Hansen’s Disease
History

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.

Oldest infection known to mankind

Synonyms: Hansen’s disease, ‘Kushtha roga’
Transmission of Leprosy

Respiratory route: inhalation of bacilli-laden
droplets

Cutaneous: skin to skin contact

GIT : ingestion of food

Intradermal : inoculation by tattoos
}
Not
Yet
Proven
Epidemiological factors
Occurs at all age groups
 Peak age of onset : Between 10 – 20 years
 Males > Females
 Children most susceptible
 Immune status ( host resistance)
 Overcrowding
 Low socioeconomic status

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
Mycobacterium Leprae
Obligate, intracellular, acid-fast bacillus
 Affinity for skin, nerves and muscle tissue
 Found in macrophages, histiocytes and
Schwann cells.
 Non cultivable
 Grown in animal models
 Closely resembles M.tuberculosis, but less
acid-fast.
 Multiplies in 11-13 days.

Classification
The Ridley Jopling classification
 Indeterminate
 Tuberculoid
 Borderline: borderline-tuberculoid,
mid-borderline,
borderline-lepromatous
 Lepromatous
Pure neural, Maculoanaesthetic - Indian
classification
Classification
Paucibacillary Leprosy(PB):
Indeterminate leprosy (I)
Tuberculoid leprosy (TT)
Borderline tuberculoid (BT)
Pure neuritic (PN)*
 Multibacillary Leprosy(MB):
Midborderline leprosy (BB)
Borderline lepromatous (BL)
Lepromatous leprosy (LL)
* Asymmetric nerve involvement with no skin
lesion and usually of tuberculoid origin.

Tuberculoid (TT)
Single or few, asymmetrical, well-defined,
erythematous or copper-coloured patches
 Sensations - Absent
 Nerves - thickened, presence of feeding nerves,
abscesses
 Skin smears - Negative
 Lepromin test - Strongly positive
 Course - Relative benign and stable, with good
prognosis.

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 asymmetric, hypopigmented or skin
coloured macules, plaques with ill defined
margins
 Presence of satellite lesion near the advancing
margin of patch
 Sensory impairment - Marked
 Nerve involvement - Marked and asymmetrical

Midborderline leprosy (BB)
Unstable form, reactions frequent
 Annular lesions with characteristic punched out
appearance (inverted saucer shaped)
 Sensory impairment - Moderate.
 Nerve involvement - Marked and asymmetrical.

Borderline lepromatous leprosy (BL)
Multiple shiny macules, papules, nodules and
plaques with sloping edges
 Sensory impairment - Slight
 Nerve involvement - Widespread and less
asymmetrical.
 Glove & stocking hypoaesthesia

Lepromatous leprosy
Hypopigmented, erythematous or coppery,
shiny macules, papules, nodules
 Lesions symmetrically distributed, small,
multiple, shiny with normal or mild sensory loss
 Leonine facies: Infiltration of skin with nodules,
loss of eyebrows and eyelashes
 Nerve involvement symmetrical; glove &
stocking anaesthesia
 Lepromin test - Negative

Indeterminate leprosy
Asymmetrical, single /multiple hypopigmented,
or faintly erythematous and ill-defined
macules.
 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
Neuritic manifestations -Tingling, heaviness
and numbness, paresis, hypotonia, atrophy,
claw hand and toes, wrist-drop, foot-drop.
No skin lesion.
 Other changes-Anhidrotic, dry glossy skin,
blisters, neuropathic ulcers, decalcification,
bone resorption.

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,
paraesthesiae or numbness.

Special forms of Leprosy
Lucio 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.
 ‘Lepra Bonita’ (Pretty leprosy)
Elderly persons with diffuse infiltration of face
smoothes out wrinkles, giving youthful
appearance.
 Histoid leprosy:
BL patients with irregular or poor treatment
compliance
Drug resistant cases

Eye Involvement in Leprosy
Lagophthalmos (partial/complete,
unilateral/bilateral)
 Conjunctivitis
 Exposure keratitis and corneal ulcers
 Madarosis, trichiasis leading to corneal
vascularity and opacity
 Dacryocystitis (acute,subacute or chronic)
 Nodules on sclera, episcleritis, scleritis
 Corneal nodules and lepromatous pearls
 Microlepromata, nodules on iris and ciliary body

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 -Icthyosis, loss of hair
and sweating.

Other features
Nasal stuffiness / crusting
 Epistaxis
 Hoarseness of voice
 Gynaecomastia
 Saddle nose
 Bone resorption
 Lymphadenopathy

Differential diagnosis of leprosy
Macular lesions
 Vitiligo
 Occupational leucoderma
 Tinea versicolor
 Pityriasis alba
 Post kala azar dermal leishmaniasis
 Naevus depigmentosus
 Scars
Differential diagnosis of leprosy
Infiltrated lesions
 Lupus vulgaris
 Lupus erythematosus
 Granuloma annulare
 Annular syphilides
 Post kala azar dermal leismaniasis (infiltrated
lesions)
 Sarcoidosis
 Psoriasis
Differential diagnosis of leprosy
Nodular lesions
 Post kala azar dermal leismaniasis
 Cutaneous leismaniasis
 Syphilis
 Onchocerciasis
 Sarcoidosis
 Leukaemia cutis
 Mycosis Fungoides
 Nodules of neruofibromatosis
Differential diagnosis of neurological conditions
Sensory impairment with or without muscle wasting
 Peripheral neuropathy
 Diabetic neuropathy
 Primary amyloidosis of peripheral nerves
 Congential sensory neuropathy
 Syringomyelia
 Tabes dorsalis
 Thoracic outlet syndrome
 Alcoholic neuropathy
Diagnosis
Cardinal signs of leprosy
 Sensory impairment in affected areas
 Enlargement of peripheral nerves associated
with signs of peripheral nerve damage
 Finding acid-fast bacilli in the lesions
Clinical examination
Type and number of skin lesions
 Sensory impairment
 Motor examination
 Nerve examination
 Sweating
 Loss of hair

Clinical examination: Sensory
Touch
Tested with wisp of cotton,nylon thread or feather.

Temperature
Tested with two test tubes – one containing hot
water and other cold

Pain
Tested by pin prick

Clinical examination : Motor

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.
Nerves
Supra/ infraorbital
 Greater auricular
 Clavicular
 Radial
 Sup. Radial cut

Ulnar
 Median
 Lateral popliteal
 Posterior tibial
 Anterior tibial
 Sural

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
Investigations
Histopathological examination
 Nerve biopsy
 Sweat function test
 Lepromin test
 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

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

Other Regimens
ROM
Comprises Rifampicin - 600 mgs,
Ofloxacin - 400 mgs,
Minocycline - 100mg
Single dose – single patch (WHO accepted)
ROM -6 (Monthly for 6 months) - Paucibacillary
ROM -12 (Monthly for 12 months) – Multibacillary

Newer Drugs / Regimens
RO - 28
 Fluoroquinlones - Nalidixic acid
 Macrolides (Clarithromycin)
 Ansamycin-Rifabutin, Rifapentine
 Dihydrofolate reductase inhibitors-Brodimoprim,
K-130
 Fusidic acid
 Beta-lactam antibiotics
 Cephalosporins
 Quinolones (Pefloxacin and Sparfloxacin

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,interleukin

Lepra Reactions
Acute episodes or bouts of exacerbations
occurring in course of chronic disease
 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 - BL & LL cases

Precipitating factors
Physiological conditions like pregnancy
 Drugs: anti-leprosy drugs, iodides
 Severe physical or mental stress
 Infections

Type I Reaction
Sub-types
- Upgrading (Reversal)
- Downgrading
 Type IV hypersensitivity reaction.
 Existing lesions worsen/New lesions may appear
 Neuritis / Nerve abscesses
 Systemic disturbances: Unusual

Type I reaction - complications
Neuritis
 Dactylitis, edema of hands & feet, inflammation
of small joints of fingers
 Corneal anesthesia, Conjunctivitis
 Sudden occurrence of claw hand, foot-drop,
facial palsy

Type II Reaction
Occurs in BL and LL cases
 Type III hypersensitivity reaction
 Erythema Nodosum Leprosum-crops of painful,
recurrent, erythematous, papulonodular lesions.
 Fever and malaise
 Iridocyclitis, episcleritis, epididymo-orchitis,
arthritis, neuritis, lymphadenitis

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

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
Analgesics
 Corticosteroids
 Antimalarials
 Clofazimine
 Thalidomide
 Miscellaneous – colchicine, zinc, cetrizine,
antimonials
 Supportive management – for eye
complications, splints etc.

Deformities in leprosy

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
Classification

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 present but vision 6/60
or better.
Grade 2
Visible deformity or damage present in hands or
feet , and vision worse than 6/60

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

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- slight puffiness and warmth in
region of metatarsal head with associated
tenderness
 Concealed ulcer - Necrosis, blisters at the site of
damage.
 Open ulceration - Frank ulcer
 Types of ulcers - Acute ulcer
Chronic ulcer
Complicated ulcer

Prevention of deformities

Early detection of nerve damage

Adequate treatment of leprosy patient

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
Physiotherapy
Splints-Indication
 Acute neuritis
 Mobile deformities(to prevent fixed deformities),
 Fixed deformities(to correct the deformities).
Splints used
 For radial neuritis-Static or dynamic wrist drop
splint
 For mobile deformity- Static or dynamic splint
 For fixed deformity-Gutter splints,finger loops etc.
Physiotherapy
Electric stimulation - Uses
 To maintain the tone of denervated muscle
 Helpful in breaking post operative adhesions
 After tendon surgery could be used as a means
of documenting nerve damage and the progress
of the nerve recovery with treatment.
Prevention and Control of leprosy
Prevention of leprosy
Early detection through survey and initiation
treatment
Families of patients to be kept under surveillance
Immunoprophylaxis -Use of leprosy vaccines
Improvement in socio-economic conditions

Control of leprosy
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, German
leprosy relief association
 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
NLEP
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

Thank you