Hansen’s Disease

CONTENTS
 History  Differential diagnosis
 Transmission of leprosy  Diagnosis
 Etiopathogenesis  Treatment
 Global and national scenario of  Lepra reactions
leprosy  Deformities
 Immunity and leprosy  Physiotherapy
 Microbiology of M.Leprae  Prevention
 Classification of leprosy  Rehabilitation in leprosy
 Clinical spectrum  MCQs
 Systemic involvement in leprosy  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 Not Yet Proven

 Transmission through breast milk

 Intradermal : inoculation by tattoos

 Incubation period: 5-7 years (on average)
 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 Clinical manifestation

 Excellent No infection
 Good Subclinical infection with spontaneous
regression
 Fair Indeterminate, pure neuritic,
tuberculoid
 Poor Mid-borderline,
borderline-lepromatous
 Very poor
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

 Obligate, non motile, nonspore forming microaerophilic intracellular, acid-

fast bacillus that forms curved or straight rods
 Components include : Cell wall, cell membrane, cytoplasm and capsule
 Affinity for skin, nerves and muscle tissue
 Found in macrophages, histiocytes and Schwann cells
 Non cultivable
 Grown in animal models(armadillo and mice)
 Closely resembles M. Tuberculosis, but less acid-fast.
 Multiplies (generation time) in 11-13 days
 Classification

Ridley Jopling classification

 Indeterminate
 Tuberculoid
 Borderline
• borderline-tuberculoid
• mid-borderline
• borderline-lepromatous
 Lepromatous
 Classification

Indian Classification

 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

 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 Vitiligo vulgaris P. Alba

dermal leishmaniasis
 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

 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
 Testing of motor power- Done clinically Monofilaments
 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  Anterior/posterior tibial

 Ulnar

 Median  Sural

 Radial  Cutaneous branch of

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

 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

 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

 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

 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, foot-

drop, 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

 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
Plantar ulcer
 Charcot joints
 Deformities : Nerve Damage

 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

 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?

E. 1982
F. 1983
G. 1984
H. 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?

E. Indeterminate
F. Lepromatous
G. Borderline tuberculoid
H. 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?

E. 6 Months
F. One Year
G. Two Years
H. 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!