Difference between revisions of "Leprosy" - New World Encyclopedia

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[[Image : Leprosy.jpg |thumb | A 24-year-old man infected with leprosy ]]
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  Caption    = A 24-year-old man infected with leprosy.
 
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{{dablink|For the malady found in the Hebrew Bible, see the article [[Tzaraath]].}}
 
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'''Leprosy''' or '''Hansen's disease''' is a chronic infectious disease caused by the [[Bacteria|bacterium]] ''[[Mycobacterium leprae]]''. Leprosy is the only known bacterial disease that infects peripheral nerves. It also affects the mucosa of the upper respiratory tract and produces skin lesions (Ryan ''et al''. 2004).If left untreated, there can be progressive and permanent damage to the skin, nerves, limbs and eyes.
 
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"Unclean! Unclean!" These were the words of lepers as they announced their presence among the unafflicted in biblical times. The mere mention of leprosy has struck fear in the hearts of people for thousands of years. Even though it is one of the least contagious of all bacterial diseases, the fear of physical disfigurement and the loss of social status that it brings, has made leprosy one of the most dreaded of all diseases. Lepers have been ostracized and put into separate colonies, where they lived as social outcasts and "untouchables" until the end of their lives.
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'''Leprosy''' or '''Hansen's disease''' is a chronic infectious [[disease]] caused by the [[Bacteria|bacterium]] ''[[Mycobacterium leprae]]'' and is the only known bacterium that infects [[peripheral nervous system|peripheral nerves]]. It also affects the mucosa of the upper respiratory tract and produces skin lesions (Ryan et al. 2004). If left untreated, there can be progressive and permanent damage to the skin, nerves, limbs and eyes.
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Many people have felt a religious calling to risk contracting the disease themselves in order to care for lepers. Some of these most noble people include Father Damien of Molokai, Hawaii; Dr. [[Albert Schweitzer]] in Lamberene, Gabon; and [[Mother Teresa]] in Calcutta, India.
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{{toc}}
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The crucial breakthrough in the cure for leprosy came when G. H. A. Hansen followed the lead of [[Robert Koch]], who first suggested that [[microorganism]]s could cause disease. When Hansen began to look into the "invisible" world for the cause of leprosy, he risked everything he had in order to help those that no one else wanted to touch.
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== History ==
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[[Image:Gerhard Hansen.jpg|thumb|right|[[Gerhard Armauer Hansen|GHA Hansen]], discoverer of ''[[Mycobacterium leprae|M. leprae]]'']]
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A disease called "leprosy" was recorded in ancient [[India]] (fifteenth century B.C.E.), in [[Japan]] (tenth century B.C.E.), and in [[Egypt]] (sixteenth century B.C.E.). Some propose that the spread of this disease to the West originated from Egypt (Souvay and Donovan 1910).
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In the sixth century C.E., Saint [[Radegund]] was praised for dedicating her life to caring for lepers.
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In 1078 C.E., a leprosarium was built in Rochester, England, and in 1084 Archbishop Lanfranc built another at Harbledown near Canterbury for the care of 100 lepers. These became known as lazar houses, based on the story of [[Lararus]], and many were built during the twelfth and thirteenth centuries (Turner et al. 1995).
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The English monk, Orderic Vitalis, writes in the twelfth century C.E., of another monk, Ralf, who was so overcome by the plight of lepers that he prayed to catch leprosy himself (which he eventually did). The leper would carry a clapper and bell to warn of his approach, and this was as much to attract attention for [[charity]] as to warn people that a diseased person was near.
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In 1873, ''Mycobacterium leprae,'' the causative agent of leprosy, was discovered by [[Gerhard Armauer Hansen|G. H. Armauer Hansen]] in Norway , making it the first [[bacterium]] to be identified as causing disease in man (Hansen 1874; Irgens 2002).
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From 1873 to 1899, [[Father Damien]] worked in the leper colony of Kalaupapa on the island of Molokai in [[Hawaii]]. He eventually contracted leprosy and died at age 49. On June 4, 1995, Pope [[John Paul II]] beatified Blessed Damien and gave him his official spiritual title.
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In 1913, Dr. [[Albert Schweitzer]] began his work in [[Lamberene, Gabon]], where he labored for more than 40 years until his death in 1965. Many of his patients were lepers. In 1953, he received the [[Nobel Peace Prize]], and spent the prize money to build a clinic for his hospital.
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In 1950, Mother Teresa started the [[Missionaries of Charity]] in [[Calcutta, India]]. She persuaded the leaders that leprosy was not contagious and got the lepers to build a colony at Titagarh that she named after [[Mahatma Gandhi]]. In 1979, she was awarded the [[Nobel Peace Prize]] for her lifelong work with the poor.
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In 1995, the [[World Health Organization]] (WHO) estimated that between two and three million individuals were permanently disabled because of leprosy (WHO 1995).
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===Etymology===
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The word "leprosy" derives from the ancient Greek words ''lepros,'' a "scale," and ''lepein,'' "to peel" (Barnhart 1995). The word came into the English language via [[Latin]] and Old French. The first attested English use is in the ''Ancrene Wisse,'' a thirteenth-century manual for nuns ''("Moyseses hond…bisemde o þe spitel uuel & þuhte lepruse."'' ''The Middle English Dictionary,'' s.v., "leprous"). A roughly contemporaneous use is attested in the Anglo-Norman ''Dialogues of Saint Gregory,'' "Esmondez i sont li lieprous" (''Anglo-Norman Dictionary,'' s.v., "leprus").
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===Tzaraath===
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The term ''[[Tzaraath]]'' from the Hebrew Bible is commonly translated as leprosy, although the symptoms of Tzaraath are not entirely consistent with leprosy and might refer to a variety of [[skin]] disorders other than Hansen's disease (Heller et al. 2003).
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In particular ''[[tinea capitis]],'' a fungal scalp infection and related infections on other body parts caused by the dermatophyte fungus ''Trichophyton violaceum,'' are abundant throughout the Middle East and North Africa today and might also have been common in biblical times. Similarly, the related agent of the disfiguring skin disease favus, ''Trichophyton schoenleinii,'' appears to have been common throughout Eurasia and Africa before the advent of modern medicine. People with severe favus and similar fungal diseases along with other skin diseases not caused by [[microorganism]]s tended to be classed as having leprosy as late as the seventeenth century in Europe (Kane et al. 1997). This is clearly shown in the painting ''Governors of the Home for Lepers at Haarlem 1667'' by [[Jan de Bray]], where a young Dutch man with a vivid scalp infection, almost certainly caused by a [[fungus]], is shown being cared for by three officials of a charitable home intended for leprosy sufferers. The use of the word "leprosy" before the mid-nineteenth century, when microscopic examination of skin for medical diagnosis was first developed, can seldom be correlated reliably with Hansen's disease as we understand it today.
  
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Leprosy has affected humanity since at least 600 [[Common Era|BCE]], and was well-recognized in the civilizations of [[History of China|ancient China]], [[ancient Egypt|Egypt]] and [[History of India|India]] (WHO 2007a ). In 1995, the [[World Health Organization]] (WHO) estimated that between two and three million individuals were permanently disabled because of leprosy (WHO 1995). A few [[leper colony|leper colonies]] still remain around the world, in countries such as [[India]], [[Vietnam]], and the [[Philippines]].
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== ''Mycobacterium leprae'' ==
  
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The age-old stigma associated with the advanced form of the disease still 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.
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''Mycobacterium leprae'' is a rod-shaped [[bacterium]] with an affinity for acid-fast stains. Its length varies from 1-8 microns and it is 0.2 microns wide. It has the longest doubling time of all known bacteria and has thwarted every effort at culture in a defined medium (Truman et al 2001). It can be grown in the foot pads of [[mice]] and [[armadillo]]s and some [[primate]]s.  
  
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== Characteristics ==
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Less than half of the genome of ''M. leprae'' contains functional [[gene]]s. Gene deletion and decay appear to have eliminated many important [[metabolism|metabolic]] activities, including siderophore production, part of the oxidative and most of the microaerophilic and anaerobic respiratory chains, and numerous catabolic systems and their regulatory circuits ( Cole et al. 1998).
  
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The clinical manifestations of leprosy vary but primarily affect the skin, nerves, and mucous membranes (Naafs et al. 2001). Patients with this chronic infectious disease are classified as having either : (1) '''paucibacillary''' (tuberculoid leprosy), (2) '''multibacillary Hansen's disease''' (lepromatous leprosy), or  (3) borderline leprosy.
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The genome sequence of a strain of ''M. leprae,'' originally isolated in Tamil Nadu and designated ''TN,'' has been completed recently. The genome sequence was found to contain 3,268,203 base-pairs (bp), and to have an average [[Guanine|G]]+[[Cytosine|C]] content of 57.8 percent, values much lower than the corresponding values for ''M. tuberculosis,'' which are 4,441,529 bp and 65.6 percent G+C. There are 1500 genes that are common to both ''M. leprae'' and ''M. tuberculosis.'' There is speculation that as ''M. leprae'' evolved it may have lost many genes (Cole et al. 2001).
  
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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.
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== Types and symptoms ==
  
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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 no nerve damage. Contrary to popular belief, Hansen's bacillus does not cause rotting of the flesh. After a long investigation by Dr. [[Paul Wilson Brand|Paul Brand]] it was discovered that insensitivity in the limbs and 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.  
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The clinical manifestations of leprosy vary but primarily affect the [[skin]], nerves, and mucous membranes (Naafs et al. 2001). Patients with this chronic infectious disease are classified as having either: (1) ''paucibacillary'' (tuberculoid leprosy), (2) ''multibacillary Hansen's disease'' (lepromatous leprosy), or (3) ''borderline leprosy.''
  
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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.
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*'''Paucibacillary Hansen's disease''' is characterized by one or more hypopigmented skin macules and anaesthetic patches, i.e., damaged [[peripheral nervous system|peripheral nerves]] that have been attacked by the human host's [[immune system|immune]] [[cell (biology)|cells]].
  
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*'''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 no [[nerve]] damage. Contrary to popular belief, Hansen's bacillus does not cause rotting of the flesh. After a long investigation by [[Paul Wilson Brand|Paul Brand]], it was discovered that insensitivity in the limbs and extremities was the reason why unfelt wounds or lesions, however minute, lead to undetected deterioration of the [[tissue]]s, the lack of [[pain]] not triggering an immediate response as in a fully functioning body.
  
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*'''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.
  
 
Recently, leprosy has also emerged as a problem in HIV patients on antiretroviral drugs (McNeil Jr. 2006).
 
Recently, leprosy has also emerged as a problem in HIV patients on antiretroviral drugs (McNeil Jr. 2006).
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== Pathophysiology ==
 
== Pathophysiology ==
  
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The exact mechanism of transmission of leprosy is not known. ''M. leprae'' has never been grown on defined media; as a result it has been difficult to study the pathogenic mechanisms. There is a theory 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, what is not clear is the role of genetics and other factors 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.
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The exact mechanism of transmission of leprosy is not known. ''M. leprae'' never has been grown on defined media; as a result it has been difficult to study the pathogenic mechanisms. There is a theory that not all people who are infected with ''M. leprae'' develop leprosy, and [[gene|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, what is not clear is the role of [[genetics]] and other factors 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.
  
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There is a belief 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 (epidemiology)|incidence studies]], infection rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per year in [[Cebu]], [[Philippines]] (Doull et al. 1942) to 55.8 per 1000 per year in a part of Southern [[India]] (Noordeen et al. 1978). Two exit routes of ''M. leprae'' from the human body 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's group has 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 (Weddell et al. 1963).  In a recent study, Job and coworkers 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 (Job ''et al''. 1999). The importance of the [[nasal mucosa]] was recognized as early as 1898 by Schäffer, particularly that of the ulcerated mucosa (Schaffer 1898).  The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy had counts ranging from 10,000 to 10,000,000 (Shepard 1960).  Pedley reported that the majority of lepromatous patients showed leprosy bacilli in their nasal secretions as collected through blowing the nose (Pedley 1973). Nasal secretions from lepromatous patients can yield as much as 10 million viable organisms per day (Davey ''et al''. 1974) . 
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There is a belief 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. 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]] (Doull et al. 1942) to 55.8 per 1000 per year in a part of Southern [[India]] (Noordeen et al. 1978).  
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The entry route of ''M. leprae'' into the human body is not definitely known , but the two most likely routes are the skin and  upper respiratory tract. With regard to the respiratory route of entry of ''M. leprae'', the evidence in its favour is on the increase in spite of the long-held belief that the skin was the exclusive route of entry. The successful transmission of leprosy through aerosols containing ''M. leprae'' in immune-suppressed mice, suggests a similar possibility in humans (Rees ''et al''. 1977).  Successful results have also been reported on experiments with  mice when ''M. leprae'' were introduced into the nasal cavity by topical application (Chehl ''et al''. 1985 ). In summary, entry through the respiratory route appears the most probable , although other routes, particularly broken skin, cannot be ruled out. The CDC notes the following assertion about the transmission of the disease: "''Although the mode of transmission of Hansen's disease remains uncertain, most investigators think that ''M. leprae'' is usually spread from person to person in respiratory droplets'' (C.D.C. 2005). 
 
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In leprosy both the reference points for measuring the incubation period and the times of infection and onset of disease are difficult to define; the former because of the lack of adequate immunological tools and the latter because of the insidious nature of the onset of leprosy. Even so, several investigators have attempted to measure the incubation period for leprosy. The minimum incubation period reported is as short as a few weeks and this is based on the very occasional occurrence of leprosy among young infants (Montestruc ''et al.'' 1954).    The maximum incubation period reported is as long as 30 years, or over, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas.  It is generally agreed that the average incubation period is between 3 to 5 years.
 
  
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== Treatment ==
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''M. leprae'' leaves  the [[human body]] through the skin and the nasal mucosa, although their relative importance in contract transmission 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. There are reports of acid-fast bacilli being found in the desquamating epithelium of the skin, but researchers could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and their contacts (Weddell et al. 1963). Fairly large numbers of ''M. leprae'' have been found in the superficial [[keratin]] layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with sebaceous secretions (Job et al. 1999). The importance of the nasal mucosa, especially the ulcerated mucosa, in transmission was recognized as early as 1898 (Schaffer 1898). The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy ranged from 10 thousand to 10 million (Shepard 1960). The majority of lepromatous patients showed leprosy bacilli in their nasal secretions (Pedley 1973), which produced as many as 10 million viable organisms per day (Davey et al. 1974).
  
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The entry route of ''M. leprae'' into the [[human body]] is not definitely known, but the two most likely routes are the skin and  upper respiratory tract. The evidence in favor of the respiratory route is on the increase in spite of the long-held belief that the skin was the exclusive route of entry. The successful transmission of leprosy through aerosols containing ''M. leprae'' in immune-suppressed [[mice]] suggests a similar possibility in humans (Rees et al. 1977). Successful results have been reported with  mice when ''M. leprae'' were introduced into their nasal cavity by topical application (Chehl et al. 1985). In summary, entry through the respiratory route appears the most probable, although other routes, particularly broken skin, cannot be ruled out. Most investigators think that ''M. leprae'' is usually spread from person to person via respiratory droplets'' (CDC 2005).
  
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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 only dapsone was used , it soon resulted in a widespread emergence of resistance. By the 1960s the world’s only known anti-leprosy drug became virtually useless.
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In leprosy, the reference points for measuring the incubation period, the times of infection, and the onset of disease are difficult to define; the former because of the lack of adequate immunological tools and the latter because of the insidious nature of the onset of leprosy. The minimum incubation period reported is as short as a few weeks, based on the very occasional occurrence of leprosy among young infants (Montestruc et al. 1954). The maximum incubation period reported is as long as 30 years, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas. It is generally agreed that the average incubation period is between 3 to 5 years.
  
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The search for more effective anti-leprosy drugs led to the use of clofazimine and rifampicin in the 1960s and 1970s (Rees ''et al.'' 1970)  and later, to avoid the danger of resistance , combined therapy was formulated using rifampicin and dapsone (Yawalkar ''et al''. 1982). 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 should be used alone because of the risk of developing resistance.
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== Treatment ==
  
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The use of MDT was slow and sporadic in most endemic countries over the next decade, due mainly to the high cost of the combined treatment. In 1985 leprosy was still considered a public health problem in 122 countries. A new impetus was provided by the 44th World Health Assembly (WHA) in 1991, that passed a resolution to eliminate leprosy as a public health problem by the year 2000. This was defined as reducing the global prevalence of the disease to less than 1 case per 100,000. The World Health Organization (WHO) was given the mandate to develop an elimination strategy by its member states .
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Until the use of [[dapsone]] pills, pioneered by Dr. [[R.G. Cochrane]] and used at the hospital compound in Carville, Louisiana in 1946, there was no effective cure for leprosy. Dapsone is only weakly bactericidal against ''[[M. leprae]]'' and it was considered necessary for patients to take the drug indefinitely. When only dapsone was used, it soon resulted in a widespread emergence of resistance. By the 1960s, the world’s only known anti-leprosy drug became virtually useless.
  
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The WHO Study Group's report on the ''Chemotherapy of Leprosy'' recommended two types of standard MDT regimen be adapted (WHO 1994). 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.
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The search for more effective anti-leprosy drugs led to the use of clofazimine and rifampicin in the 1960s and 1970s (Rees et al. 1970) and later, to avoid the danger of resistance, combined therapy was formulated using rifampicin and dapsone (Yawalkar et al. 1982). Multidrug therapy (M.D.T.), combining all three drugs, was first recommended by the World Health Organization in 1981. These three anti-leprosy drugs are still used in the standard M.D.T. regimens. None of them should be used alone because of the risk of developing resistance.
  
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Since 1995, WHO has supplied all endemic countries with free MDT in blister packs, supplied through Ministries of Health. This free provision was extended in 2000, and again in 2005, and will run until at least the end of 2010. At the country level, [[non-government organisations]] (NGOs) affiliated with the national programme will continue to be provided with an appropriate free supply of this MDT by the government.
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The use of M.D.T. was slow and sporadic in most endemic countries over the next decade, due mainly to the high cost of the combined treatment. In 1985 leprosy was still considered a public health problem in 122 countries. The World Health Assembly (W.H.A.) in 1991 passed a resolution to eliminate leprosy as a public health problem by the year 2000. This was defined as reducing the global prevalence of the disease to less than 1 case per 100,000. The World Health Organization (WHO) was given this challenge.
  
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MDT remains highly effective and patients are no longer infectious after the first monthly dose. It is safe and easy to use under field conditions due to its presentation in calendar blister packs. Relapse rates remain low, and there is no known resistance to the combined drugs (WHO 1997). They concluded that the MB duration of treatment—then standing at 24 months—could safely be shortened to 12 months "without significantly compromising its efficacy."
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The WHO recommended two types of standard M.D.T. regimen be adapted (WHO 1994). 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 were provided to WHO for the procurement and supply of M.D.T. to all endemic countries.
  
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Improving detection of the disease will allow people to begin treatment earler. The lack of education about Hansen's disease can lead people to falsely believe that the disease is highly contagious and incurable.
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Since 1995, WHO has supplied all endemic countries with free M.D.T. in blister packs. This free provision was extended in 2000, and again in 2005, and will run until at least the end of 2010. At the country level, [[non-government organizations]] (NGOs) affiliated with the national program will continue to be provided with an appropriate free supply of this M.D.T. by the government.
  
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== ''Mycobacterium leprae'' ==
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M.D.T. remains highly effective and patients are no longer infectious after the first monthly dose. It is safe and easy to use. Relapse rates remain low, and there is no known resistance to the combined drugs (WHO 1997). The WHO determined that the duration of treatment for MB leprosy could be shortened safely to 12 months "without significantly compromising its efficacy."
  
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''Mycobacterium leprae'' is a rod-shaped bacterium with an affinity for acidic stains. It's length vaires from 1-8 microns and it is 0.2 microns wide. It has the longest doubling time of all known bacteria and has thwarted every effort at culture in a defined medium (Truman ''et al''. 2001).
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Other drugs that are used include ethionamide, [[aspirin]], [[prednisone]], and [[thalidomide]] (Adam Med. Enc. 2005).
  
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Less than half of the genome contains functional [[genes]]. Gene deletion and decay appear to have eliminated many important metabolic activities, including siderophore production, part of the oxidative and most of the microaerophilic and anaerobic respiratory chains, and numerous catabolic systems and their regulatory circuits ( Cole et al. 1998).
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Improving detection of the disease will allow people to begin treatment earlier. Improving education about Hansen's disease will help people to understand that the disease is neither highly contagious nor incurable.
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The genome sequence of a strain of ''M. leprae'', originally isolated in Tamil Nadu and designated 'TN', has been completed recently. The sequence was obtained by a combined approach, employing automated [[DNA]] sequence analysis of selected [[cosmids]] and whole-genome 'shotgun' clones. The genome sequence was found to contain 3,268,203 base-pairs (bp), and to have an average G+C content of 57.8%, values much lower than the corresponding values for ''M. tuberculosis'', which are 4, 441,529 bp and 65.6% G+C.  There are 1500 genes which are common to both ''M. leprae'' and ''M. tuberculosis''. There is speculation that as ''M. leprae'' evolved it may have lost many genes (Cole ''et al.'' 2001). 
 
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Information from the completed genome may be useful to develop diagnostic skin tests, to understand the mechanism of nerve damage or drug resistance and to identify novel drug targets for rational design of new therapeutic drugs to treat leprosy and its complications.
 
  
 
== Epidemiology ==
 
== Epidemiology ==
  
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W.H.O. estimated in 1995 that worldwide, two to three million people were permanently disabled because of Hansen's disease . [[India]] has the greatest number of cases, with [[Brazil]] second and [[Myanmar]] third. W.H.O. estimates for worldwide incidence of leprosy for the following years were:
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In 2000, the [[World Health Organization]] listed 91 countries in which Hansen's disease is [[endemic (epidemiology)|endemic]]. [[India]], [[Myanmar]]. and [[Nepal]] contained 70 percent of cases. In 2002, 763,917 new cases were detected worldwide, and in that year the WHO listed [[Brazil]], [[Madagascar]], [[Mozambique]], [[Tanzania]], and [[Nepal]] as having 90 percent of Hansen's disease cases.
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*1999    640,000
 
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*2000    738,284
 
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*2002    763,917
 
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*2004    407,791
 
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*2006    220,000
 
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In 1999, 108 cases occurred in the [[United States]]. In 2000, the [[World Health Organization]] (WHO) listed 91 countries in which Hansen's disease is [[endemic (epidemiology)|endemic]]. [[India]], [[Myanmar]] and [[Nepal]] contained 70% of cases. In new cases were detected worldwide, and in that year the WHO listed [[Brazil]], [[Madagascar]], [[Mozambique]], [[Tanzania]] and [[Nepal]] as having 90% of Hansen's disease cases.
 
  
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According to recent figures from the WHO, new cases detected worldwide have decreased by approximately 107,000 cases (or 21%) from 2003 to 2004. This decreasing trend has been consistent for the past three years. In addition, the global registered prevalence of HD was 286,063 cases; 407,791 new cases were detected during 2004.
+
Hansen's disease is also tracked by the [[Centers for Disease Control and Prevention]] (CDC). Its [[prevalence]] in the [[United States]] has remained low and relatively stable. There are decreasing numbers of cases worldwide, though pockets of high prevalence continue in certain areas such as [[Brazil]], [[South Asia]] (India, Nepal), some parts of [[Africa]] ([[Tanzania]], [[Madagascar]], [[Mozambique]]), and the western [[Pacific]].
  
−
In 2006 only 220,000 cases were registered with WHO.(WHO 2007).
+
Aside from humans, other creatures that are known to be susceptible to leprosy include the [[armadillo]], mangabey [[monkey]]s, [[rabbit]]s, and [[mouse|mice]].
−
 
 
−
Hansen's disease is tracked by the [[Centers for Disease Control and Prevention]] (CDC). Its [[prevalence]] in the United States has remained low and relatively stable. There are decreasing numbers of cases worldwide, though pockets of high prevalence continue in certain areas such as [[Brazil]], [[South Asia]] ([[India]], [[Nepal]]), some parts of [[Africa]] ([[Tanzania]], [[Madagascar]], [[Mozambique]]) and the western [[Pacific]].
 
−
 
 
−
Aside from humans, other creatures that are known to be susceptible to leprosy include the [[armadillo]], [[mangabey]] [[monkey]]s, [[rabbit]]s, and [[mouse|mice]] (on their footpads).
 
  
 
=== Risk groups ===
 
=== 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 [[biochemistry|biochemical]] level.  In addition, men are two times more likely to contract leprosy than women.
+
At highest risk are those living in endemic areas with poor conditions, such as inadequate bedding, contaminated water and insufficient diet, or other diseases (e.g., [[HIV]]) that compromise immune function. Recent research suggests that there is a defect in [[immune system#Cell-mediated immune system|cell-mediated immunity]] that causes susceptibility to the disease. The region of [[DNA]] responsible for this variability may also be involved in [[Parkinson's disease]], giving rise to current speculation that the two disorders are linked in some way at the biochemical level.
  
 
=== Disease burden ===
 
=== Disease burden ===
  
−
Although annual [[Incidence (epidemiology)|incidence]]—the number of new leprosy cases occurring each year—is important as a measure of transmission, it is difficult to measure in leprosy due to its long incubation period, delays in diagnosis after onset of the disease and the lack of laboratory tools to detect leprosy in its very early stages.
+
Although ''annual incidence''—the number of new leprosy cases occurring each year—is important as a measure of transmission, it is difficult to measure in leprosy due to its long incubation period, delays in diagnosis after onset of the disease, and the lack of laboratory tools to detect leprosy in its very early stages. ''Registered prevalence'' is a better indicator of the disease burden, since it reflects the number of active leprosy cases diagnosed and receiving treatment with M.D.T. at a given point in time (WHO Study Group 1985). ''New case detection'' is another indicator of the disease burden and usually reported by countries on an annual basis. It includes cases diagnosed with onset of disease in the year in question (true incidence) and a large proportion of cases with onset in previous years (termed a backlog prevalence of undetected cases). The new case detection rate (N.C.D.R.) is defined by the number of newly detected cases, previously untreated, during a year divided by the population in which the cases have occurred.
−
 
 
−
Instead, the registered [[prevalence]] is used. Registered prevalence is a useful proxy indicator of the disease burden as it reflects the number of active leprosy cases diagnosed with the disease and retrieving treatment with MDT at a given point in time. The prevalence rate is defined as the number of cases registered for MDT treatment among the population in which the cases have occurred, again at a given point in time.<ref name=WHO_1985>{{cite journal |author= |title=Epidemiology of leprosy in relation to control. Report of a WHO Study Group |journal=World Health Organ Tech Rep Ser |volume=716 |issue= |pages=1-60 |year=1985 |pmid=3925646}}</ref>
 
−
 
 
−
New case detection is another indicator of the disease burden and usually reported by countries on an annual basis. It includes cases diagnosed with onset of disease in the year in question (true incidence) and a large proportion of cases with onset in previous years (termed a backlog prevalence of undetected cases). The new case detection rate (NCDR) is defined by the number of newly detected cases, previously untreated, during a year divided by the population in which the cases have occurred.
 
  
−
Endemic countries also report the number of new cases with established disabilities at the time of detection, as an indicator of the backlog prevalence. However, determination of the time of onset of the disease is generally unreliable, is very labour-intensive and is seldom done in recording these statistics.
+
Endemic countries also report the number of new cases with established disabilities at the time of detection, as an indicator of the backlog prevalence. However, determination of the time of onset of the disease is generally unreliable.
  
 
=== Global Situation ===
 
=== Global Situation ===
Line 153: Line 162:
 
! Start of 2004  !! Start of 2005 !! Start of 2006  !! During 2003  !! During 2004  !! During 2005
 
! Start of 2004  !! Start of 2005 !! Start of 2006  !! During 2003  !! During 2004  !! During 2005
 
|-
 
|-
−
| align="left" |{{BRA}}
+
| align="left" | [[BRAZIL]]
 
| 79,908 (4.6) || 30,693 (1.7) || 27,313 (1.5) || 49,206 (28.6) || 49,384 (26.9) || 38,410 (20.6)
 
| 79,908 (4.6) || 30,693 (1.7) || 27,313 (1.5) || 49,206 (28.6) || 49,384 (26.9) || 38,410 (20.6)
 
|-
 
|-
−
| align="left" |{{COD}}
+
| align="left" | [[DEM. REPUB. CONGO]]
 
| 6,891 (1.3) || 10,530 (1.9) || 9,785 (1.7) || 7,165 (13.5) || 11,781 (21,1) || 10,737 (18.7)
 
| 6,891 (1.3) || 10,530 (1.9) || 9,785 (1.7) || 7,165 (13.5) || 11,781 (21,1) || 10,737 (18.7)
 
|-
 
|-
−
| align="left" |{{MDG}}
+
| align="left" | [[MADAGASCAR]]
 
| 5,514 (3.4) || 4,610 (2.5) || 2,094 (1.1) || 5,104 (31.1) || 3,710 (20.5) || 2,709 (14.6)
 
| 5,514 (3.4) || 4,610 (2.5) || 2,094 (1.1) || 5,104 (31.1) || 3,710 (20.5) || 2,709 (14.6)
 
|-
 
|-
−
| align="left" |{{MOZ}}
+
| align="left" | [[MOZAMBIQUE ]]
 
| 6,810 (3.4) || 4,692 (2.4) || 4,889 (2.5) || 5,907 (29.4) || 4,266 (22.0) || 5,371 (27.1)
 
| 6,810 (3.4) || 4,692 (2.4) || 4,889 (2.5) || 5,907 (29.4) || 4,266 (22.0) || 5,371 (27.1)
 
|-
 
|-
−
| align="left" |{{ NPL}}
+
| align="left" | [[ NEPAL]]
 
| 7,549 (3.1) || 4,699 (1.8) || 4,921 (1.8) || 8,046 (32.9) || 6,958 (26.2) || 6,150 (22.7)
 
| 7,549 (3.1) || 4,699 (1.8) || 4,921 (1.8) || 8,046 (32.9) || 6,958 (26.2) || 6,150 (22.7)
 
|-
 
|-
−
| align="left" |{{TZA}}
+
| align="left" | [[TANZANIA]]
 
| 5,420 (1.6) || 4,777 (1.3) || 4,190 (1.1) || 5,279 (15.4) || 5,190 (13.8) || 4,237 (11.1)
 
| 5,420 (1.6) || 4,777 (1.3) || 4,190 (1.1) || 5,279 (15.4) || 5,190 (13.8) || 4,237 (11.1)
 
|- style="border: 1px solid #BFA3A3; margin: auto" bgcolor="#F5FFFC" | background:<tt>#F2CECE
 
|- style="border: 1px solid #BFA3A3; margin: auto" bgcolor="#F5FFFC" | background:<tt>#F2CECE
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|}
 
|}
  
−
As reported to [[WHO]] by 115 countries and territories in 2006, and published in the Weekly Epidemiological Record the global registered [[prevalence]] of leprosy at the beginning of the year was 219,826 cases. <ref name=WHO_2006>{{cite journal | author = | title = Global leprosy situation, 2006 | journal = Weekly Epidemiological Record | year = 2006 | volume = 81 | number = 32 | pages =309&ndash;16 | url= http://www.who.int/lep/resources/wer8132.pdf}}</ref> New case detection during the previous year (2005 - the last year for which full country information is available) was 296,499. The reason for the annual detection being higher than the prevalence at the end of the year can be explained by the fact that a proportion of new cases complete their treatment within the year and therefore no longer remain on the registers. The global detection of new cases continues to show a sharp decline, falling by 110,000 cases (27%) during 2005 compared with the previous year.
+
As reported to WHO by 115 countries and territories in 2006 (WHO 2006). The reason for the annual detection being higher than the prevalence at the end of the year is that new cases complete their treatment within the year and therefore no longer remain on the registers.  
  
−
'''Table 1''' shows that global annual detection has been declining since 2001. The African region reported an 8.7% decline in the number of new cases compared with 2004. The comparable figure for the Americas was 20.1%, for South-East Asia 32% and for the Eastern Mediterranean it was 7.6%. The Western Pacific area, however, showed a 14.8% increase during the same period.
+
'''Table 1''' shows that global annual detection has been declining since 2001. The African region reported an 8.7 percent decline in the number of new cases compared with 2004. The comparable figure for the Americas was 20.1 percent, for South-East Asia 32 percent, and for the Eastern Mediterranean it was 7.6 percent. The Western Pacific area, however, showed a 14.8 percent increase during the same period.
  
−
'''Table 2''' shows the leprosy situation in the six major countries which have yet to achieve the goal of elimination at the national level. It should be noted that: a) Elimination is defined as a prevalence of less than 1 case per 10,000 population; b) Madagascar reached elimination at the national level in September 2006; and c) Nepal detection reported from mid-November 2004 to mid-November 2005.
+
'''Table 2''' shows the leprosy situation in the six major countries that have yet to achieve the goal of elimination at the national level. It should be noted that: a) Elimination is defined as a prevalence of less than 1 case per 10,000 population; b) Madagascar reached elimination at the national level in September 2006; and c) Nepal detection rates are reported from mid-November 2004 to mid-November 2005.
−
<br clear="all" />
 
  
−
== History ==
+
The Leprosy Mission of Canada estimates that 4 million people are currently suffering from leprosy (L.M.C. 2007). When the WHO declares that leprosy has been eliminated, according to their definition of 1/10,000, then in a world of 6 billion people that leaves 600,000 people with leprosy.
−
[[Image:Gerhard Hansen.jpg|thumb|right|[[Gerhard Armauer Hansen|GHA Hansen]], discoverer of ''[[Mycobacterium leprae|M. leprae]]'']]
 
  
−
A very great number of ''leprosaria'', or leper hospitals, sprang up in the [[Middle ages]], particularly in England, where there were 250 by C.E. 1230.{{Fact|date=March 2007}} The first recorded leprosarium was in [[Harbledown]]. (See [[Leper colony]].) These institutions were run along monastic lines and, while lepers were encouraged to live in these monastic-type establishments, this was for their own health as well as quarantine. Indeed, some medieval sources indicate belief that those suffering from leprosy were considered to be going through [[Purgatory]] on Earth, and for this reason their suffering was considered more holy than the ordinary person's. More frequently, lepers were seen to exist in a place between life and death: they were still alive, yet many chose or were forced to completely separate themselves from mundane existence.{{Fact|date=March 2007}}
 
  
−
[[Radegund]] was noted for washing the feet of lepers. [[Orderic Vitalis]] writes of a monk, Ralf, who was so overcome by the plight of lepers that he prayed to catch leprosy himself (which he eventually did). The leper would carry a clapper and bell to warn of his approach, and this was as much to attract attention for charity as to warn people that a diseased person was near.
+
== References ==
  
−
''[[Mycobacterium leprae]]'', the causative agent of leprosy, was discovered by [[Gerhard Armauer Hansen|G. H. Armauer Hansen]] in Norway in 1873, making it the first bacterium to be identified as causing disease in man.<ref name=Hansen_1874>{{cite journal | author = Hansen GHA | title = Undersøgelser Angående Spedalskhedens Årsager (Investigations concerning the etiology of leprosy) | journal = Norsk Mag. Laegervidenskaben | year = 1874 | volume = 4| pages = pp. 1–88 | language = Norwegian }}</ref><ref name=Irgens_2002>{{cite journal |author=Irgens L |title=The discovery of the leprosy bacillus |journal=Tidsskr Nor Laegeforen |volume=122 |issue=7 |pages=708-9 |year=2002 |pmid=11998735}}</ref> Historically, individuals with Hansen's disease have been known as ''lepers'', however, this term is falling into disuse as a result of the diminishing number of leprosy patients and the [[wikt:pejorative|pejorative]] connotations of the term. The term most widely accepted among people and agencies working in the field of Hansen's disease is "people affected by Hansen's disease."
+
* A.D.A.M. Medical Encyclopedia. 2005. [http://www.drugs.com/enc/leprosy.html Leprosy]. ''Drugs.com''. Retrieved August 4, 2007.
  
−
Historically, the term ''[[Tzaraath]]'' from the [[Hebrew Bible]] is commonly translated as leprosy, although the symptoms of Tzaraath are not entirely consistent with leprosy and might refer to a variety of skin disorders other than Hansen's disease.<ref name=Heller_2003>{{cite journal |author=Heller R, Heller T, Sasson J |title=Mold: "tsara'at," Leviticus, and the history of a confusion |journal=Perspect Biol Med |volume=46 |issue=4 |pages=588-91 |year=2003 |pmid=14593226}}</ref>
+
* Barnhart, R.K. 1995. ''Barnhart Concise Dictionary of Etymology.'' New York: Harper Collins. ISBN 0062700847
  
−
In particular [[tinea capitis]] ([[fungal]] scalp infection) and related infections on other body parts caused by the [[dermatophyte]] fungus ''Trichophyton violaceum'' are abundant throughout the Middle East and North Africa today and might also have been common in biblical times. Similarly, the related agent of the disfiguring skin disease [[favus]], ''Trichophyton schoenleinii'', appears to have been common throughout Eurasia and Africa before the advent of modern medicine.  Persons with severe favus and similar fungal diseases (and potentially also with severe [[psoriasis]] and other diseases not caused by microorganisms) tended to be classed as having leprosy as late as the 17th century in Europe.<ref name=Kane_1997>{{cite book | author = Kane J, Summerbell RC, Sigler L, Krajden S, Land G | title = Laboratory Handbook of Dermatophytes: A clinical guide and laboratory manual of dermatophytes and other filamentous fungi from skin, hair and nails | publisher = Star Publishers (Belmont, CA) | year = 1997 | id = ISBN 0898631572 }}</ref> This is clearly shown in the painting ''Governors of the Home for Lepers at Haarlem 1667'' by [[Jan de Bray]] ([[Frans Hals Museum]], [[Haarlem]], [[the Netherlands]]), where a young Dutch man with a vivid scalp infection, almost certainly caused by a fungus, is shown being cared for by three officials of a charitable home intended for leprosy sufferers. The use of the word "leprosy" before the mid-19th century, when microscopic examination of skin for medical diagnosis was first developed, can seldom be correlated reliably with Hansen's disease as we understand it today.
+
* Centers for Disease Control and Prevention (CDC). 2005. [http://www.cdc.gov/ncidod/dbmd/diseaseinfo/hansens_t.htm Hansen's Disease (Leprosy)]. ''Centers for Disease Control and Prevention''. Retrieved March 22, 2007.  
  
−
The word "leprosy" derives from the ancient Greek words ''lepros'', a scale, and ''lepein'', to peel.<ref name=Barnhart_1995>{{cite book | last = Barnhart | first = Robert K. | title = Barnhart Concise Dictionary of Etymology | edition = 1st ed. | publisher = New York: Harper Collins | year = 1995 | id = ISBN 0062700847}}</ref>  The word came into the English language via Latin and Old French. The first attested English use is in the ''Ancrene Wisse,'' a 13th-century manual for nuns ("Moyseses hond..bisemde o þe spitel uuel & þuhte lepruse." ''The Middle English Dictionary,'' s.v., "leprous"). A roughly contemporaneous use is attested in the Anglo-Norman ''Dialogues of Saint Gregory,'' "Esmondez i sont li lieprous" (''Anglo-Norman Dictionary,'' s.v., "leprus").
+
* Chehl, S., C. Job, and R. Hastings. 1985. Transmission of leprosy in nude mice. ''Am J Trop Med Hyg'' 34(6): 1161-1166. PMID 3914846
  
−
== References ==
+
* Cole, S. T., R. Brosch, J. Parkhill, et al. 1998. Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence. ''Nature'' 393(6685): 537-544. PMID 9634230
  
−
*CDC 2005. Hansen's Disease (Leprosy) . Technical Information ,Centers for Disease Control and Prevention [[http://www.cdc.gov/ncidod/dbmd/diseaseinfo/hansens_t.htm]] access date = 2007-03-22
+
* Cole, S. T., K. Eiglmeier, J. Parkhill, et al. 2001. Massive gene decay in the leprosy bacillus. ''Nature'' 409(6823): 1007 - 1011. PMID 11234002
  
−
*Chehl , S.,C. Job and R. Hastings . 1985. Transmission of leprosy in nude mice . ''Am J Trop Med Hyg'' 34 (6): 1161-1166 . PMID 3914846
+
* Davey, T., and R. Rees. 1974. The nasal dicharge in leprosy: clinical and bacteriological aspects . ''Lepr Rev'' 45(2): 121-134. PMID 4608620
  
−
*Cole , S.T.,R. Brosch , J. Parkhill ''et al''. 1998. Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence. ''Nature'' 393 (6685):537-544 . PMID 9634230
+
* Doull, J. A., R. A. Guinto, R. S. Rodriguez, et al. 1942. The incidence of leprosy in Cordova and Talisay, Cebu, Philippines. ''International Journal of Leprosy'' 10: 107–131.  
  
−
*Cole , S.T., K. Eiglmeier , J. Parkhill , ''et al.'' 2001. Massive gene decay in the leprosy bacillus . Nature 409 (6823): 1007 - 1011 PMID 11234002
+
* Hansen, G. H. A. 1874. Undersøgelser Angående Spedalskhedens Årsager (Investigations concerning the etiology of leprosy). ''Norsk Mag. Laegervidenskaben'' 4: 1–88  (Norwegian)
  
 +
* Heller, R., T. Heller, and J. Sasson. 2003. Mold: "tsara'at," Leviticus, and the history of a confusion. ''Perspect Biol Med'' 46(4): 588 - 591. PMID 14593226
  
−
*Davey , T. and R. Rees . 1974 . The nasal dicharge in leprosy: clinical and bacteriological aspects . ''Lepr Rev'' 45 (2): 121-134 .PMID 4608620
+
* Icon Health Publications. 2004. ''Leprosy: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References.'' San Diego: Icon Health Publications. ISBN 0597840067
  
−
*Doull, J.A.,R.A. Guinto ,R.S. Rodriguez , et al. 1942.  The incidence of leprosy in Cordova and Talisay, Cebu, Philippines. International Journal of Leprosy 10 :107–131
+
* Irgens, L. 2002. The discovery of the leprosy bacillus. ''Tidsskr Nor Laegeforen'' 122 (7): 708-709. (Norwegian) PMID 11998735
  
−
*Job , C., J. Jayakumar ,M. Aschhoff . 1999. Large numbers of Mycobacterium leprae are discharged from the intact skin of lepromatous patients; a preliminary report. ''Int J Lepr Other Mycobact Dis''67 (2):164-167 . PMID 10472371
+
* Job, C., J. Jayakumar, and M. Aschhoff. 1999. Large numbers of ''Mycobacterium leprae'' are discharged from the intact skin of lepromatous patients; a preliminary report. ''Int J Lepr Other Mycobact Dis'' 67(2): 164-167. PMID 10472371
  
−
*McNeil Jr., D.G. 2006. Worrisome New Link: AIDS Drugs and Leprosy. New York Times 10-24-2006.[[http://www.nytimes.com/2006/10/24/health/24lepr.html]] access date = 2007-05-07
+
* Kane, J., R. C. Summerbell, L. Sigler, S. Krajden, and G. Land. 1997. ''Laboratory Handbook of Dermatophytes: A Clinical Guide and Laboratory Manual of Dermatophytes and Other Filamentous Fungi from Skin, Hair and Nails.'' Belmont, CA: Star Publishers. ISBN 0898631572
  
−
*Montestruc , E. and R. Berdonneau. 1954. 2 New cases of leprosy in infants in Martinique. ''Bull Soc Pathol Exot Filiales'' 47 (6): 781-783 (in French) PMID 14378912
+
*Leprosy Mission of Canada. 2007. [http://www.leprosy.ca/site/c.anKKIPNrEqG/b.3015375/k.34E0/News_Release__July_23_2007.htm Leprosy could cause a new threat says BBC report]. ''Leprosy Mission of Canada''. Retrieved August 5, 2007.
  
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*Naafs , B.,E. Silva ,F. Vilani-Moreno ,E. Marcos ,M. Nogueira and D.Opromolla . 2001. Factors influencing the development of leprosy: an overview. ''Int J Lepr Other Mycobact Dis'' 69 (1):26-33 . PMID 11480313
+
* McNeil, D. G. 2006. [http://www.nytimes.com/2006/10/24/health/24lepr.html Worrisome new link: AIDS drugs and leprosy]. ''New York Times'' October 24, 2006. Retrieved May 7, 2007.  
  
−
*Noordeen , S.,P. Neelan . 1978. Extended studies on chemoprophylaxis against leprosy . ''Indian J Med Res'' 67: 515-527  PMID 355134
+
* Montestruc, E., and R. Berdonneau. 1954. Two new cases of leprosy in infants in Martinique. ''Bull Soc Pathol Exot Filiales'' 47(6): 781-783 (in French) PMID 14378912
  
−
*Pedley, J. 1973. The nasal mucus in leprosy . ''Lepr Rev'' 44 (1):33-35 . PMID 4584261
+
* Naafs, B., E. Silva, F. Vilani-Moreno, E. Marcos, M. Nogueira, and D. Opromolla. 2001. Factors influencing the development of leprosy: an overview. ''Int J Lepr Other Mycobact Dis'' 69(1): 26-33. PMID 11480313
  
−
*Rees , R. and A. McDougall . 1977. Airborne infection with Mycobacterium leprae in mice . J. Med .Microbiol. 10 (1): 63-68 PMID 320339
+
* Noordeen, S., and P. Neelan. 1978. Extended studies on chemoprophylaxis against leprosy. ''Indian J Med Res'' 67: 515-527  PMID 355134
  
−
*Rees , R.J., J.M. Pearson and  M.F. Waters . 1970. Experimental and clinical studies on rifampicin in treatment of leprosy . ''Br Med J'' 5688 (1): 89-92 .PMID 4903972
+
* Pedley, J. 1973. The nasal mucus in leprosy. ''Lepr Rev'' 44(1):33-35. PMID 4584261
  
−
*Ryan, K.J., C.G. Ray (editors). 2004. ''Sherris Medical Microbiology  '' 4th ed. , pp. 451–3 . McGraw Hill . ISBN 0838585299
+
* Rees, R., and A. McDougall. 1977. Airborne infection with ''Mycobacterium leprae'' in mice. ''J. Med .Microbiol'' 10(1): 63-68 PMID 320339
  
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*Schaffer 1898.''Arch Dermato Syphilis'' 44:159–174.
+
* Rees, R. J., J. M. Pearson, and M. F. Waters. 1970. Experimental and clinical studies on rifampicin in treatment of leprosy. ''Br Med J'' 5688(1): 89-92. PMID 4903972
  
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*Shepard ,C. 1960. Acid-fast bacilli in nasal excretions in leprosy, and results of inoculation of mice. ''Am J Hyg'' 71 :147-157 PMID 14445823
+
* Rawcliffe, C. 2001. Learning to Love the Leper: aspects of institutional Charity in Anglo Norman England. ''Anglo Norman Studies'' 23: 233–252.
  
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*Truman,R.W.and J.L. Krahenbuhl. 2001. Viable M. leprae as a research reagent. ''Int. J. Lepr. Other Mycobact''. Dis.: 69(1)1- 12 PMID 11480310
+
* Ryan, K. J., and C. G. Ray, eds. 2004. ''Sherris Medical Microbiology,'' 4th ed., 451–453. McGraw Hill. ISBN 0838585299
  
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*Weddell, G.,E. Palmer . 1963. The pathogenesis of leprosy. An experimental approach , ''Leprosy Review'' 34:57-61 PMID 13999438
+
*Schaffer. 1898. ''Arch Dermato Syphilis'' 44: 159–174.
  
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*WHO  1994. Chemotherapy of Leprosy , WHO Technical Report Series 847 . [[http://www.who.int/lep/mdt/chemotherapy/en/index.html]]access date = 2007-03-24
+
* Shepard, C. 1960. Acid-fast bacilli in nasal excretions in leprosy, and results of inoculation of mice. ''Am J Hyg'' 71: 147-157. PMID 14445823
  
−
*WHO 1995 . Leprosy disabilities: magnitude of the problem . ''Weekly Epidemiological Record'' 70 (38):269- 275  .PMID 7577430
+
* Souvay, C. L, and J. F. Donovan. 1910. [http://www.newadvent.org/cathen/09182a.htm Leprosy]. ''Catholic Encyclopedia, Volume IX'' New York: Robert Appleton Company.  
  
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*WHO 1997. Seventh WHO Expert Committee on Leprosy . WHO Technical Report Series 874 . [[http://www.who.int/lep/resources/expert/en/index.html]] access date = 2007-03-24
+
* Tayman, J. 2006. ''The Colony: The Harrowing True Story of the Exiles of Molokai.'' Simon & Schuster. ISBN 074323300.  
  
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*World Health Organization (W.H.O.) 2007 [http://www.who.int/tdr/about/history_book/history_full_text.htm#leprosy_elimination] viewed on 7-4-2007
+
* Turner, B. S., and C. Samson. 1995. ''Medical Power and Social Knowledge,'' 2nd edition. London: Sage Publications. ISBN 0803975988
  
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*WHO 2007a ,Factsheet on Leprosy , [[http://www.who.int/mediacentre/factsheets/fs101/en/]] | access date = 2007-03-20
+
* Truman, R. W., and J. L. Krahenbuhl. 2001. Viable ''M. leprae'' as a research reagent. ''Int. J. Lepr. Other Mycobact'' Dis.: 69(1): 1- 12. PMID 11480310
  
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*Yawalkar, S.J.,A.C. McDougall ,J. Languillon ,S. Ghosh ,S.K. Hajra ,D.V. Opromolla  and C.J. Tonello . 1982. Once-monthly rifampicin plus daily dapsone in initial treatment of lepromatous leprosy . ''Lancet'' 8283 (1): 1199-1202 . PMID 6122970
+
* Weddell, G., and E. Palmer. 1963. The pathogenesis of leprosy. An experimental approach. ''Leprosy Review'' 34: 57-61. PMID 13999438
  
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<!-- ---------------------------------------------------------------
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* World Health Organization (WHO). 1994. [http://www.who.int/lep/mdt/chemotherapy/en/index.html Chemotherapy of Leprosy, WHO Technical Report Series 847]. ''World Health Organization''. Retrieved March 24, 2007.
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See http://en.wikipedia.org/wiki/Wikipedia:Footnotes for a
 
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discussion of different citation methods and how to generate
 
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footnotes using the <ref> & </ref> tags and the {{Reflist}} template
 
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* World Health Organization (WHO). 1995. Leprosy disabilities: Magnitude of the problem. ''Weekly Epidemiological Record'' 70(38): 269-275. PMID 7577430
  
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=== Further reading ===
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* World Health Organization (WHO) Study Group. 1985. Epidemiology of leprosy in relation to control. ''World Health Organ Tech Rep Ser'' 716: 1-60. PMID 3925646
  
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<div class="references-small" style="column-count: 2;">* {{cite book | author = Icon Health Publications | title = Leprosy: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References | edition =  | publisher =  San Diego: Icon Health Publications | year = 2004 | id = ISBN 0-597-84006-7}}
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* World Health Organization (WHO). 1997. [http://www.who.int/lep/resources/expert/en/index.html Seventh WHO Expert Committee on Leprosy. ''WHO Technical Report Series'' 874. Retrieved March 24, 2007.
  
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* {{cite book | last = Tayman | first = John | title = The Colony : The Harrowing True Story of the Exiles of Molokai | edition =  | publisher =  Simon & Schuster | year = 2006 | id = ISBN 0-7432-3300 }}
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* World Health Organization (WHO). 2006. Global leprosy situation, 2006. ''Weekly Epidemiological Record'' 81(32): 309 -316.
  
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* {{cite journal | author = Rawcliffe C | title = Learning to Love the Leper: aspects of institutional Charity in Anglo Norman England | journal = Anglo Norman Studies | year = 2001 | volume = 23 | pages = pp. 233–52 | url= }}
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* World Health Organization (WHO). 2007 [http://www.who.int/tdr/about/history_book/history_full_text.htm#leprosy_elimination Making a difference: Leprosy]. ''World Health Organization''. Retrieved July 4, 2007.
  
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* {{cite journal | author = Clark E | title = Social Welfare and Mutual Aid in the Medieval Countryside | work = Vill, Guild, and Gentry: Forces of Community in Later Medieval England | journal = ''The Journal of British Studies'' | year = 1994 | volume = 33 | issue = 4 | pages = pp. 394–6 | url= http://links.jstor.org/sici?sici=0021-9371(199410)33%3A4%3C381%3ASWAMAI%3E2.0.CO%3B2-L}}</div>
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* Yawalkar, S. J., A. C. McDougall, J. Languillon, S. Ghosh, S. K. Hajra, D. V. Opromolla, and C. J. Tonello. 1982. Once-monthly rifampicin plus daily dapsone in initial treatment of lepromatous leprosy. ''Lancet'' 8283(1): 1199-1202. PMID 6122970
  
 
== External links ==
 
== External links ==
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{{commons|Leprosy}}
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All links retrieved October 25, 2022.
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* [http://www.cdc.gov/ncidod/dbmd/diseaseinfo/hansens_t.htm Hansen's Disease (Leprosy)] - [[Centers for Disease Control and Prevention]]
 
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* [http://www.who.int/lep/en/ World Health Organization (WHO) leprosy website]
 
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* [http://www.leprosy.org/ American Leprosy Missions]
 
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* [http://bphc.hrsa.gov/nhdp/ National Hansen's Disease Programs (NHDP)]
 
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* [http://dx.doi.org/10.1371/journal.pmed.0020341 The Global Campaign to Eliminate Leprosy] article from ''PLoS Medicine''
 
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; History of leprosy
 
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* [http://www.leprosyhistory.org/ ILA Global Project on the History of Leprosy]
 
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* BBC News: [http://news.bbc.co.uk/2/hi/health/4540461.stm  Slave trade key to leprosy spread]
 
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* {{cite web | title = Interview with author John Tayman (''The Colony'') | work = IT Conversations Tech Nation  | url = http://www.itconversations.com/shows/detail975.html | format = [[MP3|MP3 audio]]: runtime = 00:23:20, 10.7 mb | date =  2006-02-07 | accessdate = 2007-03-22}}
 
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; Research
 
  
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* [http://www.cdc.gov/leprosy/ Hansen's Disease (Leprosy)] - Centers for Disease Control and Prevention.
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* [http://www.who.int/lep/en/ Leprosy elimination] - World Health Organization (WHO).
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* [http://www.leprosyhistory.org/ International Leprosy Association - History of Leprosy].
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* BBC News: [http://news.bbc.co.uk/2/hi/health/4540461.stm  Slave trade key to leprosy spread].
 
* [http://www.granuloma.homestead.com/leprosy.html Pathology Images of Leprosy and Other Granulomatous diseases] Yale Rosen, M.D.
 
* [http://www.granuloma.homestead.com/leprosy.html Pathology Images of Leprosy and Other Granulomatous diseases] Yale Rosen, M.D.
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* [http://www.infolep.org INFOLEP Leprosy Information Services]
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* [http://www.infolep.org INFOLEP Leprosy Information Services].  
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* [http://www.leprosyjournal.org/lepronline/?request=index-html ''International Journal of Leprosy and Other Mycobacterial Diseases'']
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* [http://www.leprosy-review.org.uk/ ''Leprosy Review''].
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* [http://www.leprosy-review.org.uk/ ''Leprosy Review'']
 
  
 
{{credit|129127062}}
 
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[[Category:Life sciences]]
 
[[Category:Life sciences]]
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[[Category:Health and disease]]
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[[Category:Diseases]]

Latest revision as of 21:58, 25 October 2022

A 24-year-old man infected with leprosy
Mycobacterium leprae
Scientific classification
Kingdom: Bacteria
Phylum: Firmicutes
Class: Actinobacteria
Order: Actinomycetales
Family: Mycobacteriaceae
Genus: Mycobacterium
Species: M.leprae
Binomial name
Mycobacterium leprae

"Unclean! Unclean!" These were the words of lepers as they announced their presence among the unafflicted in biblical times. The mere mention of leprosy has struck fear in the hearts of people for thousands of years. Even though it is one of the least contagious of all bacterial diseases, the fear of physical disfigurement and the loss of social status that it brings, has made leprosy one of the most dreaded of all diseases. Lepers have been ostracized and put into separate colonies, where they lived as social outcasts and "untouchables" until the end of their lives.

Leprosy or Hansen's disease is a chronic infectious disease caused by the bacterium Mycobacterium leprae and is the only known bacterium that infects peripheral nerves. It also affects the mucosa of the upper respiratory tract and produces skin lesions (Ryan et al. 2004). If left untreated, there can be progressive and permanent damage to the skin, nerves, limbs and eyes.

Many people have felt a religious calling to risk contracting the disease themselves in order to care for lepers. Some of these most noble people include Father Damien of Molokai, Hawaii; Dr. Albert Schweitzer in Lamberene, Gabon; and Mother Teresa in Calcutta, India.

The crucial breakthrough in the cure for leprosy came when G. H. A. Hansen followed the lead of Robert Koch, who first suggested that microorganisms could cause disease. When Hansen began to look into the "invisible" world for the cause of leprosy, he risked everything he had in order to help those that no one else wanted to touch.

History

GHA Hansen, discoverer of M. leprae

A disease called "leprosy" was recorded in ancient India (fifteenth century B.C.E.), in Japan (tenth century B.C.E.), and in Egypt (sixteenth century B.C.E.). Some propose that the spread of this disease to the West originated from Egypt (Souvay and Donovan 1910).

In the sixth century C.E., Saint Radegund was praised for dedicating her life to caring for lepers.

In 1078 C.E., a leprosarium was built in Rochester, England, and in 1084 Archbishop Lanfranc built another at Harbledown near Canterbury for the care of 100 lepers. These became known as lazar houses, based on the story of Lararus, and many were built during the twelfth and thirteenth centuries (Turner et al. 1995).

The English monk, Orderic Vitalis, writes in the twelfth century C.E., of another monk, Ralf, who was so overcome by the plight of lepers that he prayed to catch leprosy himself (which he eventually did). The leper would carry a clapper and bell to warn of his approach, and this was as much to attract attention for charity as to warn people that a diseased person was near.

In 1873, Mycobacterium leprae, the causative agent of leprosy, was discovered by G. H. Armauer Hansen in Norway , making it the first bacterium to be identified as causing disease in man (Hansen 1874; Irgens 2002).

From 1873 to 1899, Father Damien worked in the leper colony of Kalaupapa on the island of Molokai in Hawaii. He eventually contracted leprosy and died at age 49. On June 4, 1995, Pope John Paul II beatified Blessed Damien and gave him his official spiritual title.

In 1913, Dr. Albert Schweitzer began his work in Lamberene, Gabon, where he labored for more than 40 years until his death in 1965. Many of his patients were lepers. In 1953, he received the Nobel Peace Prize, and spent the prize money to build a clinic for his hospital.

In 1950, Mother Teresa started the Missionaries of Charity in Calcutta, India. She persuaded the leaders that leprosy was not contagious and got the lepers to build a colony at Titagarh that she named after Mahatma Gandhi. In 1979, she was awarded the Nobel Peace Prize for her lifelong work with the poor.

In 1995, the World Health Organization (WHO) estimated that between two and three million individuals were permanently disabled because of leprosy (WHO 1995).

Etymology

The word "leprosy" derives from the ancient Greek words lepros, a "scale," and lepein, "to peel" (Barnhart 1995). The word came into the English language via Latin and Old French. The first attested English use is in the Ancrene Wisse, a thirteenth-century manual for nuns ("Moyseses hond…bisemde o þe spitel uuel & þuhte lepruse." The Middle English Dictionary, s.v., "leprous"). A roughly contemporaneous use is attested in the Anglo-Norman Dialogues of Saint Gregory, "Esmondez i sont li lieprous" (Anglo-Norman Dictionary, s.v., "leprus").

Tzaraath

The term Tzaraath from the Hebrew Bible is commonly translated as leprosy, although the symptoms of Tzaraath are not entirely consistent with leprosy and might refer to a variety of skin disorders other than Hansen's disease (Heller et al. 2003).

In particular tinea capitis, a fungal scalp infection and related infections on other body parts caused by the dermatophyte fungus Trichophyton violaceum, are abundant throughout the Middle East and North Africa today and might also have been common in biblical times. Similarly, the related agent of the disfiguring skin disease favus, Trichophyton schoenleinii, appears to have been common throughout Eurasia and Africa before the advent of modern medicine. People with severe favus and similar fungal diseases along with other skin diseases not caused by microorganisms tended to be classed as having leprosy as late as the seventeenth century in Europe (Kane et al. 1997). This is clearly shown in the painting Governors of the Home for Lepers at Haarlem 1667 by Jan de Bray, where a young Dutch man with a vivid scalp infection, almost certainly caused by a fungus, is shown being cared for by three officials of a charitable home intended for leprosy sufferers. The use of the word "leprosy" before the mid-nineteenth century, when microscopic examination of skin for medical diagnosis was first developed, can seldom be correlated reliably with Hansen's disease as we understand it today.

Mycobacterium leprae

Mycobacterium leprae is a rod-shaped bacterium with an affinity for acid-fast stains. Its length varies from 1-8 microns and it is 0.2 microns wide. It has the longest doubling time of all known bacteria and has thwarted every effort at culture in a defined medium (Truman et al 2001). It can be grown in the foot pads of mice and armadillos and some primates.

Less than half of the genome of M. leprae contains functional genes. Gene deletion and decay appear to have eliminated many important metabolic activities, including siderophore production, part of the oxidative and most of the microaerophilic and anaerobic respiratory chains, and numerous catabolic systems and their regulatory circuits ( Cole et al. 1998).

The genome sequence of a strain of M. leprae, originally isolated in Tamil Nadu and designated TN, has been completed recently. The genome sequence was found to contain 3,268,203 base-pairs (bp), and to have an average G+C content of 57.8 percent, values much lower than the corresponding values for M. tuberculosis, which are 4,441,529 bp and 65.6 percent G+C. There are 1500 genes that are common to both M. leprae and M. tuberculosis. There is speculation that as M. leprae evolved it may have lost many genes (Cole et al. 2001).

Types and symptoms

The clinical manifestations of leprosy vary but primarily affect the skin, nerves, and mucous membranes (Naafs et al. 2001). Patients with this chronic infectious disease are classified as having either: (1) paucibacillary (tuberculoid leprosy), (2) multibacillary Hansen's disease (lepromatous leprosy), or (3) borderline leprosy.

  • 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 no nerve damage. Contrary to popular belief, Hansen's bacillus does not cause rotting of the flesh. After a long investigation by Paul Brand, it was discovered that insensitivity in the limbs and 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.
  • 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.

Recently, leprosy has also emerged as a problem in HIV patients on antiretroviral drugs (McNeil Jr. 2006).

Pathophysiology

The exact mechanism of transmission of leprosy is not known. M. leprae never has been grown on defined media; as a result it has been difficult to study the pathogenic mechanisms. There is a theory 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, what is not clear is the role of genetics and other factors 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.

There is a belief 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. 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 (Doull et al. 1942) to 55.8 per 1000 per year in a part of Southern India (Noordeen et al. 1978).

M. leprae leaves the human body through the skin and the nasal mucosa, although their relative importance in contract transmission 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. There are reports of acid-fast bacilli being found in the desquamating epithelium of the skin, but researchers could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and their contacts (Weddell et al. 1963). Fairly large numbers of M. leprae have been found in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with sebaceous secretions (Job et al. 1999). The importance of the nasal mucosa, especially the ulcerated mucosa, in transmission was recognized as early as 1898 (Schaffer 1898). The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy ranged from 10 thousand to 10 million (Shepard 1960). The majority of lepromatous patients showed leprosy bacilli in their nasal secretions (Pedley 1973), which produced as many as 10 million viable organisms per day (Davey et al. 1974).

The entry route of M. leprae into the human body is not definitely known, but the two most likely routes are the skin and upper respiratory tract. The evidence in favor of the respiratory route is on the increase in spite of the long-held belief that the skin was the exclusive route of entry. The successful transmission of leprosy through aerosols containing M. leprae in immune-suppressed mice suggests a similar possibility in humans (Rees et al. 1977). Successful results have been reported with mice when M. leprae were introduced into their nasal cavity by topical application (Chehl et al. 1985). In summary, entry through the respiratory route appears the most probable, although other routes, particularly broken skin, cannot be ruled out. Most investigators think that M. leprae is usually spread from person to person via respiratory droplets (CDC 2005).

In leprosy, the reference points for measuring the incubation period, the times of infection, and the onset of disease are difficult to define; the former because of the lack of adequate immunological tools and the latter because of the insidious nature of the onset of leprosy. The minimum incubation period reported is as short as a few weeks, based on the very occasional occurrence of leprosy among young infants (Montestruc et al. 1954). The maximum incubation period reported is as long as 30 years, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas. It is generally agreed that the average incubation period is between 3 to 5 years.

Treatment

Until the use of dapsone pills, pioneered by Dr. R.G. Cochrane and used at the hospital compound in Carville, Louisiana in 1946, there was no effective cure for leprosy. Dapsone is only weakly bactericidal against M. leprae and it was considered necessary for patients to take the drug indefinitely. When only dapsone was used, it soon resulted in a widespread emergence of resistance. By the 1960s, the world’s only known anti-leprosy drug became virtually useless.

The search for more effective anti-leprosy drugs led to the use of clofazimine and rifampicin in the 1960s and 1970s (Rees et al. 1970) and later, to avoid the danger of resistance, combined therapy was formulated using rifampicin and dapsone (Yawalkar et al. 1982). Multidrug therapy (M.D.T.), combining all three drugs, was first recommended by the World Health Organization in 1981. These three anti-leprosy drugs are still used in the standard M.D.T. regimens. None of them should be used alone because of the risk of developing resistance.

The use of M.D.T. was slow and sporadic in most endemic countries over the next decade, due mainly to the high cost of the combined treatment. In 1985 leprosy was still considered a public health problem in 122 countries. The World Health Assembly (W.H.A.) in 1991 passed a resolution to eliminate leprosy as a public health problem by the year 2000. This was defined as reducing the global prevalence of the disease to less than 1 case per 100,000. The World Health Organization (WHO) was given this challenge.

The WHO recommended two types of standard M.D.T. regimen be adapted (WHO 1994). 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 were provided to WHO for the procurement and supply of M.D.T. to all endemic countries.

Since 1995, WHO has supplied all endemic countries with free M.D.T. in blister packs. This free provision was extended in 2000, and again in 2005, and will run until at least the end of 2010. At the country level, non-government organizations (NGOs) affiliated with the national program will continue to be provided with an appropriate free supply of this M.D.T. by the government.

M.D.T. remains highly effective and patients are no longer infectious after the first monthly dose. It is safe and easy to use. Relapse rates remain low, and there is no known resistance to the combined drugs (WHO 1997). The WHO determined that the duration of treatment for MB leprosy could be shortened safely to 12 months "without significantly compromising its efficacy."

Other drugs that are used include ethionamide, aspirin, prednisone, and thalidomide (Adam Med. Enc. 2005).

Improving detection of the disease will allow people to begin treatment earlier. Improving education about Hansen's disease will help people to understand that the disease is neither highly contagious nor incurable.

Epidemiology

In 2000, the World Health Organization listed 91 countries in which Hansen's disease is endemic. India, Myanmar. and Nepal contained 70 percent of cases. In 2002, 763,917 new cases were detected worldwide, and in that year the WHO listed Brazil, Madagascar, Mozambique, Tanzania, and Nepal as having 90 percent of Hansen's disease cases.

Hansen's disease is also tracked by the Centers for Disease Control and Prevention (CDC). Its prevalence in the United States has remained low and relatively stable. There are decreasing numbers of cases worldwide, though pockets of high prevalence continue in certain areas such as Brazil, South Asia (India, Nepal), some parts of Africa (Tanzania, Madagascar, Mozambique), and the western Pacific.

Aside from humans, other creatures that are known to be susceptible to leprosy include the armadillo, mangabey monkeys, rabbits, and mice.

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 (e.g., HIV) that compromise immune function. Recent research suggests that there is a defect in cell-mediated immunity that causes susceptibility to the disease. The region of DNA responsible for this variability may also be involved in Parkinson's disease, giving rise to current speculation that the two disorders are linked in some way at the biochemical level.

Disease burden

Although annual incidence—the number of new leprosy cases occurring each year—is important as a measure of transmission, it is difficult to measure in leprosy due to its long incubation period, delays in diagnosis after onset of the disease, and the lack of laboratory tools to detect leprosy in its very early stages. Registered prevalence is a better indicator of the disease burden, since it reflects the number of active leprosy cases diagnosed and receiving treatment with M.D.T. at a given point in time (WHO Study Group 1985). New case detection is another indicator of the disease burden and usually reported by countries on an annual basis. It includes cases diagnosed with onset of disease in the year in question (true incidence) and a large proportion of cases with onset in previous years (termed a backlog prevalence of undetected cases). The new case detection rate (N.C.D.R.) is defined by the number of newly detected cases, previously untreated, during a year divided by the population in which the cases have occurred.

Endemic countries also report the number of new cases with established disabilities at the time of detection, as an indicator of the backlog prevalence. However, determination of the time of onset of the disease is generally unreliable.

Global Situation

Table 1: Prevalence at beginning of 2006, and trends in new case detection 2001-2005, excluding Europe
Region Registered Prevalence

(rate/10,000 pop.)

New Case Detection during the year
Start of 2006 2001 2002 2003 2004 2005
Africa 40,830 (0.56) 39,612 48,248 47,006 46,918 42,814
Americas 32,904 (0.39) 42,830 39,939 52,435 52,662 41,780
South-East Asia 133,422 (0.81) 668,658 520,632 405,147 298,603 201,635
Eastern Mediterranean 4,024 (0.09) 4,758 4,665 3,940 3,392 3,133
Western Pacific 8,646 (0.05) 7,404 7,154 6,190 6,216 7,137
Totals 219,826 763,262 620,638 514,718 407,791 296,499
Table 2: Prevalence and Detection, countries still to reach elimination
Countries Registered Prevalence

(rate/10,000 pop.)

New Case Detection

(rate/100,000 pop.)

Start of 2004 Start of 2005 Start of 2006 During 2003 During 2004 During 2005
BRAZIL 79,908 (4.6) 30,693 (1.7) 27,313 (1.5) 49,206 (28.6) 49,384 (26.9) 38,410 (20.6)
DEM. REPUB. CONGO 6,891 (1.3) 10,530 (1.9) 9,785 (1.7) 7,165 (13.5) 11,781 (21,1) 10,737 (18.7)
MADAGASCAR 5,514 (3.4) 4,610 (2.5) 2,094 (1.1) 5,104 (31.1) 3,710 (20.5) 2,709 (14.6)
MOZAMBIQUE 6,810 (3.4) 4,692 (2.4) 4,889 (2.5) 5,907 (29.4) 4,266 (22.0) 5,371 (27.1)
NEPAL 7,549 (3.1) 4,699 (1.8) 4,921 (1.8) 8,046 (32.9) 6,958 (26.2) 6,150 (22.7)
TANZANIA 5,420 (1.6) 4,777 (1.3) 4,190 (1.1) 5,279 (15.4) 5,190 (13.8) 4,237 (11.1)
Totals 112,092 60,001 53,192 80,707 81,289 67,614

As reported to WHO by 115 countries and territories in 2006 (WHO 2006). The reason for the annual detection being higher than the prevalence at the end of the year is that new cases complete their treatment within the year and therefore no longer remain on the registers.

Table 1 shows that global annual detection has been declining since 2001. The African region reported an 8.7 percent decline in the number of new cases compared with 2004. The comparable figure for the Americas was 20.1 percent, for South-East Asia 32 percent, and for the Eastern Mediterranean it was 7.6 percent. The Western Pacific area, however, showed a 14.8 percent increase during the same period.

Table 2 shows the leprosy situation in the six major countries that have yet to achieve the goal of elimination at the national level. It should be noted that: a) Elimination is defined as a prevalence of less than 1 case per 10,000 population; b) Madagascar reached elimination at the national level in September 2006; and c) Nepal detection rates are reported from mid-November 2004 to mid-November 2005.

The Leprosy Mission of Canada estimates that 4 million people are currently suffering from leprosy (L.M.C. 2007). When the WHO declares that leprosy has been eliminated, according to their definition of 1/10,000, then in a world of 6 billion people that leaves 600,000 people with leprosy.


References
ISBN links support NWE through referral fees

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