Leprosy

Cynthia Lau Sie Linh

1002059491
Prishantini Ramasamy
1002059803
Yoong Sim Yee
1002059947
 Introduction
❖ Also known as Hansen disease.

❖ A chronic bacterial infection primarily affecting the skin and peripheral nerves
usually caused by Mycobacterium leprae.

❖ The form the disease takes depends on the person’s immune response to the
infection.
 Epidemiology
❖ Affects people of all races anywhere in the world.

❖ Most common in warm, wet areas of the tropics and subtropics.

❖ Worldwide prevalence is reported to be around 5.5 million, with 80% of cases

found in 5 countries: India, Indonesia, Myanmar, Brazil and Nigeria.

❖ Infection can present at any age. [Two age peaks; 10-14 years of age and 35-44
years of age.]

❖ Rarely seen in infants and young children.

 Etiology
❖ Caused by M. leprae, an intracellular acid-fast bacillus.

❖ Grows best at cool temperatures, explaining its predilection to affect skin and
peripheral superficial nerves.

❖ Divides very slowly and takes years to reach a number sufficient to show signs of
infection.
Pathogenesis
 WHO Classification of Leprosy
Feature Paucibacillary Multibacillary
Tuberculoid Leprosy Lepromatous Leprosy

Type of lesion One or few lesions within Many lesions with marked
little tissue destruction tissue destruction

Number of acid-fast bacilli Few Many

Likelihood of transmission Low High

Cell-mediated response to Present Reduced or latent

M.leprae

Lepromin skin test Positive Negative

 Ridley and Jopling Classification
1. Tuberculoid (TT)

2. Borderline Tuberculoid (BT)

3. Borderline (BB)

4. Borderline Lepromatous (BL)

5. Lepromatous (LL)
Clinical Manifestations
1. Incubation period is 2 to 40 years (most commonly 5 to 7 years).

2. Onset is insidious and painless; first affects peripheral nervous system with persistent
or recurrent painful paresthesias and numbness without any visible clinical signs.

3. At this stage there may be transient macular skin eruptions; blister

4. Neural involvement leads to muscle weakness, muscle atrophy, severe pain, and
contractures of the hands and feet.
Types:

5. Tuberculoid (TL)

6. Lepromatous (LL)

7. Borderline (BL)

8. Reactionary State
Tuberculoid Leprosy
1. Skin lesions
a. Few well-defined hypopigmented hypoesthetic macules
(limited/localized skin involvement) with;
i. Raised edges and varying in size (from a few mm to very large lesions
covering the entire trunk)
ii. Erythematous or purple border and hypopigmented center.
iii. Often annular, enlarge peripherally
iv. Central area becomes atrophic or depressed.
v. Advanced lesions are anesthetic, devoid of skin appendages (sweat glands
or hair follicles).
vi. Any site including the face
2. Nerve lesions
a. Asymmetric nerve involvement
b. Usually a thickened nerve on the edge of the lesion
c. Large peripheral nerve enlargement frequent (ulnar, posterior auricular,
peroneal, posterior tibial nerves)
d. Nerve involvement is associated with hypoesthesia (pinprick, temperature, or
vibration) and myopath
Lepromatous Leprosy
1. Skin lesions
a. Skin-colored or slightly erythematous papules or nodules.
b. Lesions enlarge (new lesions occur and coalesce)
c. Symmetrically distributed multiple nodules, raised plaques
d. Diffuse dermal infiltrate (generalized skin involvement)
i. On the face results in loss of hair and leonine facies.
ii. Bilaterally symmetric involving the earlobes, face, arms
and buttocks, or less frequently the trunk and lower
extremities. Tongue: Nodules, plaques, or fissures

2. Nerve lesions
a. Symmetrical nerve involvement
b. More extensive than in tuberculoid leprosy

3. Other Involvement
a. Upper respiratory tract,
anterior chamber of eye, and testes
 Diffuse skin Infiltration, multiple nodular
lesions, and sensory loss are the key hallmarks
of lepromatous leprosy (LL)

← Leonine facies

↓ ↓
Nasal septum destruction Fingers & toes necrose and fall off
Borderline Leprosy

Lesions are intermediate between tuberculoid and lepromatous and are composed of macules,
papules and plaques. Anesthesia and decreased sweating are prominent in the lesions.
Reactional States

• Immunologically mediated inflammatory states, occurring spontaneously or after initiation of

therapy.

• Lepra Type 1 Reactions: Skin lesions become acutely inflamed, associated with edema and pain;
may ulcerate. Edema is most severe on the face, hands and feet

• Lepra Type 2 Reactions: Present as painful red skin nodules arising superficially and deeply;
they occur most commonly on the face and extensor limbs.

• Lucio Reaction: Occurs in patients from Mexico or Caribbean with diffuse LL. Presents as
irregularly shaped erythematous plaques; lesions may resolve spontaneously or undergo
necrosis with ulceration.
General Findings

1. Extremities:

a. Sensory neuropathy, plantar ulcers, secondary infection; ulnar and peroneal palsies

2. Charcot joints

3. Squamous cell carcinoma can arise in chronic foot ulcers

4. Nose:

a. Chronic nasal congestion, epistaxis; destruction of cartilage with saddle-nose deformity

5. Eyes:

a. Cranial nerve palsies, lagophthalmos, corneal insensitivity,uveitis, glaucoma, and cataract

formation.

6. Corneal damage
 Differential Diagnosis

❏ Sarcoidosis

❏ Hypopigmented lesions with granulomas

❏ Leishmaniasis

❏ NTM (non tuberculosis mycobacteria) infection

❏ Lymphoma

❏ Syphilis

❏ Granuloma annulare
 Lab investigation
● Slit skin smears
○ A small skin incision is made; the site is then scraped to obtain
tissue from which a smear is made and examined after Ziehl-
Neelsen staining.
○ Specimen are usually obtained from multiple sites (both
earlobes, elbows, knees. and active lesions).
● Culture
○ M. leprae has not been cultured in vitro; however, it does grow
when inoculated into the mouse foot pad. Routine bacterial
cultures is used to rule out secondary infection.
● PCR
○ M. leprae DNA detected by this technique makes the diagnosis
of early paucibacillary leprosy and identifies M. leprae after
therapy.
 Lab investigation
● Serology
○ Measure IgM antibodies to phenolic glycolipid-1(PGL-1).
● Dermapathology
○ TL shows epithelioid cell granulomas forming around dermal nerves; AFB are sparse
or absent.
○ LL shows an extensive cellular infiltrate separated from the epidermis by a narrow
zone of normal collagen.
○ Skin appendages are destroyed macrophages are filled with M. leprae, having
abundant foamy or vacuolated cytoplasm (lepra cells or Virchow cells).

Tuberculoid (TL): Localized skin involvement and/or peripheral nerve involvement; few organisms.

Lepromatous (LL): Generalized involvement including skin, upper respiratory mucous membrane, reticuloendothelial
system, adrenal glands, and testes; many bacilli.
 Diagnosis
Made if 1 or more of the cardinal findings are detected:
● Patient from endemic area
● Skin lesions characteristic of leprosy with
● Diminished or loss of sensation
● Enlarged peripheral nerves
● Finding of M. leprae in skin or less commonly other sites
 Treatment
General principles of treatment:

● Tuberculoid: Dapsone + rifampin.

● Lepromatous: Dapsone + clofazimIne + rifampin.
● Eradicate infection with anti lepromatous therapy.
● Prevent and treat reactions (prednisone or thalidomide).
● Reduce the risk of nerve damage.
● Educate patient how to deal with neuropathy and anesthesia.
● Treat complications of nerve damage.
● Rehabilitate patient into society.

Management involves a broad multidisciplinary approach including orthopedic

surgery, podiatry, ophthalmology, and physical therapy.
Thankyou