Leprosy (Hansen’s Disease)

DERMATOLOGY
LEPROSY
Group 2
By…..
1. Marwa Mohamed Ahmed Omer .
2.Mohammed Abdelgader Elsheikh
mohammed .
3.Sara Ali Hassan
4.Shima Abd Alkareem Eshag .
5.Akram Yahya Zayed
6.Marwa Mohamed Hasbelnabi .
 1.Definition of the Leprosy.
2.Learn about CAUSES.
3.Learn about PATHOGENESIS.
4.Learn about CLASSIFICATION.
5.Learn about PATHOLOGY.
6.Learn about CLINICAL FEATURES.

7.Learn about DIAGNOSIS.

The objective:- 8.Learn about COMPLICATIONS

9.Learn about TREATMENT
LEPROSY
 Leprosy (HANSEN'S DISEASE):

 Definition:
According to the WHO, it is a chronic
infectious disease caused by Mycobacterium
leprae.
It is the MOST COMMON global cause of
peripheral neuropathy.
The disease is curable if diagnosed early
The disease affects mainly:
- Skin.
- Peripheral nerves.
- Mucosal surfaces of upper respiratory tracts.
- Eyes.
 It can affect all ages and both sexes
Transmission:

It is believed that the disease is transmitted by

inhalation of bacili of mycobacterium leprae from the
respiratory tract secretions of an infected person.

• Undiagnosed patients are the main source of infection

:
 Nasal /oral Droplets
 Dermal Inoculations

:
Armadillo
 The transmit leprosy
 They act as animal model
along with monkey , mice
and rabbit
Mode of infection :
Leprosy is slow communicable disease and uncubation
period is between first exposure and appearance of signs
of disease .

Direct contact : prolonged close contact of susceptible

individuals to an open case of leprosy (demaged skin ,
nasal secretion , mucous membrane contact ).
Materno – foetal transmission
Transmission from milk from mother to infant .
Incidence :
• At highest risk are those living in endemic areas
(hot and moist) with poor conditions such as
inadequate bedding , contaminated water , and
insufficient diet , or other diseases that compromise
immune function .
• Acc to WHO – India ,Brazil , Indonesia ,
• Myanmar and Nigeria are with the most cases .
 Through out history, leprosy was a disgrace to the suffer, and
was considered by some as a punishment from heaven or a
magical curse.

 In medieval Europe , Lepers had to wear special clothes and walk

on acertain sid of the road or even tie bells around their necks
to alert people to their presence
 LEPROSY ( IS A CHRONIC
STIGMATIZING) :

BACTEARIAL DISEASE OF MAINLY THE SKIN

,PERIPHERAL NERVES ,EYES AND NOSE

CAUSES OF STIGMA
 Fear of infection.
 Multilating deformity
 Disability results from these deformities.
 Ulceration , cellulitis , scarring ,bone deformity, blindness.
 Hansen's disease caused by an exposure
to Mycobacterium leprae

the major risk factors are:

 1. Direct and close contact.
 2. Immune suppression.
 3. Environmental Factors (poor conditions).
 4. Certain genetic factors.
 Pathogenesis:
 Leprosy has low pathogenicity, the bacillus is likely
transmitted via droplets, from the nose and mouth.
 On average, the disease incubation period is 5 years
but symptoms may occur within 1 year. It can also
take as long as 20 years or even more to occur.
Leprosy mainly affects the skin, the peripheral
nerves, mucosa of the upper respiratory tract, and
the eyes.
CLASSIFICATION
CLASSIFICATION :

 Main 2 types :
 Tuberculoid types : high resistance .
 Lepromatous or low resistance
 Cass not falling in these 2 are considered as
borderline leprosy .
CLASSIFICATION

 Based on the clinical ,bacteriologic ,immunologic and

histopathologic features , leprosy is classified into main
types :
1. paucibacillary example : (Tuberculoid leprosy) (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 to
3. Multibacillary (lepromatous leprosy) (LL)
Nodules and plaques , thickened dermis ,loss of sensation , neuronal
damage , nasal congestion , epistaxis
PATHOLOGY
 The pathology due to :
 Granulomatous reaction.
 Interference with cell metabolism
The early form of all types of leprosy is known
as the indeterminate leprosy.
SCHWANN CELLS
 BACILLI
DERMIS(PILOSEBACIOUS)

LYMPHOCYTIC &MACROPHAGES
INFITERATE
RESPONSE
 3/4 self healing
 1/4 progress to determinate
 LEPROMATOUS LEPROSY(LL)
skin ,peripheral nerves, organ systems

CMI.

humeral immunity.
Pt. is very infectious
HISTOPATHLOGICAL APPEARACE

Dermis histiocytic granuloma

globi /lepra
(diagnostic)
Space bet.lesion in the dermis &
the epidermis. (diagnostic)
Large no. of the bacilli.
TUBERCULOID LEPROSY (TL)

Skin & peripheral nerves only.

CMI
Patients are not infectious.
 HISTOPATHOLOGICAL
APPEARANCE

Dermis epithelioid cell

granuloma:-

No space between lesions in the

dermis & epidermis.
Scanty bacilli.
 BORDERLINELINE LEPROSY(BL)

DIMORPHUS.
Unstable form
Intermediate immunity.
Mixed features of LL&TL.
Less severe.
Moderate no. of bacilli.
Epitheloid cell infiltrate in the dermis .
Without treatment moves towards LL or TL
CLINICAL FEATURES
Leprosy like all disease have symptoms and
signs.
Clinical symptoms
Early:
 A small patch of recent origin
either paler or redder than normal
skin.
 Numbness and tingling of hands
and/or the feet
 Burning sensation in the skin
 Slight weakness of the face hands
and feet
Late:
 More and larger skin patches.
 Painless injuries, burns or ulcers.
 Obvious nodule and or thickening of the skin.
 More severe weakness or paralyses of muscle
of face, hand or feet

NOTE:
Both early and late cases are very seldom complains of all
symptoms that are listed
:
Commonly macules or plaques
rarely papules or nodules are
seen.
More and larger skin
patches.
Painless skin patch
accompanied by loss of
sensation but not itchiness

Chronic insensate patch due to leprosy

infection
Numbness and
tingling of hands
and/or the feet
Ulcerations on hands
or feet

Chronic nonhealing
ulcer
Foot drop or clawed
hands

Characteristic clawed hand deformity

caused by ulnar involvement in leprosy
(erythema nodosum
leprosum).

Patient with erythema

nodosum leprosum  
 Signs

 There are 3 cardinal signs of leprosy, usually more than one

of these signs is present , but if you are absolutely certain
of only one of them this is sufficient to prove the diagnosis

 The cardinal signs of leprosy include hypoesthesia, skin

lesions, and peripheral neuropathy.
Peripheral nerve
hypertrophy

Peripheral nerve thickening in leprosy.

DIAGNOSIS
 DIAGNOSIS

 The diagnosis of leprosy remains primarily clinical.

 In addition to skin lesions, the presence of anesthesia or
hypoesthesia ,thickening of peripheral nerves ,and or the
presence of AFB on slit skin smears or biopsy , is noted .
 Smears are made from skin lesions, earlobes and dorsum
of the ring or middle fingers _sites of fast bacillary
replication
 Mycobacterial culture has so far proved impossible
in vitro.

 When abiopsy is required ,it is taken from a sensory

cutaneous nerve without muscular supply ,such as the
sural nerve or radial cutaneous nerve .
COMPLICATIONS
What are the potential complication of leprosy

 Delayed diagnosis and treatment can lead to serious

complication.
 These can include:
 Disfigurement
 Hair loss , particularly on the eyebrows and eyelashes
 Muscle weakness
 Permanent nerve damage in the arms and legs
 Inability to use hands and feet
 Chronic nasal congestion , nosebleeds ,and collapse of
the nasal septum
 Iritis , which is an inflammation of the iris of the
eye
 Glaucoma , an eye disease that causes damage to
optic nerve
 Blindness
 Erectile dysfunction (ED)
TREATMENT
Antileprotic drugs
 Dapsone

 Clofazimine

 Rifampicin
Before After

 Ofloxacin

 Minocycline
 Dapsone (DDS)

 Diamino diphenyl sulfone.

 Structural analogs of PABA – prevents folic acid synthesis.
 Competitive inhibitor of dihydropteroate synthase.
 Resistance – mutant genes encoding dihydropteroate
synthase.
 Oral bioavailability.
 Hemolysis in patients with G6PD deficiency.

 Nervousness ,insomnia ,blurred vision

,paresthesias , drug fever , pruritus , psychosis
,and a variety of skin rashes .
 clofazimine
 Fat soluble Riminophenazine dye.
 MOA – Bind to DNA of M. leprae ,membrane disruption
,inhibition of mycobacterial phospholipase A2 inhibition of
microbial K+ transport , generation of hydrogen
peroxide , interference with the bacterial electron
transport chain.
 Variable oral bioavailability .
 Hydrolytic dehalogenation , hydrolytic deamination
,glucuronidation ,and hydroxylation .
 AE – Acute abdominal symptoms ,skin
discolouration .

 Anti – inflammatory effectas via inhibition of

macrophages ,T cells , neutrophils , and
complement .

 Interaction
 Rifampicin
 Semisynthetic derivative of macrocyclic antibiotic rifamycin .
 Rapidily bactericidal against M. Leprae .
 B subunit of DNA – depemdent RNA polymerase – RNA
transcription .
 It is readily absorbed with an elimination half – life of – 3 hours
.
 Excreted mainly through liver in to bile and undergoes
enterohepatic circulation .
 Enzyme inducer – Auto enzyme induction , Ocp ,s , warfarin .
 Resistance .
Adverse Effects

 Rash , fever , and nausea and vomiting . Hepatitis ,

Hemolysis , hemoglobinuria ,

 Flu like syndrome

 Orange – tan discoloration of skin , urine , feces ,

saliva , tears .
 Ofloxacin

 Patients with intolerance , resistance , or clinical failure to primary

therapy (rifampicin) .
 Inhibits DNA gyrase – DNA replication and transcription .
 400mg on first day followed by 200mg \ day .

 Minocycline
 Intolerance to Clofazimine .
 30S ribosomal subunit .
 100 mg / day .
 Deposit in tooth enamel and discolor teeth .
 MDT
 Multi drug therapy (MDT) is a key element for cure .
 MDT is available free of charge from WHO
 The drugs used in WHO – MDT are a combination of
Rifampicin , Clofazimine and Dapsone for MB leprosy patients
 Rifampicin and Dapsone for PB leprosy patients
 Treatment of leprosy with only one anti leprosy drug will
always result in development of drug resistance .
 Treatment with dapsone or any other anti leprosy drug used
as monotherapy should be considered as un ethical practice .
 Treatment of Immunologic Reactions

 Type 1 reaction
Clofazimine 200 mg daily corticosteroids
 Loss of sensation or other peripheral nerve symptoms , corticosteroids
should be started immediately to prevent permanent damage .

 Type 2 reaction
May not respond to corticosteroids a lone , and the addition of drugs such
as thalidomide .
Thalidomide

 Reduce systemic concentrations of TNF- alfa ,

IL-2 , interferon

 100 – 300 mg /day

 Avoided in pregnancy and during lactation .

 PB Adult 6 months
0nce a month - At clincic
Day 1 : supervised
2 capsules of Rifampicin (300 mg ) 2
1 tablet of dapsone (100mg )
Once a day – At home
Days 2 - 28 : unsupervised
1 tablet of Dapsone (100 mg )

PB Child 6 months
Once a month – At clinic
Day 1 : supervised
2 capsules of Rifampicin(300 mg +150mg )
1 tablet of dapsone (50mg )
Once a day – At home
Days 2 -28 : unsupervised
 MB Adult 12 months
Once a month : Day 1 At clinic
2 capsules of Rifampicin (300 mg ) 2
3 capsules of clofazimine (100 mg ) 3
1 tablet of Dapsone (100mg )
Once a day : Days 2 -28 At home
1 cap of clofazimine (50 mg )
1 tablet of Dapsone (100mg )
MB Child 12 months
Once a month : Day 1 At clinic
2 capsules of Rifampicin (300 mg + 150 mg)
3 capsules of clofazimine (50 mg ) 3
1 tablet of Dapsone (50mg )
Days 2 -28 : At home
1 cap of clofazimine (50 mg ) Alternate day
1 tablet of Dapsone (50mg )
The treatment of leprosy is not only the
chemotherapy

1. PHYSICAL
2. SOCIAL AND PSYCHOLOGICAL
Thank you.