This document discusses leprosy (Hansen's disease), including its cause, epidemiology, transmission, classification, clinical features, diagnosis, and treatment. It is caused by the bacterium Mycobacterium leprae, which primarily affects the skin and peripheral nerves. Diagnosis involves examination of skin and nerves for lesions and loss of sensation. Treatment involves multidrug therapy (MDT) depending on classification as paucibacillary or multibacillary leprosy. Reactions can occur and require additional treatment such as corticosteroids.

1. DR. BIJAY KR.YADAV
Holly vision technical campus
Shankhamul, Kathmandu

2. Leprosy ( Hansen’s disease)
 A chronic infectious disease caused by the bacterium
“Mycobacterium Laprae”
 It is mainly a Granulomatous disease affecting : peripheral
nerves & mucosa of the upper respiratory tract.
 “Gerhard Henrik Armauer Hansen” was a physician which 1st
identified M. Leprae as the cause of leprosy in 1873
 Mycobacterium leprae is gram-positive & belongs to:
• kingdom: : Bacteria
• Family : Mycobacteriaceae
• Genus : Mycobacterium
• Spacies : M. leprae

3. Epidemiological factors
 Occurs at all age groups
 Peak age of onset : Between 10 – 20 years
 Males > Females
 Children most susceptible
 Immune status ( host resistance)
 Overcrowding
 Low socioeconomic status

4. Transmission of Leprosy
 Respiratory route : Inhalation of bacilli-laden droplets
 Cutaneous : Skin to skin contact
 GIT : Ingestion of food
 Intradermal : Inoculation by tattoos
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Not
Yet
Proven

6. Classification :
A. Ridley & Jopling classification: Based on
clinical, immunologic, histologic and bacteriologic
finding.
1. Tuberculoid Leprosy (TT)
2. Borderline tuberculoid leprosy (BT)
3. Borderline Borderline leprosy (BB)
4. Borderline lepromatous leprosy (BL)
5. Lepromatous leprosy (LL)

7. B. Indian classification
Non- lepromatous Indeterminate Lepromatous
•Maculo-
anesthetic
•Tuberculoid
•polyneuritic
•Indeterminate
•Borderline
•lepromatous

8. C. Therapeutic Classification (WHO)
 Paucibacillary leprosy (PB)
 Single lesion Paucibacillary leprosy (SLPB)
 Multibacillary leprosy (MB)

9. Clinical features :
Cardinal signs :
1. Hypo pigmented / erythematous skin lesions with
definite impairment of cutaneous sensations.
2. Enlargement and/ or tenderness of a peripheral nerves.
3. Skin smear for AFB Positive.

10. Indeterminate leprosy
• Solitary
• Ill-defined
• Hypo pigmented
macule
• Only partially
anesthetic

11. Tuberculoid (TT)
 Well defined
 Hypo pigmented
lesion
 Dry surface
 Moderately raised
margin.
 Completely anesthetic

12. Borderline Tuberculoid (BT)
 Erythemato-
hypochromic plaque
 Dry surface
 Raised
 Well defined margins
with satellite lesions
 Anesthetic

13. Borderline Borderline (BB)
 Erythematous
 Raised annular plaques
with central clearing and
sloping edges ( inverted
saucer appearance )
 Hypoesthetic
 Multiple, asymmetrically
thickened nerves

14. Borderline Lepromatous (BL)
 Thick erythematous
plaques on face and
ears.
 Not sharply delimited.
 No sensory
impairment.

15. Lepromatous Leprosy (LL)
 Extensive,
symmetrically
distributed
infiltration almost
coalescent macules
and plaques.
 Not anesthetic.

16. General aspect of R-J classification
Observation TT BT BB BL LL
No. of lesions Single
usually
Single or
few
Several Many Very many
Size of lesions Variable Variable Variable Variable Small
Surface of lesions Very dry Dry Slightly
shiny
Shiny Shiny
Sensation in lesion
( Not face)
Absent Mod -
markedly
diminished
Mod
diminished
Slightly
diminished
Not
affected
Hair growth in
lesions
Nil Markedly
diminished
Moderately
diminished
Slightly
diminished
Not
affected
AFB in lesions Nil Nil or
scanty
Moderate
numbers
Many Very many
(globi)
Lepromin test + + + + + or + + Negative Negative Negative

17. Diagnostic Tests
 Skin smears
 Nasal smears and nasal blows
 Skin biopsy
 Nerve biopsy
 Histamine test
 Sweating test
 Phenolic glycolipid (PGL-1)
 Polymerase chain reaction (PCR)

18. How to diagnose leprosy?
Examine skin
Check for patches
Test for sensation
Count the no. of patches
Look for damage to nerves

19. Treatment of Leprosy
 In 1982 WHO recommended
multi-drug therapy (MDT)
 Advantages of MDT: Better
cure of the disease.
 Shortened duration of
treatment.
 Better compliance by the
patient.
 Less chance of drug resistant.

20. Paucibacillary Leprosy
 Skin lesions – Not more than 5.
 Nerves - Not more than 1.
 Skin smear – Negative.
Treatment : PB leprosy (TT and BT)
 Monthly supervised: Rifampicin 600mg
 Daily, unsupervised: Dapsone 100mg.
 Duration of treatment - 6 months.

21. In Single lesion Paucibacillary leprosy (SLPB):
Only one anesthetic skin lesion and no nerve involvement &
AFB is –ve
Single dose ROM Therapy:
 (R) Rifampicin 600mg
 (O) Ofloxacin 400mg
 (M) Minocycline 100mg

22. Multibacillary Leprosy
 Skin Lesions - More than 5.
 Nerve - More then 1.
 Skin smear for AFB - Positive.
Treatment :
 Monthly, supervised : Rifampicin 600mg, Clofazamine
300mg
 Daily, unsupervised: Dapsone 100mg, Clofazamine 50mg.
 Duration of treatment: 1 year.

23. Leprosy reaction ( Reactional States )
A. Type 1 lepra reaction
B. Type 2 lepra reaction

24. Type 1 lepra Reaction
 Type 1 lepra reaction is due to
sudden improvement of Cell
mediated immunity CMI
(Upgrading or Reversal) or
worsening of CMI
(Downgrading).
 Skin lesions - Erythema,
swelling, tenderness of some or
all lesions, shiny, warm to touch.
 Fever and malaise: Unusual
 Nerve - swollen, tender and
painful. (sometimes nerve
abscesses).

25. Treatment
 Prompt treatment is of vital importance as permanent
nerve damage can occur.
 Oral Prednisone in tapering doses.
 Symptomatic treatment.
 Rest and splint.

26. Type 2 reaction
 Also known as Erythema
nodosum leprosum mediated
through humoral immunity.
 Occurs in lepromatous and few
cases of BL.
 Reaction due deposition of
antigen antibody complexes in
the lesions.
 C/F: ENL, neuritis, bone pain,
joint pain, fever, malaise,
lymphadenitis, rhinitis,
epistaxis, iritis, epididymo-
orchitis, proteinuria.

27. Treatment
 Thalidomide
 NSAIDs
 Clofazimine
 Corticosteroids (Prednisolone).