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Cutaneous leprosy

• Leprosy is a chronic granulomatous


disease, caused by Mycobacterium
leprae, which affects principally the
skin and peripheral nervous system
• Animal reservoirs of leprosy : 9-banded
armadillos & chimpanzees

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Pathophysiology:
• The areas most commonly affected by leprosy
are the superficial peripheral nerves, skin,
mucous membranes of the upper respiratory
tract, anterior chamber of the eyes, and testes.
These areas tend to be cooler parts of the
body.
• Tissue damage is caused by the degree to
which cell-mediated immunity is expressed, the
extent of bacillary spread and multiplication, the
immunologic complications (ie, lepra reactions),
and the nerve damage and its sequelae

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M leprae is an obligate intracellular acid-
fast bacillus with a unique ability to enter
nerves.
The incubation period ranges from 6
months to 40 years or longer. The average
incubation period is 2-3 years.

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Medical Diagnosis of Leprosy
• The disease is usually diagnosed on the basis
of : anesthesia of a skin lesion, thickened
nerves, and typical skin lesions.
• Prodromal symptoms are generally so slight that
the disease is not recognized until a cutaneous
eruption is present.
• Temperature is the first sensation that is lost
• The next sensation lost is light touch, then pain,
and finally deep pressure.
• A hypopigmented macule :the first cutaneous
lesion. From this stage, most lesions evolve into
the lepromatous, tuberculoid or borderline types.

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Indeterminate leprosy (IL)

– This early form causes one to a few


hypopigmented, or sometimes erythematous,
macules. Sensory loss is unusual.
– Most cases evolve from this state into one of the
other forms, depending on the patient's immunity
to the disease.
– Those with strong immunity may become cured of
disease.
– May persist in this indeterminate form.
– In those with weaker immunity, the disease
progresses to one of the other forms.

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Tuberculoid leprosy (TT)

• Skin lesions :few in number. Usually, one


erythematous large plaque is present, with
well-defined borders that are elevated and
slope down into an atrophic center.
• Another presentation involves a large
asymmetric hypopigmented macule.
• Neural involvement is common in TT; it
leads to tender, thickened nerves

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Borderline tuberculoid leprosy
(BT)
– Lesions in this form are similar to those in
the tuberculoid form, but they are smaller
and more numerous. The nerves are less
enlarged,
– Disease can remain in this stage, convert
back to the tuberculoid form, or progress.

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Borderline borderline leprosy
(BB)
– Cutaneous : numerous, red, irregularly
shaped plaques that are less well defined.
Their distribution may mimic those of the
lepromatous type, but they are more
asymmetric.
– Anesthesia : moderate.
– Regional adenopathy may be present.
– Disease may remain in this stage, improve
or worsen.

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Borderline lepromatous leprosy
(BL)

– Lesions : numerous and consist of


macules, papules, plaques, and
nodules.
– . Anesthesia : often absent.
– As with the other forms of borderline
leprosy, the disease may remain in
this stage, improve, or regress.

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Lepromatous leprosy (LL)
• Early cutaneous lesions :pale macules. Later,
infiltrations are present, with numerous
bacilli. Macular lesions : small, diffuse, and
symmetric.
• The lateral eyebrows are affected by alopecia
• Lepromatous infiltrations : diffuse, nodules
(called lepromas), or plaques. The diffuse
type results in the appearance of a leonine
facies.
• Lymphadenopathy ,hepatomegaly Stridor
,hoarseness ,osteomyelitis &Brawny edema .
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Skin Biopsy

•Epidermis
•Collections of
Foamy
macrophages
in the upper
dermis.
•Around
adnexa
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Lab. Studies:
Tissue smear test:An incision is
made in the skin, to obtain fluid from
a lesion. The fluid is placed on a
glass slide and stained by using the
Ziehl-Neelson acid-fast method to
look for organisms.The bacterial
index (BI) is then determined
– Skin biopsy: for morphologic features
and the presence of acid-fast bacilli.
– Sensory testing :Tactile and temperature
sensations should be tested.

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Lab. Studies:
• Lepromin testing
– It indicates host resistance to M leprae. and does
not not confirm the diagnosis, but they are useful
in determining the type of leprosy.
– A positive finding indicates cell-mediated
immunity,. A negative finding suggests a lack of
resistance to disease.
– To perform this test, bacillary suspension is
injected into the forearm. When the reaction is
assessed at 48 hours, it is called the Fernandez
reaction When the reaction is read at 3-4 weeks, it
is called the Mitsuda reaction.

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Reactions in
Leprosy

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Medical Classification of leprosy
• Paucibacillary or PB leprosy.: patients can be cured by
• treating the patient with two drugs for six months.
• Multibacillary or MB leprosy :patients can be cured by treating
the patient with three drugs for twelve months.
• How to tell if someone has PB or MB leprosy?
Count the skin patches
• If you find five patches or less, classify the patient as
PB.
• If you find more than five patches, classify the patient as
MB.
When a skin smear is taken
• If the skin smear is negative and the patient has five
patches or less, classify the patient as PB.
• If the skin smear is positive, classify the patient as MB,
whatever the number of skin patches.

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Therapy of Leprosy
Multiple Drug Therapy (MDT)

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Therapy for lepra reactions
• Early diagnosis and the timely initiation of
anti-inflammatory measures.
The possible precipitating factor should be
removed MDT should be continued in full
dosage without interruption.
• The principles of treatment : Rest, both
physical and mental, with appropriate
sedation.
• Analgesics and anti-inflammatory drugs:
Aspirin (acetylsalicylic acid) and
corticosteroids

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Therapy with corticosteroids
• Type 1 lepra reaction: Prednisolone should
be started with a single daily dose of 40–60
mg (maximum 1mg/kg body weight)
according to severity.
• In severe Type 2 lepra reaction: prednisolone
should be started at a dose of 20–40 mg/day.
Clofazimine :given in doses up to 300 mg
daily for one month, and then gradually
reduced.

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THANK YOU

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