This document provides a review on leprosy, including its epidemiology, causative agent, classification, symptoms, diagnosis, treatment and preventive measures. Some key points: - Leprosy is caused by Mycobacterium leprae and mainly affects India, which records the highest number of new cases globally each year. - It can be classified as paucibacillary or multibacillary depending on symptoms. Multibacillary leprosy involves more sites in the body. - Diagnosis involves skin smear tests and examination under microscopy. Treatment is multidrug therapy including dapsone, rifampicin and clofazimine over 6-12 months depending on

1. REVIEW ON LEPROSY
by
D. Santhi Krupa
Assistant Professor,
Department of pharmacology
VIJAYA INSTITUTE OF PHARMACEUTICAL SCIENCES FOR WOMEN
VV

2.  Introduction
 Epidemiology
 Causative Agent
 Classification of Leprosy
 Cardinal Features of Leprosy
 Diagnosis of Leprosy
 Treatment
 MultidrugTherapy In Leprosy
 Complications of MDT
 Relapses
 Preventive Measures
 Conclusion

3.  Leprosy is a chronic infectious disease caused by
Mycobacterium leprae, discovered by Norwegian physician
in 1873.
 The first known written reference to the disease was found
on Egyptian papyrus in about 1550 B.C. The disease was
well recognized in ancient China, Egypt, and India.

4.  According to the WHO research, India continues to
record the highest number of new leprosy cases in
the world.
 It currently has about 54% of all the new leprosy
cases in that 48,000 women and 13,610 children are
newly detected with leprosy

5.  Leprosy is a chronic infectious disease caused by
Mycobacterium leprae, an acid-fast, rod-shaped bacilli.
Different forms of existence of Mycobacterium leprae
Solid
Granular
Fragments
Globi

6.  The maximum incubation period reported is as
long as 30 years
 The average incubation period is between three
and ten years

7.  Nasal secretions
 Skin

8. Ridley Jopling Classification
Lepromatous leprosy
-Involvement of skin, nerves, reticuloendothelial
system
Tuberculoid leprosy
- Involvement of skin or nerves or both

9. Borderline leprosy
-Skin lesions are macular, infiltrated, or both,
with the earliest lesions being macules that are
erythematous or hypopigmented
Indeterminate leprosy
-single macule with uncharacteristic histology
WHO classification of Leprosy :
a) Paucibacillary (PB)
b) Multibacillary (MB)

10. According to WHO, features of Leprosy include
a) PAUCIBACILLARY (PB) PATCHES:
• Hypopigmentation
• Anesthesia (Loss of sensation)
• Dryness (Loss of sweating)
• Loss of hair growth (Not scalp hair)
• Macular/ Elevated/ Erythematous

11. b) MULTIBACILLARY (MB):
• Nasal stuffiness
• Involvement of peripheral nerves
• Upper palate perforation
• Loss of eyebrows (Madarosis)
• Lagopthalmos (unilateral/bilateral)
• Gynecomastia

12.  Skin Smears Test
 Bacteriological Examination
The
Bacteriological
index (BI)
The
Morphological
index (MI)
Thin Layer Chromatography profiles

13.  In MB patients, there will be decreased levels of SOD,
glutathione .
 They are unable to produce sufficient amount of antioxidant to
cope up with the increased oxidative stress in them.
 Providing nutritional supplementation may present a novel
approach for fast recovery. Administration of exogenous
antioxidants like vitamin C, tocopherols would prevent tissue
damage and make the patient therapeutically benefited.

14. Classification of Antileprotic drugs:
1) Sulfone - Dapsone(DDS)
2) Phenazine derivative - Clofazimine
3) Antitubercular drugs – Rifampicin, Ethionamide
4) Other antibiotics – Ofloxacin, Minocycline

15. Dapsone
 Dapsone is a competitive antagonist of
paraminobenzoic acid (PABA)
 Prevents normal bacterial utilization Of PABA for
the Synthesis Of Folic Acid
 Bacteriostatic or weakly bactericidal against
M. leprae

16. Clofazimine (CLF):
CLF was a phenazine dye, which preferentially
binds to mycobacterial DNA inhibits both
mycobacterial growth and exerts a slow bactericidal
effect on M. leprae.
Rifampicin :
It’s a highly bactericidal against M. leprae by
inhibiting bacterial RNA synthesis and blocks RNA
transcription.

17. Ofloxacin (OFLX):
 OFLX, a synthetic fluoroquinolone, acts as a
specific inhibitor of bacterial DNA gyrase and has
shown efficiency in the treatment of M. leprae .
Minocycline :
It inhibits bacterial protein synthesis by binding
into 30s and 50s ribosomal subunits of susceptible
bacteria.

18. Type of
Leprosy
Daily, Self-
Administered
Monthly
Supervised
Months of
Treatment
Multibacillary Dapsone 100 mg Rifampicin 600 mg
12
6
Paucibacillary Dapsone 100 mg Rifampicin 600 mg
Clofazimine 300 mg

20.  MDT and Drug-resistance
 Leprosy reaction and its treatment
Type 1 lepra reactions or reversal reactions are
associated with the development of M.
leprae antigenic determinants.
Type 2 lepra reactions (erythema nodosum
leprosum), are associated with circulation and
tissue deposition of immune complexes.

21.  The relapse rates after release from Dapsone
have varied from 1% to 17% for tuberculoid
leprosy and from 2% to 30% for lepromatous
leprosy.

22.  Vaccination against the leprosy bacillus may be
considered. BCG vaccination is reported to be
partially effective for protection against leprosy
 A mixed vaccine containing BCG and ICRC
bacilli is under trails for clinical use.

23. Throughout the history, the badly affected
leprosy patients are hated by the families and
communities. In present scenario with the
advancement in the treatment, most cases are
recovered. If there are new cases in India, in future
they can be reduced by using the mixed vaccines
and the severity can be decreased by detecting the
disease in the early stages by simple techniques
like TLC.

24.  Ahmad RA and Rogers HJ (1980). Plasma and
salivary pharmacokinetics of dapsone estimated by
a thin layer chromatographic method. Eur J Clin.
Pharmacol; 17:129-33
 Amuda P (2003). A study on the infectivity among
the Relieved From treatment (RFT) Leprosy patients
in Warangal. Dissertation submitted to Kakatiya
University for the partial fulfillment for the award
of M.Pharm (Pharmacology).
 Anton ES, Sandrock AW, Matthew WD (1994). A
21kDa protein of M. leprae

25.  Cochrane RG (1964). Leprosy in theory and
practice, (Cochrane RG and Davey TF, Eds) p. 613.
 Cole ST, Eiglmeier K, Parkhill J, James KD,
Thomson NR, Wheeler PR (2001). Massive gene
decay in the leprosy bacillus. Nature; 409: 1007-11.
 Cornbrooks CJ, Carey DJ, McDonald JA, Timply
R, Bunge RP (1983). Differentiation of axon-
related Schwann cells in vitro. I. Ascorbic acid
regulates basal lamina assembly and myelin
formation. Proc Nat Acad Sci., USA 80:3850–3854.
 Davey TF (1974). The nose in Leprosy: Steps to a
better understanding (editorial) Lepr. Rev., 45:97.

26.  Prabhakar MC (1987a). Investigation into cultivation of M.leprae in a
nasal mucous medium. A preliminary report. Intl J Lepr.55: 561-562.
 Prabhakar MC (1987b). Uneven distribution of M. leprae in the skin of
LL patients. China. Lepr J., 3: 27-32.
 Prabhakar MC (1994). Comparative evaluation of AAFB from the nose
and the skin of Lepromatous Leprosy patients. China Lepr J., 10: 84-
86.
 Prabhakar MC, Appa Rao AVN, Krishna DR and Ramanakar TV
(1983) How much non-infectious are the “non-infectious”
Lepromatous Leprosy patients? Lepr. India. 55: 576-583.
 Prabhakar MC, Appa Rao AVN, Krishna DR and Ramanakar TV
(1983). How much non-infectious are the “non-infectious”
Lepromatous Leprosy patients? Lepr. India. 55: 576-583.
 Prasad N (2003). Bacteraemia among the relieved from treatment
(RFT) Dissertation submitted in partial fullfillment for the award of
the degree of the master of Pharmacy in Pharmacology by Kakatiya
University, Warangal. A.P.506009.

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