LEPROSY

(Hansen's disease)
 Introduction
• Granulomatous infection, primarily of skin
and nerves.
• Nearly 10 million people are known to be
affected through out the world
• In Ethiopia 5,000 cases are estimated to
be infected each year, presented densely
populated in the highlands of Shoa,
Gojjam and Arusi.
 Etiology
• Mycobacterium leprae,
• Weakly acid fast bacilli, non motile, non toxin
producing and non spore forming bacterium
that is not yet grown in vitro.
• It prefers lower temperature for growth with
a doubling time of about 12 days.
• Man is the only reservoir.
 Transmission
• Not fully understood
• Nasal discharges from the highly infectious
individuals are believed to be the main source of
infection in the community .
• Only lepromatous leprosy cases are known to be
infectious
• Entry is through the respiratory route
• Entry of bacilli via the skin is less likely possibility
 Four important pathogenetic factors
1. Degree of specific cell mediated immunity
expressed by individuals
2. The extent of bacillary spread and
multiplication
3. The appearance of tissue-damaging
immunological complications – Leprosy
Reactions
4. The development of nerve damage and its
complications
 Classification
Ridley and Joplig
1. Tuberculoid Leprosy (TT)
2. Borderline Tuberculoid Leprosy (BT)
3. Mid-Borderline Leprosy (BB)
4. Borderline Lepromatous Leprosy (BL)
5. Lepromatous Leprosy.
 WHO Classifification
1. Paucibacillary (PB) – bacteriologically negative cases
of:
1. Indeterminate Leprosy
2. Tuberculoid Leprosy
3. Borderline Tuberculoid Leprosy.
2. Multibacillary (MB) – all smear positive cases
1. Mid-Borderline Leprosy
2. Borderline Lepromatous Leprosy
3. Lepromatous Leprosy
 Clinical Features
Indeterminate Leprosy
• Vague slightly hypopigmented or
erythematous lesion on the face, limbs or
buttock
• Nerve function is unimpaired.
• This form of leprosy may resolve
spontaneously, progress to any of the
forms o may persist indefinitely.
 Tuberculoid Leprosy
• Only nerves and skin show clinical evidence of
disease, and lesions are few, often solitary.
• The condition may be purely neural, with pain
and swelling of the affected nerve followed by
anaesthesia and/or muscle weakness.
 Tuberculoid Leprosy
• The typical lesion is a plaque which is
conspicuous, erythematous, copper coloured
or purple, with raised and clear-cut edges
sloping towards a flattened and
hypopigmented centre
• The surface is dry, hairless, insensitive and
sometimes scaly.
• There is possibility of spontaneous cure. It
never progresses to other forms.
Borderline Tuberculoid Leprosy
• Plaque, papules, or hypopigmented
macule with little or no scale.
• Multiple asymmetric lesions with
sensory loss are the rule.
• Nerves are commonly enlarged.
Borderline Tuberculoid Leprosy
• The host response is insufficient to
self-cure.
• These patients are somewhat
unstable: resistance may increase,
upgrading to TT, or decrease,
downgrading to BL
 Borderline Leprosy
• Characteristic skin changes are annular lesions
with sharply marginated interior and exterior
margins, large plaques with islands of clinically
normal skin
• It is the immunologic midpoint, or midzone,
being the most unstable area, with patients
quickly up- or downgrading to a more stable
granulomatous posture
 Borderline Lepromatous Leprosy
• Lesions resemble that of LL except they are not
absolutely symmetrical
• Resistance is too low to restrain bacillary
proliferation significantly but is still sufficient to
induce tissue-destructive inflammation,
especially in nerves.
• Bacillary invasion of the nose, larynx, eyes, and
testes is less severe than in LL.
• BL usually downgrades to LL.
 Lepromatous Leprosy
• Lack of cell-mediated immunity toward M.
leprae permits unrestricted bacillary
replication and widely disseminated,
multiorgan disease.
• Poorly defined, skin-colored nodules are the
most characteristic lesions
 Lepromatous Leprosy
• Hair loss, commonly on the eyebrows, is
evident.
• Any given skin lesion may or may not be
hyposthetic.
• Untreated LL disease is relentlessly
progressive, but this course may be altered by
reactional states.
• LLs and LLp patients frequently develop ENL;
LLp patients do not develop reversal reactions,
whereas LLs patients may.
 Leprosy Reaction
• A process by which leprosy patients develop a
sudden acute inflammatory response that
produces acute, very often painful symptoms
with loss of nerve function.
• Two principal types of reactions have been
described.
 Type 1 reaction
• Type IV hypersensitivity reaction to bacillary
antigen due to change in the host immunity
either to the tuberculoid end (Upgrading
Reaction) or towards the lepromatous end
(Downgrading Reaction).
• It occurs in borderline disease commonly
after initiation of treatment, and is
characterized by acute neuritis and/or
acutely inflammed skin lesions.
 Type 2 reaction - Erythema Nodosum
Leprosum (ENL)
• Immune complex reaction occuing in
patients with multi-bacillary disease, LL and
BL.
• They may occur spontaneously (roseolar
leprosy) or whilst on treatment.
• Sudden or gradual onset of painful red
superficial or deep nodules on the face or
extensor surface of the body is
characterstick.
 Diagnosis
The presence of one of the three cardinal
signs is diagnostic for leprosy.

1. Anesthesia over a skin lesion

2. Thickened nerve
3. Demonstration of AFB on skin slit
Treatment of Leprosy
 Principles
• Stop the infection with chemotherapy
• Prevent and treat reactions and so reduce
the risk of nerve damage
• Educate the patient to cope with existing
nerve damage, in particular anesthesia
• Treat the complications of nerve damage
• Rehabilitate the patient socially and
psychologically.
 Chemotherapy
• PB Leprosy: (Total duration is 6 months)
– Dapsone 100mg daily unsupervised
– Rifampicin 600mg monthly supervised

• MB Leprosy: (Total duration is12 months)

– Dapsone 100mg daily unsupervised
– Clofazimine 50mg daily unsupervised
– Rifampicin 600mg monthly supervised
– Clofazimine 300mg monthly supervised
 Treatment of Reactions
• Mild Reaction
– Analegesics and bed rest
• Severe Type I reaction
– Prednisonlone
• 40mg/d for 2 wks
• 30mg/d for 2 wks
• 20mg/d for 2 wks
• 15mg/d for 2 wks
• 10mg/s for 2 wks
• 5mg/d for 2 wks