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

22.02.2016 dvl

  • 1.
  • 2.
    History  Definition: Leprosyis 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’
  • 3.
    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
  • 4.
    Epidemiological factors  Occursat all age groups  Peak age of onset : Between 10 – 20 years  Males > Females  Children most susceptible  Immune status ( host resistance)  Overcrowding  Low socioeconomic status
  • 5.
    Immunity and Leprosy Hostresistance  Excellent  Good  Fair  Poor  Very poor Clinical manifestation No infection Subclinical infection with spontaneous regression Indeterminate, pure neuritic, tuberculoid Mid-borderline, borderline-lepromatous Lepromatous
  • 6.
    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.
  • 7.
    Classification The Ridley Joplingclassification  Indeterminate  Tuberculoid  Borderline: borderline-tuberculoid, mid-borderline, borderline-lepromatous  Lepromatous Pure neural, Maculoanaesthetic - Indian classification
  • 8.
    Classification  Paucibacillary Leprosy(PB): Indeterminateleprosy (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.
  • 9.
    Tuberculoid (TT)  Singleor 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.
  • 10.
    Borderline leprosy Common typeof 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.
  • 11.
    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
  • 12.
    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.
  • 13.
    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
  • 14.
    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
  • 15.
    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.
  • 16.
    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.
  • 17.
    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.
  • 18.
    Special forms ofLeprosy  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
  • 19.
    Eye Involvement inLeprosy  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
  • 20.
    Nerve Involvement inLeprosy  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.
  • 21.
    Other features  Nasalstuffiness / crusting  Epistaxis  Hoarseness of voice  Gynaecomastia  Saddle nose  Bone resorption  Lymphadenopathy
  • 22.
    Differential diagnosis ofleprosy Macular lesions  Vitiligo  Occupational leucoderma  Tinea versicolor  Pityriasis alba  Post kala azar dermal leishmaniasis  Naevus depigmentosus  Scars
  • 23.
    Differential diagnosis ofleprosy Infiltrated lesions  Lupus vulgaris  Lupus erythematosus  Granuloma annulare  Annular syphilides  Post kala azar dermal leismaniasis (infiltrated lesions)  Sarcoidosis  Psoriasis
  • 24.
    Differential diagnosis ofleprosy Nodular lesions  Post kala azar dermal leismaniasis  Cutaneous leismaniasis  Syphilis  Onchocerciasis  Sarcoidosis  Leukaemia cutis  Mycosis Fungoides  Nodules of neruofibromatosis
  • 25.
    Differential diagnosis ofneurological 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
  • 26.
    Diagnosis Cardinal signs ofleprosy  Sensory impairment in affected areas  Enlargement of peripheral nerves associated with signs of peripheral nerve damage  Finding acid-fast bacilli in the lesions
  • 27.
    Clinical examination  Typeand number of skin lesions  Sensory impairment  Motor examination  Nerve examination  Sweating  Loss of hair
  • 28.
    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
  • 29.
    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.
  • 30.
    Nerves  Supra/ infraorbital Greater auricular  Clavicular  Radial  Sup. Radial cut  Ulnar  Median  Lateral popliteal  Posterior tibial  Anterior tibial  Sural