DR,dr Luh Made Mas Rusyati SpKK (K) FINSDV

Dermatology and Venereology Department Medical Faculty

Udayana University/ Sanglah Hospital
INTRODUCTION
 Leprosy is one of the oldest disease  are still
gainning attention of WHO  the effort to reduce
leprosy has not achieved yet
 The prevalence of leprosy has decreased after
treatment modality was found  there was
assumptions that leprosy does no longer exist 
neglected disease
 Often linked with socio economic and cultural factor
 Doctors  are the leader in health care service and
capable to diagnose, to cure and prevent leprosy
DEFINITION
 Leprosy is a chronic disease caused by M. Leprae
which affected peripheral nerve, skin, oral mucosa,
respiratory track, reticulo endothelial, eyes, muscles,
bone, testical, and instead of central nervous system.
ETIOLOGY
 M. Leprae  is an acid-fast bacilli
 Positive gram
 intracellular Obligate  high affinity toward
macrophages and Schwann cell
 The Optimum temperature is 300 C
 Size : 1-8 μ X 0,2-0,5 μ
 Cannot be cultured
 Incubation period: 6 month to 40 years or more
 Average Incubation period: 4 years (tuberculoid), 10
years (lepromatous)
EPIDEMIOLOGY ( INTERNATIONAL)
 Tropic and subtropics region
 According to WHO 2015, leprosy mostly found in
India, 127 326 new cases, which is 60% of all new cases
in the world
 Brazil placed 2nd with 26.395 cases
 Indonesia is at the 3rd place with 17.202 new cases
EPIDEMIOLOGY (INDONESIA)
 Indonesia contributed to most number of MB cases,
83,4% of newly detected cases
 East Java is the most endemic area
 Bali is located near East Java
 According to Dinas Kesehatan Pemerintah Provinsi
Bali in 2014 there were 84 new cases consisted of 9 PB
cases and 75 Mb cases
PATHOGENESIS
 M. Leprae Infection rely on cellular immunity
 M. leprae Schwann cell  cell-mediated immune
response (CMI) Chronic inflammation 
perineurium swelling ischemia, fibrosis, axonal
death
 The clinical manifestation is based on cellular
immunity rather than infection intensity
CLASSIFICATION
 Madrid Classification : I, T, B, L
 Ridley-Jopling Classification : TT, BT, BB, BL, LL
 WHO Classification : PB (I, TT, mostly BT, BTA
negative) and MB (BB, BL, LL, some of them are BT, B
and L, BTA positive)
WHO Classification
PB MB

1. Skin lesion - 1-5 lesions - >5 lesion

(macula , papule - Hypopigmentati - Symmetrical
nodule) on/ erythema - Lost of sensation
- asymmetrical
- Profound Lost of
sensation

2. Nerve Damage - Affect only one - Nerve trunk

nerve
TIPE TT TIPE BT TIPE BB TIPE BL TIPE LL
Macula/ plaque Similar to TT Mix of TT & LL Mimicking LL but Lesion is
Hypopigmentation there’s still normal abundant
skin Symmetrical
Well defined margin Less stabile, shape
Plaque lesion Ill defined margin
and size is varied,
Soliter / few symmetrical,
Smooth surface
plaque
Shinny surface

Dry surface, loss of

hair , anesthetic

Periferal nerve Mild nerve

thickening, claw damage
hand, mutilation

Satelite lesion + Satelite lesion + Punched out Madarosis ->

Punched Out Lesion (+) (Facies Leonina)
Lesion (+) Keratitis & Keratitis (+)
incomplete Gynecomastia (+)
Madarosis
CLINICAL MANISFESTATION
 INTERDETERMINATE
TYPE
Hypopigmented macule,
well defined margin
Normal sensation/ slight
decrease
Perspiration and hair
growth is normal
Location : face, back, arms
extensors
TT TYPE
Erythematous macule
Soleter/Few skin lesion
Surfaces is dry, well defined
margin, anesthetic
Peripheral nerve thickening
BT TYPE
 Combination of TT and
BT, with similarity
toward TT
 Hypopigmented macule,
ill defined margin, dry
surface
 Mild nerve damage
 Satelite lesion +
BB Tipe
 Mix of TT & LL
 Less stabile, shape and size
is varied, symmetrical,
plaque
 Satelite lesion +
 Punched Out Lesion (+)
 Erythematous macule,
irregular shape, rough
surface, slightly shinny
 Satellite lesion, nerve
thickening and contracture
BL Type
 Lesion almost similar to
LL, but less in number
 Normal skin can be
found
 Erythematous infiltrate
macule, ill defined
margin
 There's plaque and
punched out lesion
LL TYPE
 Abundant lesion,
symmetrical
 No normal skin found
 Smooth surface, shinny, ill
defined margin
 Terminal stage 
thickening of skin lesion,
shinny specially on fore
head, earlobe, nose and
become madarosis 
Facies Leonina
CARDINAL SIGN OF LEPROSY
 Skin disorder : hypopigmented/ erythematous macule,
papules, plaque, nodule or infiltrate
 Anesthesia/ impairment of sensations in the area
supplied
 Thickened of nerves
 Positive slit skin smear
Diagnosed of leprosy  2 out of 4 cardinal sign or the 4
cardinal sign
OTHER CLINICAL FEATURE
 Eyes: iritis, iridocyclitis, visus disorder until blindness
 Nose: epistacsis, saddle nose,
 Bone and joint : absorbsi, mutilation, arthritis
 Tongue : ulcus, nodus
 Laryng : hoarse voice
 Testis: gynecomastia, acute epidimitis, Orchitis, atrophy
 Lymph node : lymphadenitis
 Hair: alopecia, madarosis
 Kidney: glomerulonephritis, kidney amyloidosis,
pyelonephritis, nephritis interstitial
DIFERENTIAL DIAGNOSIS
 Dermatofitosis
itchy, well defined margin, polymorf, eczema
marginatum
 Tinea Vesikolor
Hypopigmentation Macule
Pytriasis Rocea
Herald patch (medallion), Christmas tree
patern
PATIENT EXAMINATION
 Anamnesis: chief complain, history of contact with
infected person, family background, complete address
 Inspection : examined all over the body ( macule,
nodule, scar, wrinkle skin, thickening of skin, loss of
hair)
 Palpation:
 Skin disorder: nodule, infiltrate, scar, ulcus on hand
and feet
 Nerves disorder: N. Aurikularis magnus, N. Ulnaris, N.
peroneus (left/right, enlarge, regular/irregular, firm/soft,
pain on palpable/no pain)
 Nerves function test:
Examination of sensibility on the lesion
Examination motoric/Voluntary Muscle Test/VMT (n.
auricularis magnus, n. ulnaris, n. radialis, n. medianus,
n. peroneus, dan n. tibialis posterior)
 Examination of otonom nerve function (Gunawan
test)
 Slit skin smear  bacteria Index (BI)
LABORATORY EXAMINATION
1. Bacteriology examination
 Slit-skin smear on the bacil-dense body area ( ear lobe
and most active skin lesion and examination of bacilli
by using ZIEHL NEELSEN

2. Histopathology examination
 Required for indeterminate leprosy
 Biopsy can be done on new skin lesion
Serologic examination
3. Serologic examination
 Based of the formation of patient’s own antibody
affected with M.leprae
 Limited to lepromatous leprosy
 MLPA, ELISA, ML Dipstick, PCR examination
 Treatment
 MDT (Multi Drug Therapy) regiment according to WHO (1998)
recommendation:
 PB 1 Lesion
Rifampisin Ofloksasin Minosiklin

Adult 600 mg Single 400 mg Single 100 mg Single

(50-70 kg) Dose Dose Dose
Children
300 mg Single 200 mg Single 50 mg Single
(10-14
Dose Dose Dose
tahun)
Children 300 mg Single 25 mg Single
(<10 tahun) Dose Dose

ROM is not recommended to be given to expecting mother and

children < 5 year
Treatment
 MDT (Multi Drug Therapy) regiment according to WHO (1998)
recommendation:
 PB 2-5 Lesions : Consumed within 6-9 month
5-9 year 10-14 year >15 year

Supervised by
Rifampisin 300 mg/month 450 mg/month 600 mg/month
physician

Supervised by
25 mg/day 50 mg/day 100 mg/day physician

DDS
Consumed
25 mg/day 50 mg/day 100 mg/day
unsupervised
  MDT (Multi Drug Therapy) regiment according to WHO (1998)
recommendation:
 MB lesion more than 5: Finished within 12-18 month

5-9 years 10-14 years >15 years

Rifampisin Supervised by
300 mg/month 450 mg/month 600 mg/month
physician
Supervised by
25 mg/day 50 mg/day 100 mg/day physician
DDS
Unsupervised
25 mg/day 50 mg/day 100 mg/day

100 mg/ month 150 mg/month 300 mg/month Supervised by

Clofazimin physician
50 mg 2x/week 50 mg/ 2 day 50 mg/day
Unsupervised
LEPROSY REACTION
 Acute manifestation of chronic leprosy disease
 Types od reaction:
 1. Type I leprosy reaction ( Reversal reaction,
upgrading reaction, borderline reaction)
 Hypersensitivity reaction, delayed type
 Borderline because cellular immunity rises fast
 Shift of leprosy type towards PB
 Clinical manifestation: change in skin lesion, neuritis,
with or without general status
 Type II reaction (erythema nodosum Leprosum)
 MB patient
 Humoral reaction plenty of bacil are being destroyed,
turning to antigen
 Immune complex reaction deposited in the skin,
forming nodule, (erythema nodosum leprosum), eye
(iridiosychlitis, arthritis., neuritis
LEPROSY REACTION THERAPY
 Leprosy principle:
 Analgetic and sedative
- Aspirin: 600-1200 mg every 4 hours, 4-6x/day
- Paracetamol 300-1000 mg, 4-6x/day (adult)
- Chloroquine 3 x 150 mg/day
- Prednisone 30-80 mg/day single dose, in the
morning after meal or divided dose
(Severe reactionprednisone single dose divided)
 Rest and immobilization
Leprosy Disabilities/Deformities
 2 kind of mechanism leprosy deformity:
 Primary deformity caused by direct result of disease
process and infiltration of M. leprae
 Secondary deformity caused by Primary deformity due
to nerves damage (Inflamation)
Disabilities/deformities which can develop
in leprosy patient
Nerve Function
Motoric sensory otonom
Facialis Lagophthalmos
Ulnaris Claw hands of Sensory loss on
ring finger, little ulnar side of ring
Dryness and
finger finger and little
cracked due to
finger
damage of sweet
Medianus Claw hand of Sensory loss of gland and blood
thumb, fore finger, thenar eminence, flow
middle finger index and middle
finger
Radialis Wrist drop
Peroneus Drop foot
Tibialis posteriois Clawing of toes sole of the foot
numbness
WHO Grading of disabilities/deformities
Grade eyes Hand and Feet

0 No eye problem due to No deformities due to leprosy

leprosy
1 Eye problem due to Anesthesia present but not
leprosy present but visible deformity or damage
vision not severely
affected as a result of
these (vision 6/60 or
better, can count finger at
6 meters
2 Severe visual impairment Visible deformity or damage
( vision 6/60 or less, present
inability to count finger
at 6 meters)
Prevention of disabilities
 Start early treatment
 Early detection of leprosy reaction
 Management of leprosy reaction
 Monitoring and self reporting
 Exercise using aids
 Rehabilitation (reconstruction surgery)
Prevention disabilities at home
 Self care at home
 Prevention of disabilities with:
 Check eyes, hands, foot regularly
 Cover eyes, hands, foot from trauma
 Care
Eyes
Lagoftamus
 Check: using a mirror  look if there's a redness/
corpus alienum
 Cover: using sun glasses
 Care: using eye drop contain saline
Hands
Anesthesia
 Check: carefully examined the hand
 Cover : protective hand wearing
 Care : if wound present  treat and immobilization
Foot
Drop foot
 Check: carefully examined the foot
 Cover: protective foot wearing
 Care: exercises foot, stretching of foot to prevent inversion
contracture
THANK YOU