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Indonesia, as one of the largest countries in the world, spreading over more than 5.000 kilometers from east to west and containing over 17.000 islands, is quite vulnerable for a number of disease. The health care system in general is not adequately equipped to deal with many basic situations, which should be a reason to get proper information about common diseases.


Leprosy
A chronic infectious disease

Leprosy, 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 appeared 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.


Distribution of leprosy in Southeast Asia in 2003.

Characteristics

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 hypopigmented skin macules and anaesthetic patches, i.e., 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.

Cause

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. may also cause shrinking in some limbs and infected boils on genital region.

The exact mechanism of transmission of leprosy is not known: both prolonged close contact and transmission by nasal droplet have both been proposed, and, while the latter fits the pattern of disease, both remain unproved. The only other animals besides humans to contract leprosy are the armadillo, chimpanzees, sooty mangabeys, and cynomolgus macaques. The bacterium can also be grown in the laboratory by injection into the footpads of mice. There is evidence that not all people who are infected with M. leprae develop leprosy, and genetic factors have long been thought to play a role, due to the observation of clustering of leprosy around certain families, and the failure to understand why certain individuals develop lepromatous leprosy while others develop other types of leprosy. However, the role of genetic factors is not clear in determining this clinical expression. In addition, malnutrition and possible prior exposure to other environmental mycobacteria may play a role in development of the overt disease.

The most widely-held belief is that the disease is transmitted by contact between infected persons and healthy persons. In general, closeness of contact is related to the dose of infection, which in turn is related to the occurrence of disease. Of the various situations that promote close contact, contact within the household is the only one that is easily identified, although the actual incidence among contacts and the relative risk for them appear to vary considerably in different studies. In incidence studies, infection rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per year in Cebu, Philippines to 55.8 per 1000 per year in a part of Southern India.

Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not clear. It is true that lepromatous cases show large numbers of organisms deep down in the dermis. However, whether they reach the skin surface in sufficient numbers is doubtful. Although there are reports of acid-fast bacilli being found in the desquamating epithelium of the skin, Weddell et al have reported that they could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and contacts. In a recent study, Job et al found fairly large numbers of M. leprae in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with the sebaceous secretions.

Treatment

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.

Risk groups

At highest risk are those living in endemic areas with poor conditions such as inadequate bedding, contaminated water and insufficient diet, or other diseases (such as HIV) that compromise immune function. Recent research suggests that there is a defect in cell-mediated immunity that causes susceptibility to the disease. Less than ten percent of the world's population are actually capable of acquiring the disease. The region of DNA responsible for this variability is also involved in Parkinson's disease, giving rise to current speculation that the two disorders may be linked in some way at the biochemical level. In addition, men are two times more likely to contract leprosy than women.


All text in this article is available under the terms of the GNU Free Documentation License
Last revised on October 11, 2009
    
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