2. Introduction
• Leprosy is a chronic granulomatous disease caused by infection with
Mycobacterium leprae
• It is characterized by infection of skin and nerves and associated
immunological damage
• Nerve damage is responsible for repeated ulceration and paralysis
affecting hands, feet and eyes
3. Microbiology
• M. leprae is an obligate intracellular pathogen with tropism for
macrophages and Schwann cells. It cannot be propagated in culture
• The primary route of transmission is likely by the respiratory route,
either from respiratory droplets or nasal secretions
• M. leprae is acid-fast positive stained by modified Acid-Fast staining –
decolourised by 5% Sulphuric Acid
4. Microbiology
& habitat
• It is confined to humans
and nine banded
Armadillos and
sphagnum moss
• It has a generation time
of about 20 days
5. Transmission & incidence among contacts
• Most newly diagnosed patients do not have a history of contact with an affected
person
• most of those in close contact with leprosy-affected people will not develop
leprosy
• Nevertheless, attack rates for contacts are higher than in the surrounding
population, 5–10 times higher in contacts of multibacillary index cases and 2–4
times higher in paucibacillary cases
• People with untreated lepromatous leprosy may harbour billions of organisms per
gram of tissue, which are shed from nasal mucosa
• M. leprae is known to survive for many days and possibly months under optimal
conditions of high humidity and low sunlight
6. Clinical manifestations
• The presence of the cardinal signs of leprosy:
• skin lesions with definite sensory loss
• thickened peripheral nerves
• the demonstration of M. leprae on slit-skin smears or on histology
of tissue (skin or nerve)
• These cardinal signs may not be present in early Lepromatous Leprosy
• Tuberculoid = Good Lepromatous = Bad
7. Pathogenesis – Immunity & Clinical Types
Tuberculoid Borderline Lepromatous
(TT) (BT) ↔ (BB) ↔ (BL) (LL)
1. Cell-mediated immune
response
2. Antibody production
3. T cell and cytokine
response
4. M. leprae presence in
lesions
5. Histological
appearance
6. Skin lesions
1. Strong
2. Low or absent
3. Th1 pattern
4. Not detected
5. Epithelioid granulomas
6. Few asymmetrical
lesions, definite loss of
sensation
1. Intermediate and
unstable Variable
2. Variable Mixed
6. Variable number and
type of lesions
1. Weak
2. Prominent
3. Th2 pattern
4. Detected
5. Large numbers Foamy
macrophages
6. Usually many lesions,
more symmetrical, less
sensory loss in lesions
31. Microscopy – Live vs Dead bacilli
• M. leprae, similar to other mycobacteria, retains the property of
staining with carbolfuchsin when no longer alive
• It can persist in the lesions for months to years after treatment –
hence a technician examining skin smears during treatment will get
the impression that the patient is making no progress unless he can
differentiate living from dead bacilli
• Living bacilli appear as uniformly stained rods (solid-staining)
• Dead bacilli appear irregularly stained (fragmented bacilli) or as
granules (granular bacilli)
32. BI and MI – total bacilli and Live bacilli
• Bacterial (bacteriological) index (BI) - The density of bacilli in smears - that includes both
living and dead bacilli - which ranges from 1+ (1–10 bacilli per 100 high-power fields) to
6+ (>1000 bacilli per single high-power field with globi)
• Morphological index (MI) is a tedious but useful measure of viability of bacilli in smears
• This involves measuring the proportion or percentage of solid stained (uniformly and
brightly stained down their length) bacilli
• MI will tell if a patient’s leprosy is active or not, will give valuable information as to
response to treatment, and will give early intimation of bacterial resistance to
chemotherapy or of defaulting on treatment
• An increase in MI indicates a worsening of the patient’s condition, and a decrease
indicates improvement
33. Laboratory Diagnosis
• Slit-skin smears are obtained by scraping fluid from a 2–4 mm depth
of pinched blood-free skin, using the edge of the disposable scalpel
blade turned perpendicularly and reversed after slitting the skin. This
fluid is then smeared onto a microscope slide
• Most patients with leprosy will have a negative slit-skin smear
• A positive test is diagnostic and very helpful for those with early
lepromatous disease in whom cardinal clinical signs are often not
present.
• Many recommend 4 to 7 sites for skin smears, at least one being from
a skin lesion, if present, and from routine sites such as the earlobes
38. Fite stain –
better than
ZN staining
for Lepra
bacilli
• This technique combines peanut oil
with the deparaffinizing solvent
(xylene), minimizing the exposure of the
bacteria's cell wall to organic solvents,
thus protecting the precarious acid-
fastness of the organism
39. Lepra Reactions
• The pathologic immune reactions of leprosy, Type 1 - reversal reaction (RR) and Type
2 - erythema nodosum leprosum (ENL), are significant contributors to morbidity
related to leprosy
• Reactions are characterized as extension or worsening of skin lesions and symptoms
due to immunologic responses to M. leprae
• They are not drug reactions
• They do not indicate that M. leprae infection is worsening
• For patients still on multidrug therapy, it is very important to continue the therapy for
the full recommended course
• Even when bacteriologic cure has been reached, reactions can persist
40. Type 1 – Reversal Reaction
• People with the unstable borderline forms of leprosy (BT, BB, and BL) are at risk for RR
• Increased erythema and induration of preexisting lesions, as a result of spontaneous
enhancement of cell-mediated immunity in these lesions
• The most serious manifestation of reversal reaction is neuritis with sudden loss of
nerve function
• Can present as facial palsy, ulnar nerve palsy resulting in inability to extend at the
wrist, and peroneal nerve palsy with inability to flex at the ankle (footdrop).
• Patients will generally report shooting, shocklike pains in the distribution of the
nerve.
• These pains can be reproduced by palpation on examination
• Treated with corticosteroids – Prednisolone 1 mg/kg then taper
41. Type 2 – Erythema
Nodosum Leprosum
(ENL)
• ENL occurs in LL or BL leprosy
• Exact etiology is unknown
• Immune complex formation has
been associated with ENL
• Present with systemic symptoms
like fever and malaise, whereas RR
is not associated with fever
• Rx – Prednisolone and sometimes
Thalidomide
42. Lepra Reactions
• They may occur prior to, during, or after antibiotic therapy for M.
leprae and are an indication for urgent evaluation and initiation of
appropriate treatment
• Both RR and ENL immune reactions can cause acute, serious ocular
damage.
• In RR, nerve damage of the trigeminal nerve or facial nerve can cause
lagophthalmos and defective blink reflex
• ENL’s ocular manifestations include episcleritis, scleritis, and
iridocyclitis
43. Prevention of Leprosy
• The current focus of leprosy prevention and control efforts is for early diagnosis of
leprosy cases so that treatment can be initiated promptly
• This has the dual benefit -
• decreases leprosy-related disability for the patient
• decreases the time that a person could potentially transmit M. leprae
• Household contacts of people with newly diagnosed leprosy be evaluated for symptoms
and signs of leprosy
• BCG vaccination or revaccination at the time of identification as a leprosy contact gave
60-90% protection compared with contacts who did not receive BCG
44. Treatment
• Multibacillary leprosy—for adults, Duration: 24 months
• Rifampicin: 600 mg once a month—supervised
• Dapsone: 100 mg daily—self-administered
• Clofazimine: 300 mg once a month—supervised and 50 mg daily—self-
administered
• Paucibacillary leprosy— for adults, Duration: 6 months
• Rifampicin: 600 mg once a month—supervised
• Dapsone: 100 mg daily—self-administered
