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LEPROSY
Dr. Sandeep Choudhary
LEPROSY
OVERVIEW

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LEPROSY
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Introduction
Epidemiology
Bacteriology
Classification
Clinical features

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Reactions
Diagnosis
Treatment
Deformities
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
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
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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.
Epidemiology
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


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

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.
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.
Bacteriology
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
 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. 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.
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

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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)

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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
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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

(++)
Bacilli

Immunity

(++)
Immunity

(+)

(+)

(-)

(-)

LLHD
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
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
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 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
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 illdefined 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



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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) 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
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.
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


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

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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 :

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.
DIAGNOSIS
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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 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.
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.
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
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.
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
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
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
Self–advocacy
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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Dr. Sandeep Choudhary Explains Leprosy: Causes, Symptoms, Treatment

  • 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.
  • 7. WORLDWIDE PREVALENCE AT THE TURN OF CENTURY
  • 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.
  • 11.
  • 12.
  • 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)
  • 29. Indian classification      Indeterminate type Tuberculoid type Borderline type Lepromatous type Pure neuritic type
  • 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
  • 32. (+++) Immunology & bacteriology in leprosy (spectrum) (+++) Bacilli (++) Bacilli Immunity (++) Immunity (+) (+) (-) (-) LLHD
  • 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
  • 36. Indeterminate Leprosy  Earliest & transitory stage  One or two vague hypopigmented macule with definite sensory impairment.
  • 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.
  • 54.
  • 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.
  • 60. Ulnar S  Anesthesia medial 1/3 palm M Claw ring and little fingers A  Dryness medial 1/3 palm
  • 61. Median S Anesthesia lateral 2/3 palm M Claw mid + index + loss Opposition A Dryness lateral 2/3 palm
  • 62. Radial S Anesthesia dorsum hand M Wrist drop
  • 65. Posterior Tibial S Sole anesthesia M Claw Toes A Dryness in sole
  • 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.
  • 71.
  • 72. DIAGNOSIS BACTERIOLOGICAL EXAMINATION This includes : Skin Smears : Nasal Smears or blows : Nasal Scrapings :
  • 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
  • 88. TREATMENT MULTIDRUG CHEMOTHERAPY WHO RECOMMENDED REGIMENS OF CHEMOTHERAPY : PAUCIBACILLARY LEPROSY : The above regimen needs to be taken for 6months within 9 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.
  • 94. 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.
  • 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%
  • 102. CHEMOPROPHYLAXIS  Chemoprophylaxis as a public health measure is not recommended on account of lack of consistent results from various studies.
  • 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.
  • 106. DEFORMITIES IMPROVEMENT  Improvement of disabilities is achieved through the use of prostheses and orthopaedic devices, including corrective splints as well as by corrective surgery.
  • 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.