leprosy by tanta university student
TRANSCRIPT
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LEPROSY
Hansen`s Disease
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:
وسلم - عليه الله صلى النبي : - قال
من » فِرارك المجذوم ِمن فرَّصحيح» األسد حديث
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� ۖ ِه� �� َأ ال ِه5 ْي6 ِه- ِه! ًل�ا ْيي َأ7 ُخ5 ُخ�و َأي َأ8 َأ� َأ� ْي! َأا ْي2 َأ9ا َأ� َأ: ْي� َأا ْي2 ا ُخ; ِه� ْي! ُخا ُخ�م َأ9 ُخ� ِّط> َأن ُخا َأ9 � ۖ ِه� �� َأ ال ِه5 ْي6 ِه- ِه! ٰى/ َأ= ْيو َأ: ْيل ا ِهيي ْي< ُخا َأ9َأ� ) ِه.ي ِه� ْي? ُخ�� ُخ&م ُخ�. ِه-ا5 ْيم ُخ� �ل َأ ًل� َأ$ آا َأ2 َأ@ ِهل ٰىَأ6 ِه�ي َأ�5 ِه-ا � ۚ ْيم ُخ� ِه= ُخيو ُخ! ِه�ي َأ5 ُخ�9 �ِه َأ�) َأ= َأ� َأ9 َأ5 ُخ�و ُخ� ْي َأ= َأ: (49ِه!
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it is the oldest disease in history and still worldwide sociomedical and economic problem, chronic infectious diseaseas it can lead to deformities and can leave a crippled patient burdens on his family and his society .
It principally affects the skin and peripheral nerves.
Leprosy (Hansen’s disease)
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Epidemiology It is endemic in tropical and subtropical
countries .It is common and endemic in certain area in upper
Egypt e .g Assiut & Giza In lower Egypt e.g Sharkeia & Gharbeia .
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M. leprae is discovered by Hansen from Norway in 1873
Aetiology
-Mycobacterium leprae .-discovered by Hansen in Norway 1873 -It is can not be cultured in artificial media .- it can be growen in mouse footpad and armadillo .
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BACTERILOGY (cont.)
. M . Leprae are straight or slightly curved rod like bacteria
They look like M. tuberculosis stained with Ziehl – Neelsan stain . But are less acid fast and alcohol fast .
bacteriological index is the density of M leprae in smear it includes living and dead
bacilli . morphological index.is percentage of living bacilli it indicates if patient is infectious or not and response to treatment
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Mode of transmission droplet infection is main mode of infection There is personal susceptibility which decides if a contact will be
infected or not The majority of human beings have no susceptibiity
Contact through the skin (rare). Arthropod-born infection (rare). Through placenta and milk.
Leprosy is not STD or directly inherited.
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Predisposing or risk factors
Age : in all age groups .Peak of onset is 10-20 years Children are more susceptible
Sex : male to female ratio in adult was 2 : 1 last years it is going to be equal .
1.Residence in an endemic area.2.Having a blood relative with leprosy.3.Poverty (malnutrition).4.Contact with affected armadillo.
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pathogenesis
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ClassificationBased on the clinical, ibacteriologic,immunologic and histopathologicfeaturesleprosy is classified into maintypes
1.Paucibacillaryexample: (Tuberculoidleprosy) (TL) (with scanty or absent bacilli) -Skin lesions, loss of
sensation.2.Multibacillary(Border line) (with numerous bacilli)---
numerous skin lesions, loss of sensation, can go to3.Multibacillary(lepromatousleprosy) (LL).Nodules and
plaques, thickened dermis, loss of sensation, neuronal damage, nasal congestion, epistaxis.
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Classification & Clinical Presentation
Jopling Classification
Based on Host Immunity
TT BL LL
BT BB BL
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Classification & Clinical Classification & Clinical PresentationPresentation
WHO Classification
Based on Bacterial Load
Paucibacillary Multibacillary
Slit Skin Smear
Positive Negative
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LEPROSY
Paucibacillary (PB) Multibacillary (MB)
Indeterminate Leprosy (IL)
Tuberculoid Leprosy (TL)
Borderline Tuberculoid (BT)
Borderline Borderline (BB)
Borderline Lepromatous(BL)
Lepromatous Leprosy (LL)
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CLINICAL PICTURE
Indeterminate Leprosy
Tuberculoid Leprosy
Borderline Leprosy
BT BB BL
Lepromatous Leprosy
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Indeterminate Leprosy (IL)
Usually single (multiple) macule / patche. Hypopigmented or faintly erythematous. Sensation normal but sometimes imparied. The peripheral nerves normal. Slit skin smear negative.
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Indeterminate leprosy :Hypopigmented patch, sensation normal, no palpable peripheral nerve and slit skin smear negative.
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Tuberculoid Leprosy (TL)
Usually single but may be few (<5). Hypopigmented / erythematous plaque. Well defined borders. Sensation markedly imparied. Enlarged peripheral nerve. Slit skin smear negative
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Tuberculoid leprosy: Two hypopigmented patches, hypoastheticwell defined borders, palpable peripheral nerve and SSS negative.
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Tuberculoid Leprosy: Annular, erythematous, anasthetic patch with well defined and raised borders and SSS Negative.
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Borderline Leprosy (BL)(BT,BB,BL)
Few / many asymmetrical patches. Partly well-defined borders. Sensory impairments range from slight to marked. Slit skin smear usually positive. P. nerves asymmetrically enlarged. Annular plaque in leprosy are most commonly border line with
characteristic punched out internal border and sloping outer border(swiss cheese appearance)
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Borderline Tuberculoid Leprosy: Well-defined large anaesthetic patcheswith satellite lesions. SSS Negative.
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Borderline Borderline Leprosy: Less defined, asymmetrically distributed hypoaesthetic patches. SSS positive.
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Borderline Lepromatous Leprosy: Numerous, hypoaesthetic almost symmetrically distributed patches . SSS positive.
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Lepromatous Leprosy (LL)
Very numerous ill defined lesions. (macules, patches, papules,and nodules). Symmetrically distributed allover the body Loss of eyebrows and eyelashes. Leonina facies. No sensory impairments in lesions . Peripheral nerves symmetrically enlarged. Slit skin smear always positive.
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Lepromatous Leprosy: Leonine Face
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Mucous membrane involvement
Very common Usually epistaxisDryness ,rhinorrhea
and obstruction of Nose
Nerve involvementBilateral symmetrical
thickening of all nerves
Nerve fibrosis is very late in lepromatous leprosy, so loss of
sensation is also very late.Bilateral Glove and
stocking anasthesia is present in all advanced cases
of lepromatous leprosy.
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Diagnosis of Leprosy
1. Clinical Examination.2. Slit Skin Smear.3. Skin Biopsy.
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1.Clinical examination: What are the cardinal skin signs of leprosy?
1. Hypopigmented or erythematus patch / plaque
2. Complete / partial loss of sensation.3. Thickening of peripheral nerves.
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1 .History
Familial or extrafamilial contactParasthesiaNumbnessEpistaxis
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2 .Clinical examination
.I1 (E, Temperature & painxamine all modalities of sensation in the skin lesion “Touch”
.II2 (Examine peripheral nerves for Tenderness, consistency and size:
.IIIHead: Supraorbital
.IVNeck: Great auricular n..VElbows: Ulnar n.
.VIWrists: Superficial radial cut. And median n..VIIPopliteal fossa: Common peroneal n..VIIIThey may be cord-like, beaded, thinned or may show
abscess formation .
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3 .Investigations
(1 )Nicotinic acid test:“Professor Dr. El-Arini”
15 mg nicotinic acid IM injection Hypopigmented macule becomes erythematous within 10-15 mins.
*Value:Quick office test for early detection of hypopigmented lesions of leprosy.
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(2 )Bacteriological examination :
Nasal smearNot recommended) ? (:
Painful for the patient & may reveal +ve results in contacts
On treatment, lepra bacilli disappear from nasal mucus earlier than from skin.
It’s very difficult to prove the bacilli ara M. Leprae
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2.Slit Skin Smear Simple and valuable test. It is needed for diagnosis. Monitor the progress of the treatment.
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Slit Skin Smear (method).
Pinch the site tight. Incise. Scrape & collect material Smear on a slide. Air dry & fix. Stain (Z-N method)
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Slit Skin Smear (site). Ear lobe. Forehead. Gluteal region. Active edge of patch.
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Slit Skin Smear (Reporting the smear).
Bacteriological indexBacteriological index00 – – no bacilli in 100 fieldsno bacilli in 100 fields
11 :+ :+1-101-10 bacilli in 100 fieldsbacilli in 100 fields22 :+ :+1-101-10 bacilli in 10 fieldsbacilli in 10 fields
33 :+ :+1-101-10 bacilli in 1 fieldbacilli in 1 field44 :+ :+10-10010-100 bacilli in 1 fieldbacilli in 1 field
55 :+ :+100-1000100-1000 in 1 fieldin 1 field66> :+> :+10001000 bacilli field )globi(bacilli field )globi(..
Morphological indexMorphological indexThe percentage of living bacilli to the total number of bacilli in the smear.
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3 . Skin biopsy- TO verify the diagnosis & classification - The biopsy must be deep enough to include dermis
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It’s a sudden change in the clinical picture of the disease because of conflict between the bacilli and the immune system of the host.
What are the precipitating factors ?
1.1. Effective treatment.Effective treatment.2.2. Intercurrent infection.Intercurrent infection.3.3. Physical stress.Physical stress.4.4. Surgical operation.Surgical operation.5.5. Pregnancy.Pregnancy.6.6. Sometimes Sometimes
spontaneously.spontaneously.
LEPROSY REACTIONLEPROSY REACTION
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TYPES OF LEPRA REACTIONS
Type I•Change in host CMI •Seen in borderlines•Skin and nerve lesions
Type II•Antigen antibody•Seen in LL & BL leprosy•Skin, nerve & systemic involvement
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Type I Lepra Reaction(Reversal Reaction)
Seen in BT, BB & BL. Sudden onset. Eythematous & odematous changes in old
lesions. Appearing of new lesions. Tenderness & swelling of peripheral nerves.
Treatment of type I Reaction:1. Continue MDT.2. NSAID.3. Systemic corticosteroid.
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Type II Lepra Reaction (ENL) Acute onset of constitutional symptoms. Appearance of ENL-like skin lesions. Visceral manifestations includes :- Iridocyclitis, hepato-splenomegaly, epididmo-orchitis, nephritis, pleuritis, lymphadenitis & neuritis. Treatment of type II Reaction:1. Continue MDT.2. NSAID3. Thalidoamide ( clofazimine, corticosteroid )
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Lucio phenomena
Unusual reaction seen exclusively in patien from Mexico
Having diffusue leprometus form of leprometus leprosy ,who left untreated
•Patient develop recurrent crops of large and sharply marginal ulcerative lesion (lower extremities)
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COMLICATIONS OF LEPROSY
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COMLICATIONS OF LEPROSY
1. Reactions.2. Complications of peripheral nerves.3. Complications of eyes4. Complication of bones
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COMPLICATIONS OF PERIPHERAL NERVES
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Peripheral nerves
Sensory Motor Autonomic
Hypoaestesia / anaestesia Muscle paralysis Lack of sweating & sebum
Ulcers Ulnar nerve Claw handRadial nerve Wrist dropLt. popliteal Foot dropPost. tibial Claw toesFacial lagophthalmous
Dry skinCracked skin
Ulcers
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COMPLICATIONS OF EYE
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Involvment of the ophthalmic division of the (5th.) trigeminal nerve
Corneal sensation imparment
Patients ignore injuries
keratitis, conjunctivitis and ulcers
Involvment of zygomatic & temporal braches of the (7th.) facial nerve .
Lagophthalmos
Unable to close the eye (unbliking stare)
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Complications Of Bones
Bone damage in Leprosy is confined to bones of hand , feet & skull.
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In the skull two pathognomonic changes occurs
1 -Atrophy of anterior nasal spine.
Nasal collapse
2 -Atrophy of maxillary alveolar process.
Loss of upper central incisors
These two skull changes known as “facies leprosa ”
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TREATMENT
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LEPROSY IS A CURABLE DISEASE
Leprosy treatment is simple, & the drugs are supplied in backs
All you have to do is decide which course of treatment the patient needs and make
sure that he take it regularly.
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Drugs used in Leprosy treatmentWhat are the three commonly used drugs?
1. Dapson.2. Rifampicine.3. Clofazimine.
The combination of these three drugs is known as Multi Drug Therapy )MDT(
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Rifampicin is highly bactericidal 99.999% of bacilli will be killed within 3 monthly doses.
Dapsone & clofazimine are weekly bactericidal, but in combination will
kill 99.999% of bacilli within 3 months.
MDT )Chemotherapy( renders Leprosy patients non-infectious.
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MDT for PB leprosy6 months
Monthly dose Rifampicin 600mgDapsone 100 mg
Daily doseDapsone 100 mg
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Multidrug Therapy )MDT( for Paucibacillary Leprosy )PB(
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MDT for MB leprosy24 months
Monthly doseRifampicin 600mgClofazimine 300 mgDapsone 100 mg
Daily doseDapsone 100mg Clofazimine 50 mg
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Multidrug Therapy )MDT( for Multibacillary Leprosy )MB(
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Multi Drug Multi Drug TherapyTherapy
24 months
6 months
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Prophylaxis
1 -BCG Vaccine : it has protective effect as it can help until a vaccine becomes available.
3 -small dose of Dapsone can be used as prophylactic for contacts at risk , though it is liable to give chance for dapsone resistance .
But now it is the only available prophylactic measure for contacts at risk.
2- Armadillo Derived Vaccine )heat killed M.lepra( + BCG and vaccines derived from cultivable mycobacteria are now under trials .
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thanks