Hansen’s Disease “The Other Mycobacterium”

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Hansen’s Disease “The Other Mycobacterium”. Diane Rimple, MD FACEP UNM Marine and Tropical Medicine April, 2005. Basic Facts. Leprosy is caused by Mycobacterium leprae. Bacteria infection of skin eyes, testicles and peripheral nerves. Method of spread is unknown. Classification of Disease. - PowerPoint PPT Presentation

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Hansen’s Disease “The Other Hansen’s Disease “The Other Mycobacterium”Mycobacterium”

Diane Rimple, MD FACEPUNM Marine and Tropical Medicine April, 2005

Basic Facts

Leprosy is caused by Mycobacterium leprae.

Bacteria infection of skin eyes, testicles and peripheral nerves.

Method of spread is unknown

Classification of Disease

Localized disease: high host immunity (tuberculoid leprosy).

Disseminated disease: low host immunity (lepromatous leprosy).

Worldwide Epidemiology

10-15 million people afflicted, half of whom live in Africa and India.

Approximately 6000 cases in the US, 150-200 new cases reported annually.

Leprosy in Hawaii

First reported case in Hawaii in 1835 Large epidemic followed soon thereafter 1865: "Act to Prevent the Spread of Leprosy". King Kamehameha V ordered incurable leprosy

victims removed from the general population. Permanent quarantine area on the island of

Molokai.

Clinical Syndrome

Symptoms of leprosy include: Skin lesion without sensation Epistaxis Nose congestion Hair loss (eyebrows, eyelashes, body

hair)

Clinical Features to Evaluate

Number of skin lesions Size and morphology of lesions Presence of neuropathy Presence of reactional states (immune

reaction)

Clinical Features: Tuberculoid

Usually a single skin lesion Lesions are large, flat plaques Well demarcated, irregular Erythematous with raised borders and

atrophic center Hypopigmented Located on face and extremities

Clinical Features: Tuberculoid

Nerve involvement is confined to area of skin lesions.

Testicular and eye infiltration does not occur

Clinical Features: Lepromatous

Unrestrained proliferation of bacilli in skin, peripheral nerves, anterior eye and testes.

Innumerable small erythematous, symmetric hyperpigmented macules, papules and nodules.

Diffuse infiltration of face: leotine facies and loss of eyebrows (madarosis)

Clinical Features: Lepromatous

Peripheral nerves less likely to be infiltrated. Anesthesia occurs later in disease. May be

subtle. Stocking glove distribution. Testicle involvement: impotence, sterility Eye involvement: keratitis, corneal denervation Erythema nodosum leprosum: can cause iritis

and secondary glaucoma

Diagnostics

Clinical diagnosis Skin biopsy: Acid fast staining (Fite

stain) Skin smears: assess bacillary load Nerve biopsy: looking for organisms and

typical granulomas Serologic assays (ELISA or PCR)

Transmissability

Estimated risk of infection of 2-4% among close household contacts.

Tuberculoid leprosy patients do not shed the bacteria and are considered noncontagious.

Transmisability

Lepromatous patients shed bacteria in Nasal secretions Sweat Blood Breast milk Wound exudate

Treatment

Treatment is antibiotics from 6 months to several years.

Must be multidrug therapy (usually two) Rifampin and dapsone are mainstays

– Clofazimine is used for cases of dapsone resistance.

Steroid for ENL

Additional Treatments

Physical therapy: – Prevention of injury due to neuropathies.– Wound care

Psychosocial therapy:– Issues regarding societal reaction to the

disease.– Fears regarding transmissability.– Issues regarding dealing with a chronic

disease.

Prophylaxis

Vaccine is not effective Dapsone prophylaxis promotes

resistance. May delay but not prevent onset of disease

Currently, household contacts are examined regularly and any suspicious lesion is biopsied.

The Leper Colony: Kalaupapa

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