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Leprosy

Leprosy

Definition

Leprosy is a slowly progressing bacterial infection that affects the skin, peripheral nerves in the hands and feet, and mucous membranes of the nose, throat, and eyes. Destruction of the nerve endings causes the the affected areas to lose sensation. Occasionally, because of the loss of feeling, the fingers and toes become mutilated and fall off, causing the deformities that are typically associated with the disease.

Description

Leprosy is also known as Hansen's disease after G. A. Hansen, who in 1878 identified the bacillus Mycobacterium leprae that causes the disease.

The infection is characterized by abnormal changes of the skin. These changes, called lesions, are at first flat and red. Upon enlarging, they have irregular shapes and a characteristic appearance. The lesions are typically darker in color around the edges with discolored pale centers. Because the organism grows best at lower temperatures the leprosy bacillus has a preference for the skin, the mucous membranes and the nerves. Infection in and destruction of the nerves leads to sensory loss. The loss of sensation in the fingers and toes increases the risk of injury. Inadequate care causes infection of open wounds. Gangrene may also follow, causing body tissue to die and become deformed.

Because of the disabling deformities associated with it, leprosy has been considered one of the most dreaded diseases since biblical times, though much of what was called leprosy in the Old Testament most likely was not the same disease. Its victims were often shunned by the community, kept at arm's length, or sent to a leper colony. Many people still have misconceptions about the disease. Contrary to popular belief, it is not highly communicable and is extremely slow to develop. Household contacts of most cases and the medical personnel caring for Hansen's disease patients are not at particular risk. It is very curable, although the treatment is long-term, requiring multiple medications.

The World Health Organization (WHO) puts the number of identified leprosy cases in the world at about 600,000 as of the early 2000s. Seventy percent of all cases are found in just three countries: India, Indonesia, and Myanamar (Burma). The infection can be acquired, however, in the Western Hemisphere as well. There are about 5000 reported cases in the United States as of 2004, almost all of which involve immigrants from developing countries. Cases also occur in some areas of the Caribbean. Although it was thought for many years that only humans are affected by the disease, 15% of wild armadillos in southern Texas and Louisiana have been found to be infected with M. leprae.

Causes and symptoms

The organism that causes leprosy is a rod-shaped bacterium called Mycobacterium leprae. This bacterium is related to Mycobacterium tuberculosis, the causative agent of tuberculosis. Because special staining techniques involving acids are required to view these bacteria under the microscope, they are referred to as acid-fast bacilli (AFB).

When Mycobacterium leprae invades the body, one of two reactions can take place. In tuberculoid leprosy (TT), the milder form of the disease, the body's immune cells attempt to seal off the infection from the rest of the body by surrounding the offending pathogen. Because this response by the immune system occurs in the deeper layers of the skin, the hair follicles, sweat glands, and nerves can be destroyed. As a result, the skin becomes dry and discolored and loses its sensitivity. Involvement of nerves on the face, arms, or legs can cause them to enlarge and become easily felt by the doctor. This finding is highly suggestive of TT. The scarcity of bacteria in this type of leprosy leads to it being referred to as paucibacillary (PB) leprosy. Seventy to eighty percent of all leprosy cases are of the tuberculoid type.

In lepromatous (LL) leprosy, which is the second and more contagious form of the disease, the body's immune system is unable to mount a strong response to the invading organism. Hence, the organism multiplies freely in the skin. This type of leprosy is also called the multibacillary (MB) leprosy, because of the presence of large numbers of bacteria. The characteristic feature of this disease is the appearance of large nodules or lesions all over the body and face. Occasionally, the mucous membranes of the eyes, nose, and throat may be involved. Facial involvement can produce a lion-like appearance (leonine facies). This type of leprosy can lead to blindness, drastic change in voice, or mutilation of the nose. Leprosy can strike anyone; however, children seem to be more susceptible than adults.

Well-defined skin lesions that are numb are the first symptoms of tuberculoid leprosy. Lepromatous leprosy is characterized by a chronic stuffy nose due to invasion of the mucous membranes, and the presence of nodules and lesions all over the body and face.

Although patients with leprosy are commonly thought not to suffer pain, neuroapthic pain caused by inflammation of peripheral nerve endings is increasingly recognized as a major complication of the disease in many patients. Corticosteroids may be given to reduce the inflammation.

The incubation period of the leprosy bacillus varies anywhere from six months to ten years. On an average, it takes four years for the symptoms of tuberculoid leprosy to develop. Probably because of the slow growth of the bacillus, lepromatous leprosy develops even more slowly, taking an average of eight years for the initial lesions to appear.

It is still not very clear how the leprosy bacillus is transmitted from person to person; about 50% of patients diagnosed with the disease have a history of close contact with an infected family member. Since untreated patients have a large number of M. leprae bacilli in their nasal secretions, it is thought that transmission may take place via nasal droplets. The milder tubercular form of leprosy may be transmitted by insect carriers or by contact with infected soil.

The incidence of leprosy is highest in the poverty belt of the globe. Therefore, environmental factors such as unhygienic living conditions, overpopulation, and malnutrition may also be contributing factors favoring the infection.

It is also possible that genetic factors are involved in susceptibility to leprosy. In 2003, scientists conducting a genome scan of a large Vietnamese family with many cases of leprosy found that susceptibility to the disease was linked to region q25 on the long arm of chromosome 6. Further study indicated that the leprosy susceptibility gene lies within a region shared by two genes for Parkinson's disease. Further research may confirm that the emergence of leprosy in certain individuals is related to inheritance of genes for Parkinson's disease.

Diagnosis

One of the hallmarks of leprosy is the presence of AFB in smears taken from the skin lesions, nasal scrapings, or tissue secretions. In patients with LL leprosy, the bacilli are easily detected; however, in TT leprosy the bacteria are very few and almost impossible to find. In such cases, a diagnosis is made based on the clinical signs and symptoms, the type and distribution of skin lesions, and history of having lived in an endemic area.

The signs and symptoms characteristic of leprosy can be easily identified by a health worker after a short training period. There is no need for a laboratory investigation to confirm a leprosy diagnosis, except in very rare circumstances.

In an endemic area, if smears from an individual show the presence of AFB, or if he has typical skin lesions, he should definitely be regarded as having leprosy. Usually, there is slight discoloration of the skin and loss of skin sensitivity. Thickened nerves accompanied by weakness of muscles supplied by the affected nerve are very typical of the disease. One characteristic occurrence is a foot drop where the foot cannot be flexed upwards, affecting the ability to walk.

Treatment

The most widely used drug for leprosy is dapsone (DDS). However, the emergence of dapsone-resistant strains prompted the introduction of multidrug therapy, or MDT. MDT combines dapsone, rifampin (Rifadin; also known as rifampicin), and clofazimine (Lamprene), all of which are powerful antibacterial drugs. Patients with MB leprosy are usually treated with all three drugs, while patients with PB leprosy are only given rifampin and dapsone. Usually three months after starting treatment, a patient ceases being infectious, though not everyone with this disease is necessarily infectious before treatment. Depending on the type of leprosy, the time required for treatment may vary from six months to two years or more.

Each of the drugs has minor side effects. Dapsone can cause nausea, dizziness, palpitations, jaundice and rash. A doctor should be contacted immediately if a rash develops. Dapsone also interacts with the second drug, rifampin. Rifampin increases the metabolizing of dapsone in the body, requiring an adjustment of the dapsone dosage. rifampin may also cause muscle cramps, or nausea. If jaundice, flu-like symptoms or a rash appear, a doctor should be contacted immediately. The third drug, clofazimine may cause severe abdominal pain and diarrhea, as well as discoloration of the skin. Red to brownish black discoloration of the skin and bodily fluids, including sweat, may persist for months to years after use.

Thalidomide, the most famous agent of birth defects in the twentieth century, is now being used to treat complications of leprosy and similar diseases. Thalidomide regulates the immune response by suppressing a protein, tumor necrosis factor alpha.

Leprosy patients should be aware that treatment itself can cause a potentially serious immune system response called a lepra reaction. When antibiotics kill M. leprae, antigens (the proteins on the surface of the organism that initiate the body's immune system response) are released from the dying bacteria. In some people, when the antigens combine with the antibodies to M. Leprae in the bloodstream, a reaction called erythema nodosum leprosum may occur, resulting in new lesions and peripheral nerve damage. Cortisonetype medications and, increasingly, thalidomide are used to minimize the effects of lepra reactions.

In some cases, severe ulcers caused by leprosy may be treated surgically with small skin grafts.

Prognosis

Leprosy is curable; however, the deformities and nerve damage associated with leprosy are often irreversible. Preventions or rehabilition of these defects is an integral part of management of the disease. Reconstructive surgery, aimed at preventing and correcting deformities, offers the greatest hope for disabled patients. Sometimes, the deformities are such that the patients will not benefit from this type of surgery.

Comprehensive care involves teaching patients to care for themselves. If the patients have significant nerve damage or are at high risk of developing deformities, they must be taught to take care of their insensitive limbs, similar to diabetics with lower leg nerve damage. Lacking the sensation of pain in many cases, the patients should constantly check themselves to identify cuts and bruises. If adequate care is not taken, these wounds become festering sores and a source of dangerous infection. Physiotherapy exercises are taught to the patients to maintain a range of movement in finger joints and prevent the deformities from worsening. Prefabricated standardized splints are available and are extremely effective in correcting and preventing certain common deformities in leprosy. Special kinds of footwear have been designed for patients with insensitive feet in order to prevent or minimize the progression of foot ulcers.

Prevention

By early diagnosis and appropriate treatment of infected individuals, even a disease as ancient as leprosy can be controlled. People who are in immediate contact with the leprosy patient should be tested for leprosy. Annual examinations should also be conducted on these people for a period of five years following their last contact with an infectious patient. Some physicians have advocated dapsone treatment for people in close household contact with leprosy patients.

The WHO Action Program for the Elimination of Leprosy adopted a resolution calling for the elimination of leprosy around the world by the year 2005. This goal is not likely to be reached, however; a computer simulation performed for WHO by a team of Dutch researchers in 2004 indicates that leprosy is likely to persist in some parts of the world until 2020, although its incidence will continue to decline.

KEY TERMS

Endemic area A geographical area where a particular disease is prevalent.

Gangrene Death of tissue due to loss of blood supply followed by bacterial invasion and putrefaction.

Incubation period The time it takes for symptoms to develop after initial exposure to a disease-causing organism.

Lesion Any visible, local abnormality of the tissues of the skin, such as a wound, sore, rash, or boil.

Mucous membranes The inner tissue that covers or lines body cavities or canals open to the outside, such as nose and mouth. These membranes secrete mucus and absorb water and salts.

Nasal scraping Pathological material obtained for clinical study by scratching the inner surface of the nose with a clinical instrument.

Nodules A small mass of tissue in the form of a protuberance or a knot that is solid and can be detected by touch.

Pathogen Any disease-producing agent or microorganism.

Smear A specimen prepared for microscopic study by spreading the material across a slide and treating it with a specific stain.

Resources

BOOKS

Beers, Mark H., MD, and Robert Berkow, MD., editors. "Infectious Diseases Caused by Mycobacteria." In The Merck Manual of Diagnosis and Therapy. Whitehouse Station, NJ: Merck Research Laboratories, 2004.

PERIODICALS

Buschman, E., and E. Skamene. "Linkage of Leprosy Susceptibility to Parkinson's Disease Genes." International Journal of Leprosy and Other Mycobacterial Diseases 72 (June 2004): 169-170.

Jayaseelan, A., and W. Aithal. "Pinch Skin Grafting in Non-Healing Leprous Ulcers." International Journal of Leprosy and Other Mycobacterial Diseases 72 (June 2004): 139-142.

Meima, A., W. C. Smith, G. J. van Oortmarssen, et al. "The Future Incidence of Leprosy: A Scenario Analysis." Bulletin of the World Health Organization 82 (May 2004): 373-380.

Stump, P. R., R. Baccarelli, L. H. Marciano, et al. "Neuropathic Pain in Leprosy Patients." International Journal of Leprosy and Other Mycobacterial Diseases 72 (June 2004): 134-148.

ORGANIZATIONS

American Leprosy Missions. 1 ALM Way, Greenville, SC 29601. (1-800-LEPROSY).

British Leprosy Relief Association, LEPRA. Fairfax House, Causton Road, Colchester, Essex CO1 1PU, UK.

INFOLEP, Leprosy Information Services. Postbus 95005,1090 HA, Amsterdam, Netherlands. Infolep@antenna.nl.

WHO/LEP, Action Programme for the Elimination of Leprosy. 20 Avenue Appia CH-1211, Geneva 27, Suisse. http://www.who.ch/programmes/lep/lep_home.htm.

OTHER

Cherath, Lata. "Leprosy." A Healthy Me Page. http://www.ahealthyme.com/topic/topic100587076.

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Cherath, Lata; Frey, Rebecca. "Leprosy." Gale Encyclopedia of Medicine, 3rd ed.. 2006. Encyclopedia.com. 26 Jun. 2016 <http://www.encyclopedia.com>.

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Cherath, Lata; Frey, Rebecca. "Leprosy." Gale Encyclopedia of Medicine, 3rd ed.. 2006. Retrieved June 26, 2016 from Encyclopedia.com: http://www.encyclopedia.com/doc/1G2-3451600959.html

Leprosy

Leprosy

Leprosy, also called Hansen's disease, affects 10 12 million people worldwide. Caused by an unusual bacterium called Mycobacterium leprae, leprosy primarily affects humans. Leprosy is found in tropical areas, such as Africa, South and Southeast Asia, and Central and South America. In the United States, cases of leprosy have been reported in areas of Texas, California, Louisiana, Florida, and Hawaii. Leprosy can take many forms, but the most familiar form is characterized by skin lesions and nerve damage. Although leprosy is curable with various antibiotics , it remains a devastating illness because of its potential to cause deformity, especially in the facial features. Fortunately, antibiotic regimens are available to treat and eventually cure leprosy.

Mycobacterium leprae is an unusual bacterium for several reasons. The bacterium divides slowly; in some tests, researchers have noted a dividing time of once every twelve days. This differs from the dividing time of most bacteria , which is about once every few hours. M. leprae cannot be grown on culture media, and is notoriously difficult to culture within living animals. Because of these culturing difficulties, researchers have not been able to investigate these bacteria as closely as they have other, more easily cultured, bacteria. Questions remain unanswered about M. leprae; for instance, researchers are still unclear about how the bacteria are transmitted from one person to another, and are not sure about the role an individual's genetic make up plays in the progression of the disease.

Because M. leprae almost exclusively infects humans, animal models for studying leprosy are few. Surprisingly, a few species of armadillo can also be infected with M. leprae. Recently, however, wild armadillos have been appearing with a naturally occurring form of leprosy. If the disease spreads in the armadillo population, researchers will not be able to use these animals for leprosy studies, since study animals must be completely free of the disease as well as the bacteria that cause it. Mice have also been used to study leprosy, but laboratory conditions, such as temperature, must be carefully controlled in order to sustain the infection in mice.

M. leprae is temperature-sensitive; it favors temperatures slightly below normal human body temperature. Because of this predilection, M. leprae infects superficial body tissues such as the skin, bones, and cartilage, and does not usually penetrate to deeper organs and tissues. M. leprae is an intracellular pathogen; it crosses host cell membranes and lives within these cells. Once inside the host cell, the bacterium reproduces. The time required by these slow-growing bacteria to reproduce themselves inside host cells can be anywhere from a few weeks to as much as 40 years. Eventually, the bacteria lyse (burst open) the host cell, and new bacteria are released that can infect other host cells.

Researchers assume that the bacteria are transmitted via the respiratory tract. M. leprae exists in the nasal secretions and in the material secreted by skin lesions of infected individuals. M. leprae has also been found in the breast milk of infected nursing mothers. M. leprae may be transmitted by breathing in the bacteria, through breaks in the skin, or perhaps through breast-feeding.

Leprosy exists in several different forms, although the infectious agent for all of these forms is M. leprae. Host factors such as genetic make up, individual immunity , geography, ethnicity, and socioeconomic circumstances determine which form of leprosy is contracted by a person exposed to M. leprae. Interestingly, most people who come in contact with the bacterium, about three-fourths, never develop leprosy, or develop only a small lesion on the trunk or extremity that heals spontaneously. Most people, then, are not susceptible to M. leprae, and their immune systems function effectively to neutralize the bacteria. But one-fourth of those exposed to M. leprae contract the disease, which may manifest itself in various ways.

Five forms of leprosy are recognized, and a person may progress from one form to another. The least serious form is tuberculoid leprosy. In this form, the skin lesions and nerve damage are minor. Tuberculoid leprosy is evidence that the body's cellular immune responsethe part of the immune system that seeks out and destroys infected cellsis working at a high level of efficiency. Tuberculoid leprosy is easily cured with antibiotics.

If tuberculoid leprosy is not treated promptly, or if a person has a less vigorous cellular immune response to the M. leprae bacteria, the disease may progress to a borderline leprosy, which is characterized by more numerous skins lesions and more serious nerve damage. The most severe form of leprosy is lepromatous leprosy. In this form of leprosy, the skin lesions are numerous and cause the skin to fold, especially the skin on the face. This folding of facial skin leads to the leonine (lion-like) features typical of lepromatous leprosy. Nerve damage is extensive, and people with lepromatous leprosy may lose the feeling in their extremities, such as the fingers and toes. Contrary to popular belief, the fingers and toes of people with this form of leprosy do not spontaneously drop off. Rather, because patients cannot feel pain because of nerve damage, the extremities can become easily injured.

Lepromatous leprosy occurs in people who exhibit an efficient antibody response to M. leprae but an inefficient cellular immune response. The antibody arm of the immune system is not useful in neutralizing intracellular pathogens such as M. leprae; therefore, people who initially react to invasion by M. leprae by making antibodies may be at risk for developing more severe forms of leprosy. Researchers are not sure what determines whether a person will react with a cellular response or an antibody response; current evidence suggests that the cellular immune response may be controlled by a special gene . If a person has this gene, he or she will probably develop the less severe tuberculoid leprosy if exposed to M. leprae.

Treatments for leprosy have improved considerably over the past 40 years. In fact, some experts are encouraged that the drug regimens being tested in various trials throughout the world (including the United States) may eradicate leprosy completely by the year 2010. Beginning in the 1950s, an antibiotic called dapsone was used to treat leprosy, offering the first hope of a cure for persons with the disease. Dapsone's main disadvantage was that the patient had to take the medication daily throughout his or her lifetime. In addition, the M. leprae in some patients underwent genetic mutations that rendered it resistant to the antibiotic. In the 1960s, the problem of resistance was tackled with the advent of multidrug therapy. Bacteria are less likely to become resistant to several drugs given in combination. The new multidrug treatment time was also considerably shorter-typically about four years. Currently, researchers offer a new drug combination that includes an antibiotic called oflaxicin. Oflaxicin is a powerful inhibitor of certain bacterial enzymes that are involved in DNA coiling. Without these enzymes, the M. leprae cannot copy the DNA properly and the bacteria die. The treatment time for this current regimen is about four weeks or less, the shortest treatment duration so far.

One risk of treatment, however, is that antigensthe proteins on the surface of M. leprae that initiate the host immune responseare released from the dying bacteria. In some people, when the antigens combine with antibodies to M. leprae in the bloodstream, a reaction called erythema nodosum leprosum may occur, resulting in new lesions and peripheral nerve damage. In the late 1990s, the drug thalidomide was approved to treat this reaction, with good results. Because thalidomide may cause severe birth defects, women of childbearing age must be carefully monitored while taking the drug.

A promising development in the treatment and management of leprosy is the preliminary success shown by two different vaccines. One vaccine tested in Venezuela combined a vaccine originally developed against tuberculosis , called Bacille Calmette-Guerin (BCG), and heat-killed M. leprae cultured from infected armadillos. The other vaccine uses a relative of M. leprae called M. avium. The advantage of this vaccine, currently being tested in India, is that M. avium is easy to culture on media and is thus cheaper than the Venezuelan vaccine. Both vaccines have performed well in their clinical trials, leading many to hope that a vaccine against leprosy might soon be available.

The World Health Organization announced in January, 2002, that during the previous decade, the number of active cases of leprosy worldwide had been reduced by 90%. Control of leprosy still eludes six countries, Brazil, India, Madagascar, Mozambique, Myanmar and Nepal, with approximately 700,000 ongoing cases identified worldwide in 2002. In conjunction with the World Health Organization, these countries have committed to accelerating control efforts, including early access to current drug therapy. The worldwide reduction and control of leprosy stands as one of the major world health initiatives of modern times.

See also Bacteria and bacterial infection; Mycobacterial infections, atypical

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"Leprosy." World of Microbiology and Immunology. 2003. Encyclopedia.com. 26 Jun. 2016 <http://www.encyclopedia.com>.

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leprosy

leprosy Leprosy may briefly be defined as a chronic, potentially disabling disease, mainly affecting the nerves, skin, and eyes, caused by a bacillus, Mycobacterium leprae, which microscopically resembles the organism of tuberculosis. However, a better understanding of this complex disease calls for attention to (i) the long incubation period (usually 2–5 years); (ii) the remarkable diversity of clinical findings, apparently related to the level of immunity of different individuals; (iii) the frequency of adverse (damaging) immunological reactions, based on either cell-mediated or humoral (antigen–anitbody) mechanisms (iv) its propensity to produce disability and deformity, which in some cases may be severe and widespread, affecting eyes, face, or limbs; and (v) the social and psychological consequences of leprosy for the patient, the family, and the community, sometimes leading to outright stigmatization and rejection.

Leprosy is generally believed to have originated in Asia. From India, it probably spread to China in about 500 bc and then to Japan. It may have been carried from India in the fourth century bc by returning soldiers and camp followers of the Greek wars of conquest in Asia. In Europe, leprosy was active between the tenth and fifteenth centuries and then, for reasons largely unknown, steadily declined. Fear, stigma, and awareness of the disease also declined, but reappeared a few centuries later when the imperialist and colonialist activities of the countries in Western Europe revealed large numbers of cases in Africa, Asia, and Polynesia. Chaulmoogra (hydnocarpus) oil was introduced as treatment in the nineteenth century, but its beneficial effects were short-lived and it was not until the 1940s that effective chemotherapy became available. Dr G. H. Faget of the National Leprosarium at Carville, Louisiana, US, showed that a sulphone, ‘Promin’ (glucosulphone sodium) was effective intravenously in the treatment of leprosy, and this led to the use of dapsone (di-amino di-phenyl sulphone), given as tablets by mouth, on a wide scale.

The number of registered cases in the world has decreased from 5.4 million in 1985 to 700 000 recently. They are mainly in South and Cental America, Africa and the Far East. These remarkable changes have come about largely as a result of the widespread implementation of regimens of multiple drug therapy for all cases of leprosy as recommended by (WHO) in 1982. The enormous success of these regimens led to the establishment by WHO in 1994 of an Action Programme for the Elimination of Leprosy, aimed at reducing the prevalence of leprosy worldwide to less then one case per 10 000 of the population, and thus eliminating the disease as a public health problem.

A glance at the world map of prevalence suggests that the current distribution is somewhat tropical, but in the past leprosy has been quite widespread in Europe, Scandinavia, China, Korea, and Japan. The likelihood is that its development and spread are favoured by poverty and a range of poor socio-economic conditions, including over-crowding, malnutrition, illiteracy, lack of clean water, and inadequate (or non-existent) basic health services, including immunization.

For reasons which are not understood and which are in stark contrast to the situation with tuberculosis, the current HIV/AIDS pandemic has not, as yet, had an adverse effect on diagnosis, clinical management, treatment, or the control of leprosy. Coincident cases (HIV infection and leprosy in the same patient) have been reported from various countries, but there is no general evidence that HIV infection alters the clinical course of the disease or response to treatment.

Despite much research through the years, it is still impossible to grow the causative organism, Mycobacterium leprae, in laboratory culture in an artificial medium. A breakthrough was however achieved by Charles Shepard of the US Public Health Service in 1960, when he demonstrated that the bacillus could be grown in the foot-pads of laboratory mice, thus providing for the first time a model to establish the biological identity of the bacillus, assess the value of new drugs, and study drug resistance. In 1971, Eleanor Storrs and Waldemar Kirchheimer in the US reported that the 9-banded armadillo, Dasypus novemcinctus Linn., was susceptible to inoculation with bacilli of human origin, and the model was rapidly developed in the US and elsewhere to provide enormous numbers of bacilli for vaccine research and other projects. Although these endeavours have not entirely escaped the attention of animal rights activists, the general public has remained sympathetic to the importance of research and the use of animal models in order to pursue studies aimed at the prevention and treatment of leprosy in human beings.

Somewhat disappointingly, no specific vaccine against leprosy has yet been developed. It has, however, been shown that armadillo-derived, killed leprosy bacilli, in combination with BCG (Bacille Calmette-Guérin, the standard anti-tuberculosis vaccine) offers a high degree of protection, as shown in field trials in India, though not confirmed in trials in Venezuela and Malawi. Despite impressive progress, much remains to be done in the ‘final’ push towards elimination. The WHO has recently summarized the situation as follows:
‘Leprosy elimination stands at a critical and extremely difficult juncture. This is partly because the commitment to eliminate leprosy in many endemic countries is beginning to slacken (among decision-makers and in the field). Moreover, those areas that are easy to reach and to work in, have been effectively covered. The residual problem is far more difficult — from all perspectives — and is further complicated by structural inadequacies in local health services. Even today, people in many areas do not have ready access to diagnosis and MDT (including those with long-standing disease). Therefore, achievements will no longer be sustainable if significant numbers of hidden cases remain undetected and accessibility to treatment services remains difficult’

A. Colin McDougall

Bibliography

Action Programme for the Elimination of Leprosy. Status Report, 1996. WHO/LEP/96.5 World Health Organisation, Geneva, Switzerland.
Hastings, R. C. (ed.) (1985). Leprosy, ‘Medicine in the Tropics Series’. Churchill Livingstone, Edinburgh, London, Melbourne, and New York.
Jopling, W. H. and and McDougall, A. C. (1996). Handbook of Leprosy, (5th edn) CBS Publishers and Distributors, 4596/1-A, 11-Daryaganj, New Delhi, 110 002, India.

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COLIN BLAKEMORE and SHELIA JENNETT. "leprosy." The Oxford Companion to the Body. 2001. Encyclopedia.com. 26 Jun. 2016 <http://www.encyclopedia.com>.

COLIN BLAKEMORE and SHELIA JENNETT. "leprosy." The Oxford Companion to the Body. 2001. Encyclopedia.com. (June 26, 2016). http://www.encyclopedia.com/doc/1O128-leprosy.html

COLIN BLAKEMORE and SHELIA JENNETT. "leprosy." The Oxford Companion to the Body. 2001. Retrieved June 26, 2016 from Encyclopedia.com: http://www.encyclopedia.com/doc/1O128-leprosy.html

leprosy

leprosy or Hansen's disease (hăn´sənz), chronic, mildly infectious malady capable of producing, when untreated, various deformities and disfigurements. It is caused by the rod-shaped bacteriumMycobacterium leprae, first described by G. Armauer Hansen, a Norwegian physician, in 1874. The mode of transmission is not fully understood. It is thought to be transmitted by nasal discharges and skin sores, and possibly also by contaminated objects and arthropods and by infected armadillos (which are also susceptible to the disease). Only 5% of those exposed acquire the disease. The onset is intermittent and gradual; symptoms may not appear until years after exposure. It is seldom fatal, but its involvement of the peripheral nerves destroys sensation and makes the patient prone to inadvertent injury.

Types of Leprosy

There are two forms of leprosy. In the tuberculoid form of the disease the skin lesions appear as light red or purplish spots. Tuberculoid leprosy is the more benign type, even though it is accompanied by nerve involvement, which leads to numbness (usually of the extremities), contractures, and ulceration. In lepromatous leprosy the skin lesions appear as yellow or brown infiltrated nodules (protuberances) that affect the mucous membranes of the eyes, nose, and throat. There is a general thickening of the skin, especially the face and ears. Lepromatous leprosy is the more easily spread of the two.

Diagnosis and Treatment

Since Hansen identified the bacterium that causes leprosy, diagnosis has been established by isolating the bacterium from the skin lesions or the mucous membranes of the nose and identifying it under the microscope. In 2013 a simple rapid test, using a drop of a patient's blood and some reagent, was released; developed at the Infectious Disease Research Institute, Seattle, it can detect the bacterium before symptoms develop. Duration and treatment of the disease depend upon its extent and character. Patients with nodular lesions are more difficult to treat and may succumb sooner; those with the neural type of lesion, despite possible mutilation and deformity, usually live longer and even experience spontaneous periods of subsidence of the malady. Dapsone was the drug of choice for leprosy from the 1940s until 1980, but due to drug resistance and the necessity for long-term (sometimes lifelong) treatment, it has been replaced by a combination of drugs. This combination, referred to as multiple drug therapy, has been highly effective and requires a shorter treatment period. The drug thalidomide has been approved for use against a complication of leprosy called erythema nodosum leprosum, which causes fever, skin lesions, and other symptoms.

History and Incidence

Diseases that probably included the malady now known as Hansen's disease are described as leprosy in the Bible; segregation and disinfection were advocated as methods of control (Lev. 13.14). Leprosy, which may have originated in Africa or S Asia, is believed to have existed in India and Egypt earlier than 1000 BC; a skeleton that dates to c.2000 BC and that shows possible evidence of leprosy has been found in NW India. The first clearly identifiable written reference to the disease is from an Indian source c.600 BC Infectious diseases from the East—all called leprosy—later spread over most of Europe and the British Isles, and the Crusades were a factor in disseminating them still farther, so that by the 13th cent. they had reached epidemic proportions. Leprosariums were eventually established in most countries for the care of those actually afflicted with leprosy.

The disease still occurs in tropical and subtropical countries of Asia, Africa, and Latin America—mainly Brazil, S central Africa, and India—especially where crowded and unsanitary conditions contribute to its spread. Even in the more developed countries it crops up from time to time. In the United States, the disease is found mostly in Louisiana, Texas, Florida, Hawaii, as well as in California, the Northeast, and other areas where immigrants from endemic areas have settled. Although modern treatment is effective against the disease, the number of cases in the United States has increased significantly since the 1960s. The World Health Organization is working to eradicate the disease worldwide, but progress has been more slow than was anticipated.

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Leprosy

LEPROSY

LEPROSY, or Hansen's disease, is a chronic infectious disease caused by the microorganism Mycobacterium leprae, which mainly affects the skin, the peripheral nerves, and the upper respiratory tract. A complex affliction, Hansen's disease manifests itself through skin discoloration and loss of sensation in minor cases to disfigurement and physical debilitation in the most severe and advanced cases. Equally devastating have been the social stigma, rejection, and exclusion that sufferers of Hansen's disease have endured throughout history. Although popularly regarded as incurable, contagious, and mutilating, the disease is curable, it is not highly contagious, and mutilation occurs only in the most severe cases and is not an inevitable feature of the disease's course. Because of the stigma associated with the terms "leprosy" and "leper," the disease has since the 1950s been alternatively called Hansen's disease, named after Gerhard Armauer Hansen, the Norwegian physician who identified Mycobacterium leprae in 1873.

The fear of leprosy's importation by immigrants played an important role in anti-immigrant policies and racist rhetoric directed against Chinese immigrants in the 1870s and 1880s. Notable American efforts to combat leprosy abroad were led by Victor Heiser, director of health in the American colonial administration in the Philippines, and by Joseph de Veuster (Father Damien), a Belgian priest on the Hawaiian island of Molokai. Also leprosy was endemic in regional pockets of Louisiana and the upper Midwest among French Acadian and Norwegian immigrants, respectively.

Immigrants diagnosed with leprosy were often deported to their native countries. Those who could not be deported and native-born patients with leprosy were forcibly isolated in the few leprosy hospitals that existed. The Louisiana Leper Home in Carville, Louisiana, opened in 1893 and in 1921 the federal government assumed control and designated it the national leprosarium, to which all states subsequently sent patients. It became the leading American center for medical research on leprosy, culminating in the discovery in 1941 that sulfones (sulfa-based drugs) could effectively treat the disease. The leprosarium operated continuously until June 1999, when it was closed and the care of patients with leprosy moved to outpatient centers throughout the United States. Therapeutic regimens that relied exclusively on sulfones have been supplanted by multidrug therapy programs, which the World Health Organization expected will lead to the total eradication of leprosy by 2005.

BIBLIOGRAPHY

Gussow, Zachary. Leprosy, Racism, and Public Health: Social Policy in Chronic Disease Control. Boulder, Colo.: Westview Press, 1989.

Joseph, D. George. "Americans Confront the 'Loathsome' Disease: Leprosy and Tropical Medicine in Progressive Era Massachusetts." Ph.D. diss., Yale University, 2002.

Kalisch, Philip A. "Lepers, Anachronisms, and the Progressives: A Study of Stigma, 1889–1920." Louisiana Studies: An Inter-disciplinary Journal of the South 12 (1973): 489–531.

Moran, Michelle T. "Leprosy and American Imperialism: Patient Communities and the Politics of Public Health in Hawai'i and Louisiana." Ph.D. diss., University of Illinois, Urbana-Champaign, 2002.

D. GeorgeJoseph

See alsoHealth Care .

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Leprosy

LEPROSY

Evidence of leprosy (Hansen's disease) has been detected in prehistoric human remains, and the disease has been described in Biblical and other historical records dating as far back as the 2nd millennium b.c.e. It was a feared disease, and its victims were shunned because of their disfiguring stigmatacollapsed facial bones, fingers, and toes, with the hands and feet ultimately rotted away. Leprosy was among the first diseases identified as contagious. Early societies took measures to shield their healthy members from contagion: lepers were obliged to wear distinctive clothing and carry a bell to warn others of their presence, or they were segregated in lazarettos, precursors of quarantine stations and isolation hospitals. Segregation remained part of the control measures for leprosy in modern industrial nations until late in the twentieth century, and it still persists in some countries. This is a questionable practice, because the causative acid-fast bacillus that causes leprosy is only sluggishly infective. Transmission usually requires prolonged close personal contact, and children are most vulnerable. Transmission is mainly by nasal secretions, though bedbugs have been suspected as vectors.

The lepra bacillus, Mycobacterium leprae, belongs to the same family as tuberculosis. It attacks the skin and peripheral nerves, slowly destroying tissue, deforming the extremities, and disfiguring the face; it runs a natural course over many years, and death is as often due to other infections as to leprosy itself. Worldwide, ten to twelve million people suffer from leprosy, mainly in the Indian subcontinent, parts of the Middle East, and Latin America. Approximately 500,000 new cases are reported annually with about 300 cases per year in the United States, mainly among immigrants who harbored the infection on arrival. Control requires early detection and active treatment with one or more of several effective antibiotics, such as Rifampin. Once treatment is initiated, the risk of transmission is minimized. BCG vaccine confers some resistance to infection, while HIV (human immunodeficiency virus) infection increases the risk of infection with leprosy.

Leprosy is now known as Hanson's disease, named after Armauer Hanson, the Norwegian physician who discovered the cause of the disease in 1873.

John M. Last

(see also: Contagion; Isolation; Quarantine )

Bibliography

Nelson, K. E. (1998). "Leprosy." In Maxcy-Rosenau-Last Public Health and Preventive Medicine, 14th edition. ed. R. B. Wallace. Stamford, CT: Appleton & Lange.

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leprosy

leprosy (Hansen's disease) (lep-rŏ-si) n. a chronic disease, caused by the bacterium Mycobacterium leprae, that affects the skin, mucous membranes, and nerves. It is confined mainly to the tropics and is transmitted by direct contact. Symptoms mainly involve the skin and nerves. Leprosy should be treated with a combination of antibacterial drugs (including dapsone and rifampicin), to overcome the problem of resistance developing to a single drug, and reconstructive surgery can repair some of the damage caused by the disease. indeterminate l. a form of the disease in which the skin manifestations represent a combination of lepromatous and tuberculoid leprosy. lepromatous (or multibacillary) l. a contagious steadily progressive form of the disease characterized by the development of widely distributed lumps on the skin, thickening of the skin and nerves, and in serious cases by severe numbness of the skin, muscle weakness, and paralysis leading to disfigurement and deformity. Tuberculosis is a common complication. paucibacillary l. tuberculoid or indeterminate leprosy. tuberculoid l. a benign, often self-limiting, form of leprosy causing discoloration and disfiguration of patches of skin associated with localized numbness.

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leprosy

leprosy (Hansen's disease) Chronic, progressive condition affecting the skin and nerves, caused by infection with the microorganism Mycobacterium leprae. There are two main forms. Lepromatous leprosy is a contagious form in which raised nodules appear on the skin and there is thickening of the skin and peripheral nerves. In tuberculoid leprosy, there is loss of sensation in parts of the skin, sometimes with loss of pigmentation and hair. Now confined almost entirely to the tropics, leprosy can be treated with a combination of drugs, but the nerve damage is irreversible.

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Leprosy

Leprosy

What Is Leprosy?

How Common Is Leprosy?

Is the Disease Contagious?

What Are the Signs and Symptoms?

How Is Leprosy Diagnosed?

Can Leprosy Be Treated?

What Are the Complications and Course of Leprosy?

How Can Leprosy Be Prevented?

Resources

Leprosy (LEH-pro-see) is a chronic*, infectious disease that damages the skin, peripheral nerves*, and mucous membranes* of the mouth, throat, and eyes. Leprosy also is known as Hansen disease.

*chronic
(KRAH-nik) means continuing for a long period of time.
*peripheral
(puh-RIH-fer-ul) nerves are a network of nerve fibers throughout the body that send and receive messages to and from the central nervous system (the brain and spinal cord).
*mucous membranes
are the moist linings of the mouth, nose, eyes, and throat.

KEYWORDS

for searching the Internet

and other reference sources

Hansen disease

Lepromatous leprosy

Multibacillary Hansen disease

Mycobacterium leprae

Paucibacillary Hansen disease

Tuberculoid leprosy

What Is Leprosy?

His equipment was inadequate and his colleagues thought his theories were laughable. Still, Gerhard Henrik Armauer Hansen (18411912) spent day after day bent over his microscope, determined to prove that leprosy was caused by bacteria. And he did. In 1873 the Norwegian physician identified the rod-shaped bacterium Mycobacterium leprae (my-ko-bak-TEER-e-um LEH-pray) as the cause of the illness. Hansens discovery was immensely valuable in the treatment of leprosy, and it was a scientific milestonethe first proof that bacteria could cause human disease. Today, the use of the word leper is considered insulting, because it defines a person by the disease he or she has. Many advocates for people with leprosy prefer to call it Hansen disease.

The name paucibacillary (paw-sih-BAH-sih-lair-e) Hansen disease comes from the Latin word pauci, meaning few, and is used to describe a mild form of leprosy. Paucibacillary Hansen disease begins in the peripheral nerves and spreads to the skin, causing patches of skin to become numb and hypopigmented, which means that the skin has lost its coloring and appears white. Multibacillary (mul-tie-BAH-sih-lair-e) Hansen disease is a more severe form of the disease. Multibacillary Hansen disease also causes skin lesions (LEE-zhuns), or patches of damaged tissue; nodules, or lumps; and thickening of the skin. Without treatment, this type of leprosy can worsen over time, resulting in severe skin and tissue damage and disfigurement.

3,000 Years of Leprosy

Leprosy has left a trail of pain, suffering, and death that dates back thousands of years. Archeologists have uncovered skeletal remains with erosion in the bones of the nose that is characteristic of leprosy. Researchers translating from ancient Indian and Chinese texts have found descriptions of the disease. As men and armies roamed the globe in search of conquest, the germ that causes leprosy traveled with them. Researchers believe that in the first century B.C., Roman soldiers fighting in Egypt carried the disease home to Italy. In the Middle Ages, the disease spread from Italy throughout Europe. During the Crusades, a series of holy wars spanning the eleventh to the thirteenth centuries, European soldiers and pilgrims carried the disease as far as Jerusalem in the Middle East. The disease continued to follow the paths of conquering armies. The Spanish conquistadors and the slave trade brought the disease to the American continents, and European colonists probably spread the disease to islands in the Pacific Ocean.

How Common Is Leprosy?

Throughout human history leprosy has caused untold suffering. Even after Hansens groundbreaking discovery, the disease remained unchecked in many parts of the world. In 1991, the World Health Organization (WHO) began a global campaign to reduce the number of cases of leprosy. A decade later the organization announced that it had reached its goal and estimated that there were at that time 600,000 to 750,000 cases of leprosy worldwide. The disease is most common in tropical and subtropical regions, and in 2001, it remained a particular problem in Brazil, India, Madagascar, Mozambique, Nepal, and Myanmar. Leprosy is most common in densely populated areas with poor sanitation and health care, and children are at greater risk than adults of getting the disease. In the United States about 100 cases are reported each year, many of them in people who have recently immigrated.

Is the Disease Contagious?

Leprosy is contagious but does not spread easily. Researchers believe that Mycobacterium leprae is transmitted from person to person via respiratory droplets, bits of moisture that leave the mouth or nose when a person laughs, talks, sneezes, or coughs. Most people seem to have a natural immunity* that enables them to resist the disease. Of those in whom leprosy is diagnosed, most have had prolonged and close contact with someone who has an active infection. Once a person with leprosy has been taking medication for 3 or 4 days, the disease is no longer active or contagious.

*immunity
(ih-MYOON-uh-tee) is the condition of being protected against an infectious disease. Immunity often develops after a germ is introduced to the body. One type of immunity occurs when the body makes special protein molecules called antibodies to fight the disease-causing germ. The next time that germ enters the body, the antibodies quickly attack it, usually preventing the germ from causing disease.

What Are the Signs and Symptoms?

Leprosy begins as an infection in the nerve endings and spreads gradually; the skin near the infected nerves may become numb and hypopigmented. In severe cases, these skin lesions become wider and thicker. The muscles in the hands and feet can become weak or paralyzed (unable to move) because of damage to the peripheral nerves. That loss of sensation can lead to accidental injury, because a person loses the withdrawal reflex that helps protect against injury from hot or sharp objects. Left unchecked, the most severe form of the disease can progress, producing large, disfiguring nodules and enlarged facial features that give a person the lionlike appearance associated with severe leprosy.

How Is Leprosy Diagnosed?

Leprosy is not difficult to diagnose once it is suspected. A procedure in which a tiny piece of skin is scraped or cut away and then examined usually reveals the presence of Mycobacterium leprae in the multibacillary form of leprosy. (The bacteria may not be found using this method in milder, paucibacillary disease.) The procedure can be done quickly and relatively painlessly in a doctors office or clinic. It is an important part

of the diagnosis, because in the early stages of the disease leprosy lesions look very much like skin damage caused by other neurocutaneous* diseases. The presence of the characteristic lesions, accompanied by a history of living in areas where the disease is common, is what usually causes doctors to suspect the diagnosis.

*neurocutaneous
(nur-o-kyoo-TAY-nee-us) means affecting the skin and nerves.

As long ago as biblical times, people with the disfiguring signs of leprosy were cast out of their homes and villages and made to live together in isolated colonies. Even in modern times such colonies were established in the Western world, for example, on Penikese Island off Massachusetts and on the Hawaiian island of Molokai. Corbis Corporation (Bellevue)

Can Leprosy Be Treated?

Early diagnosis and treatment are key to stopping the spread of leprosy to other people and preventing long-term damage to the patient. Doctors most often prescribe multidrug therapy (MDT), combining two or three drugs that kill the bacteria: dapsone (DAP-sone), rifampicin (rye-FAM-pih-sin), and clofazimine (klo-FAY-zuh-meen). The MDT approach has been preferred since the early 1980s, when researchers noticed that the bacterium was becoming resistant to some treatments. Patients may take the drugs for as little as 6 months or as long as 2 years. Patients who have become disfigured or who experience disabilities may need surgery to correct these problems.

What Are the Complications and Course of Leprosy?

With MDT, paucibacillary Hansen disease can be cured within 6 to 12 months and multibacillary Hansen disease within 2 years. Untreated, leprosy can cause blindness, permanent nerve damage, and deformity. People may lose the use of their hands or feet, because, over time, the decreased sensation may result in repeated injuries to the limbs.

How Can Leprosy Be Prevented?

Despite centuries in which people with leprosy were vilified, shunned, and even isolated in far-off leper colonies, there is no need to separate people with leprosy from the rest of society to avoid the spread of infection. MDT treatment is more effective and far more humane, and it has been determined that leprosy is much less contagious than once was believed. Hand washing, disinfection, and monitoring of close contacts are recommended to help prevent the spread of the disease.

See also

Public Health

Resources

Book

Eynikel, Hilde. Molokai: The Story of Father Damien. Translated by Lesley Gilbert. New York: Alba House, 1999. This is the story of the Belgian priest who cared for thousands of people with leprosy who were banished to the remote island of Molokai in the Hawaiian Islands. The book was made into a movie by the same name that is available on DVD.

Organization

World Health Organization (WHO), Avenue Appia 20, 1211 Geneva 27, Switzerland. The WHO tracks efforts to eradicate leprosy and has links to fact sheets and information on the prevention and control of the disease on its website.

Telephone 011-41-22-791-2111 http://www.who.int

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leprosy

lep·ro·sy / ˈleprəsē/ • n. a contagious disease caused by the bacterium Mycobacterium leprae that affects the skin, mucous membranes, and nerves, causing discoloration and lumps on the skin and, in severe cases, disfigurement and deformities. Leprosy is now mainly confined to tropical Africa and Asia. Also called Hansen's disease.

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leprosy

leprosy now mainly confined to tropical Africa and Asia, leprosy was common in medieval Europe, and those afflicted by it were forced to live apart from the community.

Traditional allusions tend to refer to the pallor of the skin in someone suffering from the illness.

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leprosy

leprosy •radiancy •immediacy, intermediacy •expediency • idiocy • saliency •resiliency • leniency •incipiency, recipiency •recreancy • pruriency • deviancy •subserviency • transiency • pliancy •buoyancy, flamboyancy •fluency, truancy •constituency • abbacy • embassy •celibacy • absorbency •incumbency, recumbency •ascendancy, intendancy, interdependency, pendency, resplendency, superintendency, tendency, transcendency •candidacy •presidency, residency •despondency • redundancy • infancy •sycophancy • argosy • legacy •profligacy • surrogacy •extravagancy • plangency • agency •regency •astringency, contingency, stringency •intransigency • exigency • cogency •pungency •convergency, emergency, insurgency, urgency •vacancy • piquancy • fricassee •mendicancy • efficacy • prolificacy •insignificancy • delicacy • intricacy •advocacy • fallacy • galaxy •jealousy, prelacy •repellency • valency • Wallasey •articulacy • corpulency • inviolacy •excellency • equivalency • pharmacy •supremacy • clemency • Christmassy •illegitimacy, legitimacy •intimacy • ultimacy • primacy •dormancy • diplomacy • contumacy •stagnancy •lieutenancy, subtenancy, tenancy •pregnancy •benignancy, malignancy •effeminacy • prominency •obstinacy • pertinency • lunacy •immanency •impermanency, permanency •rampancy • papacy • flippancy •occupancy •archiepiscopacy, episcopacy •transparency • leprosy • inerrancy •flagrancy, fragrancy, vagrancy •conspiracy • idiosyncrasy •minstrelsy • magistracy • piracy •vibrancy •adhocracy, aristocracy, autocracy, bureaucracy, democracy, gerontocracy, gynaecocracy (US gynecocracy), hierocracy, hypocrisy, meritocracy, mobocracy, monocracy, plutocracy, technocracy, theocracy •accuracy • obduracy • currency •curacy, pleurisy •confederacy • numeracy •degeneracy • itinerancy • inveteracy •illiteracy, literacy •innocency • trenchancy • deficiency •fantasy, phantasy •intestacy • ecstasy • expectancy •latency • chieftaincy • intermittency •consistency, insistency, persistency •instancy • militancy • impenitency •precipitancy • competency •hesitancy • apostasy • constancy •accountancy • adjutancy •consultancy, exultancy •impotency • discourtesy •inadvertency • privacy •irrelevancy, relevancy •solvency • frequency • delinquency •adequacy • poignancy

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