Leprosy is caused by Mycobacterium leprae. It primarily affects the skin and peripheral nerves, causing hypopigmented patches and thickening of nerves. There are two main forms - tuberculoid leprosy, which causes localized lesions, and lepromatous leprosy, which involves multiple organs. Diagnosis involves skin smears and biopsies to identify acid-fast bacilli. Treatment involves multidrug chemotherapy regimens containing dapsone, rifampicin, and clofazimine. Prevention focuses on contact tracing, chemoprophylaxis, isolation during reactions, and rehabilitation.

2. ⦁ Leprosy is an infectious disease that causes painful white
areas on the skin and can destroy nerves and flesh
(epithelium).
⦁ Leprosy (Hansen's disease) is a nonfatal, chronic infectious
disease caused by Mycobacterium leprae, whose clinical
manifestations are largely confined to the skin, peripheral
nervous system, upper respiratory tract, eyes, and testes.
⦁ The unique tropism of M. leprae for peripheral nerves and
certain immunologically mediated reactional states are the
major causes of morbidity in leprosy.

3. ⦁ It occurs in two forms:
1. Lepromatous leprosy and
 the skin, mucous membrane, etc are involved.
2. Tuberculoid leprosy
 infiltration of nerves results in subcutaneous
nodules, anaesthesia and bleaching of the skin, trophic
ulcers, and various deformities.
⦁ Between these two forms there are
◦ borderline leprosy and
◦ indeterminate leprosy.

4. ⦁ For the purpose of convenience in the treatment, leprosy
has been divided into two forms:
⦁ Multibacillary leprosy:
◦ It is the infectious form of the disease and includes
lepromatous and borderline cases.
⦁ Paucibacillary leprosy:
◦ It is the non-infectious form and includes smear
negative, intermediate, tuberculoid and borderline cases.

5. ⦁ The disease is endemic in areas with hot and moist climates
and in poor tropical countries.
⦁ According to the WHO, 8 countries—India, China, Nepal,
Brazil, Indonesia, Myanmar (Burma), Madagascar and
Nigeria, together constitute about 80% of leprosy cases, of
which India accounts for one-third of all registered leprosy
cases globally.
⦁ In India, the disease is seen more commonly in regions like
Tamil Nadu, Bihar, Pondicherry, Andhra Pradesh, Orissa,
West Bengal andAssam.
⦁ Very few cases are now seen in Europe and the United States.

6. ⦁ It is caused by Mycobacterium leprae.
⦁ It affects mainly peripheral nerves.
⦁ It also affects the skin, muscles, eye, bones, testes and
internal organs.

7. ⦁ Leprosy is a slow communicable disease and the
incubation period between first exposure and appearance
of signs of the disease varies from 2 to 20 years (average
about 3 years).
⦁ The infectivity may be from the following sources:
⦁ 1. Direct contact with untreated leprosy patients who shed
numerous bacilli from damaged skin, nasal secretions,
mucous membrane of mouth and hair follicles.
⦁ 2. Materno-foetal transmission across the placenta.
⦁ 3. Transmission from milk of leprosy patient to the infant.

8. ⦁ Schwann cells (SCs) are a major target for infection by M.
leprae leading to injury of the nerve, demyelination, and
consequent disability and loss of axonal conductance.
⦁ M. leprae can invade SCs by a specific laminin-binding
protein.
⦁ Macrophages are one of the most abundant host cells to
come in contact with mycobacteria.
⦁ Phagocytosis of M. leprae by monocyte-derived macrophages
can be mediated by complement receptors CR1 (CD35),
CR3 (CD11b/CD18), and CR4 (CD11c/CD18).

9. ⦁ Leprosy is associated with an evolution from asymmetric
localized macules (discolored area of skin) and plaques to
nodular and indurated symmetric generalized skin
manifestations, and increasing bacterial load, and loss of
M. leprae– specific cellular immunity.
⦁ Distinguishing dermatopathologic characteristics include the
number of lymphocytes, giant cells, and AFB(Acid-Fast
Bacillus) as well as the nature of epithelioid cell
differentiation.

10. ⦁ The immune response in leprosy is T cell-mediated delayed
hypersensitivity (type IV reaction). M. leprae do not
produce any toxins but instead the damage to tissues is
immune-mediated.
⦁ This is due to following peculiar aspects in immunology of
leprosy:

11. ⦁ 1.Antigens of leprosy bacilli.
⦁ The bacterial cell wall contains large amount of M. leprae-
specific phenolic glycolipid (PGL-1) and another surface
antigen, lipo-arabinomannan (LAMN).
⦁ These antigens of the bacilli determine the immune reaction
of host lymphocytes and macrophages.
⦁ Another unique feature of leprosy bacilli is invasion in
peripheral nerves which is due to the binding of
trisaccharide of M. leprae to basal lamina of Schwann
cells

12. ⦁ 2. Genotype of the host.
⦁ Genetic composition of the host as known by MHC
class (or HLA type) determines which antigen of
leprosy bacilli shall interact with host immune cells.
⦁ Accordingly, the host response to the leprosy bacilli in
different individuals is variable.

13. ⦁ 3. T cell response.
⦁ There is variation in T cell response in different individuals
infected with leprosy bacilli:
⦁ i) activation of CD4+ T cells qnd CD8+ T cells.
⦁ ii) CD4+ T cells in lepra bacilli infected persons act not only
as helper and promoter cells but also assume the role of
cytotoxicity.
⦁ iii) The two subpopulations of CD4+ T cells (or T helper
cells)—TH 1 cells and TH 2 cells, elaborate different types of
cytokines in response to stimuli from the lepra bacilli and
macrophages.
⦁ iv) In tuberculoid leprosy, the response is largely by CD4+ T
cells, while in lepromatous leprosy although there is an excess
of CD8+ T cells (suppressor T) but the macrophages and
suppressor T cells fail to destroy the bacilli due to CD8+ T
cell defect.

14. ⦁ 4. Humoral response.
⦁ Though the patients of lepromatous leprosy have humoral
components like high levels of immunoglobulins (IgG, IgA,
IgM) and antibodies to mycobacterial antigens but these
antibodies do not have any protective role against lepra
bacilli.

15. ⦁ Tuberculoid Leprosy
⦁ It is less severe form, which encompasses Tuberculoid (TT)
Leprosy and borderline Tuberculoid (BT) Leprosy disease.
⦁ In general, these forms of leprosy result in symptoms
confined to the skin and peripheral nerves.
⦁ The skin lesions of tuberculoid leprosy consist of one or a
few hypopigmented macules or plaques that are sharply
defined and hypesthetic, often have erythematous or raised
borders, and are devoid of the normal skin organs (sweat
glands and hair follicles) and thus are dry, scaly, and
anhidrotic.
⦁ AFB are generally absent or few in number.
⦁ Tuberculoid leprosy patients may have asymmetric
enlargement of one or a few peripheral nerves.

16. ⦁ In tuberculoid leprosy, T cells breach (perforate) the
perineurium, and destruction of Schwann cells and axons may
be evident, resulting in fibrosis of the epineurium,
replacement of the endoneurium with epithelial granulomas,
and occasionally caseous necrosis.
⦁ Such invasion and destruction of nerves in the dermis by T
cells are pathognomonic for leprosy.

17. ⦁ Lepromatous Leprosy
⦁ Lepromatous leprosy patients present with symmetrically
distributed skin nodules, raised plaques, or diffuse dermal
infiltration.
⦁ Late manifestations include loss of eyebrows and eyelashes,
pendulous earlobes, and dry scaling skin, particularly on the
feet.
⦁ In LL leprosy, bacilli are numerous in the skin, where they
are often found in large clumps (globi), and in peripheral
nerves, where they initially invade Schwann cells, resulting
in foamy degenerative myelination and axonal degeneration
and later in Wallerian degeneration.
⦁ In addition, bacilli are plentiful in circulating blood and in all
organ systems except the lungs and the central nervous
system.

18. ⦁ In lepromatous leprosy, nerve enlargement and damage tend
to be symmetric, result from actual bacillary invasion, and
are more insidious but ultimately more extensive than in
tuberculoid leprosy.
⦁ They may also have signs and symptoms related to
involvement of the upper respiratory tract, the anterior
chamber of the eye, and the testes.
⦁ In untreated LL patients, lymphocytes regularly fail to
recognize either M. leprae or its protein constituents, and
lepromin skin tests are negative.
⦁ Macrophages of lepromatous leprosy patients appear to be
functionally intact; circulating monocytes exhibit normal
microbicidal function and responsiveness to IFN-.

19. The important symptoms of leprosy are;
⦁ Hypopigmented patches.
⦁ Partial or total loss of cutaneous sensation in the affected
area.
⦁ Thickening of nerves.
⦁ Presence of acid fast bacilli in skin or nasal smears.
⦁ In advanced stages, leprosy can produce deformities like:
◦ Nodules in the skin, face and ears.
◦ Ulcers in the foot.
◦ Loss of fingers or toes.
◦ Nasal depression (mood disorder), foot drop and claw toes.

20. ⦁ Specimens and Tests
⦁ Depending on the form of leprosy suspected by the treating
physician, the following specimens may be collected:
• Skin smears from the earlobes, elbows, and knees
• Skin biopsy from edges of active patches
• Nerve biopsy from thickened nerves
⦁ Skin and nerve biopsy
⦁ Biopsies are needed to definitively confirm a diagnosis of
Hansen’s disease and to classify the disease, and slit skin
smear may also be helpful in diagnosing those with
mutlibacillary disease.
⦁ Acid fast staining
⦁ The Ziehl-Neelson method using 5% sulphuric acid is used.
The presence of acid-fast bacilli confirms the diagnosis of
Hansen’s disease.

21. Chemotherapy of leprosy:
⦁ Sulphones: diamino diphenyl
Dapson
sulphone (DDS) or
⦁ Phenazine derivative: Clofazimine
⦁ Anti tubercular drug: rifampicin, ethionamide
⦁ Other drugs: ofloxacin, minocycline, clarithromycin

22. ⦁ Detection of cases of leprosy and tracing the contacts
especially children of the patient’s house.
⦁ Prevention of contact between the patient and other
normal, persons, especially children.
⦁ Prevention treatment (chemoprophylaxis) with dapsone.
⦁ Selective isolation or hospitalization of the patient
showing acute reactions or complications.
⦁ Rehabilitation of the patients with suitable work. Social
and psychological rehabilitation is also necessary.