cutaneous leprosy

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M.Yousry M.Yousry TB&leprosy TB&leprosy 1 Cutaneous leprosy 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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Skin manifestations&therapy of leprosy

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Page 1: Cutaneous Leprosy

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Cutaneous leprosyCutaneous 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: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 LeprosyMedical 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)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)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 Borderline tuberculoid leprosy (BT)(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 Borderline borderline leprosy (BB)(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 Borderline lepromatous leprosy (BL)(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)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 BiopsySkin Biopsy

•Epidermis•Collections of Foamy macrophages in the upper dermis.•Around adnexa

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Lab. Studies: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: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 Reactions in LeprosyLeprosy

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Medical Classification of leprosyMedical 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 LeprosyTherapy of LeprosyMultiple Drug Therapy (Multiple Drug Therapy (MDTMDT))

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Therapy for lepra reactionsTherapy 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 corticosteroidsTherapy 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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