Hansen’s Disease Ma. Bernadette V. Lopez-Dee Adrian B. Lorenzo.
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Transcript of Hansen’s Disease Ma. Bernadette V. Lopez-Dee Adrian B. Lorenzo.
Hansen’s Disease
Ma. Bernadette V. Lopez-DeeAdrian B. Lorenzo
Epidemiology • Global prevalence – 1.25 cases per 10,000 persons• India – 80% worldwide• Male to female ratio of occurrence – 1.5 : 1• Age of occurence – before 35 (endemic areas),
age 50 (exposure to armadillos) • Latency period – 5 years (paucibacillary), 20 years
(multibacillary)• Mode of transmission – armadillo exposure, other
cases of Hansen’s diseaseClose contact – 28 % (household contacts)
- 80 % (neighbors, social contacts)
Infectious agent
Mycobacterium leprae• Weakly acid-fast organism• Grows best at 30 C below human body core ̊�
temperature• Long generation time (12-14 days)• Unable to be cultured in vitro
Diagnosis
• Identification of infectious organism in affected tissue
• Skin biopsies: from skin or nerve lesions – stained for bacillus with Fite-Faraco stain
• Slit smears: from lesions and cooler areas of skin – stained with Acid-fast stain
organisms found – multibacillary 5 or few lesions/ negative – paucibacillary
Classification 1. Early and Indeterminate leprosy
2. Tuberculoid leprosy3. Borderline tuberculoid leprosy
4. Borderline leprosy5. Borderline lepromatous leprosy
6. Lepromatous leprosy7. Histoid leprosy
1. Early and Indeterminate Leprosy
• Insidious onset• Numbness – first manifestation in 90% of
patients• Loss of senses of cold and light touch - earliest
sensory changes • Solitary, ill-defined hypopigmented macule-
often the first lesion • Erythematous macules (cheeks, upper arms,
buttocks, thighs) –less often
1. Early and Indeterminate Leprosy
• Biopsy – usually no bacilli or only a few• Few cases remain in this state• Evolve to lepromatous, tuberculoid, or
borderline types• Good cell-mediated immunity – often resolve
spontaneously or never develop other signs and symptoms of Leprosy
2. Tuberculoid Leprosy
• Solitary lesions or few in number (5 or less)• Asymmetrical distribution• Lesions – hypopigmented or erythematous, dry,
scaly, hairless• Typical lesion – large, erythematous plaque w/
a sharply defined & elevated border that slopes down to a flattened atrophic center – “a saucer right side up”
• Common locations – face, limbs, or trunk• Lesion is anesthetic & anhidrotic
2. Tuberculoid Leprosy
• Nerve involvement – early & prominent• Greater auricular nerve & Superficial peroneal
nerve – visibly enlarged• Atrophy of interosseous muscles of hand, w/
wasting of thenar & hypothenar eminences, contracture of fingers, facial muscle paralysis, foot drop
• Evolution generally slow• Often, there is spontaneous remission in 3
years, or less if w/ treatment
2. Tuberculoid Leprosy
3. Borderline Tuberculoid Leprosy
• Similar to tuberculoid lesions, but smaller and more numerous
• Characteristic – satellite lesions around large macules or plaques
3. Borderline Tuberculoid Leprosy
4. Borderline Leprosy
Lesions:• Numerous but countable, consist of red,
irregularly shaped plaques• Small satellite lesions may surround larger
plaques• Generalized but asymmetrical• Edges are not so well defined• Nerves may be thickened and tender• Anesthesia is only moderate
4. Borderline Leprosy
5. Borderline Lepromatous Leprosy
• Lesions are symmetrical, numerous (not countable), may include macules, papules, plaques, and nodules
• Small lepromatous lesions > larger borderline type lesions
• Nerve involvement -appears later, symmetrical• Nerves - enlarged and/or tender• Sensation & sweating over individual lesions are
normal• Usually no features of full-blown leprosy (madarosis,
keratitis, nasal ulceration, leonine facies)
5. Borderline Lepromatous Leprosy
Hyperpigmentation due toClofazamine
6. Lepromatous Leprosy• Cutaneous lesions – pale lepromatous macules /
lepromatous infiltrations w/ numerous bacilli • Becomes progressively worse w/o treatment• Divided into polar form LLp & subpolar form LLs• Macular lepromatous lesions- diffuse & symmetrical
distribution, small, numerous, ill-defined, blend into surrounding skin
• No loss of sensation over lesions, nerve thickening, nor changes in sweating
• Slow, progressive hair loss – outer third of eyebrows, eyelashes, then body. Scalp hair remains unchanged.
6. Lepromatous Leprosy
Lepromatous infiltrations divide into diffuse, plaque, and nodular types
Diffuse type• Diffuse infiltration of face (forehead), madarosis,
waxy shiny appearance of skin – “varnished appearance”
• Diffuse leprosy of Lucio – 1/3 of lepromatous cases. Diffuse infiltration of skin. Localized lepromas do not form. Unique complication – Lucios’s phenomenon (erythema necroticans)
6. Lepromatous Leprosy
• Infiltrations- manifested by development of nodules called lepromas
• Early nodules – ill defined, occurs in acral parts (ears, brows, nose, chin, elbows, hands, buttocks, knees)
• Nerve involvement – variable, very slowNerve disease – bilaterally symmetrical, stocking-glove pattern (misdiagnosed as diabetic neuropathy)
6. Lepromatous Leprosy
Multiple papules and nodules Enlargement of the earlobe
7. Histoid Leprosy
• Uncommon form of multibacillary leprosy• Skin lesions – yellow-red, shiny, large papules
and nodules in dermis or subcutaneous tissue• 1- 15 mm in diameter• Appear anywhere, but favor the buttocks, lower
back, face, and bony prominences• This pattern may appear de novo, but mostly
described in patients w/ resistance to long-acting dapsone resistance
7. Histoid Leprosy