Leprosy for undergraduate medical students

Ali Gargoom
Assistant Professor of Dermatology
Faculty of Medicine
Benghazi-University
Benghazi-Libya

1. LEPROSY
Ali M. GargoomAli M. Gargoom
MB,ChB. MSc. MD
Assistant Professor Assistant Professor
Department of DermatologyDepartment of Dermatology
Faculty of Medicine.Faculty of Medicine.
Benghazi University Benghazi University

3. An ancient, chronic infectious disease An ancient, chronic infectious disease
caused by caused by Mycobacterium leprae Mycobacterium leprae . .
It principally affects the skin andIt principally affects the skin and
peripheral nerves.peripheral nerves.
Leprosy (Leprosy (Hansen’s diseaseHansen’s disease))

4. M. leprae is discovered by Hansen from Norway in 1873

5. BACTERILOGYBACTERILOGY
They are straight or slightly curved rod-like bacilli. They are straight or slightly curved rod-like bacilli.
It measure about (It measure about (3 x 0.5 micrometer)3 x 0.5 micrometer)..
Weakly Gram +ve & stained by Ziehl-Neelsen method.Weakly Gram +ve & stained by Ziehl-Neelsen method.
 M. leprae is an obligate intracellular acid-fast bacillus.M. leprae is an obligate intracellular acid-fast bacillus.
 Has never been grown in artificial media.Has never been grown in artificial media.
 It grow in nine - banded armadillo.It grow in nine - banded armadillo.

6. The nine - banded armadillo

7. BACTERILOGY BACTERILOGY (cont.)(cont.)
Replicate very slow (every 12 days once).Replicate very slow (every 12 days once).
Has an affinity for macrophages & Schwann cell.Has an affinity for macrophages & Schwann cell.
It grows best at 27-30 C, hence its predilection It grows best at 27-30 C, hence its predilection
for cooler areas of the body. for cooler areas of the body.
Skin, peripheral nerves, anterior chamber of the Skin, peripheral nerves, anterior chamber of the
eye, upper respiratory tract & testes. eye, upper respiratory tract & testes.

8. Mode of transmissionMode of transmission
The exact rout of transmission is not fully known .The exact rout of transmission is not fully known .
The spread of leprosy is believed to be via
nasal discharge (Droplets infection).(Droplets infection).
Every 1 cc of nasal secretion contains 1- 2millions lepra bacilli

9. Other modes of transmissionsOther modes of transmissions
1.Contact through the skin (rare).
2.Arthropod-born infection (rare).
3.Through placenta and milk.

Leprosy is not STD or directly inherited. Leprosy is not STD or directly inherited.

10. EpidemiologyEpidemiology
Leprosy is a disease of developing countries but affects
all races.
Registered cases of leprosy have fallen from 5.4 millions
worldwide in 1985 to below one million in 1998.
 80% of the worldwide cases are found in five countries,
namely India, Mynamar, Indonesia, Brazil and Nigeria.

11. Epidemiology (cont.)Epidemiology (cont.)
The incubation period range from 2 -5 years.The incubation period range from 2 -5 years.

Males appear to be twice common than females.Males appear to be twice common than females.
Bimodal age (10-14years & 35-44 years).Bimodal age (10-14years & 35-44 years).
Children are more susceptible to disease.Children are more susceptible to disease.
Genetic factors, e.g. HLA markers may Genetic factors, e.g. HLA markers may
determine the type of leprosy which the patient determine the type of leprosy which the patient
develops .develops .

12. 0
1000000
2000000
3000000
4000000
5000000
6000000
1985 1987 1989 1991 1993 1995 1997 1999 2001
Global Trend in Registered CasesGlobal Trend in Registered Cases

13. Predisposing or risk factorsPredisposing or risk factors
1.1.Residence in an endemic area.Residence in an endemic area.
2.2.Having a blood relative with leprosy.Having a blood relative with leprosy.
3.3.Poverty (malnutrition).Poverty (malnutrition).
4.4.Contact with affected armadillo.Contact with affected armadillo.

14. Classification & Clinical PresentationClassification & Clinical Presentation
Jopling Classification
Based on Host Immunity
TT BL LL
BT BB BL

15. Classification & Clinical Presentation Classification & Clinical Presentation
WHO Classification
Based on Bacterial Load
Paucibacillary Multibacillary
Slit Skin Smear
Positive Negative

16. LEPROSY
(Paucibacillary (PB (Multibacillary (MB
(Indeterminate Leprosy (IL
(Tuberculoid Leprosy (TL
(Borderline Tuberculoid (BT
(Borderline Borderline (BB
(Borderline Lepromatous(BL
(Lepromatous Leprosy (LL

17. CLINICAL PICTURE CLINICAL PICTURE
Indeterminate Leprosy
Tuberculoid Leprosy
Borderline Leprosy
BT BB BL
Lepromatous Leprosy

18. TT
BT BB BL LL
Skin Lesions
No. of Bacilli
Slit skin test
Immunity
Clinical spectrum of leprosy

19. Indeterminate Leprosy (IL)Indeterminate Leprosy (IL)
Usually single (multiple) macule / patche.Usually single (multiple) macule / patche.
Hypopigmented or faintly erythematous.Hypopigmented or faintly erythematous.
Sensation normal but sometimes imparied.Sensation normal but sometimes imparied.
The peripheral nerves normal.The peripheral nerves normal.
Slit skin smear negative. Slit skin smear negative.

20. Indeterminate leprosy :Hypopigmented patch, sensation normal,
.no palpable peripheral nerve and slit skin smear negative

21. Tuberculoid Leprosy (TL) Tuberculoid Leprosy (TL)
Usually single but may be few (Usually single but may be few (<<5).5).
Hypopigmented / erythematous plaque.Hypopigmented / erythematous plaque.
Varying in size from few Varying in size from few MMMM to several to several CMCM..
Well defined borders.Well defined borders.
Sensation markedly imparied.Sensation markedly imparied.
Enlarged peripheral nerve.Enlarged peripheral nerve.
Slit skin smear negativeSlit skin smear negative

22. Tuberculoid leprosy: Two hypopigmented patches, hypoasthetic
.well defined borders, palpable peripheral nerve and SSS negative

23. Tuberculoid Leprosy: Annular, erythematous, anasthetic patch with
.well defined and raised borders and SSS Negative

25. Borderline Leprosy (BL)Borderline Leprosy (BL)
(BT,BB,BL)(BT,BB,BL)
Few / many asymmetrical patches.
Partly well-defined borders.
Sensory impairments range from slight to
marked.
Slit skin smear usually positive.
P. nerves asymmetrically enlarged.

26. BLBLBBBBBTBT
Many Many Some Some FewFew(<5)(<5) .Lesion no .Lesion no
Roughly RoughlyLessLessWellWell Lesions bordersLesions borders
Slight Slight Moderate Moderate Marked Marked
Sensory Sensory
impairmentimpairment
Roughly Roughly
symmetrical symmetrical
Asymmetrical Asymmetrical Asymmetrical Asymmetrical Distribution of Distribution of
skin lesions skin lesions
Less Less
asymmetrical asymmetrical
Asymmetrical Asymmetrical Asymmetrical Asymmetrical Peripheral Peripheral
nervesnerves
MultibacillaryMultibacillary MultibacillaryMultibacillary PaucibacillaryPaucibacillary Type of leprosyType of leprosy
4+4++3 / +2+3 / +2
- - / 1+/ 1+
Slit skin smearSlit skin smear
Note: Sometimes patients may have BT/BB or BB/BL or BL/LL

27. Borderline Tuberculoid Leprosy: Well-defined large anaesthetic patches
.with satellite lesions. SSS Negative

28. Borderline Borderline Leprosy: Less defined, asymmetrically distributed
.hypoaesthetic patches. SSS positive

29. Borderline Lepromatous Leprosy: Numerous, hypoaesthetic almost
.symmetrically distributed patches . SSS positive

30. Lepromatous Leprosy (LL)Lepromatous Leprosy (LL)
Very numerous ill defined lesions.Very numerous ill defined lesions.
(macules, patches, papules,and nodules).(macules, patches, papules,and nodules).
Symmetrically distributed allover the bodySymmetrically distributed allover the body
Loss of eyebrows and eyelashes.Loss of eyebrows and eyelashes.
Leonina facies.Leonina facies.
No sensory impairments in lesions .No sensory impairments in lesions .
Peripheral nerves symmetrically enlarged.Peripheral nerves symmetrically enlarged.
Slit skin smear always positive.Slit skin smear always positive.

33. Lepromatous Leprosy: Leonine Face

34. Diagnosis of LeprosyDiagnosis of Leprosy
1.Clinical Examination.
2.Slit Skin Smear.
3.Skin Biopsy.

35. 1.Clinical examination:1.Clinical examination:
What are the cardinal skin signs of leprosy ?What are the cardinal skin signs of leprosy ?
3.Hypopigmented or erythematus patch / plaque
2. Complete / partial loss of sensation.
3. Thickening of peripheral nerves.

36. 2.Slit Skin Smear2.Slit Skin Smear
Simple and valuable test.Simple and valuable test.
It is needed for diagnosis.It is needed for diagnosis.
Monitor the progress of the treatment.Monitor the progress of the treatment.

37. Slit Skin Smear (method).
Pinch the site tight.Pinch the site tight.
Incise.Incise.
Scrape & collect materialScrape & collect material
Smear on a slide.Smear on a slide.
Air dry & fix.Air dry & fix.
Stain (Z-N method)Stain (Z-N method)

38. Slit Skin Smear (site).Slit Skin Smear (site).
Ear lobe.
Forehead.
Gluteal region.
Active edge of patch.

39. Slit Skin Smear (Reporting the smear).
Bacteriological indexBacteriological index
no bacilli in 100 fields – 0no bacilli in 100 fields – 0
bacilli in 100 fields 1-10 :+1bacilli in 100 fields 1-10 :+1
bacilli in 10 fields 1-10 :+2bacilli in 10 fields 1-10 :+2
bacilli in 1 field 1-10 :+3bacilli in 1 field 1-10 :+3
bacilli in 1 field 10-100 :+4bacilli in 1 field 10-100 :+4
in 1 field 100-1000 :+5in 1 field 100-1000 :+5
.(bacilli field (globi 1000< :+6.(bacilli field (globi 1000< :+6
Morphological indexMorphological index
The percentage of living bacilli to
the total number of bacilli in the
.smear

40. Skin Biopsy

41. Tuberculoid Leprosy (TT).
Histologically TT resemble tuberculosis.
Characterized by tuberculoid granuloma,
made up of epitheloid cell in the center
surrounded by abundant Langhans giant
cells, lymphocytes and foci of caseating
necrosis.
No acid-fast bacilli

42. Lepromatous Leprosy (LL)
Characterized by diffuse infiltration of Characterized by diffuse infiltration of
foamy macrophages in the dermis.foamy macrophages in the dermis.
Acid-fast bacill are present inside these Acid-fast bacill are present inside these
foamy cells eighter singly or in globi.foamy cells eighter singly or in globi.
There is free subepidermal zone (grenz There is free subepidermal zone (grenz
zone).zone).
Lymphocytes are scanty and giant cells Lymphocytes are scanty and giant cells
typically absent.typically absent.

43. TREATMENT

44. LEPROSY IS A CURABLE DISEASELEPROSY IS A CURABLE DISEASE
Leprosy treatment is simple, available free & Leprosy treatment is simple, available free &
the drugs are supplied in backs that contain the drugs are supplied in backs that contain
correct dose for 4 weeks.correct dose for 4 weeks.
All you have to do is decide which course of All you have to do is decide which course of
treatment the patient needs and make sure treatment the patient needs and make sure
that he take it regularlythat he take it regularly. .

45. Drugs used in Leprosy treatment
What are the three commonly used drugs?What are the three commonly used drugs?
§Dapson.Dapson.
§Rifampicine.Rifampicine.
§ClofazimineClofazimine..
The combination of these three drugs isThe combination of these three drugs is
known as Multi Drug Therapy (MDT)known as Multi Drug Therapy (MDT)

46. Rifampicin is highly bactericidal 99.999% Rifampicin is highly bactericidal 99.999%
of bacilli will be killed within 3 monthly of bacilli will be killed within 3 monthly
doses.doses.
Dapsone & clofazimine are weekly Dapsone & clofazimine are weekly
bactericidal, but in combination will bactericidal, but in combination will
kill 99.999% of bacilli within 3 months.kill 99.999% of bacilli within 3 months.
MDT (Chemotherapy) renders Leprosy
patients non-infectious.

47. MDT for PB leprosy
6 months
Monthly dose
Rifampicin 600mg
Dapsone 100 mg
Daily dose
Dapsone 100 mg

48. Multidrug Therapy (MDT) for Paucibacillary Leprosy (PB)

49. MDT for MB leprosy
24 months
Monthly dose
Rifampicin 600mg
Clofazimine 300 mg
Dapsone 100 mg
Daily dose
Dapsone 100mg
Clofazimine 50 mg

50. Multidrug Therapy (MDT) for Multibacillary Leprosy (MB)

51. Multi Drug TherapyMulti Drug Therapy
24 months
6 months

52. COMLICATIONS COMLICATIONS
OFOF
LEPROSY LEPROSY

53. COMLICATIONS OF LEPROSY
1.Reactions.
2.Complications of peripheral nerves.
3.Complications of eyes
4.Complication of bones

54. It’s a sudden change in the clinical picture of the disease because It’s a sudden change in the clinical picture of the disease because
of conflict between the bacilli and the immune system of the host.of conflict between the bacilli and the immune system of the host.
What are the precipitating factors ?
1.1.Effective treatment.Effective treatment.
2.2.Intercurrent infection.Intercurrent infection.
3.3.Physical stress.Physical stress.
4.4.Surgical operation.Surgical operation.
5.5.Pregnancy.Pregnancy.
6.6.Sometimes spontaneously.Sometimes spontaneously.
LEPROSY REACTIONLEPROSY REACTION

55. TYPES OF LEPRA REACTIONSTYPES OF LEPRA REACTIONS
Type I
•Change in host CMI
•Seen in borderlines
•Skin and nerve lesions
Type II
•Antigen antibody
•Seen in LL & BL leprosy
•Skin, nerve & systemic
involvement

56. Type I Lepra ReactionType I Lepra Reaction
(Reversal Reaction)(Reversal Reaction)
Seen in BT, BB & BL.Seen in BT, BB & BL.
Sudden onset.Sudden onset.
Eythematous & odematous changes in old lesions.Eythematous & odematous changes in old lesions.
Appearing of new lesions.Appearing of new lesions.
Tenderness & swelling of peripheral nerves.Tenderness & swelling of peripheral nerves.
Treatment of type I Reaction:Treatment of type I Reaction:
8.8.Continue MDT.Continue MDT.
9.9.NSAID.NSAID.
10.10.Systemic corticosteroid.Systemic corticosteroid.

57. Type II Lepra Reaction (ENL)Type II Lepra Reaction (ENL)
Acute onset of constitutional symptoms.Acute onset of constitutional symptoms.
Appearance of ENL-like skin lesions.Appearance of ENL-like skin lesions.
Visceral manifestations includes :- Visceral manifestations includes :-
Iridocyclitis, hepato-splenomegaly, epididmo-Iridocyclitis, hepato-splenomegaly, epididmo-
orchitis, nephritis, pleuritis, lymphadenitis & orchitis, nephritis, pleuritis, lymphadenitis &
neuritis.neuritis.

Treatment of type II Reaction:Treatment of type II Reaction:
Continue MDT.Continue MDT.
NSAIDNSAID
Thalidoamide Thalidoamide ( clofazimine, corticosteroid )( clofazimine, corticosteroid )

58. Erythema Nodosum Leprosum Erythema Nodosum Leprosum((ENL((ENL
Erythematous.Erythematous.
Tender .Tender .
Subcutaneous.Subcutaneous.
Resolve in 7 to 10 days.Resolve in 7 to 10 days.
Appear in crops.Appear in crops.
Occur any whereOccur any where
Associated with fever & joint pains.Associated with fever & joint pains.
May be vesicular, pustular & may May be vesicular, pustular & may
ulcerateulcerate

59. COMPLICATIONSCOMPLICATIONS
OF OF
PERIPHERAL NERVESPERIPHERAL NERVES

60. Peripheral nerves
Sensory Motor Autonomic
Hypoaestesia / anaestesia Muscle paralysis Lack of sweating & sebum
Ulcers Ulnar nerve Claw hand
Radial nerve Wrist drop
Lt. popliteal Foot drop
Post. tibial Claw toes
Facial lagophthalmous
Dry skin
Cracked skin
Ulcers

64. COMPLICATIONS COMPLICATIONS
OFOF
EYEEYE

65. Involvment of the ophthalmic division of the (5
th
.( trigeminal nerve
Corneal sensation imparment
Patients ignore injuries
keratitis, conjunctivitis and ulcers
Involvment of zygomatic & temporal braches of the (7
th
..( facial nerve
Lagophthalmos
(Unable to close the eye (unbliking stare

68. Complications Of BonesComplications Of Bones
Bone damage in Leprosy is confined
to bones of hand , feet & skull.

70. In the skull two pathognomonic changes occurs
.Atrophy of anterior nasal spine -1
Nasal collapse
.Atrophy of maxillary alveolar process -2
Loss of upper central incisors
These two skull changes known as ”facies leprosa ”

72. Thank you.Thank you.