Spotting the Signs:
Recognizing and
Managing 2023
Leprosy
20 January 2025
th
Dr. Ng Ting Guan
Consultantdermatologist
Departmentof Dermatology
Hospital Tengku Ampuan Rahimah
Leprosy
• Chronic infectious diseasecaused by
Mycobacterium leprae, a ects skin and
peripheralnerves
• Aka as Hansen’s disease
– Norwegian physician (Dr G A
Hansen ) discovered thebacil us in
1873
• Has stigmatised ( Leprostigma) people
a ected sinceancienttimes dueto
dis gurementit caused and lack of
understanding of its transmission
Mycobacterium leprae
• Intracellular gram positiveacid fastaerobic bacil i
– complex cell wall
– slow doubling timeof 12 to 14 days
• grow and dividewithin macrophages and Schwann cells in
peripheralnerves
• Humans arethemajor hostand reservoir
– unable to begrown on arti cialcell culture
– limited growth in mousefootpad and nine-banded armadil os.
• favours temperatureof 30 deg Celcius
– multiply in cooler partseg. ears, nose, extremities, peripheral nerves
Mechanisms of transmission
– prolonged and closecontactbetween a susceptible
individualand a bacil us-infected patient
• through inhalation of bacil i in nasalsecretion
– Main routeof transmission
• nasalmucosa
– Less commonly
• Skin erosions
– Others reported :
• Blood, verticaltransmission, breastmilk and insect
bites
Epidemiology
• Male predominancewith a male to female ratio of
1·5–2·0 to 1
• Mean Incubation period : 7 to 40 years
– Tuberculoid Leprosy : 4years
– Lepromatousleprosy : 10years
• elong incubation period makes it di cult to determine
whereor when thediseasewas contracted
Epidemiology
• After sustained exposureto M. leprae, only a subsetof
individuals develops clinicalleprosy
• Human genetic factors
– partial e ecton developmentand pattern of disease
– Di erentpopulation havedistinctgenetic susceptibilities
• Environmentalfactors : relativerisk household contacts
– Lepromatous : 8–10
– Tuberculoid : 2–4
Epidemiology
• Accordi n g
is declining to WHO, thenumber of registered leprosy patients
– 5 mil ion in 1985
– 700,000 in 2001
– 228,474 in 2010
– 213,899 in 2014
– 182,815 in 2023
• As per data of 2023 from WHO
– Brazil, Indiaand Indonesiacontinueto reportmorethan 10000new
cases
– Bangladesh, DemocraticRepublicof theCongo, Ethiopia,
Madagascar,
Somalia, Sri Mozambique,
Lankaand Myanmar,
theUnited Nepal,
Republicof Nigeria,
Tanzania)Philippines,
each
reported 1000–10000new cases
New casesin Malaysia
Target: < 1 per 100,000 population
New casesin children
Cases among children age 0-14
Target: < 3 %
Grade 2 deformity
New cases of G2D/ Total population X100,000
Target: < 0.02 Case per 100,000 population
Pathogenesis
Ridley & (TT) (BT) (BB) (BL) (LL)
Jopling TT BT BB BL LL
Madrid Tubercul
Tuberculoiodid Borderline
Borderline Lepromatous
WHO Pauci b aci
Paucibacillary l ary MultibaciMultibacillary
l ary
(smear –ve) (smear +ve)
Ridley-Jopling classi cation
Indeterminate: solitary, il -de ned,
hypopigmented macule, minimalor
no lossof sensation
Tuberculoid (TT): Borderline
well-de ned, tuberculoid (BT Borderline (BB): Borderline Lepromatous(LL):
raised margin, ): well-de ned Numerous, red, lepromatous(BL): symmetrical,
hypoaesthetic margin, irregularly numerous di usein ltrations
patch hypoaesthetic shaped plaques symmetrical withnodulesat
patchwith thatarelesswell patchessloping eyebrows, cheeks,
satellitelesions de ned towardsthe nose, chin and ear
periphery lobes
WHO classi cation
Indeterrminate Leprosy (IL)
• Children
• Single or few
hypopigmented or
erythematous macules
• Mild sensory loss +/-
• Decreased sweating
• May healor remain the
same
• 25% develop into
classi able leprosy Il -de ned hypopigmented
macule on cheek 1st sign of
leprosy
Tuberculoid Leprosy ( TT )
Lesions
• Few < four
• Erythematous, hyper-
or hypo-pigmented
plaques
• Annular/arciform
• Anaesthetic
• Dry
• Hair loss
Single erythematous annular
anaesthetic plaque (SLPB)
Tuberculoid Leprosy (TT)
Lesions
• Face, limbs or
elsewhere
• Spare intertriginous
areas and the scalp.
• Slit skin smear-
negative Dry, anaesthetic annular plaque
with hair loss
Tubercul
• Neural involvement
o i d Leprosy (TT)
– iscommon
– greatauricular nerve
– super cial peroneal nerves
– Ulnar nerve
– 5th & 7th cranial nerve
• Spontaneousresolution
– leaving pigmentary
disturbancesor scarsor Burn: medial31/2, Ulnar
deformities nerve
– 90% burntoutin 20years
– 10.9% per year
• Progression can occur
Borderline Tuberculoid Leprosy ( BT )
• Lesions like TT but
more
• Multiple nerves
involved
• Slit skin smears-neg.
• Remain in this stage,
improve or worsen
Borderline Borderline Leprosy(BB)
• Numerous, red, irregularly
shaped plaques thatare
less well de ned
• Widespread nerve
involvement
• Slit skin smear-positivefor
AFB
• Remain in this stage,
improveor worsen
Borderline
Lepromatous (BL)
• Lesions are
polymorphousnumerous &
• Asymmetrical
• Centre of l
anaestheticarge lesions -
• Positive AFB
• Remai n in this
improve or worsenstage,
Lepromatous Leprosy (LL)
• Lesions arenumerous &
polymorphous
• Symmetrical
• No sensory loss
• No thickened nerves
• Loss of lateraleyebrow
• Leoninefacies
• Nerveinvolvement- late
• Systemic disease
• Cannotconvertto theless
severetypes
Lepromatous Leprosy (LL)
• Eye
• Testicular atrophy
results in sterility and
gynecomastia.
• Lymphadenopathy and
hepatomegaly
• Larynx- Stridor and
hoarseness
• Nasal in ltration: saddle
-nose deformity.
• Kidney
DIAGNOSIS
1. Clinical
• Pureneuralleprosy
– Nerveinvolvementwithoutskin lesions
• Neuralsigns:
– Hypoesthesia
– Nerveenlargement: ulnar, radial, median, lateralperonealand
greatauricular
– Muscular wasting and weakness
– Trophic changes
2. Slit skin smear
3. Skin biopsy for HPE and Fitestain
Slit Skin Smear
Reading of Slit skin smear
• BI
– BacteriologicIndex
– Density of leprosy bacilli
– Includeboth living (solid) and dead
(fragmented)
– BI =sumof all index
no of sitestaken
• MI
– Morphological Index
– Percentageof living bacilli
– Valuableindicator of responseto
treatment
– MI = Totalno of solid bacil i X100%
Totalno of bacil i (solid + fragmented)
Skin biopsy
Lepromatous leprosy
Di usein ltration of foamy
macrophages in thedermis,
beneath a clear subepidermal
zone
Fitestain
Numerous pink-red acd-fast
bacil i in lepromatous leprosy
Managementof leprosy
• Treatment with MDT
• Management of complications
• Contact tracing and chemoprophylaxis
• Case sharing
Treatment : Multi drug therapy
Paucibacil ary Multibacil ary
MDT ( rstline) Rifampicin 600 mg monthly
Clofazimine 300 mg monthly
Dapsone 100 mg daily
Clofazimine 50 mg daily
Duration 6 month 12 month
Maximum 6 blister pack 12 blister pack within 18
duration within 9 month month
allowed Note: blisterpack
cannotbeused in
Surveil ance 5 years 15 years children< 40kg
Pengurusan Kusta Kebangsaan Edisi ketiga 2023
Side e ects of rst line MDT
Second line treatment
Indications:
• Resistanceto rstlineMDT
• Sidee ectsfrom rstlineMDT
• G6PD de ciency
Lepra reaction
• Induced by host’s immuneresponseto leprosy bacil us
• 20%–30% of thepatients may develop acuteimmunological
changes in thecourseof thedisease
Classi cation:
– Type1 reactions (Reversal)
– Type2 reactions
• Erythema nodosum leprosum (ENL)
• Lucio’s phenomenon
Lepra reaction type 1
Reversal reaction
• Typeof leprosy:
– Borderline
– BL
– BT
• swelling of someor all theleprosy
skin lesions
• New lesions may appear
• Acuteneuritis may occur
Lepra reaction type 2
Erythema Nodosum leprosum
• immunecomplexes in tissues and
blood vessels
• erythematous tender
subcutaneous nodules; may
ulcerate
• Fever, malaise, may betoxic.
Lucio's phenomenon
• rare, potential y fatalreaction seen in
untreated or inadequately treated di use
lepromatous leprosy
• an immune-mediated reaction, involving
acute, necrotizing cutaneous vasculitis
• characterized by :
– extensive, painful, purpuric skin lesions.
– ulcerations, especial y on theextremities.
WHOdeformity grade
Grade Hand and feet Eye
0 No anaesthesia No eyeproblemdueto leprosy
No visibledeformity or
damage No evidenceof visual loss
1 Anaesthesiapresent, but Eyeproblemsdueto leprosy present,
no visible butvision notseverely a ected (
deformity or damage Vision 6/60or better, can count
nger at6 meter)
2 Visibledeformity or Severevisual impairment( Vision <
damagepresent 6/60, inability to count ngersat6
meter) ; also includeslagophthalmus,
irdocylitisand corneal apacities.
Complications : Neurological involvement
Claw hand
Extensive neuropathic ulcers and footdeformities
Hand deformities and neuropathic ulcers
Lagophthalmos
Ocular involvement
seventhnerve Iridoscleritis
Corneal scar
Nodular episcleritis
Relapse
Dermatology referral
Kes-kes khas ( 3.5)
Impaired liver and renal function
HIV
Pregnantand lactating women
TB-leprosy co-infection
Examination of contact
De nition of contact
Category of contact
Chemoprophylaxis for contact
Case 1
• 16/ Sabahan girl
• c/o hypopigmented
patches on upper arm,
thigh and back for 5
years
• Hypopigmented,
hypoaesthetic patches
• ickened leftulnar
nerve
Case 1
• Slit skin smear
– Negative
• Skin biopsy
• HPE : Extensive granulomatous
in ltrates in the dermis
Case 1
Whatis the diagnosis?
• Borderline Tuberculoid (BT) Hansen
– A few hypopigmented, hypoaesthetic patches
– ickened peripheralnerves
– HPE ndings
Case 2
• 52/Indonesian man
• Construction worker
• Residing in Malaysia for >
20 years
• c/o multiple erythematous
plaques on theface, trunk,
upper limbs and lower limbs
for 1 year
Examination:
• ickenedulnar nerves
• Reducedsensation in
stockingdistribution
Case 2
• Slit skin smear
– Bacteriological index (BI) 4.0
– Morphological index (MI) 0.3
• Skin biopsy for HPE
– Di usefoamy macrophages and granuloma with positive
acid fastbacil i
Case 2
Diagnosis
• Borderline Lepromatous (BL) Hansen’s with
peripheral neuropathy
– Numerous hypoaesthetic, erythematous plaques
– ickened peripheralnerves
– Presenceof acid-fastbacil i in slit skin smear
Case 3
• 54 year old Malay referred
from HospitalSerdang
•Bilaterallower limb swelling
with ulcer on feet 1 week and
swelling of ngers
•erythematous nodules on face
and ear for 2 years
•Uncle had leprosy 40 years ago
•Numerous in ltrativenodules of
forehead, cheek and earlobes,
loss of eyebrow
Case 3
• Slit skin smear
– Bacteriological index (BI) 3.75
– Morphological index (MI) 1.5
Skin biopsy for HPE :
Di use foamy histiocytes and granuloma with
positive acid fastbacil i
CONCLUSION
•Leprosy is a chronic infectious diseasecaused by
Mycobacterium leprae
• ebacteria aretransmitted via droplets from thenoseand
mouth during closeand frequentcontactwith untreated cases
• ediseasepredominantly a ects theskin and peripheral
nerves
•If leftuntreated, it may causeprogressiveand permanent
disabilities
CONCLUSION
•Need high clinicalindex of suspicion to recognizeits diverse
clinicalmanifestations
•Leprosy is curable with multidrug therapy (MDT)
•Early diagnosis and treatmentis vitalto preventdeformities
and complications
•People a ected by leprosy can lead a normaland digni ed life
likeany other person
ank you