This document provides information about leprosy (Hansen's disease), including: - It is caused by Mycobacterium leprae and primarily affects the skin, nerves, and mucosa. - There are several classification systems including paucibacillary, multibacillary, lepromatous, tuberculoid, and borderline. Classification depends on immune response and bacterial load. - It remains a major public health problem with millions of cases worldwide, especially in India, Brazil, and African countries. Treatment involves multidrug therapy to prevent disability.

1. Dr DEEPAK CHAUDHARY
SENIOR DEMONSTRATOR
GMC AMBIKAPUR

2. Infection and Disease
 Leprosy
 Vedas
 Bible
 Fear and Social outcasts
 Hansen 1868 - Identifies First microorganism.
 Least understood and not cultured in artificial
medium

3.  It is a disease of Historical importance.
 World's oldest recorded disease
 First described KUSHTA in ancient indian text
(sushruta samhita) in 600 B.C.
 Stigmatized disease
 Gerhard Henrick Armauer Hansen discovered
mycobacterium leprae hence leprosy is also called
hansen’s disease.
 First bacterium to be identified capable of causing
human disease.
 Cannot be cultivated on culture media.
 More than 6-8 million cases of leprosy worldwide,
60% of which are in india.
What is Leprosy?

4.  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.,
 It has left behind a terrifying image in
history and human memory of mutilation,
rejection and exclusion from society.
LEPROSY

5. Mycobacterium leprare
MORPHOLOGY
 They are acid fast bacilli arranged singly, in parallel
bundles (like rolls of cigarette in a packet) or in
globular masses.
 Appear as straight or curved rods
 Size is 1 – 8 microns x 0.5 microns.
 less acid fast than tubercle bacilli.
 Live bacilli stain uniformly & appear solid.
 Dead bacilli appear as fragmented with granules.
 Intracellularly They appear as bundles of bacilli
bound together by lipid like substance THE GLIA.
 These masses are known as GLOBI. Parallel rows
of globi Presents a cigar bundle appearance.

6. GLOBI

7. GLOBI

9. Most Important
experimental
Animal

10. Structure of mycobacterium
leprae

11. Ultrastructural characteristics of M. leprae
 The ultrastructure of M. leprae is common in the
genus Mycobacterium. Electron microscopy has shown that
this bacillus has cytoplasm, plasma membrane, cell wall, and
capsule. The cytoplasm contains common structures in gram-
positive microorganisms.
 The plasma membrane has a permeable lipid bilayer
containing interaction proteins, which are the protein surface
antigens.
 The cell wall attached to the plasma membrane is composed
of peptidoglycans bound to branched chain polysaccharides,
consisting of arabinogalactans, which support mycolic acids,
and lipoarabinomannan (LAM), similarly to
other mycobacteria.
 The cell wall has a characteristic phenolic glycolipid (PGL-1).
Its carbohydrate antigenic determinant has been synthesised.
 This triglycerride binds to the basal lamina of schwann cells.

12. Resistance
 Viable for 9 -16 days in warm humid
environment.
 In moist soil for 46 days
 Direct sunlight for two hours.
 Ultraviolet light for 30 minutes.

13. Leprosy
 A chronic granulomatous disease primarily
involving Skin, Peripheral nerves, Nasal
mucosa
 Incubation period 3 -15 years.
 Source of infection- nasal discharge & skin
lesions.
 Portal of entry- inhalation of infectious aerosols,
through skin contact (damaged skin) and
prolonged close contact with infective paitents.
 Principle target cell- schwann cell, resulting in
nerve damage causing manifestations of
leprosy (anesthesia and muscle paralysis).

14. Classification ( Madrid )
 Lepromatous
 Tuberculoid
 Dimorphic/borderline
 Indeterminate.
 Type of disease is a reflection of the immune status of
the host.
 Delayed hypersensitivity determines the response of
the host to infection and production of clinical type.
 Lepromatous and tuberculoid are two extreme or polar
forms of leprosy.
 Lepromatous leprosy- CMI is absent or deficient
 Tuberculoid leprosy- CMI is intact.
 Indeterminate- between the two, can acquire any form.

15.  Borderline- Lesions clinically resemble
tuberculoid leprosy but bacteriologically
resemble lepromatous type.
 Therefore the clinical type of leprosy is not
permanent and changes with chemotherapy
and alteration in immune status of the host.

16. 1. lepromatous
 Seen where host resistance is low.
 Bacilli seen in large numbers as globi inside lepra cells or
extracellularly.
 Known as MULTIBACILLARY disease.
 Antibodies are produced, but they do not prevent bacterial
proliferation.
 Skin lesions tend to be multiple and symmetrical, preferably located
in the colder areas of the body, characterized by hypochromic,
erythematous or bright brownish spots with indefinite borders.
 As the disease progresses, lesions infiltrate forming plaques and
nodules (lepromas).
 Nodules ulcerate and bacilli invade the mucosa of nose, mouth and
upper respiratory tract and are shed in nasal and oral secretions.
 Mucous membranes, eyes, bones, joints, lymph nodes, blood
vessels, upper airways, teeth, and internal organs may be affected
 Lepromin test is negative due to deficient CMI.

17. Clinical features
 Lesions are large, diffuse and granulomatous
and multibacillary.
 Diffuse sensory nerve involvement and
patchy anaesthesia is common.
 Facial disfigurement is commonly observed.
Results in leonine facies.
 paitents are anergic to lepromin.

18. Lepromatous leprosy

19. Characteristics of clinical forms
 Lepromatous leprosy: ichthyosiform appearance of the skin of the legs and
lepromas
Lepromatous leprosy:
infiltrated face and
madarosis

20. Actas Dermosifiliogr.2013;104:554-63
 Typical leonine facies in lepromatous leprosy.

21. 2.Tuberculoid type
 Localised form of the disease and Seen in
paitents with high degree of resistance.
 CMI is intact and lepromin test is positive.
 Skin lesions are few and sharply demarcated.
 There is early neural involvement which
leads to deformities in hands and feet.
 Bacilli are scanty in lesions. This is known as
Paucibacillary disease.

22. Tuberculoid leprosy: a single,
hairless plaque with well-defined
borders.

23. Characteristics of clinical forms
 Tuberculoid leprosy: well-defined annular erythematous plaque on the dorsum of the
hand
Lepromatous leprosy: dry and barely
discernible hypochromic spots on the
arm

24. Tuberculoid leprosy (TL)

25. 3.Dimorphous/ Borderline type
 Lesions clinically resemble tuberculoid leprosy
but bacteriologically resemble lepromatous
type.
 Can shift to any spectrum depending on
chemotherapy or alterations in host resistance.

26. Characteristics of clinical forms
 Borderline leprosy: polymorphic appearance of the lesions
Borderline leprosy:
brownish erythematous
plaques (foveal spots) in the
trunk

27. 4. Indeterminate type
 There is early unstable tissue reaction not
characteristic of either lepromatous or
tuberculoid type.
 Lesions heal spontaneously in some person
and in others it may progress to lepromatous
or tuberculoid type.

28. Indeterminate leprosy: hypochromic spots with indefinite borders on the face

29. Ridley and Jopling
Classification
 Based on clinical, histopathological and
immunological findings, Ridley and jopling
classified spectrum of leprosy into 5 types:
 Tuberculoid (TT)
 Borderline Tuberculoid (BT)
 Borderline (BB)
 Boderline lepromatous (BL)
 lepromatous (LL)

32. WHO classification
 Two Groups-
 Paucibacillary & Multibacillary.
 Paucibacillary (PB):
 Includes al cases of tuberculoid types and
some cases of borderline type.
 The number of M. leprae in the body is small
(less than 1 million) and a skin smear test is
negative.
 The patient presents five or fewer skin lesions.
Most cases of leprosy are PB.

33. Multibacillary
 Includes all cases of lepromatous type and
some cases of borderline type.
 M. leprae can multiple in the body almost
without any check and is thus present in high
numbers.
 The bacillus has likely spread to almost all
areas of skin and peripheral nerves.
 A skin smear test is positive and the patient
presents more than five skin lesions.

34. EPIDEMIOLOGY
 Exclusive human disease. Only source of infection is
patient.
 Patient with untreated lepromatic leprosy my discharge
upto 8 x 10 bacilli in one nose blow.⁸
 Asymptomatic infection is quite common in endemic
areas.
 Not highly communicable. Incubation period is around 2 –
5 years.
 6 to 8 million people are affected worldwide and 600,00
new cases are estimated annually, 60% of them of which
are in india
 Mostly confined to underdeveloped areas of the tropics
and southern hemisphere (asia, africa, latin america and
the pacific)

35.  More than 80% of the world cases are observed
in india, china, myanmar, indonesia, brazil,
nigeria, madagascar and nepal.
 India has maximum prevalence with 13 of global
total. 90% cases are tuberculoid.
 Odisha & bihar have highest prevalence ( > 5 per
1000 population) and haryana the least (< 0.1 per
1000)

36. Immunity
• Innate Immunity exists against lepra bacilli in
humans.
 Infection induces both Humoral & Cellular immune
response.
 Type of leprosy is determined by status of CMI.
 CMI destroys the bacilli and determines the
recovery.
 Adequate CMI can manifest with Tuberculoid
leprosy.
 Deficient CMI develops lepromatous type of
disease.
 Lepromatous leprosy patient have large number of
CD 8+ lymphocytes in contrast to tuberculoid
lesions which contain CD 4+ cells.

37. Lepra reactions
 Lepra reactions occur in 30-50% of patients with
leprosy. They may occur before, or more often, after
the start of treatment and are induced by medicines,
stress and surgical procedures.
 There are 3 main types of reaction.
 Lepra type I (reversal) reaction
 Lepra type I (reversal) reaction often affects those with
borderline shifting toward tuberculoid type, as the cell-
mediated immune system improves in the first few
months of drug treatment or for some other reason
such as pregnancy.
 Type 1 reactions result in fever, red swollen skin, and
tender peripheral nerves.
 Treatment requires oral corticosteroids and
nonsteroidal anti-inflammatories.

38.  Lepra type II reaction
 Lepra type II reaction is also called erythema
nodosum leprosum (ENL).
 It affects those with borderline lepromatous or
lepromatous leprosy and is a humoral (antibody-
antigen) reaction to immune complexes.
 Tends to occur few months after institution of
chemotherapy.
 ENL presents as painful red nodules (lumps),
which can blister or ulcerate, accompanied by
fever, malaise, joint pain, nerve pain, eye disease
and involvement of other organs.

39. Erythema nodosum leprosum: inflammatory nodules in the
upper limb

40. Lepromin Test
 Mitsuda in 1919 – skin test – delayed hypersensitivity.
 Lepromin (antigen) is boiled extract of lepromatous tissue in
isotonic saline – rich in lepra bacilli.
 Mordern antigens are prepared from armadillo derived lepra
bacilli (lepromin A) and standardised ( 4 x 10 bacilli per ml).⁷
 Injection of 0.1 ml of lepromin in an individual causes a
biphasic reaction.
 Events in the reaction Biphasic reaction -
 Early or Fernandez Reaction – erythema and induration of
10-30 mm diameter appears 24 – 48 hours, remains for 3 –
5 days, like tuberculin reaction, little significant.

41.  Late Mitsuda reaction
 Mitsuda reaction occurs after 1 – 2 weeks,
prominent after 3 - 5 weeks with diameter of 3-
5 mm.
 Skin reaction consists of an indurated nodule.
 Histology of nodule shows nfiltration with
Lymphocytes ,Epitheloid cells and giant cells.
 Indicates CMI
 Positive mitsuda reaction indicates resistance
to leprosy.

42. Significance of Lepromin Test
 Test is not employed for Diagnosis of leprosy.
 Classification of leprosy- test is negative in
lepromatous leprosy but positive in tuberculoid
leprosy.
 Effectiveness of CMI
 To asses the prognosis and response to
therapy. Positive test indicates good
response /recovery while Negative indicates
Bad prognosis.
 To assess the resistance of individuals to
leprosy

43. Diagnosis of Leprosy
 Diagnosis must therefore be made by doing a
biopsy, in which a small piece of skin is taken
to analyse for the leprosy bacterium.
 Early diagnosis is very important because it
can prevent permanent deformities and
disability.
 For routine examination specimen are
collected from nasal mucosa, skin lesions and
ear lobules.

44. 1. Specimens
 Nasal smear
 Skin smear
 Slit skin smear
 Nerve biopsy
2. MICROSCOPY
 Diagnosis consists of demonstration of acid fast
bacilli in the lesions.
 Smears are stained by Z.N staining technique.
 5% sulphuric acid is used as decoloriser.

45. Smear Examination
 1 + (1 -10 bacilli / 100 fields)
 2 + (1-10 bacilli / 10 fields)
 3 + (1 – 10 bacilli / one field)
 4 + (10 – 100 bacilli / one field)
 5 + (100 - 1000 bacilli /field)
 6 + (> 1000 bacilli /field)
 Number of Bacilli seen in each field is
recorded as Bacillary index.

46. The bacteriological index (BI)
 This is an expression of the extent of
bacterial loads. It is calculated by counting six
to eight stained smears under the 100 x oil
immersion lens.
 Indicates the Prognosis of the Disease.
 Total score in all smears / Number of
smears
 Eg 16/8 =2
 So the index is 2

47. The Morphological index (MI)
 This is calculated by counting the numbers of
solid-staining acid-fast rods. Only the solid-
staining bacilli are viable.

48. 3. Culture
 Mouse foot pad
 Armadillo
4. Serology
 Detection of antibody against M.leprae
phenolic glycolipid antigen is a specific
diagnostic test.

49. Treatment of Leprosy
 Multidrug regime
 Paucibacillary lesions:-
 Rifampicin 600 mg / once month
 Dapsone 100 mg/day for 6 months
 Multibacillary lesions:-
 Rifampicin 600 mg / once month
 Dapsone 100 mg/day
 Clofazimine 50 mg daily
 Continue for two years.

50.  Other Drugs for Leprosy
 Ethionamide
 Prothionamide.

52. THANK YOU