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BY
VANA JAGAN MOHAN RAO M.S.Pharm, MED.CHEM
NIPER-KOLKATA
Asst.Professor, MIPER-KURNOOL
Email: jaganvana6@gmail.com
Leprosy (Hansen’s disease) is a chronic,
systemic infectious disease, affecting
primarily the peripheral nerves and
secondarily the skin, mucous membranes,
the eyes, bones, lymph nodes and viscera.
2
Discovered by Gerhard
Armauer Hansen in 1873
 Chronic granulomatous infection caused by
Acid Fast Bacteria Mycobacterium leprae
(Ml)
 Ml cannot be grown on culture media--- in vitro
drug sensitivity is not possible
 Growth and Drug susceptibility are done
by injecting inoculate in mouse foot pad
 Live dormant in macrophages but alive
 Transmitted from person to person through
nose, skin lesions of the infected persons.
 Affect mainly PNS, NS, Skin and varioustissues
3
4
Bacteria Resides in Cooler Parts of the
Body
5
Skin Peripheral Nerves
Mode of infection:
6
Leprosy is slow communicable disease and
uncubation period is between first exposure
and appearance of signs of disease.
Direct contact: Prolonged close contact of
susceptible individuals to an open case of
leprosy (damaged skin, nasal secretions,
mucous membrane contact).
Materno- foetal transmission.
Transmission from milk from mother to
infant.
Transmission
7
 Nasal/oral Droplets
 Dermal Inoculations
Armadillo
8
 They transmit
leprosy
 They act as animal
model along with
monkey, mice and
rabbit
Incidence
9
 At highest risk are those living in
endemic areas (hot and moist) with
poor conditions such as inadequate
bedding, contaminated water, and
insufficient diet, or other diseases that
compromise immune function.
 Acc to WHO- India, Brazil, Indonesia,
Myanmar and Nigeria are with the most
cases.
Classification
10
 Main 2 types:
 Tuberculoid type: highresistance.
 Lepromatous or low resistance
 Cass not falling in these 2 are
considered as borderline leprosy.
Classification
Based on the clinical, bacteriologic, immunologic and
histopathologic features, leprosy is classified into main
types:
1. Paucibacillary example: (Tuberculoid leprosy) (TL)
(with scanty or absent bacilli) - Skin lesions, loss
of sensation.
2. Multibacillary (Border line) (with numerous
bacilli)---numerous skin lesions, loss of sensation,
can go to
3. Multibacillary (lepromatous leprosy) (LL).
Nodules and plaques, thickened dermis, loss of
sensation, neuronal damage, nasal congestion,
epistaxis.
11
Symptoms
 Leprosy attacks the nervous system, particularly the
nerves of the hands, feet and face.
 In tuberculoid leprosy, skin lesions typically develop in
areas of nerve damage. Skin becomes pale, may develop a
reddish copper colour.
 Lepromatous leprosy: Loss of sensation to pin- prick or
light touch. Starts at the fingers and toes, affect a small
patch of skin to begin with, but as time passes many
skin lesions and nodules develop organdeformities.
13
The bacilli are usually absent in slit-
skin smears.
The histopathology shows tuberculoid
granulomas composed of epithelioid
cells surrounded by a zone of
lymphocytes.
Lepromin test is strongly positive.
Tuberculoid Leprosy
13
14
Tuberculoid Leprosy
Lepromatous Laprosy Cutaneous lesions
consist of macules, papules, infiltration or nodules
(lepromas).
• They are numerous, bilateral, symmetrical,
ill-defined with shiny surface.
• The sites commonly affected are the face,
arms, legs and buttocks, but may be anywhere.
15
16
Diagnosis
17
1. Clinical symptom diagnosis:
(anesthesia, nerve enlargement, and
characteristic skin lesions).
2. Slit-skin smears: Ziehl Neelson staining of
skin smear.
3. Skin biopsy. 4.
Nerve biopsy.
5. Lepromin test.
18
1. Clinical symptom diagnosis
2. Skin Smear Tests
19
Ziehl Neelsen Carbol Fuchsin Stain (ZNCF)
Absence of bacteria in smear: Paucibacillary
Presence of bacteria in smear: Multibacillary
3. Lepromin test
20
It is an immunologic test indicative of host resistance to
M. leprae.
A sample of inactivated (unable to cause infection) leprosy-
causing bacteria is injected just under the skin, usually on the
forearm
Tuberculoid: The immune system recognizes and
produces allergic reaction: Positive
Lepromatous:The immune system does not recognizes
Negative
Mechanism of Nerve Damage
21
Entry Through Blood Vessels
Inflammatory Response
Demyelination
 Sensory Loss
 Paralysis
 Deformities
Outcomes of Nerve Damage
22
Classification of Drugs
23
Sulfones: Dapsone (weak bactericidal)
MDT: Dapsone + Clofazimine + Rifampicin
Antibiotics: Ofloxacin,Clarithromycin, Minocyclin
1995:WHO Distributes MDT Drugs for Free
to WorldwidePatients
24
World leprosy day January 30 in remembrance of
25

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Leprosy

  • 1. 1 BY VANA JAGAN MOHAN RAO M.S.Pharm, MED.CHEM NIPER-KOLKATA Asst.Professor, MIPER-KURNOOL Email: jaganvana6@gmail.com
  • 2. Leprosy (Hansen’s disease) is a chronic, systemic infectious disease, affecting primarily the peripheral nerves and secondarily the skin, mucous membranes, the eyes, bones, lymph nodes and viscera. 2 Discovered by Gerhard Armauer Hansen in 1873
  • 3.  Chronic granulomatous infection caused by Acid Fast Bacteria Mycobacterium leprae (Ml)  Ml cannot be grown on culture media--- in vitro drug sensitivity is not possible  Growth and Drug susceptibility are done by injecting inoculate in mouse foot pad  Live dormant in macrophages but alive  Transmitted from person to person through nose, skin lesions of the infected persons.  Affect mainly PNS, NS, Skin and varioustissues 3
  • 4. 4
  • 5. Bacteria Resides in Cooler Parts of the Body 5 Skin Peripheral Nerves
  • 6. Mode of infection: 6 Leprosy is slow communicable disease and uncubation period is between first exposure and appearance of signs of disease. Direct contact: Prolonged close contact of susceptible individuals to an open case of leprosy (damaged skin, nasal secretions, mucous membrane contact). Materno- foetal transmission. Transmission from milk from mother to infant.
  • 8. Armadillo 8  They transmit leprosy  They act as animal model along with monkey, mice and rabbit
  • 9. Incidence 9  At highest risk are those living in endemic areas (hot and moist) with poor conditions such as inadequate bedding, contaminated water, and insufficient diet, or other diseases that compromise immune function.  Acc to WHO- India, Brazil, Indonesia, Myanmar and Nigeria are with the most cases.
  • 10. Classification 10  Main 2 types:  Tuberculoid type: highresistance.  Lepromatous or low resistance  Cass not falling in these 2 are considered as borderline leprosy.
  • 11. Classification Based on the clinical, bacteriologic, immunologic and histopathologic features, leprosy is classified into main types: 1. Paucibacillary example: (Tuberculoid leprosy) (TL) (with scanty or absent bacilli) - Skin lesions, loss of sensation. 2. Multibacillary (Border line) (with numerous bacilli)---numerous skin lesions, loss of sensation, can go to 3. Multibacillary (lepromatous leprosy) (LL). Nodules and plaques, thickened dermis, loss of sensation, neuronal damage, nasal congestion, epistaxis. 11
  • 12. Symptoms  Leprosy attacks the nervous system, particularly the nerves of the hands, feet and face.  In tuberculoid leprosy, skin lesions typically develop in areas of nerve damage. Skin becomes pale, may develop a reddish copper colour.  Lepromatous leprosy: Loss of sensation to pin- prick or light touch. Starts at the fingers and toes, affect a small patch of skin to begin with, but as time passes many skin lesions and nodules develop organdeformities. 13
  • 13. The bacilli are usually absent in slit- skin smears. The histopathology shows tuberculoid granulomas composed of epithelioid cells surrounded by a zone of lymphocytes. Lepromin test is strongly positive. Tuberculoid Leprosy 13
  • 15. Lepromatous Laprosy Cutaneous lesions consist of macules, papules, infiltration or nodules (lepromas). • They are numerous, bilateral, symmetrical, ill-defined with shiny surface. • The sites commonly affected are the face, arms, legs and buttocks, but may be anywhere. 15
  • 16. 16
  • 17. Diagnosis 17 1. Clinical symptom diagnosis: (anesthesia, nerve enlargement, and characteristic skin lesions). 2. Slit-skin smears: Ziehl Neelson staining of skin smear. 3. Skin biopsy. 4. Nerve biopsy. 5. Lepromin test.
  • 19. 2. Skin Smear Tests 19 Ziehl Neelsen Carbol Fuchsin Stain (ZNCF) Absence of bacteria in smear: Paucibacillary Presence of bacteria in smear: Multibacillary
  • 20. 3. Lepromin test 20 It is an immunologic test indicative of host resistance to M. leprae. A sample of inactivated (unable to cause infection) leprosy- causing bacteria is injected just under the skin, usually on the forearm Tuberculoid: The immune system recognizes and produces allergic reaction: Positive Lepromatous:The immune system does not recognizes Negative
  • 21. Mechanism of Nerve Damage 21 Entry Through Blood Vessels Inflammatory Response Demyelination
  • 22.  Sensory Loss  Paralysis  Deformities Outcomes of Nerve Damage 22
  • 23. Classification of Drugs 23 Sulfones: Dapsone (weak bactericidal) MDT: Dapsone + Clofazimine + Rifampicin Antibiotics: Ofloxacin,Clarithromycin, Minocyclin
  • 24. 1995:WHO Distributes MDT Drugs for Free to WorldwidePatients 24 World leprosy day January 30 in remembrance of
  • 25. 25