BAB I

INTRODUCTION

Leprosy as known as kusta is a chronic infectious disease caused by

Mycobacterium Leprae.

The disease mainly affects the skin, the peripheral nerves,

mucosa of upper respiratory tract and also the eyes. It is transmitted via droplets, from the
nose and mouth, during close and frequent contacts with untreated cases. Untreated
leprosy can cause progressive and permanent damage to the skin.
Leprosy control has improved significantly due to national and subnational
campaigns in most endemic countries. A total of 13 countries reported zero cases in 2013.
Global statistics show that 206 107 (96%) of new leprosy cases were reported from 14
countries and only 4% of new cases from the rest of the world. Indonesia still remains as
high endemic area.
Based on explanation above is important to study about leprosy to eliminate
leprosy in Indonesia by quick diagnosis and early treatment.

BAB II
LITERATURE REVIEW

2.1 HISTOLOGY OF SKIN

The skin is the largest organ of the body, typically accounting 15%-20% of total
body weight and, in adults, presenting 1,5-2 m 2 of surface to the external environment.
Also known as the integument or cutaneous layers. The skin is composed of:
1. Epidermis
An epithelial layer of ectodermal origin
Consist mainly of a stratified squamous keratinized epithelium composed of
keratinocytes.
Three less abundant epidermal cells: pigmented-producing melanocytes, antigenpresenting Langerhans cells, and tactile epithelial cells or Merkel cells.
Form the major distinction: thick (five layers) and thin skin (four layers)
Layers of epidermis: stratum basale, stratum spinosum, stratum granulosum,
stratum lucidum, stratum corneum.

2. Dermis
The connective tissue that supports the epidermis and binds it to the subcutaneous
tissue (hypodermis).
The thickness varies according to the region of the body.
Dermal papillae: projection surface that interdigitate with projection of the
epidermis. It is composed of loose connective tissue, with fibroblast, and other
connective tissue cells, such as mast cells and macrophages. Extravasations of
leukocytes are also seen. Anchoring fibrils of type VII collagen insert into the
basal lamina and bind the dermis to epidermis.
Reticular layer: thicker, composed of irregular dense connective tissue (mainly
type I collagen), and have more fibers and fewer cells than the papillary layer.
Dermis is the site of epidermal derivatives as the hair follicles and glands.
Rich supply of nerves. The effector nerves to dermal surfaces are postganglionic
fibers of sympathetic ganglion; no parasympathetic innervation is present.
Sensory afferent fibers present near hair follicle, ending at epithelial tactile cells.
3. Subcutaneous Tissue
Consists of loose connective tissue that binds the skin loosely to the subject
organs.
Also called as hypodermis or superficial fascia.
Often contains fat cells.
An extensive vascular supply promotes rapid uptake of insulin or drugs injected
into the tissue
2.2 LEPROSY
2.3.1
Definition
Leprosy is a chronic granulomatous infection and its sequel, caused by
Mycobacterium leprae.
2.3.2
Etiology
Mycobacterium leprae
Gram positive
Rod shape
Obligate aerobic bacteria
Do not form spore
Acid fast bacilli
Intracellular bacteria
2.3.3
Epidemiology
The global registered prevalence of leprosy at the beginning of 2011 stood at
192,246 cases, and 228,474 new cases were detected during the year 2010. The Indonesia
registered prevalence at the beginning 2012 are 23,169 cases and 20,023 new cases
detected.
2.3.4
Risk Factor
Endemic area: developing countries
More common in man
Rural area
Living with infected person
2.3.5

Classification

Type
Course
Skin lesions
Nerve involvement
Acid bacilli
Lepromin test
Cellular immunity

Lepromatous
progressive and malignant
nodular skin lesions
Slow symmetric
abundant
negative

Tuberculoid
benign and non progressive
macular skin lesions
severe asymmetric
few
positive

cell-mediated immunity is
markledly deficient

cell-mediated immunity is
intact

the skin infiltrated with

suppresor T cells

the skin infiltrated with

helper T cells

WHO Classification
Clinical Features on
Skin Lesion
Skin lesion
Thickening of peripheral
nerve (with or without
loss of sensation, muscle
weakness)
Skin Smear
Distribution
surface of the lesion
Margin
Nerves sensation on skin
lesion
Deformity

2.3.6

Paucibacillary (PB)

Multibacillary (MB)

1 to 5 lesion
1 nerve

More than 5 lesion

>1 nerves

AFS negative
unilateral or asymetric bilateral
dry and rough
Sharply marginated
loss of sensation

AFS positive
Symetric bilateral
smooth and shine

rapid process

occurs later

impairment

Pathogenesis

M. leprae is non toxic, the clinical manifestations of leprosy being produced by the hosts
responses or alternatively, by the accumulation of enormous numbers of bacteria, as in signs of
difuse infiltration.
The cell-wall-associated lipoproteins, ligands for the Toll-like receptor, initiate innate
immune response. Phenolic glycolipid I is a major species-specific and immunogenic constituent
of highly nonpolar outer layer of the bacillus. Entry into nerves mediated by binding of the
species-specific trisaccharide in phenolic glycolipid I to lamini-2 in the basal lamina of Schwann
cell-axon units.
2.3.7

2.3.8
Clinical Manifestation
Peripheral Nerve Changes
1. Nerve enlargement (usually perceived as asymmetry), particularly in those close to ski,
such as the great auricular, ulnar, radial cutaneous, superficial peroneal, sural and
posterior tibial.
2. Sensory impairment in the skin lesions,
3. Neuropathy, often with both sensory and motor loss (weakness and/or atrophy) and, if
long standing, also with contracture
4. Stocking-glove pattern of sensory impairment, a withering away so to speak, of the type
C fibers, involving heat and cold discrimination before loss of pain or light touch,
beginning in acral areas and, over time, extending centrally but sparing the palms, at least
for a while.
5. Anhidrosis on palms or soles, suggesting sympathetic nerve involvement.
Skin Lesion
TT BT BB LLs LLp
Other organs:
1. Insensitivity of the cornea
2. Respiratory tract: rhinitis, septal perforation, nasal collapse, hoarseness from vocal cord
nodules.
3. In men: impotence or infertility
2.3.9

Diagnosis and clinical findings

History:
a) Cardinal Signs: (leprosy positive if she/he shows one of the following sign)
Skin lesion consistent with leprosy (hypopigmentation, erythema) and with definite
sensory loss with or without
Thickening peripheral nerves
Positive skin smear
b) History of risk factors
c) Onset insidious
d) Persistent nasal stuffiness,
e) Ocular symptoms,
f) In young men loss of sexual drive or infertility
Physical Findings:
a) Dermatologist examination: determined type of skin lesion
b) Peripheral nerve examination (palpate and light touch): ulnar, peroneus communis, tibialis
posterior
c) Motoric function test: ulnar, medianus, radialis, peroneus communis, tibialis posterior.
Supporting Examination
a) Bacteriology
1. Bacteriological Index (BI)
Stained by Ziehl-Neelsen technique
Specimen: nicking the skin with sharp scalpel and scraping at the tip of earlobe.
The result are expressed on logarithmic scale:
1+: at least 1 bacillus in every 100 fields
2+: at least 1 bacillus in every 10 fields
3+: at least 1 bacillus in every field
4+: at least 10 bacilli in every field
5+: at least 100 bacilli in every field
6+: at least 1000 bacilli in every field
2. Morphology Index (MI)
Calculating the number of solid-staining acid fast rods
b) Histopathology
Biopsy

 Aim: histologic picture

Specimen: skin or thickened nerves
Appearance: epithelioid cell, datia Langerhans cells, lymphocytes.
c) Serology
Mycobacterium Leprae Particle Aglutinantion (MLPA)
ELISA
Mycobacterium leprae dipstick
d) PCR
2.3.9
Differential Diagnosis
Primary Lesion
1. Macular and patches pityriasis alba and telangectasias
2. Papular to nodula lesion dermatifibromas, eruptive histiocytomas, lymphomas,
sacoidosis.
3. Plaque mycosis fungoides, urticarial, psoriasis
4. Polymorphous vesiculobullous eruprion autoimmune blistering disease
5. Annular lesion annular eythemas, sarcoidosis, syphilis, or tinea.
Clinical consellation
1. SLE
2. Vascullitis
2.3.10
Treatment
The rational recommending three drug regimens:
1. Rifampin (bactericidal) will kill all susceptible organisms, including those resistant to
dapsone (bacteriostatic). Side effects: nefrotixic, gastrointestinal symptoms, flu-like
syndrome, skin eruption.
2. Dapsone will eventually eliminate all susceptible organisms, including those resistant to
rifampin, but it has side effects such as headache, drug eruption, hemolytic anemia,
leukopenia,
insomnia,
peripheral
neuropathy,
hepatitis
hypoalbuminemia,
methemoglobinemia.
3. Clofazimine (weakly bactericidal, mainly bacteriostatic) is added to obviate the risk of
primary dapsone resistance. Side effects: sclera icteric, brownie skin color, in high dose
consumption will appear gastrointestinal syndrome.
Age Group
Adult

Child (10-14
y.o)

Adult

Child (10-14

Rifampin
2 caps 300 mg

1 caps 300 mg
1 caps 150 mg

2 caps 300 mg

1 caps 300mg

Drug Dosage
Dapsone
MB

Clofozimin

1 tabs 100 mg

3 caps 100 mg

1 tabs 100 mg

1 caps 50 mg

1 tabs 50 mg

3 caps 100 mg

1 tabs 50 mg

1 caps 50 mg
every 2 days

PB
1 tabs 100 mg

Duration
every 1st day of the
month for 12
months
Day 2-28
every 1st day of the
month for 12
months
Day 2-28

1 tabs 100 mg

every 1st day of the

month for 6 months
Day 2-28

1 tabs 50 mg

every 1st day of the

y.o)

1 caps 150 mg
1 tabs 50 mg

1.
2.

month for 6 months

Day 2-28

2.3.11
Complication
Occular disability
Disability of hands and feet
2.3.12
Prognosis
Untreated leprosy will be progressive, with morbidity occasioned by nerve injury and a

reactional state. BT, BB, BL, and LLs may upgrade, BT, BB and BL may downgrade, and BL,
LLs, LLp may develop erythrema nodusum leprosum (ENL). Peripheral neuritis of recent onset
may improve with corticosteroid treatment.