Hansen’s Disease
Digital Lecture Series: Chapter 08
Dr. Meghana Phiske
MD, DNB, DVD, DDV
Assistant Professor
Department of Dermatology
L.T.M.M.C and L.T.M.G. Hospital Sion, Mumbai
CONTENTS
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History
Transmission of leprosy
Etiopathogenesis
Global and national scenario of
leprosy
Immunity and leprosy
Microbiology of M.Leprae
Classification of leprosy
Clinical spectrum
Systemic involvement in leprosy
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Differential diagnosis
Diagnosis
Treatment
Lepra reactions
Deformities
Physiotherapy
Prevention
Rehabilitation in leprosy
MCQs
Photoquiz
History
 Oldest infection known to mankind
 India considered as point of origin of leprosy
 First written reference appeared in Egyptian document written around
1550 BC
 Dr Gerhard Henrik Armauer Hansen first described M.leprae to be the
causative organism in 1873.
 Synonyms: Hansen’s disease, ‘Kushtha roga’
Definition :
Leprosy is a chronic systemic disease caused by Mycobacterium leprae
manifesting as development of specific granulomatous or neurotrophic
lesions in the skin, mucous membrane, eyes nerves, bones and viscera.
Transmission of Leprosy
 Respiratory route : inhalation of bacilli-laden droplets
 Cutaneous : skin to skin contact
 GIT : ingestion of food
 In utero transmission
 Transmission through breast milk
 Intradermal : inoculation by tattoos
 Incubation period : 5-7 years (on average)
Not Yet Proven
Epidemiological Factors
 Occurs at all age groups
 Peak age of onset : Between 20-30 years
 Males > Females (M:F: 2:1) (male predominance seen in adults, in
children gender distribution is nearly equal)
 Less common in children and women
 Commonest type of leprosy in children : Borderline tuberculoid
 Occurrence of disease depends on immune status
 Genetic susceptibility reported
 Migration from rural to urban areas: increase in cases
 Overcrowding, lack of personal hygiene, humidity favor disease
transmission
Global & National Scenario of Leprosy
 Registered prevalence globally(2009) : 213036
 Total cases detected in India (2011-12) : 1.27 lakh
 Annual case detection rate in India : 10.35 per one lakh population
 Increased no of new case detected (2011-12): Orissa, Gujarat,
Maharashtra, Madhya Pradesh, Andhra Pradesh
Immunity and Leprosy
Host resistance
 Excellent
 Good
 Fair
 Poor
 Very poor
Clinical manifestation
No infection
Subclinical infection with spontaneous
regression
Indeterminate, pure neuritic,
tuberculoid
Mid-borderline,
borderline-lepromatous
Lepromatous
Immunopathogenesis of leprosy
Entry of M.Leprae in the body via nose
Invasion
Multiplication in dermal lymphatics and
vascular endothelial cells
Hematogenous spread
Invasion of M.Leprae into nerves
Immunological response
Mycobacterium Leprae
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Obligate, non motile, nonspore forming microaerophilic intracellular,
acid-fast bacillus that forms curved or straight rods
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Components include : Cell wall, cell membrane, cytoplasm and capsule
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Affinity for skin, nerves and muscle tissue
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Found in macrophages, histiocytes and Schwann cells
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Non cultivable
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Grown in animal models(armadillo and mice)
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Closely resembles M. Tuberculosis, but less acid-fast.
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Multiplies (generation time) in 11-13 days
Classification
Ridley Jopling classification
 Indeterminate
 Tuberculoid
 Borderline
• borderline-tuberculoid
• mid-borderline
• borderline-lepromatous
 Lepromatous
Classification
Indian Classification
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Lepromatous
Tuberculoid
Maculoanesthetic
Borderline
Pure neuritic
Indeterminate
Classification
NLEP Classification
 Nonlepromatous
• Tuberculoid
• Maculoanesthetic
• Polyneuritic
 Indeterminate
• Borderline
• Indeterminate
 Lepromatous
• Lepromatous
Tuberculoid (TT)
 Single or few (upto 3), large,dry, asymmetrical,
erythematous / hypopigmented patches with
well-defined margins.
 Sweating – Lost
 Sensations – Absent
 Nerves - Thickened,
presence of feeding
nerves, abscesses
 Skin smears – Negative
 Lepromin test - Strongly positive
 Course-Polar TT stable and sub polar TT may
downgrade.
Borderline Leprosy
Common type of leprosy
 Subdivided into BT, BB & BL.
 Course - Unstable with variable prognosis, may progress to sub-polar
LL leprosy.
 Most prone to reactions.
 Lepromin test -Negative, weakly positive in BT.
Borderline Tuberculoid (BT)
 Few(upto 10),large, asymmetric,
hypopigmented or skin coloured macules,
plaques with ill defined margins
 Surface-Dry with hair loss
 Presence of satellite lesion near the
advancing margin of patch
 Sensory impairment - Marked
 Nerve involvement-Irregular and
asymmetrical
 Deformities are common
 Lepromin test-Weakly positive
Satellite lesion
Borderline tuberculoid leprosy
Midborderline leprosy (BB)
 Unstable form, reactions frequent
 Multiple and symmetric lesions
 Lesions range from papules, macules
and plaques
 Plaques show well demarcated
edges with characteristic punched
out centre (inverted saucer shaped)
 Face may show infiltration with
nodules on ears
 Sensory impairment - Moderate.
 Nerve involvement-Many nerves
involved and asymmetrical
Borderline lepromatous leprosy (BL)
 This type classically start as macule,
widespread and symmetrical, later
become infiltrated centrally
 Papules, nodules and plaques with
sloping edges
 Sensory impairment- Variable
(more in centre)
 Nerve involvement - Widespread and
asymmetrical
 Glove & stocking hypoaesthesia occurs late
 Lepromin reaction-Negative
 Prognosis-Variable
Lepromatous leprosy
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Lesions symmetrically distributed, small, multiple, shiny and waxy.
Macular, infiltrated, nodular, diffuse or ulcerative
Macules-Small, widespread, ill defined margins
Nodules- Arise from macules or infiltrated lesions
Sensory impairment-Normal or mild
Leonine facies- Infiltration of skin with nodules, loss of eyebrows and
eyelashes.
 Nerve involvement -Symmetrical, not markedly enlarged, fibrotic and
shrunken in late stages.
 Glove and stocking anaesthesia
 Lepromin test - Negative
Ear infiltration in lepromatous leprosy
Indeterminate leprosy
 Commonest presentation in children
(20-80%)
 Flat erythematous or hypopigmented,
asymmetrical, macules varying in number,
size and location with vague margins
 Common sites : Face, limbs, thighs
 Sensation - Normal or slightly impaired
 Peripheral nerves - Normal
 Skin smears - Negative
 Lepromin test - Unpredictable and variable
 Course - Usually self limiting, may progress
to other forms of leprosy.
Pure Neuritic leprosy
 Commonly reported from India and
Nepal
 Male preponderance seen
 Sensory loss without skin lesion
 Neuritic manifestations -Tingling,
heaviness and numbness, paresis,
hypotonia, atrophy, claw hand and toes,
wrist-drop, foot-drop.
 Other changes-Anhidrotic, dry glossy
skin, blisters, neuropathic ulcers,
decalcification, bone resorption
Dry skin in leprosy
Pure Neuritic leprosy
 Lepromin test -Slightly positive
 Course-Spontaneous regression or progression to TT leprosy
 Silent neuritis (silent neuropathy)
Sensory or motor impairment without skin signs of reversal reaction
or ENL, tenderness, paresthesia or numbness
Special forms of Leprosy
 Lucio Leprosy/Lepra Bonita’/Beautiful leprosy
Rare form of lepromatous leprosy, described in Mexico. Diffuse
widespread infiltration of skin, loss of body hair, loss of eyebrows &
eyelashes, and widespread sensory loss.
 Histoid leprosy
Seen in LL, but also in borderline and indeterminate cases.
Seen in patients taking irregular or inadequate treatment and in drug
resistant cases.
Nodules are firm, reddish or skin colored, dome shaped with shiny
skin.
Skin smears- Many bacilli seen.
 Lazarine leprosy
Diffuse ulceration seen as a part of lepra reaction in undernourished
patients.
Histoid leprosy
Eye Involvement in Leprosy
 Eyebrows/eyelashes-Madarosis, trichiasis leading to corneal vascularity
and opacity
 Facial nerve palsy- Lagophthalmos (partial/complete,
unilateral/bilateral) and ectropion
 Trigeminal nerve palsy-Exposure keratitis and vision loss
 Lacrimal gland-Dry eye and Dacryocystitis (acute, subacute or chronic)
 Cornea- Enlarged nerves, ulcers, lepromata, punctate keratitis and
pannus
 Sclera-Nodules on sclera, scleritis and episcleritis
 Uvea- Granulomatous and chronic uveitis
 Iris-Iris pearls
 Lens-Cataract
 Retina-Impaired contrast sensitivity
Nerve Involvement in Leprosy
 Sensory involvement - Anaesthesia in hands & feet, glove and stocking
anaesthesia, repeated trauma
 Motor involvement- Wasting and paralysis of muscles
 Autonomic involvement - Ichthyosis, loss of hair and sweating
Other features
 Nose : Nasal stuffiness / crusting, epistaxis, nasal deformity (Saddle
nose)
 Ear : Infiltration/nodules, ulceration
 Liver : Lepromatous hepatitis,amyloidosis
 Hoarseness of voice
 Gynaecomastia
 Bone resorption
 Lymphadenopathy
Differential Diagnosis
Macular lesions (hypopigmented)
 Vitiligo
 Occupational leucoderma
 Tinea versicolor
 Pityriasis alba
 Post kala azar dermal leishmaniasis
 Naevus depigmentosus and nevus anemicus
 Postinflammatory hypomelanosis
 Polymorphic light eruption
Differential Diagnosis
Macular lesions (erythematous)
 Pityriasis rosea
 Seborrhoeic dermatitis
 Tinea incognito
 Secondary syphilis
Differential diagnosis of hypopigmented conditions
Post kala azar
dermal leishmaniasis
Vitiligo vulgaris
P. Alba
Differential diagnosis of hypopigmented conditions
Polymorphus light eruption
P. Versicolor
Differential Diagnosis
Annular lesions
 Anular psoriasis
 Erythema multiforme
 Granuloma annulare
 Sarcoidosis
Infiltrated lesions
 Lupus vulgaris
 Lupus erythematosus
 Granuloma annulare
 Annular syphilides
 Post kala azar dermal leismaniasis (infiltrated lesions)
 Sarcoidosis
 Psoriasis
Differential diagnosis of annular lesions
Lupus vulgaris
Psoriasis vulgaris
Differential diagnosis of annular lesions
Granuloma Annulare
Tinea Corporis
Annular Syphillis
Nodular Lesions
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Post kala azar dermal leismaniasis
Cutaneous leishmaniasis
Syphilis
Sarcoidosis
Leukaemia cutis
Mycosis Fungoides
Nodules of neurofibromatosis
Kaposi’s sarcoma
Tuberous sclerosis
Differential diagnosis of nodular lesions
Neurofibromatosis
Leukemia Cutis
Differential diagnosis of neurological conditions
Sensory impairment with or without muscle wasting
 Peripheral neuropathy
 Diabetic neuropathy
 Primary amyloidosis of peripheral nerves
 Congenital sensory neuropathy
 Syringomyelia
 Tabes dorsalis
 Thoracic outlet syndrome
 Alcoholic neuropathy
 Hereditary motor and sensory neuropathy
Diagnosis
Cardinal signs of leprosy
 Anesthetic skin lesions
 Nerve enlargement
 Demonstration of M.Leprae
 Only one of these three features needed to make diagnosis
Clinical Examination
 Detailed history
 Number of skin lesions : >10, 10-15, 15-20 or numerous
 Distribution
 Size
 Colour : Hypopigmented / erythematous / coppery
 Shape : Circular, oval, irregular, annular
 Morphology : Macule / patch / plaque / papule / nodule
 Margin : Raised / flat, well / ill defined, sloping / punched out
 Surface : dry, scaly, smooth, shiny, edematous, ulcerated
Clinical Examination
 Symmetrical appearance
 Cutaneous nerve twig over the patch
 Earlobe infiltration
 Sensory impairment
 Motor examination
 Nerve examination
 Trophic ulcers
 Gynecomastia
 Loss of hair / sweating
Clinical Examination
 Sensory
 Touch : Tested with wisp of cotton
 Temperature : Tested with two test tubes
one containing hot water and other cold
 Pain : Tested by pin prick
 Semmes-Weinstein monofilament testing
 Corneal reflex : Tested with a wisp of
sterile cotton wool
 Motor
Monofilaments
 Testing of motor power- Done clinically
 Electro-diagnosis - Employed in very early cases. Electrical stimulator
using faradic and galvanic current used to test muscle power
Nerve Examination
Check for enlargement, tenderness,nodularity and
abscess and scoring system
Scoring system for enlarged nerves
Normal
0
Enlarged
+
Moderately enlarged
++
Very much enlarged
+++
Nerves
 Supra/ infraorbital
 Lateral popliteal
 Greater auricular
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Anterior/posterior tibial
 Ulnar
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Sural
 Median
 Cutaneous branch of
 Radial
radial nerve
Enlarged greater
auricular nerve
Investigations for M. Leprae
Bacteriological examination
Skin smears :
Made by slit and scrape method from the most active looking edge of skin
lesion and stained with Ziehl-Neelsen method.
Reading of smears :
Bacteriological index - Indicates density of leprosy bacilli (live & dead) in the
smears and ranges from 0 to 6+
Morphological index - It is the percentage of presumably living bacilli in
relation to total number of bacilli in the smear
Other Investigations
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Histopathological examination
Nerve biopsy
Sweat function test
Nasal mucosal smears
Nerve biopsy
Histamine tests
Lepromin test
FNAC
Animal Models : Armadillo, Thymectomised, irradiated nude mice, Korean
chipmunk etc.
Newer Investigations
 Serological assays: FLA-ABS, RIA, ELISA
 PGL, PCR
 Other techniques: Chemical, Immunological, Molecular biological,
Bioluminescent techniques, Strain specific probes
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Indications :
To confirm diagnosis in c/o inconclusive histopathological/smear reports.
To distinguish between reaction and relapse
To demonstrate M. leprae or its components
To elicit strain differentiation for molecular epidemiology
To detect drug susceptibility or resistance
Treatment
MDT-WHO
 Paucibacillary leprosy (6 months)
• Cap. Rifampicin (600 mg) monthly, supervised
• Tab. Dapsone (100 mg) daily
 Multibacillary leprosy (1 year)
• Cap. Rifampicin (600mg) monthly, supervised
• Cap. Clofazimine (300mg) monthly, supervised
• Tab. Dapsone (100mg) daily
• Cap. Clofazimine (50mg) daily
Blister packets for MDT
 Easy to use, handy and of convenient size
 Provide complete treatment
 Improve clinical attendance
 Drugs are better protected against moisture, heat and accidental damage
 Ensures quicker dispensing of the drugs
 Can be dispensed by non medical person
Blister Packets
Other New Regimens
 ROM
• Rifampicin - 600 mg
• Ofloxacin - 400 mg,
• Minocycline - 100mg
• Single dose - Single patch (WHO accepted)
 ROM-6 (Monthly for 6 months)-Paucibacillary
 ROM-12(Monthly for 12 months)-Multibacillary
 Ofloxacin based regimes
 RO (continuous treatment for 28 days)
 ROM trial (intermittent therapy)
 Moxifloxacin based regimes
Immunomodulatory Drugs
 Drugs - Levamisole, Zinc
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Antigenically related mycobacteria
B.C.G vaccine
M.leprae +B.C.G vaccine
Mycobacterium welchii vaccine
ICRC vaccine
 Other immunomodulators-Gamma interferons, interleukins
Newer Drugs / Regimens
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Fluoroquinlones (eg pefloxacin, ofloxacin, sparfloxacin, moxifloxacin)
Minocycline
Macrolides (Clarithromycin)
Ansamycin- Rifabutin, rifapentine ,isobutylpiperazinyl rifampicin, R-76-1
Cephalosporins
Beta lactamase inhibitors
Fusidic acid
Dihydrofolate reductase inhibitors-Brodimoprim, epiroprim
Hydrozone derivaties-PH-22 and PQ-22
Deoxy-Fructo-Serotonin
Lepra Reactions
 Acute episodes or bouts of exacerbations occurring in course of chronic
disease
 It is a sudden tissue response resulting from liberation of bacilli or their
products into the tissues, manifestations of which are local or systemic
 Sudden increase in activity of existing lesions, appearance of fresh lesions
with or without constitutional symptoms
 Type I reaction - All borderline cases (BT, BB,BL)
 Type II reaction - LL and sometimes BL cases
Precipitating Factors
 Pregnancy / lactation
 Drugs-Antileprosy drugs, iodides
 Severe physical or mental stress, surgical stress
 Infections
 Alcohol
Type I Reaction
 Type IV hypersensitivity reaction
 Sub - types
• Upgrading (Reversal)
• Downgrading
 Existing lesions worsen / New lesions may appear (have typical
characteristic of TT leprosy)
 Lesions become erythematosus and / or edematous and may ulcerate
 Neuritis / Nerve abscesses
 Systemic disturbances - Unusual
Type I Reaction
 Diagnosis : Clinical, histopathology (epitheloid cell granuloma, dermal
edema, plasma cells and foreign body giant cells)
 Complications : Neuritis, dactylitis, edema of hands/ feet,
corneal anesthesia, conjunctivitis, sudden occurrence of claw hand, footdrop, facial palsy
Type I reaction with enlarged nerve and nerve abscess
Type II Reaction (ENL-erythema nodosum leprosum)
 Occurs in BL and LL cases
 Type III hypersensitivity reaction
 Crops of tender, warm, recurrent, evanescent, erythematous nodules
distributed bilaterally symmetrically located on thighs ,legs and face
 Vesicular lesions can occur which break down to form ulcers (erythema
necroticans)
 ENL precedes fever, malaise, headache and joint pains
 Other manifestations : Rhinitis, epistaxis, Iridocyclitis, episcleritis,
dactylitis, epididymo-orchitis, arthritis, neuritis, bone pain and
lymphadenitis
 Diagnosis : Clinical, slit skin smears show broken bacilli, biopsy (vasculitis)
ENL and necrotic ENL
Type II Reaction - complications
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Frozen hand
Laryngitis
Non-paralytic deformity
Polyarthritis / RA-like syndrome
Multiple dactylitis
Leucocytosis, anaemia, raised ESR
Albuminuria / nephrotic syndrome
Liver / spleen enlargement
Epididimytis / orchitis, testicular atrophy / sterility
Gynaecomastia
Adrenal gland hypofunction
Eye involvement
Type 3 reaction (Lucio phenomenon)
 Rare form of reaction observed only in Lucio leprosy
 Acute ,severe, necrotizing vasculitis occurring in patients of Mexican
ancestry
 Presents as painful erythematosus patches that become necrotic and
ulcerated
Treatment of Lepra reactions
Principles of treatment
 Early initiation of treatment for reaction
 Continuation / initiation of MDT
 Removal of precipitating factor
 Rest, physical and mental
Treatment Modalities
Mild reaction
 Analgesics (aspirin or paracetamol)
Severe reaction
 Corticosteroids
 Antimalarials
 Clofazimine
 Thalidomide
 Methotrexate
 Cyclosporine
 Azathioprine
 Mycophenolate mofetil
Treatment Modalities
Supportive management
 Surgical decompression of nerves, splints / padding, treatment of steroids
/ atropine eye drops for iridocyclitis, steroids / scrotal support for
epipdidymoorchitis
Newer drugs for ENL :
 Leukotriene inhibitors, thalidomide derivatives, infliximab
Deformities/Disabilities in leprosy
 Deformity : Visible alteration in the appearance which results in
disability.
 Disability : Restriction or lack of ability to perform an activity
considered normal for a human.
 Primary : Are caused by the tissue reaction to infection with M.Lepra
e.g. leonine facies, flat-nose, claw hand.
 Secondary : Occur as a result of damage to the anesthetic parts of
the body e.g. planter ulcers, corneal ulcers.
Grading of Deformities/Disabilities : WHO disability grading
 Grade 0 :
No anaesthesia, no visible deformity or damage in hands and feet, or
no problems in eye or no visual loss.
 Grade 1 :
Anaesthesia present, but no visible deformity or damage, eye
problems due to leprosy present but vision not severely affected (6/60
or better) and can count fingers at 6 metres.
 Grade 2 :
Visible deformity or damage present in hands or feet , and severe
visual impairment (vision worse than 6/60)i.e unable to count fingers
at 6 metres or lagophthalmos or iridocyclitis or corneal opacities.
Deformities
Primary Deformities
 Leonine facies
 Loss of eyebrows and eyelashes
 Depressed nose
 Gynaecomastia
 Palatal perforation
Secondary deformities
 Corneal ulcers and opacities
 Plantar ulcers
 Palmar ulcers and ulcers on tips of fingers
 Resorption
 Charcot joints
Plantar ulcer
Deformities : Nerve Damage
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Claw hand (ulnar, median)
Clawing of the toes (posterior tibial)
Wrist-drop (radial)
Foot-drop (lateral popliteal)
Lagophthalmos, facial palsy (facial)
Trophic Ulcer : Stages
 Threatened ulcer : Process of tissue damage starts associated with
inflammation
 Presents as edema and warmth in region of metatarsal head with
associated deep tenderness and increase in inter digital gap
 Concealed ulcer : Damage to subcutaneous tissue presents as
necrosis and blisters at the site of damage
 Open ulceration : Skin breaks down and tissue damage site is
exposed to form frank ulcer
 Types of ulcers :
• Acute ulcer/ Chronic ulcer
• Complicated/uncomplicated ulcer
Prevention of Deformities
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Adequate treatment of leprosy patient
Early detection of nerve damage
Prevention of nerve damage
Protection of anesthetic hands from injury
Care of hands with weakness/paralysis
Use of protective footwear
Adequate hydration of skin
Physiotherapy
Management of Deformities
 Education of patient regarding prevention of injuries
 Daily examination of hands and feet and prompt treatment for minor
injuries
 Using adapted tools and appliances after training
 Reconstructive surgery
 Rehabilitation
Physiotherapy
Oil massage/Wax Therapy-Uses
 To make the skin soft and supple and loosen stiff joints
 As a preliminary to exercises
 To strengthen muscles and keep joints mobile
 To reduce pain in acute neuritis
 To stimulate innervated sweat glands to increase blood flow
Exercises : Active and assisted exercise : To increase the strength of muscles
and retain their tone
Electric stimulation – Uses
 To maintain the tone of denervated muscle
 Helpful in breaking post operative adhesions
 Before tendon surgery could be used as a means of documenting nerve
damage and the progress of the nerve recovery with treatment.
Splints
Indication
 Acute neuritis
 Mobile deformities(to prevent fixed deformities),
 Fixed deformities(to correct the deformities).
Various splints
 For radial neuritis-Static or dynamic wrist drop splint
 For mobile deformity- Static or dynamic splint
 For fixed deformity-Gutter splints, finger loops etc.
Splints for various deformities
Hand deformities : Gutter splints, finger loop splints, opponens splints and
adductor bands
Foot deformity : “Y” strap with spring, single elastic strap
Prevention and Control of leprosy
 Prevention of leprosy
Early detection through survey and initiation of treatment
Families of patients to be kept under surveillance
Immunoprophylaxis -Use of leprosy vaccines
Improvement in socio-economic conditions
 Leprosy control
Three activities of a leprosy control unit
• Case detection
• Case holding, including treatment
• Health education of public and patients
Prevention and Control of leprosy
 Leprosy Organizations
UNICEF LEPRA, DANIDA, SIDA, CIDA, Leprosy mission, American
leprosy mission (ALM), German leprosy relief association(GLRA),
LEPRA, Netherland leprosy relief (NLR)
 Leprosy control Programmes
National leprosy control programme (NLCP) 1954
Triad of Survey, Education and Treatment (S.E.T).
National leprosy eradication programme (NLEP) 1982
Prevention and Control of leprosy
National Leprosy Eradication Programme (NLEP), 1982
 Eradicate leprosy from the country by 2000.
 ‘Vertical’ health programme- In areas where prevalence of leprosy is
more than 5 per 1000.
 ‘Horizontal’ programme- In areas where the prevalence rate is less
than 5 per 1000.
Three main units for programme operation :
 Basic tier : Survey, education and treatment unit, leprosy control unit
and urban leprosy control unit.
 Second tier : District/zonal leprosy office.
 Third tier : Leprosy division of the state Directorate of the health
services.
Rehabilitation in Leprosy

Rehabilitation :
• Physical and mental restoration of patients to normal activities, so
that they are able to assume their place in the home, society and
industry.
• Treatment of physical disability
• Education of patient, family and public
• Rehabilitation in special homes or institutional rehabilitation
• Community based rehabilitation
MCQ’S
Q.1) What is the incubation period of leprosy?
A. 1-10 yrs
B. 11-20 yrs
C. 21-30 yrs
D. 31-40 yrs
Q.2) When was National leprosy eradication programme (NLEP) started?
A. 1982
B. 1983
C. 1984
D. 1985
MCQ’S
Q.3) What is the generation time of leprosy?
A. 1-10 days
B. 11-20 days
C. 21-30 days
D. 31-40 days
Q.4) Satellite lesion is commonly seen in which type of leprosy?
A. Indeterminate
B. Lepromatous
C. Borderline tuberculoid
D. Tuberculoid
MCQ’S
Q.5) Cardinal signs of leprosy include all except
A. Anesthetic lesions
B. Enlarged Nerves
C. Demonstration of M. Leprae
D. Trophic ulcer
Q.6) What is the duration of multi-bacillary treatment?
A. 6 Months
B. One Year
C. Two Years
D. Three Years
Photo Quiz
A 14 year old boy presented with a flexion of interphalangeal joints of
little and ring finger? What is the deformity and which nerve causes it?
Photo quiz
A 15 year old boy presented with multiple asymptomatic lesions with
asymmetric enlarged ulnar nerve. What is the likely diagnosis?
Photo Quiz
A 4 year old girl presented with aysmptomatic non scaly, whitish patch
with intact sensations. What is the likely differential diagnosis?
Thank You!