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Leprosy
Main features
• Chronic infectious disease – mycobacterium leprae
• Affects peripheral nerves / skin muscles. Eyes, bones, testes and internal organs
• 2 polar forms
Lepromatous……borderline….indeterminate…..tuberculoid
Signs
• Hypo pigmented patches
• Partial or total loss of cutaneous sensation in affected areas
• Thickened nerve
• Acid fast bacilli in skin or nasal smears
• Advanced disease; lumps in face, ears/ plantar ulcers/loss of fingers and toes/ nasal depression/ foot drop / claw toes etc
history
• Oldest disease• Lepra = scaly• Kushta roga- curse
• 1837 M leprae discovered by Hansen of Norway
• 60s and 70s discovered in Mice foot and armadillos
• 1980s mono to multi drug therapy
90% reduction in prevalence
Reasons for decrease in prevalence since 1966
• Improved management of cases
• Very low relapse rate
• High cure rates
• Absence of drug resistance
• Shorter duration of treatment with MDT
• Global Leprosy program moved from Geneva to Delhi in 2005 for SEAR has the highest numbers
WHO global strategy for decreasing disease burden and sustain leprosy control activities
• 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 in endemic countries• Strengthen routine referral services• Discontinue campaign approach• Tools and procedures that are home / community based,
integrated and socially appropriate for prevention of disabilities etc
• Promote Operational Research to improve implementation• Supportive working arrangements with partners at all
levels
http://mohfw.nic.in/National_Leprosy_Eradication_Programme/CURR_SIT.htm
Level of Elimination of leprosy (<1 case / 10K) on 31 Dec 2005
Annual new case detection rate 1.43 / 10K
Focus on High priority districts and blocks> 5 / 10K,
Disability rate 1.9%
Child proportion 10% (TN,AP, Bihar, Gujar,
Jharkand, Maharashtra, kerala, karnataka)
Epidemiological determinants- agent
• M leprae= acid fast. Extra and intra cellular• Bacterial load 1 gm of leproma- 2-7 billion• Pathogenic• Non pathogenic- M tb, BCG etc• Grows in animal= mouse / armadillos but not in
artificial medium• Source- all active cases. Esp lepromatous leprosy• Portal of exit- nose. Also ulcerated skin• Highly infections. Low pathogenic• Attack rate- 4.4 to 12% • symptomatic in 5 yrs
Epidemiological determinants- host
• Any age. Both sexes. 2.5yr baby too (active and spreading)
• Prevalence pool/ migration
• Inactivation of the disease
• Immunity – cell mediated
• Genetic factors- HLA linked genes influence the type of response
Epidemiological determinants- environment
• Presence of infectious cases• Overcrowding and lack of ventilation
Mode of transmission• Droplet• Contact• ? Insect vectors/ tattooing needles• Incubation period 3- 5 yrs for lepromatous and
less for Tuberculoid leprosy
Indian Classification
Indeterminate 1-2 patches. Sensory impairment
Bact
negative
Tuberculoid 1-2 well defined flat/ raised/hypo pig/ erythematous
Anaesthetic Bact
negative
Borderline 4 or more lesions others same as above. Usually progresses to lepromatous
anaesthetic positive
Lepromatous Diffuse infiltration or numerous other types
anaesthetic positive
Pure neuritic No skin lesion
Has only nerve involvement
negative
MADRID classification • Indeterminate• Tuberculoid -flat/ raised• Borderline• Lepromatous
RIDLEY JOPLING ( immuno histological)Tuberculoid TLBorderline Tuberculoid BTBorderline BBBorderline Lepromatous BLLepromatous LL
Clinical classification
• Pauci bacillary :1-5 lesions
• Multi bacillary: : More than 5 lesions
Obstacles
• lack of a specific and sensitive diagnostic tool,
• social stigma
• and the potential reservoir in armadilloes
Diagnosis
Clinical examination•Case taking /Interrogation•Physical examination
Bacteriological examination•Skin smear- active lesion, and ear lobe•Nasal smears or blows•Nasal scraping
Bacterial Indexnumber of bacilli in oil immersion fields (OIF) in an
average microscopeHelp in monitoring
0 No bacilli 100 OIF
1+ 1 or<1 in each mic field
2+ Bacilli found in all the fields
3+ Many bacilli in all the fields
Bacterial Index= total of indices / number of sites examinedTotal number of + in 7 sites-4 skin lesions, 1 nasal swab, both ear lobes
Pauci bacillary 2Multibacillary>2
Solid -fragmented- granular percentage
• Indicator of patient's response to treatment during the first few months--
• 200 pink stained free standing bacilli have to be counted
• Total of Mis for all sites / number of sites+ average MI for the body.
Solid rods: Uniform staining of entire organism/ parallel sides, rounded end length 5 times the width - Viable
Solid -fragmented- granular are given separately
Better indicator of response
Foot pad culture
• Inoculate material into foot pads of mice
• Demonstrate its multiplication
• 10 times more sensitive than slit skin smears- 6-9 mths
• Macrophage culture: 3-4 wks
• Helpful to detect drug resistance
• Evaluate potency of anti leprosy drugs
• Viability of baciili during treatment
Histamine test
• Detecting at an early stage peripheral nerve damage due to leprosy
• Inject 0.1 ml of 1:1000 solution of histamine phosphate or chlorhydrate in hypo pigmented patches or anaesthetic patches flare response is lost
• Indeterminate leprosy
Biopsy• Of skin• Of nerve
Immunological tests• For detecting cell mediated immunity• Tests for humoral antibodies
CMI Tests : Lepromin TestLepromin is a suspension of killed M leprae obtained from infected
human or armadillo tissue. Mitsuda / DharmendraInject Lepromin O.1 ml inner aspect of forearm . Following intradermal inoculation, Read linke for PPD• early (48 h, Fernandez) reactions and late (3-4 wk, Mitsuda)
reactions may be seen.10 mm mild 15-20 mod >20 strong• The Mitsuda reaction, a granulomatous response to the antigen,
is more consistent. 3-4 weeks.Patients with TT or BT leprosy have strong positive (>10 mm) responses,
PATIENTS WITH L L DISEASE DO NOT RESPOND.The test is not useful in the diagnosis of leprosy because most of
the population in both areas of endemic and nonendemic disease are Mitsuda positive.
The lepromin test is a guide to the cell-mediated immunity of the individual.
CMI= cell mediated immunity
• lymphocyte transformation test (LTT) and
• lymphocyte migration inhibition test (LMIT).
Response decreases steadily in the progression from subpolar TT to subpolar LL leprosy
CMI tests…
Leprosy ControlMedical measures
1. Estimation of problem
2. Early case detection
3. Multi drug therapy
4. Surveillance
5. Immuno prophylaxis
6. Chemo prophylaxis
7. Deformities health education
Leprosy control ( contd)• Social support
• Program management
• Evaluation
GOALS
1. To interrupt transmission reduce incidence
2. To treat patients.. cure.. rehab
3. To prevent formation of associated deformities
Estimation of the problem
1. Epidemiological survey
2. Random sample surveys
Prevalence among all school age children x 4 = average prevalence in the community
II.Early case detection
Aim: identify and register all cases
• Involve primary health care workers• Active community participation
Methods• Contact survey- household• if 1 per 1000 Group survey..school/slum/military• if prevalence is10 or more per 1000 :Mass surveys
House to houseRecords; standardised:. Use WHO format
Iceberg disease
III Multi Drug therapy- MDT
• Mainstay of control
• Drug resistance leprosy due to monotherapy
• Relapse of disease
Therefore MDT. Shorter treatment
Objectives:
1. To interrupt transmission by sterilizing infectious patients as rapidly as possible by bactericidal drugs
2. To ensure early detection and treatment of cases to prevent deformities
3. To prevent drug resistance
Definitions
1. Case of leprosy- person showing clinical signs with or without bacteriological confirmation, and who has not completed MDT
2. Pauci bacillary: A person with 1-5 skin lesions and/or only 1 nerve involvement
3. Multi bacillary ; A person having 6 or more skin lesions and /or more than1 nerve involvement
4. Adequate treatment: completion of regimen of multi drug therapy –
• 6 mthly doses within 9 mths for paucibacillary and • 12 mthly doses within 18 mths for multi bacillary
contd
Regular treatment: Received MDT for at least 2/3rd of the months in any interval of time
Newly diagnosed case- Diagnosed as a leprosy case and who has not taken MDT in the past
Defaulter case: A leprosy patient on MDT who has not collected treatment for 12 consecutive months
Relapsed case: successfully completed an adequate course of MDT and who subsequently develops new signs and symptoms of the disease, within during the surveillance period or thereafter.
Principles of treatment
1. Stop the infection with chemotherapy
2. Treat reactions
3. Educate the patient about leprosy
4. Prevent disability
5. Support patient socially and psychologically
DrugsName Description
Rifampicin Bactericidal -Hepatotoxic -Observe patient 1 hr after giving the drug
600mg -3 days1500 stat dose
Dapsone
DDS
Mild bactericidal.in 90 days make non infective
Haemolytic anemia, meth hb DDS syndrome
1-2 mg/kg; 100 mg OD
Clofazimine
CLF
Anti leprosy anti inflamm. Expensive. Red colouration
300 mg once a mth
Ethionamide/ protionamide
Bactericidal more expensive and toxic than DDS. Use if CLF is un acceptable
Quinalone-ofloxacin
Bactericidal. GI side effects
minocycline Inhibits bact protein synthesis CI children pregnancy
Clarithomycin Bactericidal. useful In LL
WHO Recommended regimensAdults
monthly / daily / bothMulti bacillary:
• Rifampicin-600mg monthly under supervision x 12 mths
• DDS 100 mg OD x 12 mths
• CLF 300 mg mthly supervised and 50 mg OD- for 12 mths
Pauci bacillary
• Rifampicin-600mg monthly x 6 months supervised
• DDS 100 mg OD x 6 mths
WHO Recommended regimensChildren
Multi bacillary:
• Rifampicin-450mg mthly under supervision x 12 mths
• DDS 50 mg OD x 12 mths
• CLF 150 mg mthly supervised and 50 mg alt days for 12 mths
Pauci bacillary
• Rifampicin-450mg x 6 mths supervised
• DDS 50 mg OD x 6 mths
Defaulters
• Not registered as new cases
Start a new course if she has red raised lesion/ new skin lesion/ new nerve involvement/ lepra nodules/ ENL or reversal reaction
• Drugs Shd be continued in pregnancy• Can be given to HIV positive persons• Tb, anemia
Lepra reaction
Immunologically mediated episodes. Involve nerves. Can cause deformities if not treated
1. Reversal – Type 1 Delayed Hypersensitivity reaction CMI. Usually in borderline BT BL BB cases.
2. Erythema nodosum leprosum- Type II (mild/severe) Immune complex deposition. BL and LL patients
Nodules, neuritis,High fever, ulcers and pustular, involve other organs-eye, testis, lymph node joints
• More with mono therapy than MDT• Treat with Prednisolone 12 weeks only. CLF
TYPE 1
Reversal reaction
TYPE 2 ENL
Relapse
Time interval Occurs with chemo and within 6 mths of stopping treatment
Only when chemo is discontinued after abt 5 mths
Onset Abrupt Slow Insidious
Old lesions Edematous, erythematous tender Not tender
New lesions Several appear Minimal
Ulceration May possible
Nerve involvement
Multiple+ painful and tender.Loss of nerve function
Single nerve. Painless
Gen condn May have fever jt pains. malaise Not usual
Response to steroids
Rapid Nil. Use Clofazamine
Surveillance To detect long term success and detect relapsePauci bacillary: Once an year x 2 yrsMulti bacillary : Once an year x 5 yrs
Immuno prophylaxisBCG vaccine – varying results 23-30-80%
Chemo prophylaxis
• DDS : 1-4 mg/kg for child contacts
protects 35-53%
Given 3 yrs or till index case becomes bact Neg.
ICRC – effective for 8 yrs
• Acdapsone : Inj once in 10 wks long term or short term 7 mths
• Rifampicin ??
DeformitiesCause: • Disease process- eye brows, facial• Paralysis of muscles due to nerve damage-lag ophth, claw hand, foot
drop• Injuries infection of hands and feet- mutilation, corneal ulcer
Hands and feet Eyes
Grade 0 No anaesthesia. No visible deformity
No eye problem / vision defect
Grade I Anaesthesia+
No visible deformity
eye problem present
vision defect absent
Grade II Visible deformity/ damage Severe visual impairment, lag ophthalmos, iridocyclitis and corneal opacity
Plantar ulcer
Claw hands
Prevent these by lots of care …
Preventive rehabilitation
Health education- patient / family / public
Treat by prosthesis/ surgery
Protect people at risk
Social support
Key Messages Hypopigmented patch with loss of sensation could be leprosy Like any disease Leprosy is caused by germs Leprosy is non hereditary 80% do not spread to others It is completely curable Early detection and sustained treatment Become non infectious soon after treatment is commenced Need kindness and empathy Free treatment Not a poor man’s disease Community support is essential for eradication
17 states have achieved Leprosy elimination
7 more are nearing this
Female 34.77%
Child proportion is 13.77%
Multi bacillary 39.3%
Visible deformities 1.44%
Anti leprosy activities in India
• Leprosy mission• Hindu kushth Nivaran Sangh• Gandhi memorial• Sevagram• German leprosy Relief association• Damien Foundation• Danish• JALMA central institute in Agra• Central leprosy teaching and research
institute Chenglepet
Goals of Physical Therapy for Non-Surgical patients Of Leprosy Disease
The major aim is to prevent or reduce complication, deformity and disability in body through Physical Therapy.
Means
The ways of reaching these Goals are-
By teaching the patient.
By treating and helping the patient.
Teaching:
What the disease of leprosy is?
The possible complications and deformities resulting from leprosy.
prevention of complication, deformities and disabilities.
Treating and Helping:
To respect themselves enough to take medication regularly and to take care of complications.
To protect their own anesthetic hands, feet and eyes.
To keep their skin soft and supple.
To keep their joint flexible.
To preserve all possible movements of hands and feet.
To keep their muscles strong.
To use their hands, feet and eyes safely, in daily work.
Goals of Physical Therapy for Surgical patients Of Leprosy Disease
To protect and prevent further damage and deformity.
To improve and restore function.
To improve appearance of hands, feet, face and eyes.
Surgical Techniques used in Leprosy Disease:
Tendon Transfer: Moving the distal end of the tendon to a new place so that contraction of muscle belly will produce a needed movements used to replace paralysed muscles. Example- Transfer of fore-arm muscle to make finger movements.
Tendon Lengthening: Lengthening the tendon of a muscle to permit more movement and reduce contracture. Example- Tendo Calcaneus lengthening.
Capsulotomy: To loosen tight joint capsule often done with tendon lengthening and tendon transfer to improve range of motions. Tighten the loose joint capsule using suture.
Arthrodesis: Elimination of unstable and deformed joints.
Tenodesis: Attach a piece of tendon across the joint to reduce the movement. The tendon then act as ligament. Example- Tenodesis of MCP joint to prevent hyperextension.
Physical Therapy Goals: To increase and regain range of motion. Improve muscle strength particularly in muscles to be
transferred. Clean supple skin in areas of surgery. Teach home self care. Protect tissue during wearing. Prevent/reduce swelling. Muscle re-education after tendon transfer. Safe use of any new restored skill in work.
Physical Therapy Technique:
For increasing/regaining ROM: ROM can be increased by soaking the skin or part in warm water and then performing passive movement to the part affected.
To improve strength specially in tendon transfer: Active exercise in all part in which surgery is performed.
Clean supple skin: It is provided by soaking the part in soap water, rubbing off thick skin, oiling, self massage and protecting the part from infection.
Home care: teaching skin, hand, foot and eye care to groups and individuals and teaching the patients actual home care.
Protect tissue during healing: Rest, body position and POP cast.
Prevent/Reduce swelling: Elevation, active and passive exercise.
Muscle Re-education after tendon transfer: Teaching new restored skills in movements provided by tendon transfer.
Self restored skills in daily work: Teaching patient ot use any new skill safely in specific task. Providing hand, eye and foot protection.
THE END
