WRITTEN REPORT FOR RESEARCH INSTITUTE FOR TROPICAL DISEASES May 2, 2019

Leprosy by DANIELLE VINCE D. CAPUNO

ETIOLOGY AND RISK FACTORS

Leprosy, or Hansen Disease, is a slowly progressive infection caused by Mycobacterium

leprae that mainly affects the skin and peripheral nerves. Despite its low communicability,
leprosy remains endemic among people living in several developing tropical nations.

Etiology
The causative bacterium of leprosy is Mycobacterium leprae (0.3-1 um wide and 1-8 um
long), a non-cultivable, Gram-positive, obligate intracellular, acid-fast bacillus. The bacterium is
confined in humans, armadillos, and sphagnum moss. M. leprae produces no known toxins and
is well adapted to penetrate and reside within macrophages, yet it may survive outside the
body for months. In untreated patients, only ~1% of the organisms are viable. M. leprae is the
only bacterium known to invade peripheral nerves. The unique trisaccharide of M. leprae binds
to the basal lamina of Schwann cells; this interaction is probably related to the ability of the
bacteria to invade peripheral nerves.

Risk Factors
 Birth or residence in a known endemic area
 A family member with leprosy (reflects common genetic susceptibility and/or
environmental exposure)
 Poverty

PATHOGENESIS AND PATTERNS

Pathogenesis
The source of infection and route of transmission are not known, however human
respiratory secretions or soil are likely origins. M. leprae is taken up by macrophages and
disseminates in the blood, but it replicates primarily in relatively cool tissues of the skin and
extremities. It proliferates best at 32 to 34 °C, the temperature of the human skin. Like M.
tuberculosis, M. leprae secretes no toxins, and its virulence is based on properties of its cell
wall, which is similar enough to that of M. tuberculosis that immunization with BCG confers
some protection against M. leprae infection. Cell-mediated immunity is manifested b delayed-
type hypersensitivity reactions to dermal injections of a bacterial extract called lepromin.

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Patterns
M. leprae causes two different patterns of disease, tuberculoid and lepromatous. The
helper T-lymphocyte response to M. leprae determines whether an individual has tuberculoid
or lepromatous leprosy.

a. Tuberculoid leprosy begins with localized flat, red skin lesions that enlarge and develop
irregular shapes with indurated, elevated, hyperpigmented margins and depressed pale
centers. Neuronal involvement dominates tuberculoid leprosy. Nerves become enclosed
within granulomatous inflammatory reactions. Nerve degeneration causes skin
anesthesias and skin and muscle atrophy that render the person liable to trauma of the
affected parts, leading to the development of chronic skin ulcers. Contractures,
paralyses, and autoamputation of fingers or toes may ensue. Facial nerve involvement
can lead to paralysis of the eyelids, with keratitis and corneal ulcerations.
b. Lepromatous leprosy involves the skin, peripheral nerves, anterior eye chamber, upper
airways (down to the larynx), testes, hands, and feet. The vital organs and CNS are rarely
affected, presumably because the core temperature is too high for growth of M. leprae.
Lepromatous lesions contain large aggregates of lipid-laden macrophages (lepra cells),
often filled with masses (“globi”) of acid-fast bacilli. Macular, papular, or nodular lesions
form on the face, ears, wrists, elbows, and knees. With progression, the nodular lesions
coalesce to yield a distinctive leonine facies. Most skin lesions are hypoesthetic or
anesthetic. Lesions in the nose may cause persistent inflammation and bacilli-laden
discharge. The peripheral nerves, particularly the ulnar and peroneal nerves where the
approach the skin surface, are symmetrically invaded with mycobacteria, with minimal
inflammation. Loss of sensation and trophic changes in the hands and feet follow the
nerve lesions. Lymph nodes contain aggregates of bacteria-filled foamy macrophages in
the paracortical areas and reactive germinal centers. In advanced disease, aggregates of
macrophages are also present in the splenic red pulp and the liver. The testes are
usually extensively involved, leading to destruction of the seminiferous tubules and
consequent sterility

DIFFERENTIAL DIAGNOSIS

Included in the different diagnosis of lesions that resemble leprosy are sarcoidosis,
leishmaniasis, lupus vulgaris, dermatofibroma, histiocytoma, lymphoma, syphilis, yaws,
granuloma annulare, and various other disorders causing hypopigmentation. In lepromatous
leprosy, sputum specimens may be loaded with AFB—a finding that can be incorrectly
interpreted as representing pulmonary tuberculosis.

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MANAGEMENT, PREVENTION, AND CONTROL

Antimicrobial Therapy

Vaccination
Vaccination at birth with bacille Calmette-Guerin (BCG) has proved variably effective in
preventing leprosy: the results have ranged from total inefficacy to 80% efficacy. The addition
of heat-killed M. leprae to BCG does not increase the effectiveness of the vaccine.

Chemoprophylaxis
Chemoprophylaxis with dapsone may reduce the number of tuberculoid leprosy cases
but not the number of lepromatous cases and therefore is not recommended, even for
household contacts. In addition, single-dose rifampicin prophylaxis is of doubtful efficacy.

Isolation
Because leprosy transmission appears to require close prolonged household contact,
hospitalized patients need not be isolated.

REFERENCES
 Goldsmith, L.A. et al. (2012). Fitzpatrick’s Dermatology in General Medicine. (8th Edition). United States: McGraw-Hill
Companies, Inc.
 Kasper, D.L., et al. (2018). Harrison’s Principles of Internal Medicine. (20th Edition). United States: McGraw Hill
Education.
 Kumar, K., et al. (2015). Robbins and Contran Pathologic Basis of Disease. (9th Edition). Philadephia: Elsevier Saunders.