Oldest disease known to mankind First described in ancient Indian texts as “Kustha roga” attributed ] to curse from God Leper : Greek “scaly” Hansen’s Disease – 1873 Norwegian Armauer Hansen discovered that leprosy is caused by bacterium - Mycobacterium leprae Albert Neisser (1879) – stained the organism with fuchsin & gentian violet ( AFB )

1. Leprosy(Hansen’s Disease)

2. Introduction & History
•Oldest disease known to mankind
•First described in ancient Indian
texts as “Kustha roga” attributed
to curse from God
•Leper : Greek “scaly”
Hansen’s Disease – 1873 Norwegian Armauer Hansen
discovered that leprosy is caused by bacterium -
Mycobacterium leprae
Albert Neisser (1879) – stained the organism with
fuchsin & gentian violet ( AFB )

3. Leprosy is a social disease
associated with stigma

5. Morphology
• They are Gram positive and acid fast
5% H2 SO4.
but to lesser extant than tubercle
bacilli.
• The acid-fast bacilli are arranged
singly, in parallel bundles (like rolls of
cigarettes in a packet) or in globular
masses.
• The bacilli are slender, slightly curved
or straight rods, 1-8 um X 0.2-0.5 um
in size.

6. Cultivation
• M. leprae is found only in cases of human infection.
• They have not yet been grown ion artificial media or tissue
culture.
• The generation time of leprae bacillus is found to be 12-20 days on
an average.
• When nasal scrapping from lepromatous leprosy containing lepra
bacilli are inoculated intradermally into foot pad of mouse and
kept at low temperature (20oC), a granulomatous lesion develops
at the site of injection in 1-6 months.
• When nine band armadillo is inoculated with lepra bacilli,
generalized infection develops with extensive multiplication of the
bacilli.

7. Resistance:
•M. leprae can survive in warm humid environment for 9-16 days,
• 46 days in moist soil,
•2 hours in sunlight and
•for about 30 minutes in UV light.
BacteriaResidesin
CoolerPartsoftheBody
Skin Peripheral Nerves

8. Immunocompromisedindividuals
aremoresusceptibletodisease

9. Transmission
 Nasal/oral Droplets
 Dermal Inoculations

10. Contraction of disease
• It is likely to spread through direct skin contact
(damaged skin) and air dispersement of
infectious aerosols from coughing or sneezing of
infected patient.
• Contracting the disease depends on how
susceptible the person is to the disease, how
long you are exposed, and environmental
conditions.
• Only 10 to 29% of people exposed to bacilli
actually develop leprosy.

11. Slow, chronic &progressive
Granulomatous disease of
Peripheral nerves,skin and
Muco- cutaneous tissues
(Nasal mucosa).
It affects Skin, Lungs,liver,
testes ,bones.
Leprosy
Pathogenesis

12. Pathogenesis
• The principal target cell of lepra bacilli are Schwann
cell and the resulting nerve damage causes
manifestation of leprosy, which include muscle
paralysis.
• A non-specific or Indeterminate skin lesion is the First
sign of disease.

13. Tuberculoid
Borderline
Tuberculoid
Borderline
laptomatous
Lepromatous
Classification
• Clinical manifestaion is determined by cellular immune response of
the individual to the bacilli. There are two major forms (polar
forms) of leprosy:
1. Lepromatous leprosy:
2. Tuberculoid leprosy
3. Many patients occupy an intermediate position on the spectrum,
which may be classified as borderline lepromatous (BL) which
may turn into any of the polar forms.

14. 1. Lepromatous or nodular
type:
• It is a generalized form and found in
host with low resistance.
• The bacteria disseminate
hematogenously although, the lesions
are superficial. (MULTIBACILLARY)
• Nodular Lesions are large, diffuse and
granulomatous.
• Facial disfigurement is common which
is due to extensive collagen destruction
• leading to thickening of the loose skin of
the forehead, lips and ears, resulting the
classic leonine facies.
Leonine face

16. • Localized form of disease and found in patient
with high degree of resistance where cell
mediated immunity is intact
Skin lesions:
•The skin lesions are few and characterized by
non- elevated macular, hyperpigmented,
anasthetic patches on the trunk, face and
limbs.
•Bacilli are scanty or absent (Paucibacillary).
M. leprae invades sensory nerves leading to
patchy anaesthesia in the lesion. Localized
anaesthesia often leads to injury and severe
bacterial infection of hand and feet,
sometimes producing deformities. Infectivity is
low. Lepromin test is positive.
Patient shows a delayed type hypersensitivity
and disease progression is slow .
Tuberculoid leprosy

20. Symptoms
Tuberculoid Leprosy Symptoms
• Severe pain
• Muscle weakness
• Skin stiffness and
dryness
• Loss of fingers and toes
• Eye problems
• Blindeness
• Enlarged nerves
• Thickened skin on face
• Nasal stuffiness
• Bloody nose
• Laryngitis
• Collapsing of the nose
• Swelling of the lymph nodes
in the groin and armpits
• Scarring of the testes that
leads to infertility
• Enlargement of male breasts
There is two ways leprosy is presented:
Lepromatous Leprosy Symptom

21. Tuberculoid Lepromatous
CMI to M leprae +++ ---
Lepra bacilli in tissue -/+ ++++
Lepromin test +++ ---
CD4/CD8 > 1 <1
Plasma cells in lymphoid
tissue
+ ++++
Lymphocytic ifiltration of
lesion
++++ ---
Lesion Scaly Nodular

23. MechanismofNerveDamage
Scollard, DM et al. 2006. “The continuing challenges of leprosy.”
Clinical microbiology reviews 19, no. 2: 338-81.
1. EntryThrough
BloodVessels
2. Inflam
matory
Response
3. Demyelination

24.  SensoryLoss
 Paralysis
 Deformities
OutcomesofNerveDamage
Brought to you by

26. SensoryLossCanLeadto
SecondaryInfectionsandSevere
Deformities

27. Lepromin test
•Detects delayed hypersensitivity
•Described by Mitsuda (1919)
•Prepared from boiled bacilli-rich lepromatous
lesions
•Biphasic reaction:
•Fernandez reaction: erythema & induration
in 24-48 h
•Mitsuda reaction: indurated skin nodule,
may ulcerate; starts in 1-2 weeks, peaks in 4
weeks

28. Lepromin test
•Not used for diagnosis
• To classify the lesions (+ve in tuberculoid, -ve
in lepromatous)
•To assess prognosis & response to treatment
(+ve reaction – good prognosis)

29. •Lab. Diagnosis
Specimens :
1. Scrapings from
Lesion ,Nasal mucosa and ear lobule
Z-N staining.
Acid fast bacilli
Live bacilli : Solid, uniformly stained.
Dead bacilli :Fragmented and granular.

30. 1. Bacteriological index:
2. Morphological index(% of uniformly stained bacilli)
= Uniformly stained bacilli X 100
Total number of bacilli
• Bacteriological index ranges from 1 to 6+ as shown below:
• 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+
• 100-1,000 bacilli per filed = 5+
• More than 1,000 bacilli, clumps and groups in every field = 6+

31. 2. Skin & Nerve biopsy.
3. Lepromin test : To know prognosis.
Not for diagnosis.
5. Serological test :
ELISA .
6. Molecular diagnosis: Identifying DNA codes for
65 & 18-kDa M.leprae proteins.

32. Multibacillary or Lepromatous Laprorosy

33. TREATMENT

34. 1941:Discoveryof Dapsone
 Inhibitsnucleicacid
synthesis

35. 1960’s:Rifampicinand
ClofazimineDiscovered
 Rifampicin (Rifampin):
InhibitRNA synthesis
 Clofazimine:
Anti-
inflam
matory

36. 1981:WHO ProposesMulti-
DrugTherapy (MDT)
 Combinationof DAPSONE,
RIFAMPICIN, and CLOFAZIMINE
+ +

37. 1995:WHO DistributesMDTDrugs
forFreetoWorldwidePatients

38. 1999:GlobalAlliancetoEliminate
LeprosyAsaPublicHealth Problem

39. Treatment
Type of
leprosy
Drug Dose Frequency Total
duration
Paucibacillary Rifampicin
Dapsone
600 mg
100 mg
Monthly
Daily
6 months
Multibacillary Rifampicin
Dapsone
Clofazimine
600 mg
100 mg
300 mg
+ 50 mg
Monthly
Daily
Monthly
Daily
2 years
or more

43. Lepers are outcasts……