Leprosy 140131074236 Phpapp01

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LEPROSY

Dr. Sandeep Choudhary


LEPROSY
OVERVIEW
LEPROSY
Introduction Reactions
Epidemiology Diagnosis
Bacteriology Treatment
Classification Deformities
Clinical features Rehabilitation
NLEP
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.
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-Bukharis Muslim Hadith (volume 1, 2.443) documented
Prophet Mohammeds 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 Hansens disease.
Leprosy control started with the use of chaulmoogra oil and for
the last three decades, MDT has been the main tool against
leprosy.
Epidemiolo
gy
WORLDWIDE AND INDIA
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.
WORLDWIDE
PREVALENCE AT THE
TURN OF CENTURY
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.
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 Apr13 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.
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.
Bacteriolo
gy
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: (5 X 0.5 )
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
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)
The Leprosy Bacteria
Reservoir of infection
Main reservoir : Human being
Lepromatous case> Non lepromatous
cases

Animal reservoirs
9-banded armadillos

Chimpanzees

Mangabey monkeys

Sphagnum moss
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
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.
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.
VIRULENCE FACTOR

The bacterium's complex cell wall contains


large amounts of an M. lepraespecific
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.
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.
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
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
CLASSIFICATION
OF
LEPROSY
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
Various Classifications
Indian Classification :
clinicobacteriological
Madrid Classification :
clinicobacteriological
Ridley Jopling classification :
immunohistological
Classification by WHO Study Group on
Chemotherapy of Leprosy :
clinicobacteriological.
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)
Indian classification

Indeterminate type
Tuberculoid type
Borderline type
Lepromatous type
Pure neuritic type
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
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
Immunology &
bacteriology in leprosy
(+++) (spectrum) (+++)

Bacilli Immunity
(++) (++)
Bacilli Immunity

(+) (+)

(-) (-)
LLHD
WHO
Classification(1981,87,93)
Clinical Paucibacillary Multi Bacillary
Feature on Leprosy Leprosy
Skin Lesion PB MB
Including macular 1 to 5 lesion More than 5 lesion
flat lesion, papules & Asymmetrical Symmetrical
nodules distribution distribution
Definite loss of Loss of sensation
sensation may or may not be
BI <2 at all sites present
in the initial skin BI >= 2 at any site
smear in the initial skin
smear
W H O classification
(For chemotherapy M.
leprae)
Paucibacillary Multibacillary
Indeterminate - I Mid borderline BB

Tuberculoid TT Borderline
Borderline Lepromatous BL
Tuberculoid BT Lepromatous LL
If any of these have All smear positive
positive bacterial cases
index they should be
classified as
multibacillary for
multidrug therapy
Clinical
Feature
Indeterminate Leprosy
Earliest & transitory stage
One or two vague hypopigmented macule
with definite sensory impairment.
Indeterminate Leprosy

If untreated may progress towards


tuberculoid, borderline or lepromatous
leprosy
Spontaneous regression may occur
Bacteriologically Negative
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
Tuberculoid Leprosy
Borderline Tuberculoid
Four or more lesions, asymmetrically distributed
Macules or plaques of variable sizes with well or
ill-defined margins & satellite lesions
Peripheral nerves enlarged asymmetrically
Sensation: hypoesthesia
SS for AFB: may or may not be positive.
Lepromin test may be weakly positive
Borderline Tuberculoid
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
Borderline Borderline
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
Borderline Lepromatous
Lepromatous Leprosy
Numerous macules, plaques, nodules or
diffusely infiltrated lesions, shiny, smooth,
symmetrically distributed on face, trunk
and extremities with ill-defined margin
which may be slightly hypopigmented or
erythematous
Symmetrical nerve enlargement is seen
Sensation: normal
SS for AFB: numerous seen
Lepromin test - negative
Lepromatous Leprosy
Ear lobes involvement
Diffuse thickening of the skin, with loss
of hair (eyebrows and eyelashes) :
madarosis.
Saddle nose deformity
Leonine facies
Clinical, Bacteriologic, Pathologic, and
Immunologic Spectrum of Leprosy
Feature Tuberculoid (TT, BT) Borderline (BB, BL) Lepromatous (LL)
Leprosy Leprosy Leprosy
Skin lesion One or a few sharply Intermediate between BT- Symmetric, poorly
defined annular and LL-type lesions; ill- marginated, multiple
asymmetric macules or defined plaques with an infiltrated nodules and
plaques with a tendency occasional sharp margin; plaques or diffuse
toward central clearing, few or many in number infiltration; xanthoma-like
elevated borders or dermatofibroma
papules; leonine facies
and eyebrow alopecia

Nerve lesion Skin lesions anesthetic Hypoesthetic or Hypoesthesia a late sign;


early; nerve near lesions anesthetic skin lesions; nerve palsies variable;
sometimes enlarged; nerve trunk palsies, at acral, distal, symmetric
nerve abscesses most times symmetric anesthesia common
common in BT
BI(Bacteriological index) 0-1+ 3-5+ 4-6+
lymphocytes 2+ 1+ 0-1+
Macrophage Epitheloid Epitheloid in BB,usually Foamy change is the
differentiation undiff but may have rule,may be
foamy changes in BL undifferentiated in early
lesions
Langhans giant cells 1-3+ - -
Lepromin skin test +++ - -
Lymphocyte Generally positive 1 to 10 1 to 2
transformation test
CD4 : CD8 ratio 1.2 BB(NT),BL:0.48 0.50
PGL1 antibodies 60 85 95
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
non-nodular 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.
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.
Nerve
involvement in
Leprosy
M. Leprae : superficial nerve
involvement

W Britton
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.
Face
Facial Nerve
Lagophthalmos
Facial droop

Trigeminal Nerve
Corneal anesthesia
NERVE DAMAGE
UPPER LIMB
Ulnar S Anesthesia medial 1/3 palm
M Claw ring and little fingers
A Dryness medial 1/3 palm
Median S Anesthesia lateral 2/3 palm
M Claw mid + index + loss
Opposition
A Dryness lateral 2/3 palm
Radial S Anesthesia dorsum hand
M Wrist drop
NERVE DAMAGE

LOWER LIMB
Lateral (common) Popliteal
Foot drop
Posterior Tibial
S Sole anesthesia
M Claw Toes
A Dryness in sole
CASE DEFINITION
Leprosy is clinically defined by one or more of the
following cardinal features :
I. Hypopigmented patches
II. Partial or total loss of cutaneous sensation in affected area.

III. Presence of thickened nerves and

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.
DIAGNOSIS
HISTORY
CLINICAL EXAMINATION
BACTERIOLOGICAL EXAMINATIONS
FOOT-PAD CULTURE
HISTAMINE TEST
BIOPSY
IMMUNOLOGICAL TEST
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
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.
Nerve palpation
DIAGNOSIS
BACTERIOLOGICAL EXAMINATION
This includes :
Skin Smears :

Nasal Smears or blows :

Nasal Scrapings :
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.
DIAGNOSIS
BACTERIAL INDEX
DIAGNOSIS
BACTERIAL INDEX
DIAGNOSIS
BACTERIAL INDEX
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 patients
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 patients response to
treatment.
DIAGNOSIS
FOOT-PAD CULTURE
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 :
1. Detecting drug resistance.
2. Evaluating the potency of anti-leprosy drugs.
3. Detecting the viability of bacilli during treatment.
Newer in vitro macrophage culture which
takes only 3 4 weeks.
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.
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.
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.
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.
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.


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)
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
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.
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
TREATMENT
MULTIDRUG CHEMOTHERAPY
WHO RECOMMENDED REGIMENS OF
CHEMOTHERAPY :
PAUCIBACILLARY LEPROSY :

The above regimen needs to be taken for


6months within 9 months
TREATMENT
MULTIDRUG CHEMOTHERAPY
Treatment regimen for children 10-14
years :
MULTIBACILLARY LEPROSY

Rifampicin : 450mg once monthly under supervision


Dapsone : 50mg daily self administered
clofazimine : 150mg once monthly under supervision
50mg every other day self-
administered

PAUCIBACILLARY LEPROSY

Rifampicin : 450mg once a month under supervision


Dapsone : 50mg daily self administered.
TREATMENT
MULTIDRUG CHEMOTHERAPY
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
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
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.
TREATMENT
MULTIDRUG CHEMOTHERAPY
Ethionamide and Prothionamide : highly
bactericidal killing 98 percent of viable
bacilli in 3 to 4 days. Relatively more
expensive and more toxic.
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.
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.
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.
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.
LEPRA REACTIONS
TREATMENT

Prednisolone regimen Add clofazimine in ENL

40mg daily for first 2 weeks 100mg tds x 4 weeks


30mg daily or week 3 and 4

20mg daily for week 5 and 6 100mg bd x 4weeks


15mg daily for week 7 and 8

10mg daily for week 9 and 10 100mg od x 4 weeks


5mg daily for week 11 and 12

For neuritis, treatment with Should be prolonged to four


prednisolone weeks from
20mg onwards
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.
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%
CHEMOPROPHYLAXIS
Chemoprophylaxis as a public health
measure is not recommended on account
of lack of consistent results from various
studies.
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.
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.
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.
DEFORMITIES
IMPROVEMENT
Improvement of disabilities is achieved
through the use of prostheses and
orthopaedic devices, including corrective
splints as well as by corrective surgery.
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..
REHABILITATION

Basic principles of CBR includes :


Participation

Empowerment

Raising awareness

Selfadvocacy

Gender sensitivity and special needs

Partnerships

Sustainability
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.
Thank You

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