pathophysiology of leprosy

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Leprosy (Hansen’s Disease) (Lepi: scales on the fish) 1

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Page 1: Pathophysiology of Leprosy

Leprosy

(Hansen’s Disease)

(Lepi: scales on the fish)

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Page 2: Pathophysiology of Leprosy

Discovered by

Gerhard

Armauer

Hansen in

1873

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Page 3: Pathophysiology of Leprosy

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.

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Page 4: Pathophysiology of Leprosy

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 various tissues

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Page 5: Pathophysiology of Leprosy

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Page 6: Pathophysiology of Leprosy

Bacteria Resides in

Cooler Parts of the Body

Skin Peripheral Nerves

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Page 7: Pathophysiology of Leprosy

Mode of infection: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.

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Page 8: Pathophysiology of Leprosy

Transmission

Nasal/oral Droplets

Dermal Inoculations

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Page 9: Pathophysiology of Leprosy

Armadillo

They transmit

leprosy

They act as animal

model along with

monkey, mice and

rabbit

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Page 10: Pathophysiology of Leprosy

Incidence

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.

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Page 11: Pathophysiology of Leprosy

Classification

Main 2 types:

Tuberculoid type: high resistance.

Lepromatous or low resistance

Cass not falling in these 2 are considered

as borderline leprosy.

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Page 12: Pathophysiology of 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.

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Page 13: Pathophysiology of Leprosy

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. Organ deformaties 13

Page 14: Pathophysiology of Leprosy

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

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Page 15: Pathophysiology of Leprosy

Tuberculoid Leprosy

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Page 16: Pathophysiology of Leprosy

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.

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Lepromatous Laprosy

Page 17: Pathophysiology of Leprosy

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Page 18: Pathophysiology of Leprosy

Diagnosis

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.

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Page 19: Pathophysiology of Leprosy

1. Clinical symptom diagnosis

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Page 20: Pathophysiology of Leprosy

2. Skin Smear TestsZiehl Neelsen Carbol Fuchsin Stain (ZNCF)

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Absence of bacteria in smear: Paucibacillary

Presence of bacteria in smear: Multibacillary

Page 21: Pathophysiology of Leprosy

3. Lepromin test

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

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Page 22: Pathophysiology of Leprosy

Mechanism of Nerve Damage

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Entry Through Blood VesselsInflammatory ResponseDemyelination

Page 23: Pathophysiology of Leprosy

Sensory Loss

Paralysis

Deformities

Outcomes of Nerve Damage

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Page 24: Pathophysiology of Leprosy

Classification of Drugs

Sulfones: Dapsone (weak bactericidal)

MDT: Dapsone + Clofazimine + Rifampicin

Antibiotics: Ofloxacin, Clarithromycin,

Minocyclin

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Page 25: Pathophysiology of Leprosy

1995: WHO Distributes MDT Drugs for

Free to Worldwide Patients

World leprosy day January

30 in remembrance of

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Page 26: Pathophysiology of Leprosy

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