Leprosy is caused by Mycobacterium leprae, an acid-fast bacillus that attacks cutaneous tissue and peripheral nerves, producing a cellular immune response that results in skin lesions, anesthesia, infection, and deformities. Leprosy isn’t highly contagious, but transmission can occur from continuous, close contact, possibly via nasal droplets or by skin breaks (with a contaminated hypodermic or tattoo needle, for example). The incubation period ranges from 2 to 40 years, with an average of 5 to 7 years. Early clinical indications of skin lesions and muscular and neurologic deficits are usually sufficiently diagnostic in patients from endemic areas.

Complications of leprosy include fever, malaise, lymphadenopathy, ulceration into muscle and fascia, secondary bacterial infection, and amyloidosis.

M. leprae attacks the peripheral nervous system, especially the ulnar, radial, facial, deep fibular, and posterior popliteal nerves. Bacilli damage the skin’s fine nerves, causing anesthesia, anhidrosis, and dryness. If a large nerve trunk is infected, motor nerve damage, weakness, and pain occur, followed by peripheral anesthesia, muscle paralysis, or atrophy. In later stages, clawhand, footdrop, and ocular complications (corneal insensitivity and ulceration, conjunctivitis, photophobia, and blindness) can occur. Injury, ulceration, infection, and disuse of the deformed parts cause scarring and contracture. Neurologic complications occur in both lepromatous and tuberculoid leprosy but are less extensive and develop more slowly in the lepromatous form. Lepromatous leprosy can invade tissue in every organ of the body, but the organs remain functional.