Leprosy is caused by Mycobacterium leprae, an obligate intracellular organism. It manifests as a spectrum of diseases from lepromatous leprosy (LL) to tuberculoid leprosy (TT), with severity inversely related to cell-mediated immunity status. Diagnosis is by clinical signs and microscopy examination of skin/nerve lesions. Treatment involves multidrug regimens over 6-12 months. Prevention focuses on active case finding, effective treatment, and reducing transmission through awareness and early detection of cases.

1. Leprosy
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2. Learning objectives
At the end of the session, the audience will be able to
understand:
– Clinical manifestations, classification, complications,
lab diagnosis and treatment of M.leprae.
– Differences between lepromatous leprosy and
tuberculoid leprosy.
– Prevention of leprosy
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3. INTRODUCTION
• Mycobacterium leprae - causative agent of leprosy; a
disease of antiquity, having been recognized since long
time :
 Vedic times in India (described as Kushta Roga in
Sushruta Samhita, 600 BC)
 Biblical times in the Middle East
 Hippocrates, 460 BC.
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4. INTRODUCTION
(Cont..)
• G. H. Armauer Hansen (1873) - discovery of lepra bacilli
• Shepard (1960) – multiplying lepra bacilli in footpads of mice kept at a low
temperature (20°C).
• World Leprosy Day is celebrated on 30 January, the anniversary of Mahatma
Gandhi's death
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5. INTRODUCTION (Cont..)
• This year theme of World Leprosy Day
2021 is “Beat Leprosy, End Stigma and
advocate for Mental Wellbeing ”.
• The day was initiated in 1954 by French
philanthropist and writer, Raoul
Follereau, as a tribute to the life of
Mahatma Gandhi who had compassion
for people afflicted with leprosy
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6. •History of leprosy
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7. 7

8. •CLINICAL
MANIFESTATIONS
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9. CLINICAL
MANIFESTATIONS
• Chronic granulomatous disease of humans -
involving cooler parts of the body (skin, peripheral
nerves, upper respiratory tract, eyes, and testes,
etc.).
• Capable of affecting any tissue or organs causing
bony deformities and disfigurements in untreated
cases.
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10. CLINICAL
MANIFESTATIONS
• Incubation period: long incubation period - 5–7
years (vary between 2 and 40 years)
• Attributed to longer generation time of lepra bacilli -
12–13 days as compared to 14 hours for tubercle
bacillus.
• Lepromatous cases - longer incubation period than
tuberculoid cases.
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11. Classification of Leprosy
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12. Clinical Classification
• Paucibacillary (PB) leprosy: A case of leprosy which
fulfills all the criteria—
 (i) 1 to 5 skin lesions,
 (ii) no nerve involvement, and
 (iii) slit-skin smear negative for lepra bacilli
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13. Clinical Classification (Cont..)
• Multibacillary (MB) leprosy: A case of leprosy which
fulfills any one of the criteria—
 (i) >5 skin lesions; or
 (ii) nerve involvement (neuritis); or
 (iii) slit-skin smear positive for lepra bacilli.
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14. Differences between
lepromatous leprosy and
tuberculoid leprosy
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15. Differences between
lepromatous leprosy and
tuberculoid leprosy
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16. Differences between
lepromatous leprosy and
tuberculoid leprosy
A B
A. Nodular lesions of lepromatous leprosy; B. Hypopigmented skin lesions of
tuberculoid leprosy (arrow showing).
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17. Other Categories of Leprosy
• Borderline type-symmetric bilaterally distributed lesions with widespread
small macules, papules, and nodules of various sizes and shapes. These
lesions are mostly lepromatous in nature but also contain aspects of
tuberculoid lesions
• Indeterminate type- early form of leprosy that consists of a single skin lesion
with slightly diminished sensation to touch. It will usually progress to one of
the major types of leprosy.
• Pure neuritic type- no skin lesions. Larger nerve trunks or their branches are
enlarged. There is a sensory loss in the areas of distribution of the nerves
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18. •IMMUNE
RESPONSE
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19. IMMUNE RESPONSE
• Innate immunity: High degree – to lepra bacilli - minority
of those infected develop clinical disease
• Cell-mediated immune response: Plays a vital role in the
control of the disease.
 People with low CMI - develop LL type of lesions
 People with intact CMI develop TT type lesions.
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20. IMMUNE RESPONSE
• Humoral immune response:
• Antibodies – minor role in disease control as M.
leprae is intracellular.
• In LL patients - exaggerated TH2 response - releases
cytokines that cause polyclonal B cell activation
producing high titer of antibodies—(both specific
and nonspecific).
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21. •COMPLICATIONS
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22. COMPLICATIONS
• Complications in leprosy patients may be of two types—
 Deformities
 Hypersensitive response (called lepra reactions).
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23. Deformities
• 25% of untreated cases develop deformities - may arise
due to—
 (1) Nerve injury - muscle weakness or paralysis, or
 (2) Disease process (facial deformities or loss of
eyebrow), or
 (3) Injury -> ulcers-> infection.
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24. Deformities
Common deformities include:
• Face: Leonine facies, sagging face, loss of
eyebrow/eye lashes, saddle nose and corneal
opacity and ulcers
• Hands: Claw hand and wrist drop
• Feet: Foot drop, clawing of toes, inversion of foot,
and plantar ulcers.
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25. Deformities
Deformities seen in untreated lepromatous leprosy:
A.Saddle nose-leonine facies,eyebrow alopecia; B.Autoamputation; C.Corneal opacity.
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26. Lepra Reactions
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27. Lepra Reactions
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28. •EPIDEMIOLOGY
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29. EPIDEMIOLOGY
Source of infection:
• Multibacillary (LL and BL) cases - most important
sources of infection.
• Asymptomatic cases - have a role in transmission.
• Tuberculoid leprosy - do not transmit infection
efficiently
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30. EPIDEMIOLOGY
Mode of transmission:
• Unknown
• Suspected as Nasal droplet infection (aerosols containing M.
leprae) - most common mode.
• Contact transmission (skin):
 Direct contact from person to person
 Indirect contact with infected soil, fomites - clothes and
linens.
• Direct dermal inoculation during tattooing.
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31. EPIDEMIOLOGY
• Communicability: Leprosy - not highly
communicable - Intimate and prolonged contact
is necessary for transmission.
• Environmental factors - people of rural areas,
moist soil, humidity and overcrowding.
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32. 32

33. •National
strategies to
control leprosy 33

34. National strategies to control
leprosy
• NLEP- National Leprosy Eradication Program
lays protocols to Detect-Treat-Control
leprosy
• WHO, ILEP(International Federation of Anti-
Leprosy Associations) along with NGO
support NLEP
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35. Goals of NLEP
•To reduce Prevalence rate to less than 1/10,000 population
•To reduce Grade II Disability % < 1 among new cases at
National level
•To reduce Grade II disability cases < 1 case per million
population at National level.
•Zero disabilities among new paediatric cases
•Zero stigma and discrimination against person affected by
leprosy. 35

36. Institutes Of National
Importance
• JALMA(Japanese Leprosy Mission for Asia)- Agra
• Regional Leprosy Training And Research Institute
• CLTRI(central Leprosy Teaching And Research
Institute)- Chengalpattu, Tamil Nadu
• Schieffelin Institute of Health – Research
and Leprosy Centre (SIH-R & LC) - Vellore, Tamil
Nadu
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37. •LABORATORY
DIAGNOSIS
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38. LABORATORY
DIAGNOSIS
1. Smear Microscopy
2. Mouse Foot Pad Cultivation
3. Antibody Detection
4. Test for Detecting CMI (Lepromin Test)
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39. 1. Smear Microscopy
• Done to demonstrate the acid-fast bacilli
in the lesions.
• Less acid-fast - stained by Ziehl–Neelsen
technique - 5% sulfuric acid for
decolorization.
• Under oil immersion - red acid-fast
bacilli, arranged singly or in groups (cigar
like bundles/globi). 39

40. • Live bacilli - uniformly stained with parallel
sides and round ends and length is five
times the width
• Dead bacilli - less uniformly stained and
have fragmented and granular appearance.
• Virchow’s lepra cells or foam cells
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41. Grading of the Smear
• 1–10 bacilli in 100 OIF =1+
• 1–10 bacilli in 10 OIF = 2+
• 1–10 bacilli per OIF = 3+
• 10–100 bacilli per OIF = 4+
• 100–1000 bacilli per OIF = 5+
• >1000 bacilli or bacilli in clumps and globi in each OIF =
6+
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42. Grading of the Smear
• Bacteriological index (BI): Total number of bacilli (live
and dead) per oil immersion field
• Morphological index (MI): Percentage of uniformly
stained bacilli out of the total number of bacilli counted
 MI is a better marker to monitor the treatment
response
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43. 2. Mouse Foot Pad Cultivation
• Not cultivable either in artificial culture media
or in tissue culture due to loss of genes in
metabolic pathways such as energy metabolism
• Only certain way - by inoculating the specimens
into foot pad of mice and keeping at 20°C for 6–
9 months.
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44. 2. Mouse Foot Pad Cultivation
• Advantages:
 10 times more sensitive than microscopy
 Detecting drug resistance & Evaluating potency of
drugs
 detects viability of bacilli
• Disadvantages: Time-consuming (6–9 months) & ethical
issues
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45. • Other animals - Nine banded Armadillo
(Dasypus novemcinctus) - also used.
• However, red squirrels (Sciurus vulgaris)
with leprosy-like lesions in the British
Isles M. leprae & M. lepromatosis DNA
was detected recently
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46. 3. Antibody Detection
• FLA-ABS (Fluorescent Leprosy Antibody Absorption Test):
 To identify subclinical cases
 Antibodies detected irrespective of duration and stage of
the disease
 92% sensitive and 100% specific
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47. 3. Antibody Detection
• ELISA detecting IgM antibodies to PGL-1
(phenolic glycolipid-1) antigen of M. Leprae
- found in 95% of patients with untreated LL
& titre decreases with effective therapy
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48. 4. Test for Detecting CMI
(Lepromin Test)
• Demonstrates delayed hypersensitivity reaction
against the lepra antigen.
• Also indicates an intact host’s CMI.
• Procedure: Lepromin antigen - injected
intradermally to forearm and reading is taken at
two occasions.
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49. 4. Test for Detecting CMI
(Lepromin Test)
• At 48hr (Early or Fernandez reaction): Induration (>10
mm) - corresponds to DTH reaction to lepra antigen and
indicates past exposure to lepra bacilli.
• At 21 days (Late or Mitsuda reaction): A nodule of >5
mm – subsequently ulcerates
 If positive - patient’s CMI is intact
 If negative - absence of CMI
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50. Treatment of Leprosy
• Recommended drugs: Dapsone, rifampicin
and clofazimine
• Alternate drugs: Ethionamide, quinolones
(ofloxacin), minocycline and clarithromycin.
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51. Treatment of Leprosy
• WHO Regimen (2018)
• 3-drug regimen: WHO recommends a 3-drug regimen of
rifampicin, dapsone and clofazimine for all leprosy patients.
 Dapsone (100 mg) - daily, self-administered
 Rifampicin (600 mg) - once a month under supervision
 Clofazimine (300 mg) - once a month under supervision,
and by 50 mg daily, self-administered
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52. Treatment of Leprosy
• Duration of treatment—6 months for
paucibacillary leprosy and 12 months for
multibacillary leprosy
• Follow-up - annually for 2 years for
paucibacillary leprosy and for five years for
multibacillary leprosy.
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53. •PREVENTION
OF LEPROSY
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54. PREVENTION OF
LEPROSY
• Active case finding and effective treatment of cases.
• BCG(Bacille Calmette-Guérin) vaccine: No effective
vaccine available so far.
• MIP vaccine: Killed leprosy vaccine – developed by a
team led by Dr G.P. Talwar at the AllMS, New Delhi
India in 2018, using Mycobacterium indicus pranii
(MIP).
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55. PREVENTION OF
LEPROSY
• Chemoprophylaxis: Dapsone – to high-risk
household contacts of tuberculoid patients, but
not for lepromatous patients; hence not
recommended
• Hospitalized patients need not be isolated as
transmission requires prolonged contact.
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56. Summary
• M. Leprae is an obligate, intracellular
organism, which is acid fast with 5% H2SO4
• EXACT MOT is unknown, aerosol droplets and direct
contact with infected skin contribute to transmission
• Leprosy manifests as spectrum of
diseases(LL,TT,Borderline)
• Severity of leprosy is inversely related to
status of CMI
• Diagnosis is by Clinical signs + microscopy
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57. References
• Essentials Of Medical Microbiology- Apurba S
Sastry & Sandhya Bhatt
• Anantanarayan & Paniker Textbook Of
Microbiology
• Reservoirs And Transmission Routes Of
Leprosy; A Systematic Review- Thomas
Ploemacher et al
• WHO.int
• Challenges in Implementation National Leprosy
Eradication Programme-MOHFW
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58. -Thank you 58