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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.
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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 • 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.
