|Classification and external resources|
A 24-year-old man from Norway, infected with leprosy, 1886.
|eMedicine||med/1281 derm/223 neuro/187|
Leprosy, also known as Hansen's disease (HD), is a chronic infection caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis. Initially infections are without symptoms and typically remain this way for 5 to as long as 20 years. Symptoms that develop include granulomas of the nerves, respiratory tract, skin, and eyes. This may result in a lack of ability to feel pain and thus loss of parts of extremities due to repeated injuries. Weakness and poor eyesight may also be present.
There are two main types of disease based on the number of bacteria present: paucibacillary and multibacillary. The two types are differentiated by the number of poorly pigmented numb skin patches present, with paucibacillary having five or fewer and multibacillary having more than five. The diagnosis is confirmed by finding acid-fast bacilli in a biopsy of the skin or via detecting the DNA by polymerase chain reaction. It occurs more commonly among those living in poverty and is believed to be transmitted by respiratory droplets. It is not very contagious.
Leprosy is curable with treatment. Treatment for paucibacillary leprosy is with the medications dapsone and rifampicin for 6 months. Treatment for multibacillary leprosy consists of rifampicin, dapsone, and clofazimine for 12 months. These treatments are provided for free by the World Health Organization. A number of other antibiotics may also be used. Globally in 2012 the number of chronic cases of leprosy was 189,000 and the number of new cases was 230,000. The number of chronic cases has decreased from some 5.2 million in the 1980s. Most new cases occur in 16 countries, with India accounting for more than half. In the past 20 years, 16 million people worldwide have been cured of leprosy.
Leprosy has affected humanity for thousands of years. The disease takes its name from the Latin word lepra, which means "scaly", while the term "Hansen's disease" is named after the physician Gerhard Armauer Hansen. Separating people in leper colonies still occurs in countries like India, where there are more than a thousand; China, where there are hundreds; and in the continent of Africa. However, most colonies have closed. Leprosy has been associated with social stigma for much of history, which remains a barrier to self-reporting and early treatment. World Leprosy Day was started in 1954 to draw awareness to those affected by leprosy.
- 1 Signs and symptoms
- 2 Cause
- 3 Pathophysiology
- 4 Diagnosis
- 5 Prevention
- 6 Treatment
- 7 Epidemiology
- 8 History
- 9 Society and culture
- 10 References
- 11 External links
Signs and symptoms
Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external sign. Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs and eyes. Contrary to folklore, leprosy does not cause body parts to fall off, although they can become numb or diseased as a result of secondary infections; these occur as a result of the body's defenses being compromised by the primary disease. Secondary infections, in turn, can result in tissue loss causing fingers and toes to become shortened and deformed, as cartilage is absorbed into the body.
Mycobacterium leprae and Mycobacterium lepromatosis are the causative agents of leprosy. M. lepromatosis is a relatively newly identified mycobacterium isolated from a fatal case of diffuse lepromatous leprosy in 2008.
Due to extensive loss of genes necessary for independent growth, M. leprae and M. lepromatosis are obligate pathogens, and unculturable in the laboratory, a factor that leads to difficulty in definitively identifying the organism under a strict interpretation of Koch's postulates. The use of non-culture-based techniques such as molecular genetics has allowed for alternative establishment of causation.
While the causative organisms have to date been impossible to culture in vitro, it has been possible to grow them in animals.
Several genes have been associated with a susceptibility to leprosy. It is believed that around 95% of people are naturally immune. Recent research suggests that there is a defect in cell-mediated immunity that causes susceptibility to leprosy. 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.
At highest risk are those living in areas with polluted water and poor diet or people suffering from diseases that compromise immune function.
Although the mode of transmission of leprosy remains uncertain, many think that M. leprae is usually spread from person to person in nasal droplets. Studies have shown that leprosy can be transmitted to humans by armadillos. Leprosy is not known to be either sexually transmitted or highly infectious after treatment. Approximately 95% of people are naturally immune and sufferers are no longer infectious after as little as two weeks of treatment.
The precise mechanism of transmission of leprosy is unknown; however, both prolonged close contact and transmission by nasal droplet are thought to be implicated. In addition to humans, leprosy has been observed in the nine-banded armadillo, (which, it has recently been confirmed, is among the primary sources of new cases of leprosy in the population of North America), and three species of non-human primates. The bacterium can also be grown in the laboratory by injection into the footpads of mice. There is evidence that not all people who are infected with M. leprae develop leprosy, and genetic factors have long been thought to play a role, due to the observation of clustering of leprosy around certain families, and the failure to understand why certain individuals develop lepromatous leprosy while others develop other types of leprosy. It is estimated that due to genetic factors, only 5% of the population is susceptible to leprosy. This is mostly because the body is naturally immune to the bacteria, and those persons that do become infected experience severe allergic reactions to the disease. However, the role of genetic factors is not entirely clear in determining this clinical expression. In addition, malnutrition and prolonged exposure to infected persons may play a role in development of the overt disease.
The most widely held belief is that the disease is transmitted by contact between infected persons and healthy persons. In general, closeness of contact is related to the dose of infection, which in turn is related to the occurrence of disease. Of the various situations that promote close contact, contact within the household is the only one that is easily identified, although the incidence among contacts and the relative risk for them appear to vary considerably in different studies. In incidence studies, infection rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per year in Cebu, Philippines to 53 per 1000 per year in part of Western India to 55.8 per 1000 per year in a part of Southern India
Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not clear. Lepromatous cases show large numbers of organisms deep in the dermis, but 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 (sloughing of superficial layer of skin) of the skin, Weddell et al. had reported in 1963 that they could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and contacts. In a recent study, Job et al. found fairly large numbers of M. leprae in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with the sebaceous secretions.
The importance of the nasal mucosa was recognized as early as 1898 by Schäffer, in particular that of the ulcerated mucosa. The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy was demonstrated by Shepard as large, with counts ranging from 10,000 to 10,000,000. Pedley reported that the majority of lepromatous patients showed leprosy bacilli in their nasal secretions as collected through blowing the nose. Davey and Rees indicated that nasal secretions from lepromatous patients could yield as much as 10 million viable organisms per day.
The entry route of M. leprae into the human body is also not definitively known: The skin and the upper respiratory tract are most likely. While older research dealt with the skin route, recent research has increasingly favored the respiratory route. Rees and McDougall succeeded in the experimental transmission of leprosy through aerosols containing M. leprae in immune-suppressed mice, suggesting a similar possibility in humans. Successful results have also been reported on experiments with nude mice when M. leprae were introduced into the nasal cavity by topical application. In summary, entry through the respiratory route appears the most probable route, although other routes, particularly broken skin, cannot be ruled out.
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 disease's slow onset. 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. 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 three and five years.
Per the World Health Organization, diagnosis in an endemic area is based on one of the following cardinal signs:
- Skin lesion consistent with leprosy and with definite sensory loss
- Positive skin smears
Skin lesions can be single or multiple, usually hypopigmented although occasionally reddish or copper colored. The lesions may be macules (flat), papules (raised), or nodular. Sensory loss at the skin lesion is important because this feature can help differentiate from other causes of skin lesions such as tinea versicolor.
Thickened nerves are associated with leprosy and can be accompanied by loss of sensation, muscle weakness. However, without the characteristic skin lesion and without the sensory loss and/or muscle weakness is not considered a reliable sign of leprosy.
Diagnosis in the U.S. is often delayed because healthcare providers are unaware of leprosy and its symptoms. Early diagnosis and treatment prevents nerve involvement, the hallmark of leprosy, and the disability it causes.
There are many kinds of leprosy but there are common symptoms, including: runny nose; dry scalp; eye problems; skin lesions; muscle weakness; reddish skin; smooth shiny diffuse thickening of facial skin, ear, and hand; loss of sensation in fingers and toes; thickening of peripheral nerves; and flat nose due to destruction of nasal cartilage. There is also phonation and resonation of sound during speech. Often there is atrophy of the testes and impotency.
There are several different approaches for classifying leprosy; however, parallels exist.
- The World Health Organization system distinguishes "paucibacillary" and "multibacillary" based upon the proliferation of bacteria("pauci-" refers to a low quantity.)
- The SHAY scale provides five gradations.
- The ICD-10, though developed by the WHO, uses Ridley-Jopling and not the WHO system. It also adds an indeterminate ("I") entry.
- In MeSH, three groupings are used.
|WHO||Ridley-Jopling||ICD-10||MeSH||Description||Lepromin test||Immune target|
borderline tuberculoid ("BT")
|A30.1, A30.2||Tuberculoid||It is characterized by one or more hypopigmented skin macules and anaesthetic patches, where skin sensations are lost because of damaged peripheral nerves that have been attacked by the human host's immune cells.||Positive||bacillus (Th1)|
|Multibacillary||midborderline or borderline ("BB")||A30.3||Borderline||Borderline leprosy is of intermediate severity and 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.|
|Multibacillary||borderline lepromatous ("BL"),
and lepromatous ("LL")
|A30.4, A30.5||Lepromatous||It is associated with symmetric skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting in nasal congestion and epistaxis (nose bleeds), but, typically, detectable nerve damage is late.||Negative||plasmid inside bacillus
 (Th2)
There is a difference in immune response to the tuberculoid and lepromatous forms.
Leprosy may also be divided into the following types::344–346
Medications can decrease the risk of those living with people with leprosy from acquiring the disease and likely those with whom people with leprosy come into contact outside the home. There are however concerns of resistance, cost, and disclosure of a person's infection status when doing follow up of contacts, thus the WHO however recommends that people who live in the same household be examined for leprosy and only be treated if symptoms are present.
The Bacillus Calmette–Guérin (BCG) vaccine offers a variable amount of protection against leprosy in addition to tuberculosis. It appears to be 26 to 41% effective (based on controlled trials) and about 60% effective based on observational studies with two doses possibly working better than one. Development of a more effective vaccine is ongoing as of 2011.
A number of leprostatic agents are available for treatment. For paucibacillary (PB or tuberculoid) cases treatment with daily dapsone and monthly rifampicin for six months is recommended. While for multibacillary (MB or lepromatous) cases treatment with daily dapsone and clofazimine along with monthly rifampicin for twelve months is recommended.
Multi-drug therapy (MDT) remains highly effective, and people 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.
Globally in 2012 the number of cases of leprosy was 180,000. In 2011 the approximate number of new cases diagnosed was 220,000. The number of cases has decreased significantly from the 1960s to the 2010s.
In 1995 two to three million people were estimated to be permanently disabled because of leprosy. India has the greatest number of cases, with Brazil second and Myanmar third. In 2000, the World Health Organization (WHO) listed 91 countries in which leprosy is endemic. India, Burma, and Nepal contained 70% of cases. India reports over 50% of the world's leprosy 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 leprosy cases. Although the number of cases worldwide continues to fall, 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.
While the number of cases of leprosy was in the tens of millions in the 1960s, a series of national (The International Federation of Anti-Leprosy Associations) and international (the WHO's "Global Strategy for Reducing Disease Burden Due to Leprosy") initiatives have reduced the total number and the number of new cases the disease.
Although the number of new leprosy cases occurring each year is important as a measure of transmission, it is difficult to measure due to leprosy's long incubation period, delays in diagnosis after onset of the disease, and the lack of laboratory tools to detect it in the 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 receiving 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.
New case detection is another indicator of the disease that is 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).
Endemic countries also report the number of new cases with established disabilities at the time of detection, as an indicator of the backlog prevalence. Determination of the time of onset of the disease is, in general, unreliable, is very labor-intensive, and is seldom done in recording these statistics.
Evidence of leprosy dates back to ancient Egypt in 4000 BC and was discussed by Hippocrates in 460 BC. It was recognized in the civilizations of ancient China, Egypt, Israel, and India. The earliest proven human case was verified by DNA taken from the shrouded remains of a man discovered in a tomb next to the Old City of Jerusalem dated by radiocarbon methods to 1–50 AD.
The term leprosy is derived from either the Indo-European term lap, which means the removal of scales, or the Greek word for "scales", lepia. Historically, people infected were often confined against their will in leper colonies and in Medieval Europe were required to carry a bell to identify their presence. Attempted treatments have included arsenic, elephants' teeth, creosote, and mercury.
The causative agent of leprosy, Mycobacterium leprae, was discovered by G. H. Armauer Hansen in Norway in 1873, making it the first bacterium to be identified as causing disease in humans. The first effective treatment (promin) became available in the 1940s. In the 1950s dapsone was introduced. The search for further effective anti-leprosy drugs led to the use of clofazimine and rifampicin in the 1960s and 1970s. Later, Indian scientist Shantaram Yawalkar and his colleagues formulated a combined therapy using rifampicin and dapsone, intended to mitigate bacterial resistance. Multidrug therapy (MDT) combining all three drugs was first recommended by the WHO in 1981. These three anti-leprosy drugs are still used in the standard MDT regimens.
Leprosy was once believed to be highly contagious and was treated with mercury—all of which applied to syphilis, which was first described in 1530. It is possible that many early cases thought to be leprosy could actually have been syphilis. Effective treatment first appeared in the late 1940s. Resistance has developed to initial treatment. It was not until the introduction of MDT in the early 1980s that the disease could be diagnosed and treated successfully within the community.
Many English translations of the Bible translate tzaraath as "leprosy," a confusion that derives from the use of the koine cognate "Λέπρα" (which can mean any disease causing scaly skin) in the Septuagint. Ancient sources such as the Talmud (Sifra 63) make clear that tzaraath refers to various types of lesions or stains associated with ritual impurity and occuring on cloth, leather, or houses as well as skin. While it may sometimes be a symptom of the disease described in this article, but has many other causes as well.
Society and culture
Between 1995 and 1999, WHO, with the aid of the Nippon Foundation, supplied all endemic countries with free Multi-Drug Treatment (MDT) in blister packs, channelled through ministries of health. This free provision was extended in 2000 and again in 2005 with donations by the MDT manufacturer Novartis through WHO. In the latest agreement signed between the company and WHO in October 2010, the provision of free MDT by WHO to all endemic countries will now run until at least the end of 2015. At the national level, non-government organizations (NGOs) affiliated with the national programme will continue to be provided with an appropriate free supply of this WHO-supplied MDT by the government.
Stigma in India
People with leprosy in India, like many parts of the world, suffer under some of the worst conditions and stereotypes. Depending on the level of disfigurement, a leper could receive harsher stigma and ostracism. People with leprosy earn less: 16–44% of them report their pay dropped as a result of having leprosy. Women suffer greater restrictions and social stigma than men. Leprosy prevents mothers from getting too close to their children out of fear that they could infect them. In a report, 49% of women stopped breast-feeding their babies as a result of having leprosy. Doctors and other health care providers and NGOs are working hard to educate people about the disease. In one study when leprosy treatment and education were mixed in with the local healthcare program, the attitudes towards the disease were somewhat alleviated as people had a better understanding of it. Now the disease prevalence has been reduced to less than 1 per million population in most parts of the country.
- Saint Damien DeVeuster, a Roman Catholic priest from Belgium, ministered to the people with leprosy who had been placed under a government-sanctioned medical quarantine on the island of Molokaʻi in the Kingdom of Hawaiʻi.
- Baldwin IV of Jerusalem was a Christian king of Latin Jerusalem, afflicted with leprosy. Baldwin, and the effects of his disease, were portrayed in the film Kingdom of Heaven.
- Vietnamese poet Han Mac Tu
- Ōtani Yoshitsugu, a Japanese daimyo
- "Leprosy Fact sheet N°101". World Health Organization. Jan 2014.
- "New Leprosy Bacterium: Scientists Use Genetic Fingerprint To Nail 'Killing Organism'". ScienceDaily. 2008-11-28. Retrieved 2010-01-31.
- Suzuki K, Akama T, Kawashima A, Yoshihara A, Yotsu RR, Ishii N (February 2012). "Current status of leprosy: epidemiology, basic science and clinical perspectives.". The Journal of dermatology 39 (2): 121–9. doi:10.1111/j.1346-8138.2011.01370.x. PMID 21973237.
- "Global leprosy situation, 2012". Wkly. Epidemiol. Rec. 87 (34): 317–28. August 2012. PMID 22919737.
- Rodrigues LC, Lockwood DNj (June 2011). "Leprosy now: epidemiology, progress, challenges, and research gaps.". The Lancet infectious diseases 11 (6): 464–70. doi:10.1016/S1473-3099(11)70006-8. PMID 21616456.
- Walsh F (2007-03-31). "The hidden suffering of India's lepers". BBC News.
- Lyn TE (2006-09-13). "Ignorance breeds leper colonies in China". Independat News & Media. Retrieved 2010-01-31.
- Byrne, Joseph P. (2008). Encyclopedia of pestilence, pandemics, and plagues. Westport, Conn.[u.a.]: Greenwood Press. p. 351. ISBN 9780313341021.
- McMenamin, Dorothy (2011). Leprosy and stigma in the South Pacific : a region-by-region history with first person accounts. Jefferson, N.C.: McFarland. p. 17. ISBN 9780786463237.
- Kenneth J. Ryan, C. George Ray, editors. (2004). Ryan KJ, Ray CG, ed. Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 451–3. ISBN 0-8385-8529-9. OCLC 52358530 61405904.
- "Lifting the stigma of leprosy: a new vaccine offers hope against an ancient disease". Time 119 (19): 87. May 1982. PMID 10255067.
- Kulkarni GS (2008). Textbook of Orthopedics and Trauma (2 ed.). Jaypee Brothers Publishers. p. 779. ISBN 9788184482423.
- "Q and A about leprosy". American Leprosy Missions. Retrieved 2011-01-22. "Do fingers and toes fall off when someone gets leprosy? No. The bacillus attacks nerve endings and destroys the body's ability to feel pain and injury. Without feeling pain, people injure themselves on fire, thorns, rocks, even hot coffee cups. Injuries become infected and result in tissue loss. Fingers and toes become shortened and deformed as the cartilage is absorbed into the body."
- McMurray DN (1996). Mycobacteria and Nocardia. in: Baron's Medical Microbiology (Baron S et al., eds.) (4th ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1. OCLC 33838234.
- Bhattacharya S, Vijayalakshmi N, Parija SC (1 October 2002). "Uncultivable bacteria: Implications and recent trends towards identification". Indian journal of medical microbiology 20 (4): 174–7. PMID 17657065.
- Meredith, Anna; Del Pozo, Jorge; Smith, Sionagh; Milne, Elspeth; Stevenson, Karen; McLuckie, Joyce (September 2014). "Leprosy in red squirrels in Scotland". Veterinary Record 175 (11): 285–286. doi:10.1136/vr.g5680.
- "Functional Haplotypes That Produce Normal Ficolin-2 Levels Protect against Clinical Leprosy". Oxford Journals. Retrieved March 8, 2014.
- Buschman E, Skamene E (Jun 2004). "Linkage of leprosy susceptibility to Parkinson's disease genes" (PDF). International journal of leprosy and other mycobacterial diseases 72 (2): 169–70. doi:10.1489/1544-581X(2004)072<0169:LOLSTP>2.0.CO;2. ISSN 0148-916X. PMID 15301585. Retrieved January 31, 2011.
- Lockwood DN, Lambert SM (January 2011). "Human immunodeficiency virus and leprosy: an update.". Dermatologic clinics 29 (1): 125–8. doi:10.1016/j.det.2010.08.016. PMID 21095536.
- "Probable Zoonotic Leprosy in the Southern United States". The New England Journal of Medicine. Retrieved April 28, 2011.
- "Armadillos linked to leprosy in humans". CNN. 2011-04-28.
- Truman RW, Singh P, Sharma R, Busso P, Rougemont J, Paniz-Mondolfi A, Kapopoulou A, Brisse S, Scollard DM, Gillis TP, Cole ST (April 2011). "Probable Zoonotic Leprosy in the Southern United States". The New England Journal of Medicine (Massachusetts Medical Society) 364 (17): 1626–1633. doi:10.1056/NEJMoa1010536. PMC 3138484. PMID 21524213.
- "Leprosy". WHO. 2009-08-01. Retrieved 2010-01-31.
- Rojas-Espinosa O, Løvik M (2001). "Mycobacterium leprae and Mycobacterium lepraemurium infections in domestic and wild animals". Rev. - Off. Int. Epizoot. 20 (1): 219–51. PMID 11288514.
- Hastings RC, Gillis TP, Krahenbuhl JL, Franzblau SG (1988-07-01). "Leprosy". Clin. Microbiol. Rev. 1 (3): 330–48. PMC 358054. PMID 3058299.
- Alcaïs A, Mira M, Casanova JL, Schurr E, Abel L (2005). "Genetic dissection of immunity in leprosy". Curr. Opin. Immunol. 17 (1): 44–8. doi:10.1016/j.coi.2004.11.006. PMID 15653309.
- "AR Dept of Health debunks leprosy fears". 2008-02-08. Retrieved 2008-04-08.
- Kaur H, Van Brakel W; Van Brakel (2002). "Dehabilitation of leprosy-affected people—a study on leprosy-affected beggars". Leprosy review 73 (4): 346–55. PMID 12549842.
- Doull JA (1942). "The incidence of leprosy in Cordova and Talisay, Cebu, Philippines". International Journal of Leprosy 10: 107–131.
- Noordeen SK, Neelan PN; Neelan (1978). "Extended studies on chemoprophylaxis against leprosy". Indian J Med Res 67: 515–27. PMID 355134.
- "What Is Leprosy?" THE MEDICAL NEWS | from News-Medical.Net - Latest Medical News and Research from Around the World. Web. 20 Nov. 2010. <http://www.news-medical.net/health/What-is-Leprosy.aspx>.
- Weddell G, Palmer E; Palmer (1963). "The pathogenesis of leprosy. An experimental approach". Leprosy Review 34: 57–61. PMID 13999438.
- Job CK, Jayakumar J, Aschhoff M; Jayakumar; 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): 164–7. PMID 10472371.
- Arch Dermato Syphilis 1898; 44:159–174
- Shepard CC (1960). "Acid-fast bacilli in nasal excretions in leprosy, and results of inoculation of mice". Am J Hyg 71: 147–57. PMID 14445823.
- Pedley JC (1973). "The nasal mucus in leprosy". Lepr Rev 44 (1): 33–5. PMID 4584261.
- Davey TF, Rees RJ; Rees (1974). "The nasal discharge in leprosy: clinical and bacteriological aspects". Lepr Rev 45 (2): 121–34. PMID 4608620.
- Rees RJ, McDougall AC; McDougall (1977). "Airborne infection with Mycobacterium leprae in mice". J Med Microbiol 10 (1): 63–8. doi:10.1099/00222615-10-1-63. PMID 320339.
- Chehl S, Job CK, Hastings RC; Job; Hastings (1985). "Transmission of leprosy in nude mice". Am J Trop Med Hyg 34 (6): 1161–6. PMID 3914846.
- Montestruc E, Berdonneau R; Berdonneau (1954). "2 New cases of leprosy in infants in Martinique". Bull Soc Pathol Exot Filiales (in French) 47 (6): 781–3. PMID 14378912.
- "Diagnosis of Leprosy." WHO. from http://www.who.int/lep/diagnosis/en/ accessed on 14 July 2014.
- U.S. Department of Health and Human Services, Health Resources and Services Administration. (n.d.). National Hansen's disease (leprosy) program Retrieved from http://www.hrsa.gov/hansens/
- Smith DS (2008-08-19). "Leprosy: Overview". eMedicine Infectious Diseases. Retrieved 2010-02-01.
- Singh N, Manucha V, Bhattacharya SN, Arora VK, Bhatia A; Manucha; Bhattacharya; Arora; Bhatia (June 2004). "Pitfalls in the cytological classification of borderline leprosy in the Ridley-Jopling scale". Diagn. Cytopathol. 30 (6): 386–8. doi:10.1002/dc.20012. PMID 15176024.
- Ridley DS, Jopling WH; Jopling (1966). "Classification of leprosy according to immunity. A five-group system". Int. J. Lepr. Other Mycobact. Dis. 34 (3): 255–73. PMID 5950347.
- Modlin RL (June 1994). "Th1-Th2 paradigm: insights from leprosy". J. Invest. Dermatol. 102 (6): 828–32. doi:10.1111/1523-1747.ep12381958. PMID 8006444.
- James, William D.; Berger, Timothy G.; and others (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0.
- Jardim MR, Antunes SL, Santos AR, Nascimento OJ, Nery JA, Sales AM, Illarramendi X, Duppre N, Chimelli L, Sampaio EP, Sarno EP; Antunes; Santos et al. (July 2003). "Criteria for diagnosis of pure neural leprosy". J. Neurol. 250 (7): 806–9. doi:10.1007/s00415-003-1081-5. PMID 12883921.
- Mendiratta V, Khan A, Jain A; Khan; Jain (2006). "Primary neuritic leprosy: a reappraisal at a tertiary care hospital". Indian J Lepr 78 (3): 261–7. PMID 17120509.
- Ishida Y, Pecorini L, Guglielmelli E; Pecorini l; Guglielmelli e (July 2000). "Three cases of pure neuritic (PN) leprosy at detection in which skin lesions became visible during their course". Nihon Hansenbyo Gakkai Zasshi 69 (2): 101–6. doi:10.5025/hansen.69.101. PMID 10979277.
- Mishra B, Mukherjee A, Girdhar A, Husain S, Malaviya GN, Girdhar BK; Mukherjee; Girdhar; Husain; Malaviya; Girdhar (1995). "Neuritic leprosy: further progression and significance". Acta Leprol 9 (4): 187–94. PMID 8711979.
- Talwar S, Jha PK, Tiwari VD; Jha; Tiwari (September 1992). "Neuritic leprosy: epidemiology and therapeutic responsiveness". Lepr Rev 63 (3): 263–8. PMID 1406021.
- Rodrigues LC, Lockwood DNj; Lockwood (June 2011). "Leprosy now: epidemiology, progress, challenges, and research gaps". Lancet Infect Dis 11 (6): 464–70. doi:10.1016/S1473-3099(11)70006-8. PMID 21616456.
- Duthie MS, Gillis TP, Reed SG; Gillis; Reed (November 2011). "Advances and hurdles on the way toward a leprosy vaccine". Hum Vaccin 7 (11): 1172–83. doi:10.4161/hv.7.11.16848. PMC 3323495. PMID 22048122.
- Setia MS, Steinmaus C, Ho CS, Rutherford GW; Steinmaus; Ho; Rutherford (March 2006). "The role of BCG in prevention of leprosy: a meta-analysis". Lancet Infect Dis 6 (3): 162–70. doi:10.1016/S1473-3099(06)70412-1. PMID 16500597.
- Merle CS, Cunha SS, Rodrigues LC; Cunha; Rodrigues (2010). "BCG vaccination and leprosy protection: Review of current evidence and status of BCG in leprosy control". Expert Review of Vaccines 9 (2): 209–222. doi:10.1586/ERV.09.161. PMID 20109030.
- "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002.
- WHO (1995). "Leprosy disabilities: magnitude of the problem". Weekly Epidemiological Record 70 (38): 269–75. PMID 7577430.
- Surgery grants for leprosy sufferers in India. Times of India. February 2, 2009.
- "About ILEP". ILEP. Retrieved 2014-08-25.
- World Health Organization. (1985). "Epidemiology of leprosy in relation to control. Report of a WHO Study Group". World Health Organ Tech Rep Ser (Geneva: World Health Organization) 716: 1–60. ISBN 92-4-120716-7. OCLC 12095109. PMID 3925646.
- al.], edited by Andrew Baum ... [et (1997). Cambridge handbook of psychology, health and medicine. Cambridge, Angleterre: Cambridge University Press. p. 521. ISBN 9780521436861.
- "DNA of Jesus-Era Shrouded Man in Jerusalem Reveals Earliest Case of Leprosy". ScienceDaily. 2009-12-16. Retrieved 2010-01-31.
- Braun-Falco, Otto; Plewig, Gerd; Helmut Heinrich, Wolff; Burgdorf, Walter H.C. (2000), Dermatology (2nd revised ed.), Berlin: Springer, p. 221, ISBN 9783540594529
- Cox, Carol Turkington, Jeffrey S. Dover ; medical illustrations, Birck (2007). The encyclopedia of skin and skin disorders (3rd ed.). New York, NY: Facts on File. p. 211. ISBN 9780816075096.
- Irgens LM (2002). "The discovery of the leprosy bacillus". Tidsskr nor Laegeforen 122 (7): 708–9. PMID 11998735.
- Rees RJ, Pearson JM, Waters MF; Pearson; Waters (1970). "Experimental and Clinical Studies on Rifampicin in Treatment of Leprosy". Br Med J 688 (1): 89–92. doi:10.1136/bmj.1.5688.89. PMC 1699176. PMID 4903972.
- Yawalkar SJ, McDougall AC, Languillon J, Ghosh S, Hajra SK, Opromolla DV, Tonello CJ; McDougall; Languillon; Ghosh; Hajra; Opromolla; Tonello (1982). "Once-monthly rifampicin plus daily dapsone in initial treatment of lepromatous leprosy". Lancet 8283 (1): 1199–1202. doi:10.1016/S0140-6736(82)92334-0. PMID 6122970.
- Syphilis through history Encyclopædia Britannica
- "Communicable Diseases Department, Leprosy FAQ". World Health Organization. 2006-05-25. Retrieved 2010-01-31.
- Japan repealed its "Leprosy Prevention Laws" in 1996 but former patients still reside in sanatoriums. "Koizumi apologises for leper colonies". BBC News. May 25, 2001. and Ex-Hansen's disease patients still struggling with prejudice Japan Times June 7, 2007.
- Rafferty, Joy. "Curing the Stigma of Leprosy." Leprosy Review. 76 (2005): 119–126. Web. 8 Dec. 2011. <http://www.kit.nl/-/INS/24155/(57698)-ILS/KIT-ILS-Dossiers.pdf>.
- Tayman, John (2007). The Colony: The Harrowing True Story of the Exiles of Molokai. New York: Simon and Schuster. ISBN 978-0-7432-3301-9.
- Hamilton, Bernard (2000). The leper king and his heirs: Baldwin IV and the Crusader Kingdom of Jerusalem. Cambridge, UK: Cambridge University Press. ISBN 0-521-64187-X.
- Cung giu Nguyên (1955). "Contemporary Vietnamese Writing". Books Abroad (University of Oklahoma) 29 (1): 19–25. doi:10.2307/40093803. JSTOR 40093803.
- Bryant A (1995). Sekigahara 1600: The Final Struggle for Power (Campaign Series, 40). Osprey Publishing (UK). ISBN 1-85532-395-8. Retrieved 2010-02-28.
|Wikimedia Commons has media related to Leprosy.|
- Leprosy at DMOZ
- Dr. George J. Hill Leprosy Collection, Marshall University Virtual exhibit of books on leprosy.