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HEALTH CENTER INTERNATIONAL RESEARCH

http://healthcenterinternationalresearches.webs.com/

Dr. Maddalena Frau

Leprosy

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Leprosy orHansen's disease (HD) is a chronic disease caused by the bacteriaMycobacteriumleprae andMycobacterium lepromatosis. Named after physician Gerhard Armauer Hansen,leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upperrespiratory tract; skin lesions are the primary external sign. Left untreated, leprosy can beprogressive, 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 aresult of secondary infections; these occur as a result of the body's defenses being compromisedby the primary disease. Secondary infections, in turn, can result in tissue loss causing fingers andtoes to become shortened and deformed, as cartilage is absorbed into the body.

Although the mode of transmission of Hansen's disease remains uncertain, most investigatorsthink thatM. leprae is usually spread from person to person in respiratory droplets. Studies haveshown that leprosy can be transmitted to humans by armadillos. Leprosy is now known to beneither sexually transmitted nor highly infectious after treatment. Approximately 95% of peopleare naturally immune and sufferers are no longer infectious after as little as 2 weeks of treatment.

The minimum incubation period reported is as short as a few weeks, based on the veryoccasional occurrence of leprosy among young infants. The maximum incubation periodreported is as long as 30 years, or over, as observed among war veterans known to have beenexposed for short periods in endemic areas but otherwise living in non-endemic areas. It isgenerally agreed that the average incubation period is between three and five years.

Leprosy has affected humanity for over 4,000 years, and was well-recognized in the civilizationsof ancient China, Egypt, and India. In 1995, the World Health Organization (WHO) estimatedthat between 2 and 3 million people were permanently disabled because of leprosy at that time.In the past 20 years, 15 million people worldwide have been cured of leprosy. Although theforced quarantine or segregation of patients is unnecessary in places where adequate treatments

are available, many leper colonies still remain around the world in countries such as India (wherethere are still more than 1,000 leper colonies), China, Romania, Egypt, Nepal, Somalia, Liberia,Vietnam, and Japan. Leprosy was once believed to be highly contagious and was treated withmercuryall of which applied to syphilis, which was first described in 1530. It is now thoughtthat many early cases of leprosy could have been syphilis.

The age-old social stigma associated with the advanced form of leprosy lingers in many areas,and remains a major obstacle to self-reporting and early treatment. Effective treatment forleprosy appeared in the late 1930s with the introduction ofdapsone and its derivatives. Leprosybacilli resistant to dapsone soon evolved and, due to overuse of dapsone, became widespread. Itwas not until the introduction of multidrug therapy (MDT) in the early 1980s that the diseasecould be diagnosed and treated successfully within the community.

MDT for multibacillary leprosy consists of rifampicin, dapsone, and clofazimine taken over 12months. Dosages adjusted appropriately for children and adults are available in all primary healthcentres in the form of blister packages. Single dose MDT for single lesion leprosy consists ofrifampicin, ofloxacin, and minocycline. The move toward single-dose treatment strategies hasreduced the prevalence of disease in some regions, since prevalence is dependent on duration oftreatment.

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World Leprosy Day was created to draw awareness to leprosy and its sufferers.

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 lowquantity.)

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.

WHORidley-

Jopling

ICD-

10MeSH Description

Lepromin

test

Immune

target

Paucibacillary

tuberculoid("TT"),borderlinetuberculoid("BT")

A30.1,A30.2

Tuberculoid

It is characterized byone or more

hypopigmented skinmacules andanaesthetic patches,where skin sensationsare lost because ofdamaged peripheralnerves that have beenattacked by the humanhost's immune cells.

Positivebacillus(Th1)

Multibacillarymidborderlineor borderline("BB")

A30.3 Borderline

Borderline leprosy isof intermediate

severity and is the mostcommon form. Skinlesions resembletuberculoid leprosy butare more numerous andirregular; large patchesmay affect a wholelimb, and peripheralnerve involvementwith weakness and lossof sensation is

common. This type isunstable and maybecome more likelepromatous leprosy ormay undergo a reversalreaction, becomingmore like thetuberculoid form.

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Multibacillary

borderlinelepromatous

("BL"), andlepromatous("LL")

A30.4,A30.5 Lepromatous

It is associated withsymmetric skin lesions,nodules, plaques,thickened dermis, andfrequent involvement

of the nasal mucosaresulting in nasalcongestion andepistaxis (nose bleeds),but, typically,detectable nervedamage is late.

Negative

plasmid

insidebacillus(Th2)

There is a difference in immune response to the tuberculoid and lepromatous forms.

Hansen's disease may also be divided into the following types::344-346

Early and indeterminate leprosy Tuberculoid leprosy Borderline tuberculoid leprosy Borderline leprosy Borderline lepromatous leprosy Lepromatous leprosy Histoid leprosy Diffuse leprosy of Lucio and Latap

This disease may also occur with only neural involvement, without skin lesions. This disease is

also known as Hansen's Disease.

Skin lesions are the primary external sign. Left untreated, leprosy can be progressive, causingpermanent damage to the skin, nerves, limbs, and eyes.

Diagnosis in the U.S. is often delayed because healthcare providers are unaware of leprosy andits symptoms. Early diagnosis and treatment prevents nerve involvement, the hallmark ofleprosy, and the disability it causes.

There are many kinds of leprosy but there are common symptoms. These include runny nose, dryscalp, eye problems, skin lesions, and muscle weakness.

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Mycobacterium leprae

Mycobacterium leprae, one of the causative agents of leprosy. As acid-fast bacteria,M. lepraeappear red when a Ziehl-Neelsen stain is used.

Main article: Mycobacterium leprae

At highest risk are those living in endemic areas with poor conditions such as inadequate

bedding, contaminated water, and insufficient diet, or other diseases that compromise immunefunction. However, though hard evidence is limited, and fringe publications have madepassionate claims to the contrary, professional studies show little evidence that HIV is animportant factor in increasing the risk of leprosy infection. It is presumed that this might bebecause of differences between the modes of immunity involved. However, it is plain that thetwo infections and their signs and progressions need not be fully independent, so the mattershould be regarded with reserve. For example, a Medscape clinical presentation reports that HIVinfection neither is a risk factor for acquisition nor for increased virulence of leprosy, but thatlatent cases of leprosy may emerge after starting HAART. Lewis, F. S. et al. ; DermatologicManifestations of Leprosy Clinical Presentation

Recent research suggests that there is a defect in cell-mediated immunity that causessusceptibility to Hansen's disease. Less than ten percent of the world's population is capable ofacquiring the disease. The region of DNA responsible for this variability is also involved inParkinson disease, giving rise to current speculation that the two disorders may be linked in someway at the biochemical level. In early 2003, an international team of scientists conducted agenome scan in Vietnamese multiplex leprosy families and found that susceptibility to leprosywas significantly linked to region q25 on the long arm of chromosome 6. Further confirmation ofthe chromosome 6 locus was provided by high-resolution linkage mapping in simplex leprosyfamilies. Now, in a continuation of these findings, the team has pinpointed the chromosome 6susceptibility locus to the 5' regulatory promoter region shared by both the Parkinson's diseasegene PARK2 and its co-regulated gene PACRG. According to The Leprosy Mission Canada,

most people-about 95% of the population-are naturally immune to the disease.

The mechanism of transmission of leprosy is prolonged close contact and transmission by nasaldroplet. In addition to humans, leprosy has been observed in nine-banded armadillo, (which, ithas recently been confirmed, are among the primary sources of new cases of leprosy inAmericans), and three species of primates. The bacterium can also be grown in the laboratory byinjection into the footpads of mice. There is evidence that not all people who are infected withM. leprae develop leprosy, and genetic factors have long been thought to play a role, due to the

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observation of clustering of leprosy around certain families, and the failure to understand whycertain individuals develop lepromatous leprosy while others develop other types of leprosy. It isestimated that due to genetic factors, only 5% of the population is susceptible to leprosy. This ismostly because the body is naturally immune to the bacteria, and those persons that do becomeinfected 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 andprolonged 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 personsand healthy persons. In general, closeness of contact is related to the dose of infection, which inturn 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 incidenceamong contacts and the relative risk for them appear to vary considerably in different studies. Inincidence studies, infection rates for contacts of lepromatous leprosy have varied from 6.2 per1000 per year in Cebu, Philippines to 53 per 1000 per year in part of Western India to 55.8 per1000 per year in a part of Southern India.[

Two exit routes ofM. leprae from the human body often described are the skin and the nasalmucosa, although their relative importance is not clear. Lepromatous cases show large numbersof organisms deep in the dermis, but whether they reach the skin surface in sufficient numbers isdoubtful. Although there are reports of acid-fast bacilli being found in the desquamatingepithelium (sloughing of superficial layer of skin) of the skin, Weddell et al. had reported in1963 that they could not find any acid-fast bacilli in the epidermis, even after examining a verylarge number of specimens from patients and contacts. In a recent study, Job et al. found fairlylarge numbers ofM. leprae in the superficial keratin layer of the skin of lepromatous leprosypatients, suggesting that the organism could exit along with the sebaceous secretions.

The importance of the nasal mucosa was recognized as early as 1898 by Schffer, in particularthat of the ulcerated mucosa. The quantity of bacilli from nasal mucosal lesions in lepromatousleprosy 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 nasalsecretions as collected through blowing the nose. Davey and Rees indicated that nasal secretionsfrom lepromatous patients could yield as much as 10 million viable organisms per day.

The entry route ofM. leprae into the human body is also not definitively known: The skin andthe upper respiratory tract are most likely. While older research dealt with the skin route, recentresearch has increasingly favored the respiratory route. Rees and McDougall succeeded in theexperimental transmission of leprosy through aerosols containingM. leprae in immune-suppressed mice, suggesting a similar possibility in humans. Successful results have also beenreported on experiments with nude mice whenM. leprae were introduced into the nasal cavity bytopical application. In summary, entry through the respiratory route appears the most probableroute, although other routes, particularly broken skin, cannot be ruled out. The CDC notes thefollowing assertion about the transmission of the disease: "Although the mode of transmission ofHansen's disease remains uncertain, most investigators think thatM. leprae is usually spreadfrom person to person in respiratory droplets."

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In leprosy, both the reference points for measuring the incubation period and the times ofinfection and onset of disease are difficult to define, the former because of the lack of adequateimmunological tools and the latter because of the disease's slow onset. Even so, severalinvestigators have attempted to measure the incubation period for leprosy. The minimumincubation 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 longas 30 years, or over, as observed among war veterans known to have been exposed for shortperiods in endemic areas but otherwise living in non-endemic areas. It is generally agreed thatthe average incubation period is between three and five years.

Prevention

Because leprosy can be cured with medicines, an early diagnosis will often reduce leprosysymptoms and complications. Therefore, while prevention of leprosy is not always possible,especially where leprosy is endemic, control should be possible.

An early diagnosis of help reducing the severeness and complications caused by the disease asleprosy can be cured with medicines. Although the prevention is often difficult especially in theplaces where it is endemic, control can be possible. People in immediate contact with leprosypatients should examine themselves for the infection. Annual examinations for at least five yearsshould be conducted for such people following their very last contact with the leprosy patient.

In a recent trial, a single dose of rifampicin reduced the rate at which contacts acquired leprosy inthe two years after contact by 57%; 265 treatments with rifampicin prevented one case of leprosyin this period. A non-randomized study found that rifampicin reduced the number of new casesof leprosy by 75% after three years.

BCG offers a variable amount of protection against leprosy as well as against tuberculosis.

Efforts to overcome persistent obstacles to the elimination of the disease include improvingdetection, educating patients and the population about its cause, and fighting social taboos abouta disease that has caused its patients throughout history to be considered "unclean" or "cursed byGod" as outcasts. Leprosy is not a hereditary disease. Where taboos are strong, patients may beforced to hide their condition (and avoid seeking treatment) to avoid discrimination. The lack of

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awareness about Hansen's disease can lead people to believe (falsely) that the disease is highlycontagious and incurable.

The ALERT hospital and research facility in Ethiopia provides training to medical personnelfrom around the world in the treatment of leprosy, as well as treating many local patients.

Surgical techniques, such as for the restoration of control of movement of thumbs, have beendeveloped.

In 1988, Jacinto Convit was nominated for the Nobel Prize in Medicine, for developing a vaccineto fight leprosy, by combining a tuberculosis (TB) vaccines with Mycobacterium Leprae.

MDT anti-leprosy drugs: standard regimens

Enough synthetic pharmaceuticals that are effective against leprosy have by now been identified,and support a flexible choice of treatments. The WHO Study Group's report on the

Chemotherapy of Leprosy in 1993 recommended two types of standard MDT regimen beadopted. The first was a 24-month treatment for multibacillary (MB or lepromatous) cases usingrifampicin, clofazimine, and dapsone. The second was a six-month treatment for paucibacillary(PB or tuberculoid) cases, using rifampicin and dapsone. At the First International Conference onthe Elimination of Leprosy as a Public Health Problem, held in Hanoi the next year, the globalstrategy was endorsed and funds provided to WHO for the procurement and supply of MDT toall endemic countries.

The disease was known in Ancient Greece as elephantiasis (elephantiasis graecorum). At varioustimes blood was considered to be a treatment either as a beverage or as a bath. That of virgins orchildren was considered to be especially potent. This practice seems to have originated with the

Ancient Egyptians but was also known in China. This practice persisted until at least 1790, whenthe use of dog blood was mentioned inDe Secretis Naturae. Paracelsus recommended the use oflamb's blood and even blood from dead bodies was used.

Snakes were also used, according to Pliny, Aretaeus of Cappadocia, and Theodorus. Gaucherrecommended treatment with cobra venom. Boinet, in 1913, tried increasing doses of bee stings(up to 4000). Scorpions and frogs were used occasionally instead of snakes. The excreta ofAnabas (the climbing fish) was also tried.

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Alternative treatments included scarification with or without the addition of irritants includingarsenic and hellebore. Castration was also practiced in the Middle Ages.

A common pre-modern treatment of leprosy was chaulmoogra oil.

The oil has long been used in India as an Ayurvedic medicine for the treatment of leprosy andvarious skin conditions. It has also been used in China and Burma, and was introduced to theWest by Frederic John Mouat, a professor at Bengal Medical College. He tried the oil as an oraland topical agent in two cases of leprosy and reported significant improvements in an 1854paper.

This paper caused some confusion. Mouat indicated that the oil was the product of a treeChaulmoogra odorata, which had been described in 1815 by William Roxburgh, a surgeon andnaturalist, while he was cataloging the plants in the East India Companys botanical garden inCalcutta. This tree is also known as Gynocardia odorata. For the rest of the 19th century, thistree was thought to be the source of the oil. In 1901, Sir David Prain identified the true

chaulmoogra seeds of the Calcutta bazaar and of the Paris and London apothecaries as comingfrom Taraktogenos kurzii, which is found in Burma and Northeast India. The oil mentioned inthe Ayurvedic texts was from the treeHydnocarpus wightiana, known as Tuvakara in Sanskritand chaulmugra in Hindi and Persian.

The first parenteral administration was given by the Egyptian doctorTortoulis Bey, personalphysician to the Sultan Hussein Kamel of Egypt. He had been using subcutaneous injections ofcreosote for tuberculosis and in 1894 administered subcutaneous injection of chaulmoogra oil ina 36-year-old Egyptian Copt who had been unable to tolerate oral treatment. After 6 years and584 injections, the patient was declared cured.

An early scientific analysis of the oil was carried out by Frederick B. Powerin London in 1904.He and his colleagues isolated a new unsaturated fatty acid from the seeds, which they named'chaulmoogric acid'. They also investigated two closely related species:HydnocarpusanthelminticaandHydnocarpus wightiana. From these two trees they isolated bothchaulmoogric acid and a closely related compound, 'hydnocarpus acid'. They also investigatedGynocardia odorata and found that it produced neither of these acids. Later investigationshowed that 'taraktogenos' (Hydnocarpus kurzii) also produced chaulmoogric acid.

Another difficulty with the use of this oil was administration. Taken orally it is extremelynauseating. Given by enema may cause peri-anal ulcers and fissures. Given by injection the drugcaused fever and other local reactions. Despite these difficulties, a series of 170 patients werereported in 1916 by Ralph Hopkins, the attending physician at the Louisiana Leper Home inCarville, Louisiana. He divided the patients into two groups - 'incipient' and 'advanced'. In theadvanced cases, 25% (at most) showed any improvement or arrest of their condition; in theincipient cases, 45% reported an improvement or stabilization of the disease (mortality rateswere 4% and 8%, respectively). The remainder absconded from the Home apparently inimproved condition.

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Given the apparent usefulness of this agent, a search began for improved formulations. VictorHeiser the Chief Quarantine Officer and Director of Health for Manila and Elidoro Mercado thehouse physician at the San Lazaro Hospital for lepers in Manila decided to add camphor to aprescription of chaulmoogra and resorcin, which was typically given orally at the suggestion ofMerck and Company in Germany to whom Heiser had written. They found that this new

compound was readily absorbed without the nausea that had plagued the earlier preparations.

Heiser and Mercado in 1913 then administered the oil by injection to two patients who werecured of the disease. Since this treatment was administered in conjunction with other materials,the results were not clear. A further two patients were treated with the oil by injection withoutother treatments and again appeared to be cured of the disease. The following year, Heiserreported a further 12 patients but the results were mixed.

Less toxic injectable forms of this oil were then sought. Between 1920 and 1922, a series ofpapers were published describing the esters of these oils. These may have been based on thework of Alice Ball - the record is not clear on this point and Ms Ball died in 1916. Trials of these

esters were carried out in 1921 and appeared to give useful results.

These attempts had been preceded by others. Merck of Darmstadt had produced a version of thesodium salts in 1891. They named this sodium gynocardate in the mistaken belief that the originof the oil was Gynocardia odorata. Bayer in 1908 marketed a commercial version of the estersunder the name 'Antileprol'.

To ensure a supply of this agent Joseph Rock, Professor of Systematic Botany at the College ofHawaii, traveled to Burma. The local villagers located a grove of trees in seed, which he used toestablish a plantation in 2,980 trees on the island of Oahu, Hawaii between 1921 and 1922.

The oil remained a popular treatment despite the common side effects until the introduction ofsulfones in the 1940s. Debate about its efficacy continued until it was discontinued.

Modern drug treatment

MDT patient packs and blisters

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Epidemiology

Worldwide, two to three million people are estimated to be permanently disabled because ofleprosy. India has the greatest number of cases, with Brazil second and Myanmar third.

In 1999, the world incidence of Hansen's disease was estimated to be 640,000. In 2000, 738,284cases were identified. In 2000, the World Health Organization (WHO) listed 91 countries inwhich Hansen's disease is endemic. India, Burma, and Nepal contained 70% of cases. Indiareports over 50% of the world's leprosy cases. In 2002, 763,917 new cases were detectedworldwide, and in that year the WHO listed Brazil, Madagascar, Mozambique, Tanzania, andNepal as having 90% of Hansen's disease cases.

Although annual incidencethe number of new leprosy cases occurring each yearisimportant as a measure of transmission, it is difficult to measure in leprosy due to its longincubation period, delays in diagnosis after onset of the disease, and the lack of laboratory toolsto detect leprosy in its very early stages. Instead, the registered prevalence is used. Registeredprevalence is a useful proxy indicator of the disease burden, as it reflects the number of activeleprosy cases diagnosed with the disease and receiving treatment with MDT at a given point intime. The prevalence rate is defined as the number of cases registered for MDT treatment amongthe 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 anannual 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 backlogprevalence of undetected cases).

Endemic countries also report the number of new cases with established disabilities at the time ofdetection, as an indicator of the backlog prevalence. Determination of the time of onset of thedisease is, in general, unreliable, is very labor-intensive, and is seldom done in recording thesestatistics.

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G. H. A. Hansen, discoverer ofM. leprae

DNA taken from the shrouded remains of a man discovered in a tomb next to the Old City ofJerusalem shows him to be the earliest human proven to have suffered from leprosy. The remains

were dated by radiocarbon methods to 1-50 C.E.

After the end of the 17th century, Norway, Iceland and England were the countries in WesternEurope where leprosy was a significant problem. During the 1830s, the number of lepers inNorway, Iceland and England rose rapidly, believed to be caused by frequent visits of sailorswho visited Western India, causing an increase in medical research into the condition, and thedisease became a political issue. Norway appointed a medical superintendent for leprosy in 1854and established a national register for lepers in 1856, the first national patient register in theworld. Mycobacterium leprae, the causative agent of leprosy, was discovered by G. H. Armauer

Hansen in Norway in 1873, making it the first bacterium to be identified as causing disease inhumans. The principal opposition to Hansen's view that leprosy was an infectious disease camefrom his father-in-law, Daniel Cornelius Danielssen who considered it a hereditary disease andhad stated this in his book, Trait de la Spedalskhed ou Elephantiasis des Grecs - the standardreference book on leprosy from 1848 until the death of Danielssen in 1895.

Hansen observed a number of nonrefractile small rods in unstained tissue sections. The rodswere not soluble in potassium lye, and they were acid- and alcohol-fast. In 1879, he was able tostain these organisms with Ziehl's method and the similarities with Koch's bacillus(Mycobacterium tuberculosis) were noted. There were three significant differences betweenthese organisms: (1) the rods in the leprosy lesions were extremely numerous, (2) they formed

characteristic intracellular collections (globii), and (3) the rods had a variety of shapes withbranching and swelling. These differences suggested that leprosy was caused by an organismrelated to but distinct fromMycobacterium tuberculosis.

He worked at St. Jrgens Hospitalin Bergen, founded early in the fifteenth century. St. Jrgensis today a museum,Lepramuseet, it can be argued the best-preserved leprosy hospital inNorthern Europe.

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References

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2. ^abc"New Leprosy Bacterium: Scientists Use Genetic Fingerprint To Nail 'KillingOrganism'".ScienceDaily. 2008-11-28. Retrieved 2010-01-31.

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4. ^ab"Lifting the stigma of leprosy: a new vaccine offers hope against an ancient disease".Time119 (19): 87. May 1982.PMID10255067.

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6. ^"Q and A about leprosy". American Leprosy Missions. Retrieved 2011-01-22. "Dofingers and toes fall off when someone gets leprosy? No. The bacillus attacks nerveendings 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 becomeinfected and result in tissue loss. Fingers and toes become shortened and deformed as thecartilage is absorbed into the body."

7. ^City of Houston Government Center, Health and Human Services. (n.d.). Hansen'sdisease (leprosy) Retrieved fromhttp://www.houstontx.gov/health/ComDisease/hansens.html

8. ^"Probable Zoonotic Leprosy in the Southern United States". The New England Journalof Medicine. Retrieved April 28, 2011.

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