Mycobacterium leprae notes from Mahon.

1. Mycobacterium leprae
Mycobacterium leprae is the causative agent of Hansen disease (leprosy), an infection of skin, mucous
membranes, and peripheral nerves. The disease is rare in the United States and other Western
countries, yet it remains a major problem in other parts of the world. At one time, the World Health
Organization (WHO) estimated that 11 million people had Hansen disease. However, the WHO
launched an eradication program, and since 1985 the incidence of Hansen disease has been reduced
by about 90%. Since 1995 the WHO has provided treatment free of charge to all patients with Hansen
disease. Globally, the annual incidence has steadily declined since 2001 to about 210,758 cases in
2014.

2. Currently, India, Brazil, and Indonesia account for over 80% of all new cases. In the United
States, generally fewer than 100 cases are reported annually; which are often acquired abroad.
Despite its reputation, Hansen disease is not highly contagious. The most important mode of
transmission is not known, but the disease can be transmitted by direct contact and inhalation
of aerosols from skin lesions. Shedding from the nasal passage is another route of transmission.
The two major forms of the disease are tuberculoid leprosy and lepromatous leprosy. Symptoms
of tuberculoid leprosy include skin lesions and nerve involvement that can produce areas with
loss of sensation. Patients eventually exhibit an effective cellmediated immune (CMI) response.

3. • The optimal growth temperature for M. leprae is approximately 30° C, and because the patient mounts an
adequate immune response, the bacteria tend to remain in the extremities. Spontaneous recovery often
occurs with tuberculoid leprosy. Conversely, patients with lepromatous leprosy have a strong humoral-
mediated immune response but not an effective CMI response. The disease is slowly progressive, and if
untreated, it can be life-threatening. It is characterized by disfiguring skin lesions and progressive, symmetric
nerve damage.

4. • Lesions of the mucous membranes of the nose can lead to destruction of the cartilaginous septum, resulting
in nasal and facial deformities. Current therapy recommended for lepromatous leprosy consists of a
combination of diaminodiphenylsulfone (dapsone) and rifampin for a minimum of 6 months. For tuberculoid
leprosy, clofazimine is added, and treatment should be continued for 12 months.

5. • Laboratory diagnosis of Hansen disease depends on the microscopic demonstration of AFB from skin biopsy
specimens. M. leprae has not been grown on artificial media. In patients with tuberculoid leprosy, organisms
are extremely rare and may not be detected in skin scrapings or biopsy specimens. However, AFB are usually
abundant in samples from patients with lepromatous leprosy (Fig. 26.5). M. leprae is not as acid fast or
alcohol fast as in the case of other mycobacteria; as such, a weaker decolorizer consisting of 10% sulfuric
acid is recommended instead of the standard acid-ethanol decolorizer. The bacteria are rod shaped, usually
1 to 7 µm long and 0.3 to 0.5 µm wide. The entire smear should be examined under oil immersion field
(×1000) for the presence of the microorganisms. PCR assays are also available to definitively detect the
bacteria.