This document summarizes information about Mycobacterium leprae and leprosy (Hansen's disease). It discusses how leprosy is caused by M. leprae, mainly affecting the skin, nerves, and respiratory tract. Key points include that leprosy is an ancient disease, most infectious in its lepromatous form. Diagnosis involves examination of skin and nerve lesions as well as lab tests to identify acid-fast bacilli. Treatment involves multidrug therapy to prevent deformities and control transmission.

1. MYCOBACTERIUM LEPRAE

2. It is a chronic infectious
disease caused by M.leprae,
an acid fast, rod shaped
bacillus.
It mainly affects the skin,
peripheral nerves, and mucosa
of the respiratory tract etc…

3. HISTORY
One of the oldest and most
dreaded disease known to
mankind.
Discovered by Dr.Gerhard
Armauer Hansen in 1873 in
Norway.
Hansen’s disease
The term leprosy was taken
from a Latin word, ‘lepra’
means scaly.

5. EPIDEMIOLOGY
Age
All ages,from early infancy to very old age
Youngest age reported is 1 and half months
Sex
Both
Males more than females,2:1
Source of infection
Patient

6. MYCOBACTERIUM
LEPRAE

7. MORPHOLOGY
• Slender,straight or slightly curved rods
• Size – 1-8µmx0.2-0.5 µm.
• Occurs characteristically in clumps or
bundles(globi)
• Acid fast bacilli
• Live bacilli, solid uniform structure.
• Dead appear as fragmented
with granules.

8. CULTIVATION
Not possible to cultivate – media, tissue culture
Generation time – 12–13 days[20 days]
Cultivation
Foot pad of mice
Nine-banded armadillo (Dasypus novemcinctus)
Chimpanzees
Monkeys
Slender loris
Indian pangolin
Chipmunks
Golden hamsters
European hedgehog
Adaptation in artificial media – ICRC bacillus [Indian Cancer Research Center]

9. CULTIVATION
1.FOOT PAD OF MICE

10. 2.NINE BANDED ARMADILLO

11. ANTIGENIC STRUCTURE
Cell wall – 1.Peptidoglycan layer
2.Lipoarabinomannan
layer(LAM-B)
3.Mycosides(PGL-1)
LAM-B highly immunogenic.
PGL-1 Protects pathogens against host
cell enzymes and suppress CMI.

12. TRANSMISSION
-Nasal droplets
-Contact transmission

13. RISK FACTORS
Close contact
Immunosuppression
Malnutrition
Genetics

14. PATHOGENESIS
Chronic granulomatous disease
Patient is the only source of
infection-nasal discharge&skin
lesion
Mostly affects the cooler parts of
the body skin, eyes and nasal
mucosa.
Incubation period- long&variable

16. SIGNS AND SYMPTOMS
Skin
Discolored patches on skin
Dry skin
Painless ulcers on the soles of feet
Painless swelling or lumps on the face and ear lobes

17. TYPES OF LEPROSY

18. LEPROMATOUS TYPE
Generalized form
Found in individuals with low resistance
Severe and prognosis is poor.
More infectious
Lepromin test – negative (CMI )
Nodular lesions on face,ear lobes,hands, feet and less
commonly on trunk.
Bacilli are shed in sweat , nasal and oral secretions
Continous bacteremia is commonly seen

19. TUBERCULOID TYPE
Localised form.
Seen in patients with high degree of resistance
Skin lesions are few- face, limb and trunk.
Consists of non elevated hypo or
hyperpigmented macular patches
Bacilli are very few & absent in tissues
Lepromin test- positive.
Diagnosis – clinical& histological findings.

20. DIMORPHOUS TYPE
Clinically resemble tuberculoid leprosy
INDETERMINATE TYPE
Neither characteristic of tuberculoid not
lepromatous type.
Lesions heals spontaneously

21. RIDLEY & JOPLING’S
CLASSIFICATION
On the basis of clinical , histopathological
and immunological findings
1. Tuberculoid(TT)
2. Borderline tuberculoid(BT)
3. Borderline(BB)
4. Borderline lepromatous(BL)
5. Lepromatous(LL)

22. WHO CLASSIFICATION
Classification depends upon number of skin
lesions and involvement of nerves
Paucibacillary
When there are ≤5 skin lesions and
no/one nerve trunk involvement.
Multibacillary
6 or more skin lesions and more than
one nerve trunk involvement.

24. Complications
Complications in leprosy patients may be of two types- deformities and
allergic response ( called lepra reactions types, I and II)
Deformities
Abou t 25% of untreated cases develop deformities in due course of time
which may arise due to-(1) nerve injury leading to muscle weakness or
paralysis, or (2) disease process (facial deformities or loss of eyebrow), or
(3) infection or injury (ulcers).
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.

25. LAB DIAGNOSIS
SPECIMENS
Nasal mucosa
Skin lesions
Ear lobes
Total 6 specimens are collected .
Including 4 from skin [buttocks , chin , cheek , forehead] one from nasal
mucosa and ear lobule
Slit and scrape method[ skin cleansed with spirit in order to remove any
saprophytic acid fast bacilli
Skin is punched tightly to minimise bleeding
Cut of 5mm long is made with scalpel , wipe of blood or lymph
Bottom and sides of slit are scrapped with point of blade

26. ACID FAST STAINING
5% H2SO4
1-10 bacilli in 100 fields =1+
1-10 bacilli in 10 fields = 2+
1-10 bacilli per field =3+
10-100 bacilli per field =4+
100-1000 bacilli per field = 5+
More than 1000 bacilli, clumps& globi in every
field=6+

27. BACTERIOLOGICAL INDEX(BI)
 No of total bacilli in a tissue.
BI= NO. of pluses(+) scored in all smears
Number of smears
MORPHOLOGICAL INDEX(MI)
 % of uniformly stained bacilli out of the total
number of bacilli counted

28. LEPROMIN TEST
Described by
Mitsuda in 1919.
Intradermal inj of
0.1ml of lepromin
Biphasic response

30. EARLY REACTION OF
FERNANDEZ
Consists of erythema and induration
developing hours and usually remains for 3-
5 days
Is a delayed type hypersensitivity reactions
Greater than 10mm diameter after 48 hrs
considered as positive
Do not indicate active infection

31. LATE REACTION OF MITSUDA
Appears in 1-2 weeks after
injection
Reaction appears in the form of
nodule that may ulcerate
Takes few weeks to heal
Reading taking after 21 days
Nodule of more than 5 mm :
positive
Positive Mitsuda indicates
resistance to leprosy

32. ANIMAL INOCULATION
Foot pad of mice
Nine banded armadillo
Tissue from LL containing leprae bacilli
inoculated intradermally into footpad of
mouse kept at 20 degree . A granuloma
develops at site in 1-6 months
Inoculation with lepra bacilli animal
develops a generalized infection with
extensive multiplication of bacilli and
lesions resembles LL

33. SEROLOGICAL TESTS
Detection of anti-phenolic glycolipid-1(antiPGL-1)
antibodies.
Latex agglutination
MLPA
ELISA

34. AURAMINE STAINING FOR
VIABILITY
To assess the metabolic activity of m.leprae
in clinical samples
MOLECULAR METHODS
Real time PCR
For detection of M.leprae DNA from clinical
samples
For treatment monitoring

35. TREATMENT

36. PREVENTION
Early diagnosis & treatment with MDT.
Surveillance of contacts
Health education
Vaccination - BCG

37. NATIONAL LEPROSY
ERADICATION PROGRAMME
Launched in 1983.
Vision -Leprosy free india by 2030.
India has achieved leprosy elimination at
National level in Dec 2005(PR<1/10000
population)

38. THANK YOU