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1
PREPARED BY: PUNIT PATEL
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
3
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
7
Examine skin
Check for patches
Count the number of patches
Test for sensation
Check for damage to nerves
8
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
10
 Sulfones
 Dapsone, Sulfoxone, Acedapsone
 Phenazine derivative
 Clofazimine
Antitubercular drug
 Rifampicin
Antibiotics
 Fluoroquinolones – Ofloxacin, Sparfloxacin
 Macrolides – Clarithromycin
 Tetracyclines - Minocycline
11
 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
13
 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
15
 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]
16
 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
17
 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.
18
 Pharmacokinetics-
 Oral absorption variable
 excreted in feces
 plasma half life 60-70hrs
19
 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
20
 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.
21
 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
22
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
24
25

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Leprosy

  • 2. 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
  • 3. 3
  • 4. 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
  • 5. 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
  • 6. 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
  • 7. 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 7
  • 8. Examine skin Check for patches Count the number of patches Test for sensation Check for damage to nerves 8
  • 9. 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
  • 10. 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 10
  • 11.  Sulfones  Dapsone, Sulfoxone, Acedapsone  Phenazine derivative  Clofazimine Antitubercular drug  Rifampicin Antibiotics  Fluoroquinolones – Ofloxacin, Sparfloxacin  Macrolides – Clarithromycin  Tetracyclines - Minocycline 11
  • 12.  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
  • 13. 13
  • 14.  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
  • 15.  Uses  In treatment and prevention of Pneumocystis carinii pneumonia in AIDS patient 15
  • 16.  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] 16
  • 17.  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 17
  • 18.  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. 18
  • 19.  Pharmacokinetics-  Oral absorption variable  excreted in feces  plasma half life 60-70hrs 19
  • 20.  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 20
  • 21.  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. 21
  • 22.  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 22
  • 23. 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
  • 24. • 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 24
  • 25. 25