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Leprosy is a chronic granulomatous
infectious disease that attacks the nervous
system caused by acid fast bacilli
Mycobacterium leprae
M. leprae lies within the macrophages and
remain dormant
Leprosy cause deficiency in cell mediated
immunity
2

Leprosy attacks the different parts of the body
Leprosy destroys neurons in these areas, taking
feeling away from them
Leprosy also causes cartilage in those areas to
get absorbed back into the body, causing
fingers, toes, ears and nose to disappear
Leprosy also causes large bumps in the skin
that do not feel pain and do not heal
4

Infection usually transmitted from person to person
due to shedding of bacilli
To avoid leprosy, avoid close contact with someone
who has untreated leprosy
5

In the first stages of Leprosy, people’s lives are
not very affected, but eventually, people lose
their fingers and toes and become disfigured
Not only are the victims of Leprosy physically
disabled, but emotionally as well
In the later stages of leprosy, people lose their
sight, as well as most of the feeling in their
body
6

Nerve is
damaged and
broken by
leprosy
infection.
Large bumps (legions)
on the skin that do not
heel and cannot feel
pain.
Nerve
Leprosy infection
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Examine skin
Check for patches
Count the number of patches
Test for sensation
Check for damage to nerves
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Pale or slightly reddish patch
Loss of sensation in the patch
Signs of damage to nerves
Loss of sensation in hands/feet
weakness of muscles of hands/feet/face
visible deformity of hands/feet/face
9

The diagnosis is made based on finding definite
loss of sensation in one or more patches.
1-5 patches is paucibacillary (PB), more than 5
patches is multibacillary (MB) leprosy
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 Sulfones
 Dapsone, Sulfoxone, Acedapsone
 Phenazine derivative
 Clofazimine
Antitubercular drug
 Rifampicin
Antibiotics
 Fluoroquinolones – Ofloxacin, Sparfloxacin
 Macrolides – Clarithromycin
 Tetracyclines - Minocycline
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 M.O.A.
 Inhibition of bacterial folic acid synthesis
 Dapsone acts against bacteria and protozoa in the
same way as sulphonamides.
 That is by inhibiting the synthesis of dihydrofolic acid
through competition with para-amino-benzoate for the
active site of dihydropteroate synthetase
 Has antiinflammatory properties
12

 Pharmacokinetics
 Well absorbed orally
 widely distributed throughout the body fluids and tissues
 acetylated in liver excreted in bile, undergoes
enterohepatic circulation
 It tends to remain in skin,muscle,kidney and liver up to the
three weeks after the therapy is stopped
 70% excreted through urine
 Plasma half life 1-2 days
14

 Uses
 In treatment and prevention of Pneumocystis carinii
pneumonia in AIDS patient
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 Side effect
 During treatment of lepromatous laprosy some reactive
episodes may occur called as lepra reactions
 (1)Type 1 lepra reaction
 (2)Type 2 lepra reactions(erythema nodosum
leprosum)
 Type 1 reactions delayed hypersensitivity reactions due
to M leprae antigens [type 4 hypersensitivity reactions]
 Type 2 reactions represent a humoral antibody
response[type 3 hypersensitivity reaction]
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 Adverse effects
 Nonhaemolytic anaemia and methaemoglobinaemia in
G6PD deficient
 Mild – nausea
 loss of appetite
 pruritus
 reversible neuropathy & hepatotoxicity
 drug fever
 Not given when hb% is below 7
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 M.O.A.
 Phenazine dye which binds with mycobacterial DNA &
Inhibit mycobacterial growth
 Leprostatic with anti-inflammatory action
 It bind to mycobacterial DNA leading to disruption of
the cell cycle and eventually prevents the growth of
the bacterium.
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 Pharmacokinetics-
 Oral absorption variable
 excreted in feces
 plasma half life 60-70hrs
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 Side effect
 Red brown discolouration of skin
 Abdominal pain with loose stools due to deposition of
crystals in intestinal mucosa
 Avoided in pregnancy
 Mild – Conjunctival pigmentation & phototoxicity
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 MOA-
 It binds to and inhibits bacterial DNA dependent RNA polymerase
so that it can not synthesize new RNA
 Mammalian RNA does not binds with drug , host cells unaffected
 The drug is bactericidal
 Pharmacokinetics-
 well absorbed on oral administration.
 Penetrates all tissue, tubercular cavities, placenta & protein
binding.
 Excreted through liver into bile & undergo enterohepatic
circulation.
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 Side effect
 Hepatitis –major adverse effect
 Ocasionally- rashes, Gi disturbances, dizziness &
fatigue.
 Flu like syndromes- fever, chills,myalgias &
thrombocytopenia.
 Imparts harmless red colour urine.
 Resistance devlop after prolong use
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Category and
Type of patient
Duration of
Treatment
Drug regimen
Multibacillary
Leprosy
(Lepromatous)
For 24 months
If RMP
resistance
Dapsone 100 mg daily +
Clofazimine 50 mg daily with
300 mg once a month +
Rifampicin 600 mg once a
month
Clofazimine 50 mg daily +
Ofloxacin 400 mg daily +
Minocycline 100 mg daily for 6
m
Then Clofazimine + Ofloxacin
for 18 months
Paucibacillary
Leprosy
(Tuberculoid)
6 months
If Dapsone not
tolerated
Dapsone 100 mg daily +
Rifampicin 600 mg once a
month
Clofazimine 50 mg daily and
300 mg once a month may be
substituted in place of Dapsone23

• Red coloured urine
• Darkening of skin
• Severe itching of skin
• This is due to rifampicin. Lasts
only for few hours Reassure the
patient that this is harmless
• This is due to clofazimine.
Reassure the patient that this will
disappear after treatment is
completed
• This is due to allergy to one of the
drugs (commonly to dapsone).
Stop all medicines and refer to
hospital
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Leprosy

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