Abraham G.

Assistant Professor of Tropical Dermatology

Dermatology course for Public Health officer
June, 2025
 Introduction
• A chronic granulomatuos infectious disease
caused by mycobacterium leprae
• The body parts affected by leprosy includes
superficial peripheral nerves, skin, mucus
membrane of URT, eyes & testes.
• Scalp, axillae, groin and lumbar skin tend to
be spared
• Slowly progressive disease
 Introduction cont…
• Although it seldom kills, leprosy is
nonetheless a deforming & stigmatizing
disease
• Early Dx & prompt therapy are the key
stones in the strategy to control this chronic
infectious disease
• Leprosy is an exemplary model for the
understanding of CMI in humans
 Etiology
• Mycobacterium Leprae
• Non cultivable, Gm +ve, obligate intracellular AFB

• Has a predilection for skin & peripheral nerves

• Grows best at Temperature 30*c
• Doubling time of 12 days
• The only bacterium known to invade peripheral
nerves
• Causes lepromatous like illness in wild armadillo
Fig. 1 Armadillo
WHO Long term vision (2021-2030)

Zero leprosy: zero infection and disease, zero disability, zero

stigma and discrimination
• Goal
– Elimination of leprosy (defined as interruption of
transmission)

• Global targets for 2030

– 120 countries with zero new autochthonous cases
– 70% reduction in annual number of new cases detected
– 90% reduction in rate per million population of new cases
with grade-2 disability (G2D)
– 90% reduction in rate per million children of new child cases
with leprosy
 Contiud…..
• Europe: low incidence

• India: 2/3 of the world leprosy burden

• Although leprosy can occur at all ages most cases appear on

the endemic area before the age 35

• Peak incidence is at age 10 – 14 yrs

• Although men & women are equally affected, the

lepromatous form of leprosy is seen twice as often in men as
in women
Prevalence rate of leprosy, 2005
 Pathogenesis
• M.leprae is an obligate intracellular micro-
organism (lives with in cells particularly
macrophages & Schwann Cells)
• When macrophages encounter m.leprae they
produce cytokines such as IL-1, TNF-α and IL-
12
• Studies in humans have shown that a
predominantly Th1 CD4+ T-cell response is
seen in p’ts with TT
• This response produces IL-2, IFN-γ and TNF-
β that maintain inflammation
 Cont……
• With LL, a predominantly TH2 response leads to
the release of a different set of cytokines (IL-4, IL-5,
IL-10 and IL-13), which suppress macrophage
activity
• Susceptibility & type of response appear to
correlate with specific HLA
• Individuals with HLA-DR2 and HLA-DR3 are more
likely to develop Tubercloid form
• Those with HLA-DQ1 develop Lepromatous form
• Entery in to nerves is mediated by the binding of
the species specific trisaccharide in phenolic
glycolipid-l to laminin -2 in the basal lamina of
schwann cell axon unit.
 Transmission
• Three requirements for spread of leprosy
are:
 Contagious person
 A susceptible person
 Close or intimate contact
• The mode of transmission remains
controversial
 Cont….
a. Respiratory:
- Nasal discharges from Un-Rxed LL p’ts are the
main source of infection
- Current evidences favor respiratory
transmission
b. Conginental :
- There appear to be a genetic bases for
susceptibility to acquire leprosy
c. Percutaneous :
- Rarely tattooing or other penetrating injury to
the skin can be route of infection
 Cont…
 It is believed that more than 90% of persons
exposed to M.leprae are able to resist the
infection
 Incubation period -> 4 – 10 yrs (average)
Up to 5 yrs for TT
May be 20 yrs or longer for LL
 Clinical manifestation
• Leprosy often presents with hypo pigmented or
slightly erythematous patch lesion with lose of
sensation & enlarged nerves

• The 1st c/m in 90% of p’ts is numbness

• S/sx of leprosy can vary depending on the

individual response to m.leprae .
 Classification
• The Ridley-Jopling classification
TT ← BT ↔ BB ↔ BL ↔ LLs LLp
– Tuberculoid (TT)
– Borderline tuberculoid (BT)
– Borderline (BB)
– Borderline lepromatous (BL)
– Lepromatous leprosy (LL)
• The WHO classification
– Paucibacillary leprosy(PB)
– Multibacillary leprosy(MB)
* Purely neural leprosy
 Conti…..
 Clinical
 Bacteriological
 Immunological
Histological
 Cont…
1- Tubercloid (TT)
 Lesions are few; often solitary
 Annular plaque lesion (due to peripheral
propagation) – scaly, dry, hairless
 A tubercloid lesion is anesthetic or
hypestetic & anhidrotic
 Cont…..
May be purely neural (pain & swelling of
affected nerves), muscle weakness/wasting
 Immunity is sufficient to self cure but Rx is
recommended.
No upgrading or downgrading
 M.leprea is not detectable
 Cont….

Fig. 8 A solitary, anesthetic, and annular

lesion of polar tuberculoid leprosy, which Fig.9 Tuberculoid leprosy (TT).
had been present for 3 months. Its sharp Face of Pakistani lady showing
margines, erythema, and scale are more erythematous
evident than its elevation. The central red
dots are the sequelae or foot prints of testing plaque with a well-defi ned active
for pinprick perception when it is absent.(if edge, and a small satellite lesion.
present, the p’t with draws, preventing On the face, such lesions may not
overtly purpuric consequences)
be anaesthetic.
 Cont…
2- Borderline Tubercloid (BT)
Multiple asymmetric lesion
 Solitary lesions are not rare
 The primary lesions are plaque and papule
Annular configuration is common
Impaired sensation in the skin is the rule
 Immunity is strong but not sufficient self cure
 Upgrading or downgrading
 Cont….

Fig.10 Borderline tuberculoid Fig. 11 Borderline tuberculoid leprosy. Back

of Nigerian man showing large,
leprosy. Arm of an Indian
well-defi ned, scaly macules with some
woman. A large, scaly macule marginal elevation. Extensive disease, such as
is developing secondary this, may seriously impair sweating and heat
ichthyotic change. control.
 Cont…
3- Borderline Borderline (BB)
 Rare because of instability
 It is an immunologic mid point
 Characteristic skin changes are annular
lesions with sharply marginated internal &
external margin
Swiss cheese appearance.
 Cont…

Fig. 12 Leprosy: borderline-type A 31-yearold

Vietnamese female. Geographic shaped plaque on
the buttock with raised red indurated margins and central
clearing. There is extension of the infection indicated by
the erythematous papules beyond the margins.
 Cont…
4- Borderline leprematous (BL)
 Variable in its clinical presentation
 1/3 of patients have annular lesion
- Poorly marginated outer
- Sharply marginated inner
 Resistance is too low
 Nerve trunk palsy have their highest prevalence in
BL
 Cont…

Fig.13 Borderline lepromatous leprosy. Multiple

erythematous plaques are seen, some with central
clearing.
 Cont…
5- Leprematous Leprosy (LL)
 Lack of cell-mediated immunity toward M. leprae permits
unrestricted bacillary replication and widely disseminated,
multiorgan disease

 The cutaneous lesions of LL consist of mostly hypo-pigmented

macule, diffuse infiltration of the skin

 Infiltration of the skin of the fore head can lead to leonine face

 Characterized initially by multiple, poorly defined, erythematous

macule, papules & plaques
 Cont…
The most common sites of involvement are face,
buttock & lower extremities

 Fingers may became crooked or short

 Hair loss on eye borrow, madarosis

 Nose became collapse due to septal perforation,

saddle nose, widening of the nasal root
 Cont….

Acquired icthayosis of lower extremities

 Anesthesia in stocking or glove distribution

 Ocular manifestations such as lagophthtalmos

 Cont….

Lepromatous leprosy (LL). Face of an Lepromatous leprosy (LL). Face of an

Anglo-Indian man showing diffuse Ethiopian child showing typical pattern
of late lepromatous infi ltration. Note
infiltration of the skin and the collapsed nasal bridge and the infi
appearance of nodules on nose and ltration of the tongue.
lip.
 Cont…
 Indeterminate leprosy
 An early lesion appearing
before the host makes a
definitive immunologic
commitment to cure or overt
granulomatous response
 Hypo-pigmented macule/patch
with or with out associated
sensory loss.
Indeterminate leprosy. Face of a Nepali child
showing vague hypopigmented patch with some
central healing. Note the mark of a recent slit-skin
smear.
 Cont…
Histoid leprosy

 Clinically distinct variant of LL

 The skin lesions appear as

yellow-red, shiny papules
&nodules in dermis & s/c
tissue.
 Summery of leprosy classification

Table .1 Classification of leprosy. Adapted from A Guide to Leprosy Control, 2nd ed. Geneva: World Health Organization, 1988:27-28.
LL,lepromatous leprosy;BL,borderline LL;BB,mid-borderline leprosy; BT,borderline TT;TT, tuberculoid leprosy; I, indeterminate.
 Cont…
WHO classification of Leprosy

• Pauci Bacillary (PB)

 If the result of skin smear is –ve & there are five
or fewer lesion the p’t is called PB
• Multi bacillary (MB)
 If M.leprae are found in skin smear the p’t is said
to be MB.
Multiple symmetrical lesions.
 Relapsing leprosy
• MB p’ts who are non complient or whose disease develops
drug resistance are prone to relapse
• Such individuals present in several ways including
 A reprise of their initial presentation
 A flacid dermatofibroma like lision(histoidleprosy)
 A reactional state
 A posture of high resistance than their initial presentation
Eg. An initially LLs p’ts having BL or even BT disease
 Related findings
 Pregnancy
 Precipitating factor for leprosy in 10-25% of
women p’ts
 Untreated, lactating BL &LL p’ts have viable bacilli
in their milk but no risk has been identified in
infants ingesting such bacilli.
 Cont….
 Acquired immunodeficiency syndrome

leprosy has not been regarded as an Opportunistic

infection
 How ever, recent reports of leprosy being diagnosed
as DTH reaction in the setting of HAART suggest that
current view may need revision.
Early Diagnosis & prompt therapy are the key
stones in the strategy to control this chronic
infectious disease
Diagnosis of leprosy must be considered in any
patient with neurologic and cutaneous lesions
Diagnosis of leprosy can be made
 Clinically
 Laboratory
 History
 On the History the following should be included

 General information
 Name, sex, age, complete address, distance from home
to the clinic and occupation.
 History of onset, duration of symptoms,
 History of contact with a leprosy patient;
 Painless wounds/burns; burning sensation;
 Weakness in picking or holding objects or closing
eyelids;
 Unusual sensation in hands and feet (numbness,
tingling);
 history of previous leprosy treatment.
 Physical Examination
Assess for physical signs of leprosy in 3 general
areas:
Cutaneous lesions,
Neuropathies, and
Eyes, hands , and feet for disabilties.
 Skin Examination
 Examination must always be carried out with adequate
light (preferably natural light)

 Sufficient privacy for the patient to feel at ease

 Inform client about the examination

 Ask the client to remove all garments,

 Examine systematically from

 head to neck to shoulders,

 then arms, trunk, buttocks, hands and finally legs and feet
Examine for the presence hypo pigmented
macules patches , plaque, nodules, skin
infiltrations
Presence of loss of sensation in the hypo
pigmented patches
Count the number of skin lesions.
Sensation of skin lesion is tested with a wisp
of cotton-wool
Nerve Palpation
 Nerves are palpated to check for
 Enlargement and/or
 Tenderness

 Palpate the nerves starting from the head and going down to
the feet. Compare the right and left sides
 When palpating a nerve, always use the pulp of two or

three fingers;
 The nerves should be rolled over the surface of the
underlying bone.
Greater auricular nerve
Cross interiorly and superiorly
across sternocleidomastoid muscle
toward the ear lobe.
 Ulnar nerve
 Forearm of the patient is bent at
90 – 110*.
 The examiner uses his Lt hand to
palpate the Rt ulnar nerve and his Rt
hand to palpate Lt ulnar nerve.

 In the olecranon groove, b/n the

olecranon & the medial epicondyle
of the humerus.
 Radial cutaneous nerve
 It can be rolled under the tips
of the examiners fingers .

 As it cross the lateral border

of the radius just proximal to
the wrist
 Median nerve
 Is felt in front of the wrist when wrist joint is
semi-flexed

 It is often difficult to palpate.

 Peroneal nerve
In the poplitial fossa

It can be palpated as it

pass round the neck of
the fibula.
 Nerve Function Testing
After diagnosis of leprosy is made, nerve functions tests
must be carried out:
 Voluntary Muscle Testing (VMT)
 Sensory Testing (ST)
 Autonomic nerve function test for dryness
of palms and soles
 Voluntary Muscle Testing (VMT)
VMT is done to check Muscle strength of eye, hands and
feet.

The strength should be graded as

oStrong (S),
oWeak (W) or
oParalyzed (P).
 VMT of the eyes:

 Ask the patient to close his/her eyes lightly as in sleep.

 Observe whether or not the closure on both eyes is complete.

 Inability to fully close the eye is called lagophthalmos

 If there is lagophthalmos, measure the lid gap in mm

 if the closure is normal ,record ‘0’ mm.

 VMT of the hands and feet
 Check for range of movement
 If movement is normal, test for resistance

Little finger in test of ulnar nerve function

Straight Thumb up test of median nerve function

Wrist up test of radial nerve function

Foot up test of peroneal nerve function

 COMPARE the right hand with the left hand always.

 Sensory Testing (ST)
 Sensory testing is done to check the presence of

sensation in the eyes, hands and feet

Sensation of the eyes (cornea):

 ASK patient to blink his/her eyes.

 Observe the patient's spontaneous blinking while talking to him/her.

 If there is a blink, corneal sensation is normal.

 If there is no blink, the eye is at risk

Sensation of palms and soles

ST on palms and soles should be done with a ball-point pen.

The tests are done on ten standard points

 Examination for eyes, hands,&feet disabilities.
• Visual acuity
- look for injury of cornea & loss of vision.
 Patients should also examined for hand and feet complications.
 Palmo plantar hyperkeratosis/cracks/ dryness-
 Ulcers on the palms or soles -Venous insufficiency, 2ry to endothelial
involvement of deep vein valves./trauma/
 Clawed fingers-
 Foot drop-
 Wrist drop-
 Shortening &scaring in fingers and toes with sensation loss.
Leprosy complication in summary
 Laboratory examinations
1.Slit-skin smears
• Fite stain demonstrating numerous bacilli,
some of which are clumped.

• bacillary index (BI) = 5

 Mitsuda /Lepromin test

• It is a non-specific test of occasional value in

classifying a case of leprosy.

• It is strongly positive(85%) in TT, weakly

positive in BT, negative in BB, BL and LL, and
unpredictable in IL.

• Lepromin 0.1 mL, is injected intradermally

 Histiologies of leprosy

• In this classification, epithelioid cells and

lymphocytes at the tuberculoid end of the
spectrum give place to macrophages, which
• Appear increasingly foamy as the LL pole is
reached.

TT ← BT ↔ BB ↔ BL ↔ LLs LLp
 TT leprosy
• The granuloma invades the papillary zone
and may even erode the epidermis.
• a dermal granulomatous infiltrate is seen that
may have a linear pattern as it follows the
course of a nerve.
• Epithelioid cells and Langhans giant cells are
surrounded by lymphocytes.
• The cutaneous nerves are edematous.
• There is an absence of organisms.
Indeterminate leprosy
- a scattered non-specific
histiocytic and lymphocytic
infiltration with some
concentration around skin
appendages.

-no granuloma

-No virchow cells.

-Rarely single bacillus will be

found with in dermis.
 Diagnosis
The presence of one of the three cardinal signs is
diagnostic for leprosy :

1. Anesthesia over a hypopigmented skin lesion

2. Enlarged peripheral nerve/s with impairment of

sensations in the area supplied

3. Demonstration of AFB on skin slit smear

 For Rx purpose diagnosed as
follows;
 MB leprosy- six or more skin lesion
- positive skin smear result.
 PB leprosy – 1 to 5 skin lesions. Smear –Ve for
AFB .

Purely neural leprosy
=> Patients who don’t have any skin lesion, who have clearly thickened
nerves with or with out signs of nerve damage.

 If only one nerve is affected & nerve biopsy is

negative treat as PB.
 If two nerves or more nerves affected nerve biopsy is
 Differential diagnosis
 With out careful examination , leprosy can
easily be mistaken for a number of skin
diseases. Likewise some skin diseases can
be mistaken for leprosy.
 If pts are examined carefully, mistakes in
diagnosis should not occur.

 None of cardinal signs of leprosy are found

in common skin diseases.
 Macules and patches
 Pityriasis alba-
 Birthmarks-
 Vitiligo
 Pityriasis versicolor
 Tinea facia/T.corporis
 Onchocerciasis
 Nutritional deficiencies
 Dermatofibroma – has “dimple” sign unlike LL.
 DCL
 PKDL- has the same distrubution like LL.
 slit smear AFB, /leishmania slit smear conferm
Dx.
 Seconary Syphilis
P. Alba • Indeterminate leprosy
Tuberculoid or borderline
tuberculoid (TT/BT) leprosy.
Upper arm of Indian
man, showing typical dry,
hairless, hypopigmented
plaque with scaly,
erythematous
edge. Such lesions are usually
anaesthetic
 Borderline leprosy (BL).

 BT down-grading to BL.

Typical well-defi ned

hypopigmented macules of

BT leprosy and many small

lesions, some of which are
papular.

 Slit-skin smears
showed acid-fast bacilli (AFB) +Ve
 Annular plaques
Granuloma annulare
Sarcoidosis
 cutaneous tuberculosis
Mycosis fungoides –
 -Psoriasis,
 PROGNOSIS AND CLINICAL COURSE
• In un Rx leprosy, the only pt’s who will self-cure are those
with TT, or BT pt’s who upgrade to TT.
• Otherwise, the disease will be progressive, with morbidity
occasioned by nerve injury and a reactional state.
• BT, BB, BL, & LLs may upgrade, BT, BB & BL may
downgrade, and BL, LLs & LLp may develop ENL.
• Treatment arrests much of disease activity, but S-GPSI may
progress.
• Peripheral neuritis of recent onset may improve with
corticosteroid treatment.
 Treatment
Leprosy is treated with Mult Drug Therapy(MDT)
• MDT- is the use of two or three anti-leprosy drugs to treat leprosy.

• Transmission of Leprosy is interrupted after first dose of MDT.

• Drugs – Rifampicin(R),Clofazimine(C), Dapsone(DDS)

 Treatment continued…….
There are five main principles of treatment:
 Stop the infection with chemotherapy
 Treat reactions and reduce the risk of nerve damage.
 Educate the patient to cope with existing nerve damage,
in particular anaesthesia
 Treat the complications of nerve damage
 Rehabilitate the patient socially and psychologically

 All leprosy patients should be given an appropriate

multidrug combination.
.
 PB-MDT regimen
-it is prescribed to all cases classified
as PB-leprosy for 6 months duration
Drugs child <10 yrs 10-14 yrs > 15 yrs

Rifampicin 3oomg 450mg 600mg

monthly monthly monthly

Dapsone 25mg daily. 50mg daily 100 mg daily

 MB-MDT regimen
-it is prescribed to all cases classified
as MB-leprosy for 12 months duration.
Drugs child <10 yrs 10-14 yrs >15 yrs
Rifampicin 3oomg 450mg 600mg montly
monthly monthly
Clofazimine 100 mg 150mg 300mg
monthly monthly monthly
Clofazimine 50 mg twice a 50mg daily 50mg daily
wk.
Dapsone 25mg daily. 50mg daily 100 mg daily
 Treatment of special cases
During pregnancy & breast –feeding
- MDT regimens are safe ,for both mother and child,
should be continued during this time.
Rx for pt’s with Hiv infection.
-Rx is the same with the same duration.
Rx for pts’ with leprosy and TB
- Pts with TB &leprosy requires both standard Rx.
- once the TB- Rx is completed ,the pt should
continue his/her MDT.
- skip monthly dose of Rifampicin in the MDT.
 Relapse and it’s Mgt.
Relapses after the complete course of MDT are very
rare!.
• MB pts’ who are non-compliant or whose disease
develops drug resistance are prone to relapse.
 a reprise of their initial presentation.
 Histoid lesions
 A reactional state.
 A posture higher resistance than their initial presentation
Ex, LLs pts having BL 0r even BT .
• Difficult to differentiate from leprosy reaction.
Rx - Relapsed MB pts are also retreated with MDT
regardless of any change in classification.
 Preventions & control
• Unlike TB no prophylaxis treatment for leprosy.
• Vaccination against M.leprae (BCG) – has
estmated to protect with 50%.
• Combining BCG and killed M. leprae is one
approach. Leprosy
• Early diagnosis , treating and monitoring the
pts for the leprosy reaction prevents disabilities.
• Educate the leprosy pts how to protect them
selves from eye, hand, foot damage due to loss
of sensation.