PhotobucketLeprosy, or Hansen’s disease, is a chronic infectious disease caused by the bacterium Mycobacterium leprae. Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external symptom. Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs, and eyes. Contrary to popular conception, leprosy does not cause body parts to simply fall off, and it differs from tzaraath, the malady described in the Hebrew Scriptures and previously translated into English as leprosy.

Historically, leprosy has affected humanity since at least 600 BC, and was well-recognized in the civilizations of ancient China, Egypt and India. In 1995, the World Health Organization (WHO) estimated that between two and three million individuals were permanently disabled because of leprosy. Although the forced quarantine or segregation of patients is unnecessary—and can be considered unethical—a few leper colonies still remain around the world, in countries such as India, and Vietnam.

The age-old social stigma associated with the advanced form of leprosy lingers in many areas, and remains a major obstacle to self-reporting and early treatment. Effective treatment for leprosy appeared in the late 1940s with the introduction of dapsone and its derivatives. However, leprosy bacilli resistant to dapsone gradually evolved and became widespread, and it was not until the introduction of multidrug therapy (MDT) in the early 1980s that the disease could be diagnosed and treated successfully within the community.

Etiologic agent

Mycobacterium Leprae


The clinical manifestations of leprosy vary but primarily affect the skin, nerves, and mucous membranes. Patients with this chronic infectious disease are classified as having paucibacillary (tuberculoid leprosy),multibacillary Hansen’s disease (lepromatous leprosy), or borderline leprosy.
Borderline leprosy (also termed multibacillary), of intermediate severity, is the most common form. Skin lesions resemble tuberculoid leprosy but are more numerous and irregular; large patches may affect a whole limb, and peripheral nerve involvement with weakness and loss of sensation is common. This type is unstable and may become more like lepromatous leprosy or may undergo a reversal reaction, becoming more like the tuberculoid form.
Paucibacillary Hansen’s disease is characterized by one or more hypo pigmented skin macules and anesthetic patches, damaged peripheral nerves that have been attacked by the human host’s immune cells.

Multibacillary Hansen’s disease is associated with symmetric skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting in nasal congestion and epistaxis (nose bleeds) but typically detectable nerve damage is late.
Contrary to popular belief, Hansen’s bacillus does not cause rotting of the flesh; rather, a long investigation by Paul Brand yielded that insensitivity in the limbs extremities was the reason why unfelt wounds or lesions, however minute, lead to undetected deterioration of the tissues, the lack of pain not triggering an immediate response as in a fully functioning body. Recently, leprosy has also emerged as a problem in HIV patients on antiretroviral drugs.

Mode of transmission

Existing clinical, scientific, and epidemiological knowledge on the mode of transmission of human leprosy is reviewed under the following headings: a. the release of viable organisms from the host into the environment. b. The presence of viable organisms so released into the environment. c. Entry into the new human host and distribution within the body. d. Production of clinical illness. It is concluded that much of the published evidence deals with one, or rather few, parameters, whose relationship to the overall scheme of transmission is uncertain. Although it is beyond doubt that most leprosy bacilli emerge from the nose and nasal secretions, probably entering the environment in droplets, little is known of their mode of survival in the environment or their entry into the new host. Existing data certainly does not provide a full “model” of leprosy transmission, and it is suggested that further work attempting to clarify the relative importance of the component events in transmission may have to rely increasingly on epidemiological methods.

It also emerges that consideration of the immunological factors bearing on whether or not infections causes’ clinical illness is important in elucidating the mechanism of leprosy transmission.


Mycobacterium leprae is the causative agent of leprosy. An intracellular, acid-fast bacterium, M. leprae is aerobic, gram-positive, and rod-shaped, and is surrounded by the waxy cell membrane coating characteristic of Mycobacterium species.

Due to extensive loss of genes necessary for independent growth, M. leprae is unculturable in the laboratory, a factor which leads to difficulty in definitively identifying the organism under a strict interpretation of Koch’s postulates. The use of non-culture-based techniques such as molecular genetics has allowed for alternative establishment of causation.


Until the development of dapsone, rifampin, and clofazimine in the 1940s, there was no effective cure for leprosy. However, dapsone is only weakly bactericidal against M. leprae and it was considered necessary for patients to take the drug indefinitely. Moreover, when dapsone was used alone, the M. leprae population quickly evolved antibiotic resistance; by the 1960s, the world’s only known anti-leprosy drug became virtually useless.

The search for more effective anti-leprosy drugs to dapsone led to the use of clofazimine and rifampicin in the 1960s and 1970s. Later, Shantaram Yawalkar and colleagues formulated a combined therapy using rifampicin and dapsone, intended to mitigate bacterial resistance. Multidrug therapy (MDT) and combining all three drugs was first recommended by a WHO Expert Committee in 1981. These three anti-leprosy drugs are still used in the standard MDT regimens. None of them are used alone because of the risk of developing resistance.

Because this treatment is quite expensive, it was not quickly adopted in most endemic countries. In 1985 leprosy was still considered a public health problem in 122 countries. The 44th World Health Assembly (WHA), held in Geneva in 1991 passed a resolution to eliminate leprosy as a public health problem by the year 2000 — defined as reducing the global prevalence of the disease to less than 1 case per 100,000. At the Assembly, the World Health Organization (WHO) was given the mandate to develop an elimination strategy by its member states, based on increasing the geographical coverage of MDT and patients’ accessibility to the treatment.

The WHO Study Group’s report on the Chemotherapy of Leprosy in 1993 recommended two types of standard MDT regimen is adapted. The first was a 24-month treatment for multibacillary (MB or lepromatous) cases using rifampicin, clofazimine, and dapsone. The second was a six-month treatment for paucibacillary (PB or tuberculoid) cases, using rifampicin and dapsone. At the First International Conference on the Elimination of Leprosy as a Public Health Problem, held in Hanoi the next year, the global strategy was endorsed and funds provided to WHO for the procurement and supply of MDT to all endemic countries.


The best way to prevent the spread of leprosy is the early diagnosis and treatment of people who are infected. For household contacts, immediate and annual examinations are recommended for at least five years after last contact with a person who is infectious.

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