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Medieval love of squirrel fur may have helped spread leprosy, study reveals

Oct 25 2017

DNA of Jesus-era shrouded man in Jerusalem reveals earliest case of leprosy

Dec 9 2009

What is Leprosy?

Nov 17 2009

New Leprosy Bacterium: Scientists Use Genetic Fingerprint To Nail 'Killing Organism'

Nov 1 2008

Signs and symptoms

Common symptoms present in the different types of leprosy include a 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; a flat nose from the destruction of nasal cartilages; and changes in phonation and other aspects of speech production.⁴⁴ In addition, atrophy of the testes and impotence may occur.⁴⁵

Leprosy can affect people in different ways.⁴⁶ The average incubation period is five years.⁴⁷ People may begin to notice symptoms within the first year or up to 20 years after infection.⁴⁸ The first noticeable sign of leprosy is often the development of pale or pink coloured patches of skin that may be insensitive to temperature or pain.⁴⁹ Patches of discolored skin are sometimes accompanied or preceded by nerve problems including numbness or tenderness in the hands or feet.⁵⁰⁵¹ Secondary infections (additional bacterial or viral infections) can result in tissue loss, causing fingers and toes to become shortened and deformed, as cartilage is absorbed into the body.⁵²⁵³ A person's immune response differs depending on the form of leprosy.⁵⁴

Approximately 30% of people affected with leprosy experience nerve damage.⁵⁵ The nerve damage sustained is reversible when treated early but becomes permanent when appropriate treatment is delayed by several months. Damage to nerves may cause loss of muscle function, leading to paralysis. It may also lead to sensation abnormalities or numbness, which may lead to additional infections, ulcerations, and joint deformities.⁵⁶

Cause

M. leprae and M. lepromatosis

Mycobacterioum leprae and Mycobacterium lepromatosis are the mycobacteria that cause leprosy.⁵⁷ M. lepromatosis is a relatively newly identified mycobacterium isolated from a fatal case of diffuse lepromatous leprosy in 2008.⁵⁸⁵⁹ M. lepromatosis is indistinguishable clinically from M. leprae.⁶⁰ M. leprae is an aerobic, rod-shaped, acid-fast bacterium with a waxy cell envelope characteristic of the genus Mycobacterium.⁶¹ M. leprae and M. lepromatosis are obligate intracellular pathogens and cannot grow or be cultured outside of host tissues.⁶²⁶³ However, they can be grown using research animals such as mice and armadillos.⁶⁴⁶⁵

Naturally occurring infections have been reported in nonhuman primates (including the African chimpanzee, the sooty mangabey, and the cynomolgus macaque), armadillos,⁶⁶ and red squirrels.⁶⁷ Multilocus sequence typing of the armadillo M. leprae strains suggests that they were of human origin for at most a few hundred years.⁶⁸ Thus, it is suspected that armadillos first acquired the organism incidentally from early European explorers of the Americas.⁶⁹ This incidental transmission was sustained in the armadillo population, and it may be transmitted back to humans, making leprosy a zoonotic disease (spread between humans and animals).⁷⁰

Red squirrels (Sciurus vulgaris), a threatened species in Great Britain, were found to carry leprosy in November 2016.⁷¹ It has been suggested that the trade in red squirrel fur, highly prized in the medieval period and intensively traded, may have been responsible for the leprosy epidemic in medieval Europe.⁷² A pre-Norman era skull excavated in Hoxne, Suffolk, in 2017 was found to carry DNA from a strain of M. leprae which closely matched the strain carried by modern red squirrels on Brownsea Island.⁷³⁷⁴

Risk factors

The greatest risk factor for developing leprosy is contact with another person infected by leprosy.⁷⁵ People who are exposed to a person who has leprosy are 5–8 times more likely to develop leprosy than members of the general population.⁷⁶ Leprosy occurs more commonly among those living in poverty.⁷⁷ Not all people who are infected with M. leprae develop symptoms.⁷⁸⁷⁹

Conditions that reduce immune function, such as malnutrition, other illnesses, or genetic mutations, may increase the risk of developing leprosy.⁸⁰ Infection with HIV does not appear to increase the risk of developing leprosy.⁸¹ Certain genetic factors in the person exposed have been associated with developing lepromatous or tuberculoid leprosy.⁸²

Transmission

Transmission of leprosy occurs during close contact with those who are infected.⁸³ Transmission of leprosy is through the upper respiratory tract.⁸⁴⁸⁵ Older research suggested the skin as the main route of transmission, but research has increasingly favored the respiratory route.⁸⁶ Transmission occurs through inhalation of bacilli present in upper airway secretion.⁸⁷

Leprosy is not sexually transmitted and is not spread through pregnancy to the unborn child.⁸⁸⁸⁹ The majority (95%) of people who are exposed to M. leprae do not develop leprosy; casual contact such as shaking hands and sitting next to someone with leprosy does not lead to transmission.⁹⁰⁹¹ People are considered non-infectious 72 hours after starting appropriate multi-drug therapy.⁹² Two exit routes of M. leprae from the human body that are 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.⁹³ Humans can acquire a leprosy infection from armadillos by handling them or consuming armadillo meat.⁹⁴⁹⁵ The mechanism is not fully understood.⁹⁶⁹⁷⁹⁸

Genetics

Not all people infected or exposed to M. leprae develop leprosy, and genetic factors are suspected to play a role in susceptibility to an infection.⁹⁹ Cases of leprosy often cluster in families, and several genetic variants have been identified.¹⁰⁰ In many who are exposed, the immune system can eliminate the leprosy bacteria during the early infection stage before severe symptoms develop.¹⁰¹ A genetic defect in cell-mediated immunity may cause a person to be susceptible to develop leprosy symptoms after exposure to the bacteria.¹⁰² 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 at the biochemical level.¹⁰³

Mechanism

Most leprosy complications are the result of nerve damage. The nerve damage occurs from direct invasion by the M. leprae bacteria and a person's immune response resulting in inflammation.¹⁰⁴ The molecular mechanism underlying how M. leprae produces the symptoms of leprosy is not clear,¹⁰⁵ but M. leprae has been shown to bind to Schwann cells, which may lead to nerve injury including demyelination and a loss of nerve function (specifically a loss of axonal conductance).¹⁰⁶ Numerous molecular mechanisms have been associated with this nerve damage including the presence of a laminin-binding protein and the glycoconjugate (PGL-1) on the surface of M. leprae that can bind to laminin on peripheral nerves.¹⁰⁷

As part of the human immune response, white blood cell-derived macrophages may engulf M. leprae by phagocytosis.¹⁰⁸ In the initial stages, small sensory and autonomic nerve fibers in the skin of a person with leprosy are damaged.¹⁰⁹ This damage usually results in hair loss to the area, a loss of the ability to sweat, and numbness (decreased ability to detect sensations such as temperature and touch). Further peripheral nerve damage may result in skin dryness, more numbness, and muscle weaknesses or paralysis in the area affected.¹¹⁰ The skin can crack and if the skin injuries are not carefully cared for, there is a risk for a secondary infection that can lead to more severe damage.¹¹¹

Diagnosis

In countries where people are frequently infected, a person is considered to have leprosy if they have one of the following two signs:

• Skin lesion consistent with leprosy and with definite sensory loss.¹¹²
• Positive skin smears.¹¹³

Skin lesions can be single or many, and usually hypopigmented, although occasionally reddish or copper-colored.¹¹⁴ The lesions may be flat (macules), raised (papules), or solid elevated areas (nodular).¹¹⁵ Experiencing sensory loss at the skin lesion is a feature that can help determine if the lesion is caused by leprosy or by another disorder such as tinea versicolor.¹¹⁶¹¹⁷ Thickened nerves are associated with leprosy and can be accompanied by loss of sensation or muscle weakness, but muscle weakness without the characteristic skin lesion and sensory loss is not considered a reliable sign of leprosy.¹¹⁸ In some cases, the presence of acid-fast leprosy bacilli in skin smears is considered diagnostic; however, the diagnosis is typically made without laboratory tests, based on symptoms.¹¹⁹ If a person has a new leprosy diagnosis and already has a visible disability caused by leprosy, the diagnosis is considered late.¹²⁰

In countries or areas where leprosy is uncommon, such as the United States, diagnosis of leprosy is often delayed because healthcare providers are unaware of leprosy and its symptoms.¹²¹ Early diagnosis and treatment prevent nerve involvement, the hallmark of leprosy, and the disability it causes.¹²²¹²³ There is no recommended test to diagnose latent leprosy in people without symptoms.¹²⁴ Few people with latent leprosy test positive for anti PGL-1.¹²⁵ The presence of M. leprae bacterial DNA can be identified using a polymerase chain reaction (PCR)-based technique.¹²⁶ This molecular test alone is not sufficient to diagnose a person, but this approach may be used to identify someone who is at high risk of developing or transmitting leprosy such as those with few lesions or an atypical clinical presentation.¹²⁷¹²⁸ New approaches propose tools to diagnose leprosy through artificial intelligence.¹²⁹

Classification

Several different approaches for classifying leprosy exist. There are similarities between the classification approaches.

• The World Health Organization (WHO) system distinguishes patients with 5 or fewer skin lesions and no bacilli in a skin smear as "paucibacillary" ("pauci-" refers to a small quantity) from patients with more lesions or detected bacilli as "multibacillary".¹³⁰
• The Ridley-Jopling scale provides five gradations.^131132133
• The ICD-10, though developed by the WHO, uses Ridley-Jopling and not the WHO system. It also adds an indeterminate ("I") entry.¹³⁴
• In MeSH, three groupings are used.

Leprosy may also occur with only neural involvement, without skin lesions.^{140141142143144145}

Complications

Leprosy may cause the victim to lose limbs and digits but not directly. M. leprae attacks nerve endings and destroys the body's ability to feel pain and injury. Without feeling pain, people with leprosy have an increased risk of injuring themselves. Injuries become infected and result in tissue loss. Fingers, toes, and limbs become shortened and deformed as the tissue is absorbed into the body.¹⁴⁶

Prevention

Early disease detection is important, since physical and neurological damage may be irreversible even if cured.¹⁴⁷ Medications can decrease the risk of those living with people who have leprosy from acquiring the disease and likely those with whom people with leprosy come into contact outside the home.¹⁴⁸ The WHO recommends that preventive medicine be given to people who are in close contact with someone who has leprosy.¹⁴⁹ The suggested preventive treatment is a single dose of rifampicin in adults and children over 2 years old who do not already have leprosy or tuberculosis.¹⁵⁰ Preventive treatment is associated with a 57% reduction in infections within 2 years and a 30% reduction in infections within 6 years.¹⁵¹

The Bacillus Calmette–Guérin (BCG) vaccine offers a variable amount of protection against leprosy in addition to its closely related target of tuberculosis.¹⁵² 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.¹⁵³¹⁵⁴ The WHO concluded in 2018 that the BCG vaccine at birth reduces leprosy risk and is recommended in countries with high incidence of TB and people who have leprosy.¹⁵⁵ People living in the same home as a person with leprosy are suggested to take a BCG booster which may improve their immunity by 56%.¹⁵⁶¹⁵⁷ Development of a more effective vaccine is ongoing.^158159160161

A novel vaccine called LepVax entered clinical trials in 2017 with the first encouraging results reported on 24 participants published in 2020.¹⁶²¹⁶³ If successful, this would be the first leprosy-specific vaccine available.

Treatment

Several leprostatic agents are available for treatment. A three-drug regimen of rifampicin, dapsone, and clofazimine is recommended for all people with leprosy, for six months for paucibacillary leprosy and 12 months for multibacillary leprosy.¹⁶⁴ Multidrug therapy (MDT) remains highly effective, and people are no longer infectious after the first monthly dose.¹⁶⁵ MDT is safe and easy to use under field conditions because it is available in calendar-labelled blister packs.¹⁶⁶ The treatment does pose compliance challenges for young children who find swallowing multiple solid pills difficult.¹⁶⁷ Post-treatment relapse rates remain low.¹⁶⁸

The combination treatment accelerates treatment and decreases the chance of creating drug-resistant bacteria. All three drugs in the three-drug regimen are antibacterial, with rifampicin being the most potent. Rifampicin is scheduled monthly since it interferes with dapsone by inducing its increased metabolism.¹⁶⁹

Resistance to the three-drug regimen has been reported in several countries, although the number of cases is small.¹⁷⁰ People with rifampicin-resistant leprosy may be treated with second-line medications such as fluoroquinolones, minocycline, or clarithromycin, but the treatment duration is 24 months because of their lower bactericidal activity.¹⁷¹ Evidence on the potential benefits and harms of alternative regimens for drug-resistant leprosy is not available.¹⁷²

For people with nerve damage, protective footwear may help prevent ulcers and secondary infection.¹⁷³ Canvas shoes may be better than PVC boots.¹⁷⁴ There may be no difference between double rocker shoes and below-knee plaster.¹⁷⁵ Topical ketanserin seems to have a better effect on ulcer healing than clioquinol cream or zinc paste, but the evidence for this is weak.¹⁷⁶ Phenytoin applied to the skin improves skin changes to a greater degree when compared to saline dressings.¹⁷⁷

Outcomes

Although leprosy has been curable since the mid-20th century, left untreated it can cause permanent physical impairments and damage to a person's nerves, skin, eyes, and limbs.¹⁷⁸ Despite leprosy not being very infectious and having a low pathogenicity, there is still significant stigma and prejudice associated with the disease.¹⁷⁹ Because of this stigma, leprosy can affect a person's participation in social activities and may also affect the lives of their family and friends.¹⁸⁰ People with leprosy are also at a higher risk for problems with their mental well-being.¹⁸¹ The social stigma may contribute to problems obtaining employment, financial difficulties, and social isolation.¹⁸² Efforts to reduce discrimination and reduce the stigma surrounding leprosy may help improve outcomes for people with leprosy.¹⁸³

Epidemiology

Main article: Epidemiology of leprosy

In 2018, there were 208,619 new cases of leprosy recorded, a slight decrease from 2017.¹⁸⁴ In 2015, 94% of the new leprosy cases were confined to 14 countries.¹⁸⁵ India reported the greatest number of new cases (60% of reported cases), followed by Brazil (13%) and Indonesia (8%).¹⁸⁶ Although the number of cases worldwide continues to fall, there are parts of the world where leprosy is more common, including Brazil, South Asia (India, Nepal, Bhutan), some parts of Africa (Tanzania, Madagascar, Mozambique), and the western Pacific.¹⁸⁷ About 150 to 250 cases are diagnosed in the United States each year.¹⁸⁸

In the 1960s, there were tens of millions of leprosy cases recorded when the bacteria started to develop resistance to dapsone, the most common treatment option at the time.¹⁸⁹¹⁹⁰ International (e.g., the WHO's "Global Strategy for Reducing Disease Burden Due to Leprosy" and the International Federation of Anti-Leprosy Associations) and national initiatives have reduced the total number and the number of new cases of the disease.¹⁹¹¹⁹²

The number of new leprosy cases is difficult to measure and monitor because of leprosy's long incubation period, delays in diagnosis after the onset of the disease, and lack of medical care in affected areas.¹⁹³ The registered prevalence of the disease is used to determine disease burden.¹⁹⁴ 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.¹⁹⁵ 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.¹⁹⁶

History

Main article: History of leprosy

Historical distribution

Using comparative genomics, in 2005, geneticists traced the origins and worldwide distribution of leprosy from East Africa or the Near East along human migration routes. They found four strains of M. leprae with specific regional locations:¹⁹⁸ Monot et al. (2005) determined that leprosy originated in East Africa or the Near East and traveled with humans along their migration routes, including those of trade in goods and slaves. The four strains of M. leprae are based in specific geographic regions where each predominantly occurs:¹⁹⁹

• strain 1 in Asia, the Pacific region, and East Africa;
• strain 2 in Ethiopia, Malawi, Nepal, north India, and New Caledonia;
• strain 3 in Europe, North Africa, and the Americas;
• strain 4 in West Africa and the Caribbean.

This confirms the spread of the disease along the migration, colonisation, and slave trade routes taken from East Africa to India, West Africa to the New World, and from Africa to Europe and vice versa.²⁰⁰

Skeletal remains discovered in 2009 represent the oldest documented evidence for leprosy, dating to the 2nd millennium BC.²⁰¹²⁰² Located at Balathal, Rajasthan, in northwest India, the discoverers suggest that if the disease did migrate from Africa to India during the 3rd millennium BC "at a time when there was substantial interaction among the Indus Civilization, Mesopotamia, and Egypt, there needs to be additional skeletal and molecular evidence of leprosy in India and Africa to confirm the African origin of the disease".²⁰³ A proven human case was verified by DNA taken from the shrouded remains of a man discovered by researchers from the Hebrew University of Jerusalem in a tomb in Akeldama, next to the Old City of Jerusalem dated by radiocarbon methods to the first half of the 1st century.²⁰⁴

The oldest strains of leprosy known from Europe are from Great Chesterford in southeast England and date back to AD 415–545. These findings suggest a different path for the spread of leprosy, meaning it may have originated in western Eurasia. This study also indicates that there were more strains in Europe at the time than previously determined.²⁰⁵

Discovery and scientific progress

Literary attestation of leprosy is unclear because of the ambiguity of many early sources, including the Indian Atharvaveda and Kausika Sutra, the Egyptian Ebers Papyrus, and the Hebrew Bible's various sections regarding signs of impurity (tzaraath).²⁰⁶ Leprotic symptoms are attested in the Indian doctor Sushruta's Compendium, originally dating to c. 600 BC but only surviving in emended texts no earlier than the 5th century BC. Symptoms consistent with leprosy were possibly described by Hippocrates in 460 BC.²⁰⁷ However, Hansen's disease probably did not exist in Greece or the Middle East before the Common Era.^208209210 In 1846, Francis Adams produced The Seven Books of Paulus Aegineta which included a commentary on all medical and surgical knowledge and descriptions and remedies to do with leprosy from the Romans, Greeks, and Arabs.²¹¹²¹²

Leprosy did not exist in the Americas before colonization by modern Europeans²¹³ nor did it exist in Polynesia until the middle of the 19th century.²¹⁴ The causative agent of leprosy, M. leprae, was discovered by Gerhard Armauer Hansen in Norway in 1873, making it one of the first species of pathogenic bacteria identified.²¹⁵

Treatment

Chaulmoogra tree oil was used topically to manage Hansen's disease for centuries. Chaulmoogra oil could not be taken orally without causing nausea or injected without forming an abscess.²¹⁶ Leprosy was once believed to be highly contagious and was treated with mercury, as was syphilis, which was first described in 1530. Many early cases thought to be leprosy could actually have been syphilis.²¹⁷ In 1915, Alice Ball, the first black woman to graduate from the University of Hawai'i with a masters in chemistry, discovered how to make the oil water soluble.²¹⁸ This technique led to marked improvements in patients with Hansen's disease who were treated in Hawai'i.²¹⁹

The first effective drug (promin) became available in the 1940s.²²⁰ In the 1950s, dapsone was introduced. The search for further effective antileprosy drugs led to the use of clofazimine and rifampicin in the 1960s and 1970s.²²¹ Later, Indian scientist Shantaram Yawalkar and his colleagues formulated a combined therapy using rifampicin and dapsone, intended to mitigate bacterial resistance.²²² Combining all three drugs was first recommended by the WHO in 1981. These three drugs are still used in the standard MDT regimens.²²³ Resistance has developed to initial treatment. Until the introduction of MDT in the early 1980s, leprosy could not be diagnosed and treated successfully within the community.²²⁴

The importance of the nasal mucosa in the transmission of M. leprae was recognized as early as 1898 by Schäffer, in particular, that of the ulcerated mucosa.²²⁵[verification needed] The mechanism of plantar ulceration in leprosy and its treatment was first described by Ernest W. Price.²²⁶

Etymology

The word "leprosy" comes from the Greek word "λέπος (lépos) – skin" and "λεπερός (leperós) – scaly man".

Society and culture

Treatment cost

Between 1995 and 1999 the WHO, with the aid of the Nippon Foundation, supplied all endemic countries with free MDT in blister packs, channeled through ministries of health.²²⁷ This free provision was extended in 2000 and again in 2005, 2010, and 2015 with donations by the MDT manufacturer Novartis through the WHO.²²⁸²²⁹ At the national level, non-governmental organizations (NGOs) affiliated with the national program will continue to be provided with an appropriate free supply.²³⁰

Historical texts

Written accounts of leprosy date back thousands of years. Various skin diseases translated as leprosy appear in the ancient Indian text, the Atharava Veda, by 600 BC.²³¹ Another Indian text, the Manusmriti (200 BC), prohibit contact with those infected with the disease and make marriage to a person infected with leprosy punishable.²³²

The Hebraic root tsara or tsaraath (צָרַע, – tsaw-rah' – to be struck with leprosy, to be leprous) and the Greek (λεπρός – lepros), are of broader classification than the more narrow use of the term related to Hansen's Disease.²³³ Any progressive skin disease (a whitening or splotchy bleaching of the skin, raised manifestations of scales, scabs, infections, rashes, etc.) — as well as generalized molds and surface discoloration of any clothing, leather, or discoloration on walls or surfaces throughout homes — all came under the "law of leprosy" (Leviticus 14:54–57).²³⁴ 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 occurring on cloth, leather, or houses, as well as skin. Traditional Judaism and Jewish rabbinical authorities, both historical and modern, emphasize that the tsaraath of Leviticus is a spiritual ailment with no direct relationship to Hansen's disease or physical contagions. The relation of tsaraath to "leprosy" comes from translations of Hebrew Biblical texts into Greek and ensuing misconceptions.²³⁵

All three Synoptic Gospels of the New Testament describe instances of Jesus healing people with leprosy (Matthew 8:1–4, Mark 1:40–45, and Luke 5:12–16). The Bible's description of leprosy is congruous (if lacking detail) with the symptoms of modern leprosy, but the relationship between this disease, tzaraath, and Hansen's disease has been disputed.²³⁶ The biblical perception that people with leprosy were unclean can be found in a passage from Leviticus 13:44–46. While this text defines the leper as impure, it does not explicitly make a moral judgement on those with leprosy.²³⁷ Some early Christians believed that those affected by leprosy were being punished by God for sinful behavior. Moral associations have persisted throughout history. In the 6th century Pope Gregory the Great and Isidore of Seville considered people with the disease to be heretics.²³⁸

Middle Ages

The social perception of leprosy in the general population was mixed. On one hand, people feared getting infected with the disease and thought of people suspected of leprosy to be unclean, untrustworthy, and occasionally morally corrupt.²³⁹ On the other hand, Jesus' interaction with lepers, the writing of church leaders, and the Christian focus on charitable works led to viewing the lepers as "chosen by God"²⁴⁰ or seeing the disease as a means of obtaining access to heaven.²⁴¹

Early medieval understanding of leprosy was influenced by early Christian writers such as Gregory of Nazianzus and John Chrysostom, whose writings were later embraced by Byzantine and Latin writers.²⁴² Gregory, for example, composed sermons urging Christians to assist victims of the disease, and he condemned pagans or Christians who justified rejecting lepers on the allegation that God had sent them the disease to punish them. As cases of leprosy increased in the Eastern Roman Empire, becoming a major health issue, the ecclesiastic leaders discussed how to assist those affected as well as how to change the attitude of society towards them. They also tried this by using the name "holy disease" instead of the commonly used "elephant's disease" (elephantiasis), implying that God did not create this disease to punish people but to purify them for heaven.²⁴³ Although not always successful in persuading the public and a cure was never found by Greek medicians, they created an environment where victims could get palliative care and were never expressly banned from society, as sometimes happened in western Europe. Theodore Balsamon, a 12th-century jurist in Constantinople, noted that lepers were allowed to enter the same churches, cities, and assemblies that healthy people attended.²⁴⁴

As the disease became more prevalent in western Europe in the 5th century, efforts began to set up permanent institutions to house and feed lepers. These efforts were, inclusively, the work of bishops in France at the end of the sixth century, such as in Chalon-sur-Saône.²⁴⁵ The increase in hospitals or leprosaria (sing. leprosarium) that treated people with leprosy in the 12th and 13th century seems to indicate a rise in cases,^246247248 possibly in connection with the increase in urbanisation²⁴⁹ as well as returning crusaders from the Middle East.²⁵⁰ France alone had nearly 2,000 leprosaria during this period.²⁵¹ Additionally to the new leprosia, further steps were taken by secular and religious leaders to prevent further spread of the disease. The third Lateran Council of 1179 required lepers to have their own priests and churches²⁵² and a 1346 edict by King Edward expelled lepers from city limits. Segregation from mainstream society became common, and people with leprosy were often required to wear clothing that identified them as such or carry a bell announcing their presence.²⁵³ As in the East, it was the Church who took care of the lepers due to the persisting moral stigma and who ran the leprosaria.²⁵⁴²⁵⁵ Although the leprosaria in Western Europe removed the sick from society, they were never a place to quarantine them or from which they could not leave: lepers would go beg for alms for the upkeep of the leprosaria or meet with their families.²⁵⁶²⁵⁷

Multiple groups in Western Europe from the Middle Ages faced social ostracization and discrimination that was justified, in part, due to claims that they were the descendants of lepers. These groups included the Cagots and the Caquins.^258259260

19th century

Norway was the location of a progressive stance on leprosy tracking and treatment and played an influential role in European understanding of the disease. In 1832, Dr. JJ Hjort conducted the first leprosy survey, thus establishing a basis for epidemiological surveys. Subsequent surveys resulted in the establishment of a national leprosy registry to study the causes of leprosy and to track the rate of infection. Early leprosy research throughout Europe was conducted by Norwegian scientists Daniel Cornelius Danielssen and Carl Wilhelm Boeck. Their work resulted in the establishment of the National Leprosy Research and Treatment Center. Danielssen and Boeck believed the cause of leprosy transmission was hereditary. This stance was influential in advocating for the isolation of those infected by sex to prevent reproduction.^261262263

Though leprosy rates were on the decline in the Western world by the 1860s, authorities frequently embraced isolation treatment due to a combination of reasons, including fears of the disease spreading from the Global South, efforts by Christian missionaries and a lack of understanding concerning bacteriology, medical diagnosis and how contagious the disease was.²⁶⁴ The rapid expansion of Western imperialism during the Victorian era resulted in westerners coming into increasing contact with regions where the disease was endemic, including British India. English surgeon Henry Vandyke Carter observed isolation treatment for leprosy patients first-hand while visiting Norway, applying these methods in British India with the financial and logistical assistance of Protestant missionaries. Colonialist and religious viewpoints of the disease continued to be a major factor in the treatment and public perception of the disease in the Global South until decolonization in the mid-20th century.²⁶⁵

20th and 21st century

See also: Leprosy in India

In 1898, the colonial government in British India enacted the Leprosy Act of 1898, which mandated the compulsory segregation of people with leprosy by authorities in newly established leper asylums, where they were segregated by sex to prevent sexual activity. The act, which proved difficult to enforce, was repealed in 1983 by the Indian government after MDT had become widely available in India. In 1983, the National Leprosy Elimination Programme, previously the National Leprosy Control Programme, changed its methods from surveillance to the treatment of people with leprosy. India still accounts for over half of the global disease burden. According to WHO, new cases in India during 2019 diminished to 114,451 patients (57% of the world's total new cases).²⁶⁶²⁶⁷ Until 2019, Indians could justify a petition for divorce with their spouse's diagnosis of leprosy.²⁶⁸

The National Leprosarium at Carville, Louisiana, known in 1955 as the Louisiana Leper Home, was the only leprosy hospital in the mainland United States. Leprosy patients from all over the United States were sent to Carville to be kept in isolation away from the public, as not much about leprosy transmission was known at the time and stigma against those with leprosy was high. The Carville leprosarium was known for its innovations in reconstructive surgery for those with leprosy. In 1941, 22 patients at Carville underwent trials for a new drug called promin. The results were described as miraculous, and soon after the success of promin came dapsone, a medicine even more effective in the fight against leprosy.²⁶⁹ Leprosy incidence peaked in the United States in 1983, followed by a steep decline.²⁷⁰ However, case numbers have been slowly rising again since 2000. In 2020, 159 cases were reported in the country.²⁷¹

Stigma

See also: Leprosy stigma and Leper colony stigma

Despite now effective treatment and education efforts, leprosy stigma continues to be problematic in developing countries where the disease is common. Leprosy is most common amongst impoverished populations where social stigma is likely to be compounded by poverty. Fears of ostracism, loss of employment, or expulsion from family and society may contribute to a delayed diagnosis and treatment.²⁷²

Folk beliefs, lack of education, and religious connotations of the disease continue to influence social perceptions of those affected in many parts of the world. In Brazil, for example, folklore holds that leprosy is a disease transmitted by dogs, or that it is associated with sexual promiscuity, or that it is a punishment for sins or moral transgressions (distinct from other diseases and misfortunes, which are in general thought of as being according to the will of God).²⁷³ Socioeconomic factors also have a direct impact. Lower-class domestic workers who are often employed by those in a higher socioeconomic class may find their employment in jeopardy as physical manifestations of the disease become apparent. Skin discoloration and darker pigmentation resulting from the disease also have social repercussions.²⁷⁴

In extreme cases in northern India, leprosy is equated with an "untouchable" status that "often persists long after individuals with leprosy have been cured of the disease, creating lifelong prospects of divorce, eviction, loss of employment, and ostracism from family and social networks."²⁷⁵

Public policy

The World Health Organization maintains an Expert Committee on Leprosy since 1954, and a goal of the WHO is to "eliminate leprosy." In 2016 the organization launched "Global Leprosy Strategy 2016–2020: Accelerating towards a leprosy-free world".²⁷⁶²⁷⁷ Elimination of leprosy is defined as "reducing the proportion of (people with) leprosy in the community to very low levels, specifically to below one case per 10,000 population".²⁷⁸ Diagnosis and treatment with multidrug therapy are effective, and a 45% decline in disease burden has occurred since MDT has become more widely available.²⁷⁹ The organization emphasizes the importance of fully integrating leprosy treatment into public health services, effective diagnosis and treatment, and access to information.²⁸⁰ The approach includes supporting an increase in health care professionals who understand the disease, and a coordinated and renewed political commitment that includes coordination between countries and improvements in the methodology for collecting and analysing data.²⁸¹

Interventions include:²⁸²

• Early detection of cases focusing on children to reduce transmission and disabilities.
• Enhanced healthcare services and improved access for people who may be marginalized.
• For countries where leprosy is endemic, further interventions include an improved screening of close contacts, improved treatment regimens, and interventions to reduce stigma and discrimination against people who have leprosy.

In some instances in India, community-based rehabilitation is embraced by local governments and NGOs alike. Often, the identity cultivated by a community environment is preferable to reintegration, and models of self-management and collective agency independent of NGOs and government support have been desirable and successful.²⁸³

Notable cases

• Josephine Cafrine of Seychelles (1877–1907) had leprosy from age 12 and kept a journal that documented her struggles and suffering.^284285286 It was published as an autobiography in 1923.^287288289290
• Saint Damien De Veuster (1840–1889), a Catholic priest from Belgium, contracted leprosy and ministered to lepers who had been placed under a government-sanctioned medical quarantine on Molokaʻi in the Kingdom of Hawaiʻi.²⁹¹
• Baldwin IV of Jerusalem (1161–1185), Catholic king of Latin Jerusalem, had leprosy.²⁹²
• Ingeborg Grytten (c. 1668 – after 1705), Norwegian writer whose leprosy is thought to have influenced her poetry, which is characterized by a strong religious faith in God's salvation.²⁹³
• Josefina Guerrero (1917–1996), Filipino World War II spy who used the Japanese fear of her leprosy to listen to their battle plans and deliver the information to the American forces under Douglas MacArthur.²⁹⁴
• King Henry IV of England (r. 1399–1413) possibly had leprosy.²⁹⁵
• Vietnamese poet Hàn Mặc Tử (1912–1940)²⁹⁶
• Ōtani Yoshitsugu (1558 or 1565–1600), a Japanese daimyō (feudal lord).²⁹⁷
• British writer Peter Greave (1910–1977).
• Popular Indian actress Dimple Kapadia (1957–present) was diagnosed with leprosy a few months before the shoot of the 1973 musical romance film, Bobby (1973 film). She later recovered completely and went on to have a successful acting career.²⁹⁸

In media

• August 1891 — the short story collection Life's Handicap by Rudyard Kipling has a story "The Mark of the Beast" in which a traveller on horseback literally stumbles into a leper colony in India.²⁹⁹
• 1909 — Jack London published "Koolau the Leper" in his Tales of Hawai'i about Molokai and people consigned to it circa 1893.
• 1959 — James Michener's novel Hawaii dramatizes Molokai's leper settlement, including Father Damien.
• 1959 — Ben-Hur depicts the title character's mother, Miriam, and younger sister, Tirzah, are imprisoned by the Roman Empire. When they are freed years later, they have leprosy and leave town for the Valley of the Lepers, rather than stay and reunite with Ben-Hur. They leave the colony, and when Jesus dies on the cross, they are miraculously cured.
• 1960 — English author Graham Greene's novel A Burnt-Out Case is set in a leper colony in Belgian Congo. The story is also predominantly about a disillusioned architect working with a doctor on devising new cures and amenities for mutilated victims of lepers; the title, too, refers to the condition of mutilation and disfigurement in the disease.³⁰⁰
• 1962 — Forugh Farrokhzad made a 22-minute documentary about a leprosy colony in Iran titled The House Is Black. The film humanizes the people affected and opens by saying that "there is no shortage of ugliness in the world, but by closing our eyes on ugliness, we will intensify it."
• 1977 — The lead character in The Chronicles of Thomas Covenant by Stephen R. Donaldson suffers from leprosy. His condition seems to be cured by the magic of the fantasy land he finds himself in, but he resists believing in its reality, for example, by continuing to perform a regular visual surveillance of extremities as a safety check. Donaldson gained experience with the disease as a young man in India, where his father worked in a missionary for people with leprosy.
• 2006 — Moloka'i is a novel by Alan Brennert about a leper colony in Hawaii. This novel follows the story of a seven-year-old girl taken from her family and put on Molokai's leper settlement.
• 2009 — Squint: My Journey with Leprosy is a memoir by Jose P. Ramirez.³⁰¹

Infection of animals

Between 15 and 20% of nine-banded armadillos (Dasypus novemcinctus) in the south-central United States carry M. leprae.³⁰²³⁰³ As a result of their low body temperature their tissues commonly contain massive numbers of organisms which help in the dissemination of the infection. Armadillos were first demonstrated in 1971 to develop leprosy after inoculation with M. leprae.³⁰⁴ Because of armadillos' armor, skin lesions are difficult to ascertain.³⁰⁵ Abrasions around the eyes, nose, and feet are the most common signs. Infected armadillos make up a large reservoir of M. leprae and may be a source of infection for some humans in the United States or other locations in the armadillos' home range. In armadillo leprosy, lesions do not persist at the site of entry in animals; M. leprae multiply in macrophages at the site of inoculation and lymph nodes.³⁰⁶

Armadillos have been used in immunological research to fight leprosy. Some notable reagents include recombinant interleukin-2 and recombinant interferon-gamma reagents.³⁰⁷ Additionally, they have been key and have been useful models of leprosy for studies regarding neuropathy.³⁰⁸ In clinical procedures such as electrophysiological nerve conduction tests Armadillo's nerve function has been properly assessed.³⁰⁹ Despite the studies mentioned regarding Armadillo's relationship to neuropathy and other effects of leprosy, there is still a lack of proper study on armadillos, and in conducting more armadillo-specific regents our understanding of leprosy’s effects on armadillos and possible humans can be found. Armadillos are a key component of modern-day research on leprosy.

There is a stigma surrounding armadillos and the carrying of leprosy. Because many people do not understand armadillos very well it is common for people to think of them as being dangerous to society and as a result valuing their lives less than other animals. It has become more common in parts of America for people to eat raw or undercooked armadillo, making the chances high that if not properly handled with care, one may become infected.³¹⁰

An outbreak in chimpanzees in West Africa is showing that the bacteria can infect another species and also possibly have additional rodent hosts.³¹¹ Studies have demonstrated that the disease is endemic in the UK red Eurasian squirrel population, with M. leprae and M. lepromatosis appearing in different populations. The M. leprae strain discovered on Brownsea Island is equated to one thought to have died out in the human population in mediaeval times.³¹² Despite this, and speculation regarding past transmission through trade in squirrel furs, there does not seem to be a high risk of squirrel to human transmission from the wild population. Although leprosy continues to be diagnosed in immigrants to the UK, the last known human case of leprosy arising in the UK was recorded over 200 years ago.³¹³

It has been shown that leprosy can reprogram cells in mouse³¹⁴³¹⁵ and armadillo³¹⁶³¹⁷ models, similar to how induced pluripotent stem cells are generated by the transcription factors Myc, Oct3/4, Sox2, and Klf4. A notable study conducted by Charles Shepard used mice to find how leprosy, an infection that has a preference for cooler areas of the body, would work in a warm-blooded animal. This mice study helped further the understanding of how leprosy works in humans. This was called "The Mouse Model."³¹⁸ The main findings were that even in mice whose immune systems were severely impaired and at a perceived high risk of developing leprosy, the body was still in most cases able to fight off leprosy. The findings suggest that in mice, the body will use their body's energy to fight leprosy.³¹⁹ Using The Mouse Model Shepard was able to conduct new research regarding leprosy. This model can now be used as a tool to further study M. leprae.³²⁰ The Mouse Model takes a more easily accessible animal model to better understand this complex disease. There are a few other up-and-coming models for M. leprae including the use of other animals including but not limited to mammals, birds, and cold-blooded animals.³²¹ These animals do not tend to give as great results as armadillos and mice as different animals have different levels of disease resistance.

Further reading

• Pam Fessler (2020). Carville's Cure: Leprosy, Stigma, and the Fight for Justice. Liveright. ISBN 978-1631495038.
• Guidelines for the diagnosis, treatment and prevention of leprosy. World Health Organization (WHO) (Report). October 2018. hdl:10665/274127. ISBN 978-92-9022-638-3.

External links

References

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