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LEPROSY
Dawn Ambrose
Department of Dermatology
Hospital Kuala Lumpur
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LEPROSYFirst described in India
In 600 BC
A chronic infectiousdisease principallyaffecting
Skin Peripheral nerves Upper respiratory tracts
Eyes
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Leprosy
Worldwide estimate of 5.5 million cases
Registered cases 600 000 world-wide Tropics and subtropics 15 endemic countries
Asia (India, Nepal, Myanmar)Africa (Madagascar, Mozambique)
Latin America (Brazil) 90% registered cases in the world
1991, WHO Leprosy Elimination programme Prevalence rate of
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Leprosy
Race
all racesAfrican blacks: tuberculoid leprosy
Light skin & Chinese: lepromatous type
Recent study
chromosome 6- that increase susceptibility Confirm chromosone 10 that determine clinical types
Sex:
male:female ratio of 2:1
Age
10-14 & 35-44 year-old
rare in infants
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Leprosy
Mode of transmission- inhalation, droplet Incubation period
3-7 years
6 months to 40 years or longer
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PathogenesisM. lepraeenter body
Sub-clinical infectionSpontaneous
healing
Indeterminate leprosy
Lepromatous Borderline Tuberculoidleprosy leprosy leprosy
Cell-mediated immunity
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Tuberculoid (TT)well-defined, raised granularmargin, hypoaesthetic patch
Borderlinetuberculoid (BT)well-defined margin,hypoaesthetic patch with
satellite lesions
Borderlinelepromatous (BL)numerous symmetrical patchessloping towards the periphery
Lepromatous (LL)symmetrical, diffuse infiltrationswith nodules at eyebrows,cheeks,nose, chin and ear lobes
Indeterminatesolitary, ill-defined, hypopigmentedmacule, minimal or no loss ofsensation
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Global Situation
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Indeterrminate Leprosy(IL)
Children Single or fewhypopigmented orerythematous macules
Mild sensory loss +/- Decreased sweating May heal or remain the
same
25% develop intoclassifiable leprosy Ill-defined hypopigmentedmacule on cheek 1stsign ofleprosy
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Tuberculoid Leprosy ( TT )
Lesions
Few < four Erythematous, hyper-
or hypo-pigmented
plaques Annular/arciform Anaesthetic Dry
Hair lossSingle erythematousannular anaestheticplaque (SLPB)
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Tuberculoid Leprosy (TT)
Lesions
Face, limbs orelsewhere
Spare intertriginousareas and the scalp.
Slit skin smear-negative
Lepromin test
Positive indicates host
resistance (CMI)
Dry, anaesthetic annularplaques with hair loss
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Tuberculoid Leprosy (TT) Neural involvement
is common
great auricular nerve
superficial peroneal nerves
Ulnar nerve
5th & 7th cranial nerve
Spontaneous resolution leaving pigmentary
disturbances or scars ordeformities
90% burnt out in 20 years
10.9% per year
Progression can occur
Burn: medial 31/2, Ulnarnerve
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Borderline Tuberculoid Leprosy ( BT )
Lesions like TT butmore
Multiple nervesinvolved
Slit skin smears-neg. Lepromin test- weak
positive
Remain in this stage,improve or worsen
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Borderline Borderline Leprosy(BB)
Numerous, red,irregularly shapedplaques that are less welldefined
Widespread nerveinvolvement
Slit skin smear-positivefor AFB
Lepromin test - neg. Remain in this stage,
improve or worsen
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Borderline LepromatousLeprosy (BL)
Lesions are numerous& polymorphous
Asymmetrical
Centre of largelesions - anaesthetic
Positive AFB Lepromin test
negative Remain in this stage,
improve or worsen
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Lepromatous Leprosy (LL)
Lesions are numerous &polymorphous
Symmetrical No sensory loss
No thickened nerves Loss of lateral eyebrow Leonine facies Nerve involvement - late
Systemic disease Cannot convert to the
less severe types
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Lepromatous Leprosy (LL)
Eye Testicular atrophy
results in sterility andgynecomastia.
Lymphadenopathyand hepatomegaly Larynx- Stridor and
hoarseness
Nasal infiltration:saddle-nosedeformity.
Kidney
L t L
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Lepromatous Leprosy(Teleconsultation)
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Diagnosis of Leprosy
Anaesthetic skin lesions: leprosy unless proven otherwise
Slit skin smears: BI.MI BI (bacteriological index)
number of AFB per high power field
MI( morphological index) % solid staining AFB & considered viable bacilli.
Skin biopsy
Think of thepossibility of Leprosy
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Management of Leprosy
General principles
Multiple drug therapy ( MDT ) for all patients Patient education to dispel myths of disease and
to ensure compliance Curable
Treatment break transmission chain and preventdeformities
Possible side effects of drugs
Reactions can occur
Identify and treat Leprosy reactions Treat complications of nerve damage
Rehabilitate patients
Notify the cases
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TreatmentWHO Multi-drug therapy regime
Paucibacillary
Rifampicin 600mg monthly (supervised)Dapsone 100mg daily 6 months
Clofazimine 50mg daily
Multibacillary
Rifampicin 600mg monthly (supervised)Clofazimine 300mg monthly (supervised) 2 yearsDapsone 100mg dailyClofazimine 50mg daily
T M l i
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Sungai Buloh Augmented Regime
Paucibacillary
Rifampicin 600mg monthly (supervised)Dapsone 100mg daily 1 yearClofazimine 50mg daily
Multibacillary
Intensive phase :Rifampicin 600mg daily
Clofazimine 100mg daily 3 weeks orDapsone 100mg daily till MI=0
Maintenance phase :Rifampicin 600mg monthly (supervised)Clofazimine 300mg monthly (supervised) 3 year or tillDapsone 100mg daily smear -veClofazimine 50mg daily
Treatment - Malaysia
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Immunological reactions in leprosy
Immunological reactions inleprosy up to 30% of patients under
treatment develop reactions
Precipitating factors: anti-leprosy drugs other drugs eg. progesterone,
vitamin A
infections
anaemia mental / physical stress surgery pregnancy, child birth
Type 1 (Reversal) reaction
Type 2 reaction (ENL)
Complications of Leprosy
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Neuropathic ulcer Claw hand Extensive neuropathic ulcersand foot deformities
Bilateral lagophthalmos Corneal opacity
Leonine facies
Complications of Leprosy
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Summary
Hansens disease is now a curable disease with theavailability of potent and effective treatment
Early detection and treatment prevent morbidity However, it is still a public health problem in Malaysia,
especially with the influx of immigrants and foreignworkers in recent years
Current statistics of cases probably only represent thetip of the iceberg
Undetected and untreated cases serve as a reservoir forthe disease which is an obstacle of disease eradication Improving health education to the public as well as to
the medical personnel may be an answer to the successof control and eradication of Hansens disease
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THANK YOU