Department of Physiotherapy, SHUATS, Prayagraj

1. Submitted To :
Mrs.Surabhi Srivastava
Assistant Professor
Department of Physiotherapy
SHUATS
Presented By:
Anash Fatima
21BPHY011
Department Of Physiotherapy
3 Year

2. Contents
 Introduction about Leprosy
 Incidence of Leprosy
 Risk Factors
 Mode of transmission
 Immunology of leprosy
 Pathogenesis
 Classification of leprosy
 Signs and Symptoms
 Complications
 Diagnosis
 Treatment
 References

3. LEPROSY

4. INTRODUCTIO
N
 Leprosy, also known as Hansen's disease, is a chronic
infectious disease caused by Mycobacterium leprae an
acid fast, rod shaped bacillus.
 It mainly affects the skin, peripheral nerves, and
mucosa of the respiratory tract etc.
 Leprosy was renamed Hansen’s disease after
Norwegian Scientist Gerhard Henrik Armauer Hansen,
who in 1873 discovered the slow-growing bacterium
now known as Mycobacterium leprae as the cause of
the illness.
 Leprosy is known to occur at all ages ranging from
early childhood to old age.
 Leprosy is curable and treatment during early stages
can prevent disability.

5. INCIDENCE
 Leprosy is a neglected tropical disease (NTD)
which still occurs in more than 120 countries, with
more than 2,00,000 new cases reported every year.
 More prevalent in countries like India, China,
Nepal, Brazil, Indonesia, Myanmar, Madagascar
and Nigeria.
 India still makes up 58.8% of the world's leprosy
cases.
 More commonly in states of Tamil Nadu, Bihar,
Puducherry, Andhra Pradesh, Odisha, West Bengal
and Assam.

6.  According to the World Health Organization,
approximately 2,08,000 people have leprosy
(Hansen's disease) around the globe, with most
cases found in Asia and Africa.
 In the United States, about 100 people receive a
leprosy (Hansen's disease) diagnosis every year.

7. RISK FACTORS
 Close Contact- Close contacts with leprosy
patients increases the risk of contracting the
disease.
 Armadillo Contact -Armadillo's serve as a
reservoir for disease, and armadillo contact
increases the risk of transmission of disease.
 Genetic Risk Factors
 Immunosuppression

8.  Endemic Regions -People living in endemic
regions along with poor hygiene and poor
nutritional status are at increased risk of
contracting leprosy
 Age
 Poverty
Incubation Period
 The latent period of the disease is variable and is
unusually long. It can last from a few weeks to up
to 20 years. However, the average incubation
period of the disease is 2-7 years. Moreover, it has
been observed that patients with paucibacillary
(PB) leprosy have a shorter incubation period.

9. MODE OF TRANSMISSION
 Direct contact with untreated patient who shed numerous
bacilli from
 Nasal secretion
 Damaged skin
 Mucous membrane of mouth
 Hair follicles
 The disease is not spread through casual contact with a
person who has leprosy like shaking hands or hugging,
sharing meals or sitting next to each other.
 Materno-foetal transmission across the placenta
 From infected Armadillo Contact.

10. IMUNNOLOGY OF LEPROSY
 The immune response in leprosy is T-cell Mediated
(CMI) delayed Hypersensitivity type IV.
 Person with ‘GOOD’ CMI response (NORMAL CD4-T
HELPER CELLS) develops milder & localised form of
the disease (Tuberculoid Leprosy) with less bacterial
load.
 Whereas, in persons with ‘WEAK OR ABSENT’ CMI
(LOW CD4-T HELPER CELLS), develop
disseminated wide spread disease (Lepromatous
Leprosy) with high bacterial load.

11. PATHOGENESIS
 Bacilli enter the body usually through respiratory
system
 After entering the body, bacilli migrate towards the
neural tissue and enter Schwann cells.
 Can also be found in macrophages, muscle cells and
endothelial cells of blood vessels.
 Slow multiplication inside cells & tissues with lower
temperature (about 12 – 14 days for one bacterium to
divide into two)
 Further progress depends on the immunological status
of the infected person.

12. Effect of strong cell mediated immunity
 Granuloma formation in cutaneous nerve
 Inflammation within the epineurium causes
compression and destruction of unmyelinated sensory
and autonomic fibers.
 Myelinated motor fibers are the last to get affected
producing motor impairment.
 Severe inflammation may result in caseous necrosis
within the nerve.
 Sensory loss – 30% of sensory fibers are destroyed
 M. leprae may escape from nerve to adjacent skin at
any time and cause classical skin lesion(s).

13. Effect of depressed Cell Mediated Immunity
 Bacilli multiply unchecked in schwann cells and
destroy the nerve.
 Bacilli liberated by infected and destroyed cells are
engulfed by histiocytes.
 Wandering macrophages - travel to other tissues,
through blood, lymph or tissue fluid.

14. M.Laprae bacteria
Enter through respiratory tract
Good CMI response
Schwann cells in cooler places(cutaneous nerves and peripheral nerve trunks
of limbs and face) bacilli multiply in the Schwann cells
DISSEMINATED DISEASE
(BB,BL,LL)
Weak CMI response
No Signs and
Symptoms
Signs and
Symptoms:
Skin, Nerve
Leisons (IL,TT,BT)

15. CLASSIFICATION OF LEPROSY
 According to WHO, leprosy can be classified on
the basis of clinical manifestations and skin smear
results.
 In the classification based on skin smears, patients
showing negative smears at all sites are said to
have paucibacillary leprosy (PB).
 While those showing positive smears at any site
are said to have multibacillary leprosy (MB).

17. Indeterminate leprosy (IL)
 Shows as a hypopigmented or erythematous macule
with little to no sensation. Bacilli are not usually found
in this biopsy. If the lesion shows not to be fully
developed, it should develop into another type within
the leprosy spectrum.
Borderline lepromatous leprosy (BL)
 Lesions, in this case, include erythematous macules,
nodules, or papules that show no distinct pattern of
appearance on the body. Though normal patches of skin
can be found, the delineation of the lesions is not clear
and spread out. Larger sized lesions are shown to have
a disproportionate distribution

18. Tuberculoid leprosy (TT)
 This presents with large hypopigmented or
erythematous lesions with clear demarcation and
raised margins. Plaque presentation was shown to be
scaly.
Borderline tuberculoid (BT)
 BT is defined as macules with a “target” appearance
in lesions. In this specific disease, the number of
lesions is higher than TT and usually shows on one
side of the body. When referencing the previously
mentioned WHO classification, these types of
lesions are considered “paucibacillary.”

19.  Significantly progressed cases present with body hair
loss along with nodular enlargement of earlobes.
 Mucosal invasion can resemble stuffiness, similar to the
common cold.
 A perforated septum or collapse could occur unless
treatment is readily sought after. Also, asymptomatic
presentation is possible with sporadic bacteremia during
this disease.
 M. leprae, in this case, progresses with focal lesions in
several organs. Some situations show organisms to be
present in the liver or marrow after biopsies have been
requested. Involvement with testicles and larynx is also
possible.
Lepromatous
leprosy (LL)

20. SIGNS AND SYMPTOMS
The disease can cause skin symptoms such as:
 A large, discolored lesion on the chest of a person with
Hansen’s disease.
 Discolored patches of skin, usually flat, that may be
numb and look faded (lighter than the skin around)
 Growths (nodules) on the skin
 Thick, stiff or dry skin
 Painless ulcers on the soles of feet
 Painless swelling or lumps on the face or earlobes
 Loss of eyebrows or eyelashes

21. Symptoms caused by damage to the nerves
are:
 Numbness of affected areas of the skin
 Muscle weakness or paralysis (especially in the hands
and feet)
 Enlarged nerves (especially those around the elbow
and knee and in the sides of the neck)
 Eye problems that may lead to blindness (when facial
nerves are affected)

22. Enlarged nerves below the skin and dark
reddish skin patch overlying the nerves
affected by the bacteria on the chest of a
patient with Hansen’s disease.
A large, discolored lesion on the
chest of a person with Hansen’s
disease.

23. COMPLICATIONS
 Muscle paralysis
 Trophic ulcer
 Testicular atrophy
 Amyloidosis
 Blindness
 Charcot joints
 Loss of eyebrows
 Keratitis
 Scleritis
 Loss of sensation with corneal ulceration with scarring .

24. DIAGNOSIS
Lepromin skin test
 The lepromin skin test is used to determine what type of
leprosy a person has.
How the Test is Performed
 A sample of inactive (cannot cause infection) leprosy-
causing bacteria is injected just under the skin, often on the
forearm, so that a small lump pushes the skin up. The lump
indicates that the antigen has been injected at the correct
depth.
 The injection site is labeled and examined 3 days, and
again 28 days later to see if there is a reaction.
How to Prepare for the Test
 People with dermatitis or other skin irritations should have
the test performed on an unaffected part of the body.

25. Normal Results
o People who don't have leprosy will have little or
no skin reaction to the antigen. People with a
particular type of leprosy, called lepromatous
leprosy, will also have no skin reaction to the
antigen.
What Abnormal Results Mean
o A positive skin reaction may be seen in people
with specific forms of leprosy, such as
tuberculoid and borderline tuberculoid leprosy.
People with lepromatous leprosy will not have a
positive skin reaction.

26. TREATMENT
Treatment
 Leprosy is a curable disease. The currently
recommended treatment regimen consists of three
drugs: Dapsone, Rifampicin and Clofazimine.
 The combination is referred to as multi-drug therapy
(MDT). The duration of treatment is 6 months for PB
and 12 months for MB cases.
Prevention
 WHO recommends tracing household contacts along
with neighborhood and social contacts of each patient,
accompanied by the administration of a single dose of
rifampicin as preventive chemotherapy.

27. LEONINE FACES