10 Leprosy

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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