal secretions can excrete as much as 10 million viable organisms per day. Viability of M. Leprae outside the human host : M. Leprae can survive up to 7 to 9 days in nasal secretions , in shady places .Slide 30: Portal of Entry : As such portal of entry of M. Leprae into human body is not definitely known, the two portals of entry seriously considered are the skin and the upper respiratory tract. Although entry through respiratory route appears most probable, other routes, particularly broken skin, cannot be ruled out.Slide 31: The period between the time of entry of the organism and the time of onset of clinical signs is called incubation period. As such, in Leprosy, these two reference points for measuring the incubation period are difficult to define. The former ( Time of entry of the organism ) because of the lack of adequate immunological tools and the latter ( time of onset of clinical signs ) because of the insidious nature of the onset of Leprosy.Slide 32: The incubation period in Leprosy is variable. It could be as small as 6 months or as long as 30 years. It is believed that the incubation period could be an average of 3 – 5 years .Slide 33: Diagnosis of leprosy can be done on the basis of cardinal signs. Presence of any one of the cardinal signs is sufficient to diagnose. Absence of any cardinal sign , after few months of treatment , does not rule out Leprosy. Cardinal SignsSlide 34: Hypo pigmented or reddish colour skin patch (es) with definite loss of sensation . Definite loss of sensation includes Complete Loss of sensation & Partial Loss of sensationSlide 35: 2. Thickness and / or tenderness of peripheral nerves.Slide 36: 3. Demonstration of acid-fast bacilli in skin smears .Slide 37: Out of these three cardinal signs , presence of any one is sufficient to diagnose a case of Leprosy. As per GOI and WHO guidelines , skin smear examination has now been stopped . Now only two cardinal signs are available to diagnose a case of Leprosy.Slide 38: Once you diagnose a case of Leprosy, then you have to examine the patient thoroughly.Slide 39: Clinical Examination includes : 1. Case History. 2. Skin Examination 3. Nerve Examination Clinical ExaminationSlide 40: Remember the cardinal sign : Loss of sensation on patch is a cardinal sign of Leprosy ( PB Leprosy ) . It may or may not be present in MB Leprosy ( BL & LL ). Hypo pigmented or reddish colour skin patch(es) with definite loss of sensation . ( B ) Skin Examination :Slide 41: While doing skin examination , you may find any of the followings : 1. Flat patch 2. Raised Patch or Plaque 3. Diffuse infiltration 4. NodulesSlide 42: The simplest and quickest way : To use the tip of your finger to touch the patient. Testing for Anaesthesia Using your ring or little finger pulp, touch the patient very gently. If you can feel it, he should be able to do so also.Slide 43: Remember the cardinal sign : Thickness and / or tenderness of peripheral nerves. ( C ) Nerve Examination : In the absence of any other signs of leprosy on skin , nerve thickening alone without sensory loss and / or muscle weakness , is often not a reliable sign of Leprosy .Slide 44: Principles of Nerve Palpation : This involves two aspects : 1. Palpation of Nerves for thickening or tenderness. 2. Assessment of Nerve function.Slide 45: The ‘ sites of predilection ’ at which the peripheral nerves are most commonly enlarged and palpable in Leprosy.Slide 46: Nerve function assessment is useful to identify any impairment of nerve function . 2. Assessment of Nerve Function : Identification and management of impaired nerve function is important for prevention of disability in Leprosy patients . 2. Assessment of Nerve Function :Bacteriological Examination: Bacteriological Examination Skin smears Nasal smears Nasal scrapings Bacterial Index :- indicates the density of leprosy bacilli in smears and include both living (solid staining) and dead (fragmented)bacilli. Morphological index :- The percentage of solid (living) staining bacilli in a stained smear referred to as MI. Foot pad culture Hisatamine test Biopsy Immunological Tests (Lepromin test)Slide 48: Classification of Leprosy Classification of Leprosy WHO Classification Clinical ClassificationSlide 49: WHO Classification : As per WHO classification, Leprosy is classified into two types for the purpose of treatment . This classification is based on the number of skin lesions and nerve involvement . 1. Paucibacillary Leprosy ( PB ) 2. Multibacillary Leprosy ( MB )Slide 50: Skin Lesions : Paucibacillary Leprosy ( PB ) 1 to 5 lesions Asymmetrical Definite Loss of sensation > 5 lesions Towards Symmetrical Loss of sensation ( May be / May not be )` Nerve Lesions: Only 1 nerve involved 2 or more nerve involved Multibacillary Leprosy ( MB )Slide 51: Clinical Classification : Ridley and Joppling classified leprosy clinically into the following : 1. Tuberculoid ( TT ) 2. Borderline Tuberculoid ( BT ) 3. Mid Borderline ( BB ) 4. Borderline Lepromatous ( BL ) 5. Lepromatous ( LL ) BB Leprosy is immunologically the least stable , and therefore the rarest .Slide 52: Pure Neural Leprosy : In all forms of leprosy , at least one peripheral nerve is attacked by M. Leprae , though this may not have any clinical evidence . Leprosy can involve nerves without any skin changes . This unusual occurrence is called Pure Neural Leprosy . Paucibacillary leprosy(PBL): Paucibacillary leprosy(PBL) From “Leprosy” book by Yawalkar 2002Multibacillary leprosy(MBL): Multibacillary leprosy(MBL) From “Leprosy” book by Yawalkar 2002Leprosy: Leprosy Figure 22.8Slide 60: Hypopigmented flat patch Well defined borders BI - 0Slide 91: Lepromatous LeprosySlide 92: Lepromatous LeprosySlide 93: Lepromatous LeprosySlide 94: Lepromatous LeprosySlide 95: Lepromatous LeprosySlide 96: Lepromatous LeprosySlide 97: PB MB PB MDT 1. Rifampicin 2. Dapsone MB MDT 1. Rifampicin Dapsone Clofazimine Duration of treatment 1 year 6 months Treatment for LeprosySlide 98: MDT Drugs : * Rifampicin is the most important drug and highly bactericidal. Therefore, it is included in the treatment of both types of Leprosy. * Clofazimine and Dapsone are mainly bacteriostatic drugs but they have very very low bactericidal action also.Slide 99: Clofazimine A weak Bacteriocidal Mode of Action : * Interferes with DNA metabolism of M.leprae. * Has anti-inflammatory property if given in high doses. * It is anticholinergic, hence there is loss of sweating resulting in dry skin. Dose : 50 mg daily in adults. Side effects : ( Uncommon ) * Reddish brown discolouration of skin . ( dose related-reversible ) * Ichthyosis. * Abdominal pain while on large doses for a long period.Slide 100: Dapsone A weak Bacteriocidal Mode of Action : * Interferes with folic acid metabolism of M.leprae. Dose : 1-1.5 mg / kg body wt. daily Side effects : ( Uncommon ) * Drug hypersensitivity . * Hepatotoxicity * Exfoliative dermatitis ( Dapsone syndrome ) * Haemolytic anaemia.Slide 101: MDT should not be given when there is : 1. Jaundice : If the patient has jaundice, you will have to wait till the jaundice subsides. 2. Anaemia : If the patient is anaemic, treat the anaemia first. Enquire... Before starting MDTSlide 102: 3. Tuberculosis : If the patient is taking Rifampicin, ensure that he continues to take Rifampicin in the dose required for the treatment of Tuberculosis along with other drug regimen required for the treatment of Leprosy. 4. Allergy to Sulpha Drugs : If the patient is known to be allergic to Sulpha drugs, Dapsone should be avoided.Slide 103: PB MDT ( Adult ) : Supervised dose on day 1 At clinic Rifampicin 600 mg Dapsone 100 mg Unsupervised dose- At home : Dapsone 100 mg daily for 27 daysSlide 104: MB MDT ( Adult ) : Supervised dose on day 1 Rifampicin 600 mg Clofazimine 300 mg Dapsone 100 mg Unsupervised dose : Clofazimine 50 mg daily Dapsone 100 mg daily , both for 27 daysSlide 105: PB MDT ( Child 10 –14 yrs. ) : Supervised dose on day 1 Rifampicin 450 mg Dapsone 50 mg Unsupervised dose : Dapsone 50mg daily for 27 daysSlide 106: MB MDT ( Child 10 –14 yrs. ) : Supervised dose on day 1 Rifampicin 450 mg Clofazimine 150 mg Dapsone 50 mg Unsupervised dose : for 27 days Clofazimine 50 mg on alternate days Dapsone 50 mg dailySlide 107: Lesions of BB Leprosy Before starting treatment Lesions of BB Leprosy After treatmentSlide 108: Lesions of BB Leprosy Before starting treatment Lesions of BB Leprosy After treatmentSlide 109: After stopping the treatment , advice the patient to report to clinic in case of any event like reappearance of patches or nerve pain. Side Effects of Anti Leprosy Drugs Practically No side effects in the doses and duration given in WHO regimens.Slide 110: Leprosy reaction is an acute inflammatory event occurring in the course of the disease, which produces painful symptoms. Reactions in LeprosySlide 111: The occurrence of Leprosy reactions are not MDT drug reaction & also does not mean that MDT drugs are not being effective, and therefore, MDT should not be stopped during the reaction.Slide 112: Reactions are the part of the natural course of the disease and can occur frequently and may be severely damaging in untreated Leprosy. Treatment with Leprosy significantly reduces the frequency and severity of the reactions.Slide 113: Type 1 Lepra Reaction Inflammation in existing patch Borders are raised and clear .Slide 114: Type 1 Lepra Reaction Inflammation in existing patches Borders are raised and clear . Oedema over hands .Slide 115: Type 1 Lepra Reaction Inflammation in existing patches Borders are raised and clear .Slide 116: Type 1 Lepra Reaction Inflammation in existing patches Borders are raised and clear . Inflammation in great auricular nerve also .Slide 117: Type 2 Lepra Reaction ENL nodules on faceSlide 118: Type 2 Lepra Reaction ENL nodules on Fore arm & front of chest.Slide 119: Type 2 Lepra Reaction Pustular ENL nodule Pink coloured ENL nodules on the backSlide 120: Type 2 Lepra Reaction ENL nodules on faceSlide 121: Type 2 Lepra Reaction ENL nodules on faceSlide 122: Type 2 Lepra Reaction Pink coloured ENL nodules on both hands Few ENLs show desquamationSlide 123: Management of Lepra Reactions 1. Continue anti – leprosy treatment 2. Rest - Physical rest - Mental rest - Rest to the affected part ( nerve ) 3. Care of the pain – Analgesics & Anti – inflammatory 4. Corticosteroid Therapy 5. Other anti – reactional drugs : Clofazimine, Thalidomide 6. Surgery – For recurrent neuritis not responding to corticosteroidSurveillance: Surveillance (a) PB Leprosy :- at least once a year for a minimum of 2 years after completion of treatment (b) MB Leprosy :- at least once a year for a minimum period of 5 years after completion therapy.Immunoprophylaxis: Immunoprophylaxis BCG vaccine can provide protection against clinical leprosySlide 126: Disability in LeprosySlide 127: Most of the disabilities that occur in Leprosy are preventable. Therefore, it is very important to prevent these disabilities from occurring. Leprosy is associated with intense stigma because of the disabilities and deformities that result from Leprosy.Slide 128: Primary – These disabilities occur as a direct result of a nerve damage ,or Invasion of bacilli. e.g. loss of sensation , claw hand etc. Secondary – These occur as a result of neglected primary disabilities . e.g. Non healing planter ulcer , contractures etc. There are two types of disabilities in Leprosy :Slide 129: Disability Primary Direct result of Secondary OR Result of Neglected Primary Disability Nerve Damage Bacterial InvasionSlide 130: Primary Disability Motor fibres Sensory fibres Autonomic fibres Paralysis Anaesthesia Dryness Bacterial Invasion of tissues Saddle Nose Loss of eyelashes Loss of eyebrow Leonine Face Thickened Earlobes Nerve Damage M a y o c c u r I n Leads to Leads to Leads toSlide 131: Illustrations of Primary DisabilitySlide 132: Lagophthalmos : Inability to close the eyes due to paralysis of zygomatic branch of facial nerveSlide 133: Ulnar Claw Clawing of little and ring finger , due to involvement of ulnar nerveSlide 134: Total Claw Hand Clawing of all the fingers , due to involvement of ulnar nerve , and median nerveSlide 135: Wrist Drop Dropping of wrist , due to involvement of radial nerve .Slide 136: Claw Toes Clawing of all the toes due to involvement of posterior tibialis nerveSlide 137: Primary Disability Secondary Disability Result of Neglected Primary DisabilitySlide 138: Ulcers in hand : Patient is having anaesthesia in hand , and therefore has developed ulcers due to contact with hot objects .Slide 139: Non healing ulcers in feet : Patient is having anaesthesia in soles of feet , and therefore has developed ulcers due to pressure on pressure points .Slide 140: Prevention of Disabilities ( POD )Slide 141: FOOTWEAR (MCR)Slide 142: Protective footwear for insensitive feet Characteristics of ideal footwear : Have a soft insole to provide padding / cushion. Have a hard outer sole to prevent pins / thorns from piercing the foot. Have adjustable straps. Be well fitting. Be culturally and cosmetically acceptable. Deformed feet will require specially designed footwear.Slide 143: No. of Total RCS Camps :14 No. of Total Operations:6307 During current year regular RCS are being done. Reconstructive Surgery Activities under DPMR Before During RCS AfterSlide 144: Elimination of Leprosy, & IntegrationSlide 145: It is well known that two initiatives : 1. The introduction of WHO recommended MDT in the 1980s and 2. The 1991 resolution of World health assembly to eliminate Leprosy as a public health problem made possible the remarkable progress the world has seen in the battle against Leprosy. Elimination of LeprosySlide 146: Elimination : Now, our goal is to achieve elimination of Leprosy as a public health problem in India. Elimination of Leprosy aims at reducing the disease burden to very low levels so that after reaching such low levels the disease will disappear over a period of time. This very low level has been defined by WHO as a level of prevalence of less than 1 case per 10000 population.Slide 147: Elimination is the achievement of low levels of disease ( prevalence less than 1 case per 10000 population ) while Eradication has a more precise meaning. Making total disappearance of the organism for complete stopping of transmission of disease is Eradication. Elimination of Leprosy Elimination Vs. Eradication :Slide 148: Eradication aims at : 1. Zero disease 2. Zero transmission 3 Zero disease agent in the world In the case of Leprosy, eradication is not possible in view of limitations of technology, neither is it necessary as Leprosy, unlike other diseases like Small pox and Poliomyelitis, is not likely to result in outbreaks and widespread dissemination after reaching very low levels of prevalence.Slide 149: Simplified Information System ( SIS )Slide 150: Following are the indicators which are essential for monitoring of elimination of Leprosy : Elimination IndicatorsSlide 151: 1. Prevalence Rate ( P. R. ) 2. A. New Case Detection Rate ( N. C. D. R. ) 3. Child proportion among new cases 4 .Visible deformed case proportion among new cases 5. MB proportion among new cases 6. Female proportion among new casesSlide 152: 7. SC new case detection rate 8. ST new case detection rate 9. Patient month blister calendar packs stock 10. Proportion of health sub – centres providing MDT 11. Absolute number of patients made RFTSlide 153: 1. Prevalence Rate Total number of Leprosy cases on treatment at a given point of time in a PHC area is known as Prevalence rate. P. R. = X 10000 Total no. of Leprosy cases on treatment Total Mid – year population of PHCSlide 154: 2. Annual New Case Detection Rate The total number of cases newly detected during a year in an area is known Annual New Case Detection Rate. N. C. D. R. = X 10000 Total no. of Leprosy cases newly detected Total Mid – year population of PHCSlide 157: Thank You You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.