Leprosy

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A 24-year-old man infected with leprosy
For the malady found in the Hebrew Bible, see the article Tzaraath.

Leprosy or Hansen's disease is a chronic infectious disease caused by the 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.


Mycobacterium leprae
Scientific classification
Kingdom: Bacteria
Phylum: Firmicutes
Class: Actinobacteria
Order: Actinomycetales
Family: Mycobacteriaceae
Genus: Mycobacterium
Species: M.leprae
Binomial name
Mycobacterium leprae


Leprosy has affected humanity since at least 600 B.C.E., and was well-recognized in the civilizations of ancient China, Egypt and 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 colonies still remain around the world, in countries such as India, Vietnam, and the Philippines.

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.

Characteristics

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 Dr. 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 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.

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 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) . 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). 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.

Treatment

Until the development of dapsone, rifampin, and clofazimine in the 1940s there was no effective cure for leprosy. However, dapsone is only weakly bactericidal against M. leprae and it was considered necessary for patients to take the drug indefinitely. Moreover, when 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 (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.

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 .

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.

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.

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."

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.

Mycobacterium leprae

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).

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). 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). 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

In 2000, the World Health Organization listed 91 countries in which Hansen's disease is endemic. India, Myanmar and Nepal contained 70% 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% 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 (such as HIV) that compromise immune function. Recent research suggests that there is a defect in cell-mediated immunity that causes susceptibility to the disease. Less than ten percent of the world's population are actually capable of acquiring the disease. The region of DNA responsible for this variability is also involved in Parkinson's disease, giving rise to current speculation that the two disorders may be linked in some way at the biochemical level. In addition, men are two times more likely to contract leprosy than women.

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.

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 (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 (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.

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 W.H.O. 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 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.

History

GHA Hansen, discoverer of 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.[citation needed] 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 normal existence.[citation needed]

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.

Mycobacterium leprae, the causative agent of leprosy, was discovered by G. H. Armauer Hansen in Norway in 1873, making it the first bacterium to be identified as causing disease in man (Hansen 1874)(Irgens 2002). Historically, individuals with Hansen's disease have been known as lepers, however, this term is falling into disuse as a result of the dimin-ishing number of leprosy patients and the pejorative connotations of the term.

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 (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 17th 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-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.

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 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").

References
ISBN links support NWE through referral fees

  • Barnhart , R.K. . 1995. Barnhart Concise Dictionary of Etymology , 1st ed. New York: Harper Collins . ISBN 0062700847
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Further reading

* Icon Health Publications (2004). Leprosy: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. San Diego: Icon Health Publications. ISBN 0-597-84006-7. 
  • Tayman, John (2006). The Colony : The Harrowing True Story of the Exiles of Molokai. Simon & Schuster. ISBN 0-7432-3300. 
  • Rawcliffe C (2001). Learning to Love the Leper: aspects of institutional Charity in Anglo Norman England. Anglo Norman Studies 23: pp. 233–52.

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