The document provides an overview of leprosy, including its introduction, epidemiology, bacteriology, classification, and clinical features. It is caused by Mycobacterium leprae, which mainly involves the peripheral nerves and skin. Worldwide prevalence has dropped significantly due to multidrug therapy. In India, over 12 million people have been cured of leprosy. Leprosy exists on a spectrum from tuberculoid to lepromatous forms based on immunity and bacterial load. Clinical classification systems help determine treatment and prognosis.
3. INTRODUCTION
Chronic granulomatous infectious disease.
Caused by Mycobacterium leprae
Mainly involves the peripheral nerves and skin
Other organs may involve:
Mucosa of mouth
Upper respiratory tract
Eyes
Bones & Muscles.
Testes etc.
Commonly involves every organ except :
CNS, Ovary and Lungs.
4. Historical aspect of leprosy
One of the Oldest and most dreaded disease known to Mankind.
Earliest description from India in 600BC
Kustha Roga & attributed to punishment or curse of God
Al-Bukhari’s Muslim Hadith (volume 1, 2.443) documented
Prophet Mohammed’s apparent dread of leprosy in his
statement: “Escape from the leprous the way you escape from a lion”
Word leper comes from Greek word “scaling”
M. leprae was discovered by Gerhard Henrik Armauer Hansen
in 1873 in Norway. Hence referred to as Hansen’s disease.
Leprosy control started with the use of chaulmoogra oil and for
the last three decades, MDT has been the main tool against
leprosy.
6. Distribution
Prevalence
Worldwide distribution but essentially a disease of developing
countries.
The prevalence rate has dropped by 90 percent from
21.1cases/10000 in 1985 to <1/10000 in 2000.
Out of 122 countries, only 2 countries still have to reach the
elimination goal :
Brazil and East Timor
To date there has been no resistance to antileprosy medicines
when used as MDT.
8. Leprosy Situation in India
The goal of leprosy elimination at National level (i.e. PR of <1 case/10,000
population) as set by National Health Policy 2002 had been achieved in the month
of December 2005.
9. Leprosy Situation in India 2012-13
A total of 1.35 lac new cases were detected during
2012-13 i.e, ANCDR of 10.78/lac population
Prevalence was 0.92 lac cases as on 1st Apr’13 i.e, PR of
73/10000 population.
Multibacillary cases were 49.92 percent
Female cases were 37.72 percent, children 9.93 percent
3.45 percent cases were with visible deformity
33 states/UTs have already achieved the PR of <1
case/10000.
Chhattisgarh(1.69), Dadra & Nagar Haveli(2.93) are yet
to achieve the goal.
10. Leprosy Situation in India 2012-13
Three States viz. Bihar, Maharashtra and West Bengal
which have achieved elimination earlier have shown
slight increase in P.R. (1-1.2) in the current year due to
the effect of SAP-2012.
This brings the total number of persons affected by
Leprosy cured of the disease in the country with MDT
from the beginning till date to 12.80 million.
14. Lepra bacilli
Gram positive Obligate intracellular bacillus - due to its large
pool of non functional genes.
Acid fast stained with modified Fite stain or ZN stain
Short, thick, pink stained rods of Size: (5µ X 0.5 µ )
Occurs characteristically in clumps or bundles( “globi”)
Affinity for Schwann cells & cells of R-E system .
M. leprae grows best in cooler tissues (the skin, peripheral
nerves, anterior chamber of the eye, upper respiratory tract,
and testes), sparing warmer areas of the skin (the axilla, groin,
scalp, and midline of the back).
Optimal temp. for growth is 30-33 centigrade
15. M. leprae remains one of the few bacterial species
that still has not been cultivated on artificial
medium or tissue culture and produces no known
toxins, but can grow in
Nude mouse
Nine banded armadillos(best)
17. Reservoir of infection
Main reservoir : Human being
Lepromatous case> Non lepromatous cases
Animal reservoirs
9-banded armadillos
Chimpanzees
Mangabey monkeys
Sphagnum moss
18. Portal of exit
Major portal of exit : Nasal Mucosa
LL cases harbour millions of M. leprae in their nasal
mucosa discharged when they sneeze or blow nose.
Ulcerated or broken skin of bacteriologically
positive cases
19. Mode of transmission
Transmission by inhalation
Droplet infection(most common)
Transmission by contact
Skin to skin contact with infectious cases
Contact with soil or fomites
Other Routes
Insect Vectors e.g.. Mosquito, Bedbugs
Tattooing needles
NB : Breast feeding and Transplacental infection do not
occur.
20. Incubation period
Long incubation period
Ranged: 2 to 40 years or more
Average: 3-5 years
Generation time : 12 days.
Infectivity : Leprosy is a highly infectious disease with low
pathogenicity. Among household contacts of lepromatous
cases about 5 to 12 percent is expected to show signs of
leprosy within 5 yrs.
21. VIRULENCE FACTOR
The bacterium's complex cell wall contains large amounts
of an M. leprae–specific phenolic glycolipid (PGL-1),
which is detected in serologic tests. The unique
trisaccharide of M. leprae binds to the basal lamina of
Schwann cells; this interaction is probably relevant to the
fact that M. leprae is the only bacterium to invade
peripheral nerves.
22. Host Factors
Leprosy affects all age groups but incidence generally
rises to a peak between 10 to 20 years of age and then
fall.
Higher incidence is seen in males, more marked among
adults, more marked among lepromatous cases.
Cell Mediated Immunity is responsible for resistance to
infection with M.leprae. In lepromatous leprosy there is
complete breakdown of CMI.
23. Environmental factors
Humidity favors survival of M. leprae in environment
M. leprae remain viable in
Dried nasal secretions for 9 days
Moist soil at room temperature for 46 days
Overcrowding & lack of ventilation within households
24. Social factors
Often called a “social disease”
In addition to the physical effects of the disease,
patients have also suffered severe social stigma and
ostracism from their families, communities, and even
health professionals to such an extent that leprosy has
been known since ancient times as “the death before
death”.
Social factors:
Poverty
Poverty related circumstances
Overcrowding
Poor housing
Lack of personal hygiene
26. IMPORTANCE OF CLASSIFICATION
Identify the infectious cases – Epidemiological
importance - Principal targets for treatment
Identify the patients likely to develop the deformities
and determine the prognosis
Frame the line of treatment
Helpful in planning and evaluation of leprosy control
activities
27. Various Classifications
Indian Classification : clinicobacteriological
Madrid Classification : clinicobacteriological
Ridley Jopling classification : immunohistological
Classification by WHO Study Group on Chemotherapy
of Leprosy : clinicobacteriological.
28. Ridley- Jopling 1966
(Research purposes)
Most widely accepted
Divides Leprosy cases into five groups according
to their position on an immunohistological scale.
It can be used only when full research facilities
are available :
Tuberculoid (TT)
Borderline Tuberculoid (BT)
Borderline Borderline (BB)
Borderline Lepromatous (BL)
Lepromatous (LL)
30. Immunity in leprosy
LL - multibacillary state with
multiple lesions due to low
immune response
(+)
TT -paucibacillary
state, few lesions due
to high immune
response
(-)
LLHD
BLHD
BBHD
BTHD
TTHD
31. Contd..
Borderline forms (BB, BT and BL) lie between these
two poles and are immunologically unstable, tending
to move towards one of the polar forms
33. WHO
Classification(1981,87,93)
Clinical Feature on
Skin Lesion
Including macular flat
lesion, papules & nodules
Paucibacillary
Leprosy
PB
1 to 5 lesion
Asymmetrical
distribution
Definite loss of
sensation
BI <2 at all sites in the
initial skin smear
Multi Bacillary
Leprosy
MB
More
than 5 lesion
Symmetrical distribution
Loss of sensation
may or may not be present
BI >= 2 at any site in the
initial skin smear
34. W H O classification
(For chemotherapy – M. leprae)
Paucibacillary
Indeterminate - I
Tuberculoid – TT
Borderline Tuberculoid – BT
If any of these have positive
bacterial index they should be
classified as multibacillary
for multidrug therapy
Multibacillary
Mid borderline – BB
Borderline Lepromatous –
BL
Lepromatous – LL
All smear positive cases
37. Indeterminate Leprosy
If untreated may progress towards tuberculoid,
borderline or lepromatous leprosy
Spontaneous regression may occur
Bacteriologically Negative
38. TUBERCULOID LEPROSY
Single or a few lesions
Asymmetrically distributed on trunk and limbs
Sharply defined, dry, flat or raised, erythematous or
hypopigmented, and are anesthetic.
One or two nerves may be enlarged near the skin
lesion
SS for AFB: Negative
Lepromin test may be strongly positive
40. Borderline Tuberculoid
Four or more lesions, asymmetrically distributed
Macules or plaques of variable sizes with well or illdefined margins & satellite lesions
Peripheral nerves enlarged asymmetrically
Sensation: hypoesthesia
SS for AFB: may or may not be positive.
Lepromin test may be weakly positive
42. Borderline Borderline
Multiple erythematous macules & plaques
Various sizes and shapes with punched out center and
ill defined slopping outer margin
Tend to be symmetrical
Nerves may be asymmetrically enlarged
Sensation:+/-
SS for AFB: seen +/-
Lepromin test-usually negative, may be doubtful
44. Borderline Lepromatous
Numerous, symmetrically distributed lesions
Hypopigmented or erythematous irregularly shaped
maculopapular, infiltrative nodules, or plaques, with
smooth surfaces & ill defined borders, sloping outwards
Nerves may be symmetrically or asymmetrically enlarged
Sensation:+/-
SS for AFB: numerous seen
Lepromin test -negative
46. Lepromatous Leprosy
Numerous macules, plaques, nodules or diffusely
infiltrated lesions, shiny, smooth, symmetrically
distributed on face, trunk and extremities with illdefined margin which may be slightly hypopigmented
or erythematous
Symmetrical nerve enlargement is seen
Sensation: normal
SS for AFB: numerous seen
Lepromin test - negative
49.
Diffuse thickening of the skin, with loss of hair
(eyebrows and eyelashes) : madarosis.
Saddle nose deformity
Leonine facies
50. Clinical, Bacteriologic, Pathologic, and Immunologic
Spectrum of Leprosy
Feature
Tuberculoid (TT, BT) Leprosy
Borderline (BB, BL) Leprosy
Lepromatous (LL) Leprosy
Skin lesion
One or a few sharply defined
annular asymmetric macules or
plaques with a tendency toward
central clearing, elevated borders
Intermediate between BT- and
LL-type lesions; ill-defined
plaques with an occasional sharp
margin; few or many in number
Symmetric, poorly marginated,
multiple infiltrated nodules and
plaques or diffuse infiltration;
xanthoma-like or dermatofibroma
papules; leonine facies and
eyebrow alopecia
Nerve lesion
Skin lesions anesthetic early; nerve
near lesions sometimes enlarged;
nerve abscesses most common in
BT
Hypoesthetic or anesthetic skin
lesions; nerve trunk palsies, at
times symmetric
Hypoesthesia a late sign; nerve
palsies variable; acral, distal,
symmetric anesthesia common
BI(Bacteriological index)
0-1+
3-5+
4-6+
lymphocytes
2+
1+
0-1+
Macrophage differentiation
Epitheloid
Epitheloid in BB,usually undiff
but may have foamy changes in
BL
Foamy change is the rule,may be
undifferentiated in early lesions
Langhans giant cells
1-3+
-
-
Lepromin skin test
+++
-
-
Lymphocyte transformation test
Generally positive
1 to 10
1 to 2
CD4 : CD8 ratio
1.2
BB(NT),BL:0.48
0.50
PGL1 antibodies
60
85
95
51.
52. Other Variants of Leprosy
HISTOID LEPROSY : variant of LL with better
CMI. Usually seen in patients with incomplete
chemotherapy or acquired drug resistance.
Characterized by presence of spindle shaped histiocytes
in tissue section.
LUCIO LEPROSY : mimics myxedema, diffuse nonnodular type of leprosy ch. by melancholy look, thick
shiny skin, widespread sensory loss, hoarseness of voice
and ulceration of nasal mucosa.
LAZARINE LEPROSY : seen in association with
HIV.
53. General Findings
Eye : The anterior chamber can be invaded in LL with
resultant glaucoma and cataract formation.
Iritis/Iridocyclitis
Testes : May be involved in LL with resultant
hypogonadism.
Systemic involvement – Respiratory, Bones, Kidneys,
Lymph glands, etc.
56. M. Leprae : superficial nerve involvement
W Britton
57. Nerve Involvement
Neural involvement leads to muscle weakness, muscle
atrophy, severe neuritic pain, and contractures of the
hands and feet.
Ulnar nerve is most commonly involved , least common
is radial.
Most common cranial nerve involved is Trigeminal.
>30 percent neural loss required for loss of sensation.
First sensation to go is thermal (cold>fine touch).
Proprioception is usually preserved.
66. CASE DEFINITION
Leprosy is clinically defined by one or more of the
following cardinal features :
Hypopigmented patches
II. Partial or total loss of cutaneous sensation in affected area.
III. Presence of thickened nerves and
I.
IV.
Presence of AFB in the skin or nasal smears
It also includes : patients who started MDT but did not
receive for 12 consecutive months and subsequently
presents with signs of active disease as well as patient
who relapse after completing a full course of treatment.
68. DIAGNOSIS
HISTORY
History should include the following points :
Patients Bio data : name, age, sex, address
Presenting complaints
Family history of leprosy
Contact with leprosy cases
Previous history of treatment for leprosy, if any
69. DIAGNOSIS
CLINICAL EXAMINATION
Physical examination should include :
A thorough inspection of the body surface(skin).
Palpation of commonly involved superficial nerves:
1.Ulnar N. near the medial epicondyle.
2.Greater Auricular N as it turns over SCM muscle.
3.Lateral Popliteal N.
4.Dorsal branch of
Radial N.
Testing for :
1.Loss of sensation : heat, cold, pain, touch .
2.Paresis or paralysis of muscles of hands and feet.
73. DIAGNOSIS
BACTERIAL INDEX
Bacterial index is the only objective way of monitoring
benefit of treatment.
According To Ridley’ Logarithmic Scale It Ranges
From 0 To 6+ and is based on the no. of bacilli seen in
an average microscopic field.
B 0 stands for no bacilli in any of 100 oil immersion
field.
77. DIAGNOSIS
MORPHOLOGICAL INDEX
The MI is calculated after examining 200 pink-stained
free standing bacilli.
The percentage of solid staining bacilli in a stained
smear is referred to as MI.
It is a valuable indicator of the patient’s response to
treatment during the first few months and helps to
signal drug resistance.
SOLID FRAGMENTED GRANULAR(SFG)
PERCENTAGE : similar to MI but a more sensitive
indicator of the patient’s response to treatment.
78. DIAGNOSIS
FOOT-PAD CULTURE
1.
2.
3.
Only certain way of identifying M. Leprae.
10 times more sensitive at detecting the bacilli than slit
skin smear.
Time consuming : requires 6 to 9 months.
Used for :
Detecting drug resistance.
Evaluating the potency of anti-leprosy drugs.
Detecting the viability of bacilli during treatment.
Newer in vitro macrophage culture which takes only 3 –
4 weeks.
79. DIAGNOSIS
HISTAMINE TEST
Reliable test for detecting at an early stage peripheral
nerve damage due to leprosy.
Method : carried out by injecting 0.1ml of a 1:1000
solution of histamine phosphate into hypopigmented
patches or in areas of anesthesia.
Result : in normal person it gives rise to a wheal
surrounded by erythematous flare(Lewis triple
response). In case of leprosy where the nerve supply is
destroyed, flare response is lost.
Particularly useful in cases of indeterminate leprosy.
80. DIAGNOSIS
BIOPSY
Usually resorted to when there is high clinical
suspicion but the other test are unyielding. It also
gives information about the bacterial content of
skin.
81. DIAGNOSIS
IMMUNOLOGICAL TESTS
Tests for cell mediated immunity(CMI)
LEPROMIN TEST
Tests for humoral antibodies(serological tests)
FLA-ABS test : used for detecting subclinical infections. 92.3
percent sensitive and 100 percent specific in detecting specific
antibodies in all types leprosy irrespective of type and duration of
disease.
Monoclonal antibodies
Others : RIA, ELISA.
82. DIAGNOSIS
LEPROMIN TEST
Method : it is performed by injecting 0.1ml of lepromin
into inner aspect of the forearm. The reaction is read at 48
hours and 21 days. Two types of reaction have been
described :
EARLY REACTION(FERNANDEZ REACTION) :
an inflammatory reaction develops within 24 to 48 hours and this
tends to disappear in 3 to 4 days. If the diameter of the red area is
more than 10mm the test is considered positive. It is a delayed type
hypersensitivity reaction to soluble constituents of lepra bacilli and
indicates whether or not a person has been sensitized by exposure
to and infection by lepra bacilli.
83. DIAGNOSIS
LEPROMIN TEST
LATE REACTION(MITSUDA REACTION) : It is
characterized by the appearance of a nodule which
becomes apparent in 7 to 10 days and reaches its
maximum in 3 to 4 weeks. The test is read at 21 days. If
the nodule is more than 5 mm it is considered positive. It
is induced by the bacillary component and indicates cell
mediated immunity.
In the first six months of life most children are lepromin
negative
BCG vaccination is capable of converting lepra reaction
from negative to positive.
84. DIAGNOSIS
LEPROMIN TEST
VALUE OF LEPROMIN TEST :
Useful tool for evaluating the immune status of leprosy patients.
Aid to classify the type of disease.
Estimating the prognosis
Strongly positive in a typical tuberculoid case and getting weaker
towards the lepromatous end, the typical lepromatous case being
lepromin negative indicating failure of CMI.
The greatest drawback being high false positive and false negative
cases hence not used as a diagnostic test.
OTHER TESTS FOR CMI :
Lymphocyte transformation test(LTT)
Leucocyte migration inhibition test(LMIT)
85. TREATMENT
MULTIDRUG CHEMOTHERAPY
In the absence of effective of primary prevention by a
leprosy vaccine leprosy control is based on effective
multidrug chemotherapy(secondary prevention).
OBJECTIVES :
To interrupt transmission of infection
Early detection and treatment of cases to prevent deformities
To prevent drug resistance
86. TREATMENT
MULTIDRUG CHEMOTHERAPY
In multidrug regimens only bactericidal drugs are
used :
First line drugs : rifampicin, dapsone, clofazimine,
ethionamide and prothionamide.
Second line drugs : quinolones, minocycline,
clarithromycin.
87. TREATMENT
MULTIDRUG CHEMOTHERAPY
WHO RECOMMENDED REGIMENS OF
CHEMOTHERAPY :
MULTIBACILLARY LEPROSY
Rifampicin
: 600mg once monthly under supervision
Dapsone
: 100mg daily self administered
clofazimine : 300mg once monthly under supervision
50mg daily self-administered
Where clofazimine is unacceptable due skin coloration it may
be substituted by 250 to 375mg daily dose of ethionamide or
prothionamide.
The above regimen needs to taken for 12 months within 18
months
89. TREATMENT
MULTIDRUG CHEMOTHERAPY
Treatment regimen for children 10-14 years :
MULTIBACILLARY LEPROSY
Rifampicin
Dapsone
clofazimine
: 450mg once monthly under supervision
: 50mg daily self administered
: 150mg once monthly under supervision
50mg every other day self-administered
PAUCIBACILLARY LEPROSY
Rifampicin
Dapsone
: 450mg once a month under supervision
: 50mg daily self administered.
91. TREATMENT
MULTIDRUG CHEMOTHERAPY
Important points :
MDT is not contraindicated in patients with HIV
infection.
MDT is safe during pregnancy.
Drugs are excreted in breast milk but no reports of
adverse reaction except for mild discoloration of infants
skin by clofazimine
Leprosy is exacerbated during pregnancy, it is important
that MDT is continued
92. TREATMENT
MULTIDRUG CHEMOTHERAPY
Drugs
Rifampicin : highly bactericidal, a single 1500mg dose
kills 99 percent of viable organisms
Toxic effects includes anorexia, nausea, vomiting,
abdominal discomfort and orange discoloration of body
secretions. It is hepatotoxic
Dapsone : weakly bactericidal.
Adverse effects include hemolytic anemia,
methemoglobinemia, agranulocytosis, hepatitis,
neuropathy, psychosis and rarely…
93. TREATMENT
MULTIDRUG CHEMOTHERAPY
DDS syndrome ch. by fever, maculopapular rash, enlarged
lymph nodes, hepatitis and exfoliative dermatitis.
Clofazimine : was originally synthesized for TB. Less
effective than dapsone but has added advantage of
preventing lepra reaction. More expensive but less toxic
which includes dark red discoloration of skin, mucus
membranes, sweat and urine.
95. LEPRA REACTIONS
During the course of leprosy, immunological mediated
episodes of acute or subacute inflammation known as
reaction may occur.
There are two types of reactions :
Type 1 or Reversal reaction
Type 2 or erythema nodosum leprosum
Both types can occur before the start of MDT, during
treatment or after completion of treatment.
96. LEPRA REACTIONS
REVERSAL REACTION
In reversal reaction the leprosy skin lesions themselves
become inflamed red, swollen and painful.
It is type of delayed type of hypersensitivity.
Occurs in both PB and MB
Nerves may be enlarged, tender and painful with loss of
function.
General symptoms are uncommon
Do not affect other organs.
97. LEPRA REACTIONS
ERYTHEMA NODOSUM LEPROSUM
In ENL new inflamed, red nodules appear under the
skin, while the original lesions remain same. Commonly
on face, arm and legs & bilaterally symmetrical. They
appear in crops and subside within few days even
without treatment
It is antigen antibody reaction.
Seen in MB cases only.
Nerves may be affected but is uncommon
Other organs like testis, eye, kidney may be affected
General symptoms of fever, joint pain, red eyes and
watering may be associated.
98. LEPRA REACTIONS
TREATMENT
Because of high risk of permanent nerve damage
reversal reaction needs to be promptly diagnosed and
treated adequately
Standard 12 wk. regimen of prednisolone is the
treatment of choice.
ENL varies in severity, duration and organ
involvement, and can be treated with prednisolone as
reversal reaction.
Treatment includes bed rest, splinting of affected
nerves, analgesics and prednisolone.
99. LEPRA REACTIONS
TREATMENT
Prednisolone regimen
Add clofazimine in ENL
40mg daily for first 2 weeks
30mg daily or week 3 and 4
100mg tds x 4 weeks
20mg daily for week 5 and 6
15mg daily for week 7 and 8
100mg bd x 4weeks
10mg daily for week 9 and 10
5mg daily for week 11 and 12
100mg od x 4 weeks
For neuritis, treatment with prednisolone
20mg onwards
Should be prolonged to four weeks from
100. LEPRA REACTIONS
TREATMENT
For pregnant women prednisolone should be started at
30mg dose instead of 40mg and limit the course for
10weeks in PB cases and 20 weeks for MB cases.
For children dose should be started at 1mg/kg of body
wt. per day.
Thalidomide : was reintroduced for the treatment of ENL,
mainly because of its antipyretic action. WHO does not
recommend the use of thalidomide in leprosy. Prednisolone is
more effective in controlling ENL and associated neuritis,
clofazimine is the drug of choice for the management of
chronic, recurrent ENL reactions. Another drug claimed to be
useful in ENL is pentoxyfylline.
101. IMMUNOPROPHYLAXIS
Till date there is no effective vaccine against leprosy
The vaccine undergoing trials are :
BCG –34.1% PROTECTION
BCG+KILLED M.LEPRAE – 64.0%
M.W – 25.7%
ICRC – 65.5%
103. DEFORMITIES
As a single disease entity leprosy is the foremost cause
of deformities and crippling.
Approx. 25 percent of cases who are not properly
treated at an early stage develop deformities of hands
and feet.
Deformities may results from the disease process, or
from muscle paralysis due nerve damage, or due to
injuries or infections.
104. DEFORMITIES
Face
Masked face, facies leonina, sagging face, lagopthalmos,
madarosis(eyebrows, cilliary) corneal ulcers and opacities,
perforated nose, depressed nose, nodules on ears and
elongated lobules
Hands
Claw hand, wrist drop, ulcers, absorption of digits, thumb web
contracture, hollowing of interosseus space, swollen hand
Feet
Plantar ulcers, foot drop, inversion of foot, clawing of toes,
absorption of toes, collapsed foot, swollen foot and callosities
Others
Gynaecomastia and perforation of palate.
105. DEFORMITIES
PREVENTION
Measures include care of dry and denervated skin of
palms and soles.
Treating wounds, ulcers, and cracks in palms & soles
Use of protective gloves and footwear
Prevent joint stiffness in case of paralysis
Protection of eyes
Periodic check up for progression of disease.
107. REHABILITATION
Rehabilitation includes all the measures used for
reducing the impact of disability for an individual,
enabling him/her to achieve independence, social
integration, a better quality of life and self actualization.
Community Based Rehabilitation (CBR) is a strategy
within community development for the rehabilitation,
equalization of opportunities, poverty alleviation and
social inclusion of all the people with disabilities. It is
implemented with combined efforts of people with
disability, their families, community, social and
government organisation..
108. REHABILITATION
Basic principles of CBR includes :
Participation
Empowerment
Raising awareness
Self–advocacy
Gender sensitivity and special needs
Partnerships
Sustainability
109. NATIONAL LEPROSY
ERADICATION PROGRAMME
The history of anti leprosy work in India goes back to 1874
when the mission to lepers(leprosy mission) was founded by
Bailey at Chamba, HP
The NLCP was launched in 1954 later converted to NLEP in
1983
The prevalence rate was 57cases/10000 population in 1981
which declined to 5.7/10000 in 2000
In Dec 2005 India achieved the target of leprosy elimination
envisaged in NHP 2002, when PR was brought down to
<1/10000.
Chhattisgarh and Dadra & Nagar haveli are yet to reach the
target.