Hansen's Disease (Leprosy) | CDC Hansen's Disease (Leprosy) ShareCompartir Hansen's disease (also known as leprosy) is a long-lasting infection caused by bacteria. The disease was once feared as a highly contagious and devastating disease. Now, however, the disease is very rare and easily treated. Early diagnosis and treatment usually prevent disability related to the disease. Leprosy (Hansen's Disease) | NIH: National Institute of Allergy and Infectious Diseases share with facebook share with twitter share with linkedin Leprosy (Hansen's Disease) Leprosy (Hansen's Disease) is a chronic infectious disease that primarily affects the peripheral nerves, skin, upper respiratory tract, eyes, and nasal mucosa (lining of the nose). The disease is caused by a bacillus (rod-shaped) bacterium known as Mycobacterium leprae. Why Is the Study of Leprosy (Hansen's Disease) a Priority for NIAID?

At the beginning of 2010, the registered prevalence of leprosy in the world was 211,903 cases, and 244,796 new cases were detected during 2009, as reported by 141 countries (World Health Organization [WHO]). Since the 1980s, when the WHO initiated its Leprosy Elimination Project, more than 14 million cases have been cured. However, the number of new cases being detected annually is raising the unanswered questions about the infection source, transmission, and incubation period of leprosy. How Is NIAID Addressing This Critical Topic? Researchers are exploring more avenues than ever before in the search for solutions to leprosy, now that the genome of M. leprae has been sequenced. NIAID goals are to discover reservoirs of infection, routes of transmission, and incubation periods so the disease can be stopped before patients even have symptoms. New tests for early detection of leprosy before nerve damage occurs are now being developed. Innovative research efforts are addressing such issues as transmission and the true extent of leprosy incidence.

Studies are focusing on the areas of early detection (prior to developing clinical symptoms), prevention of nerve damage, surveillance of areas where drug resistance is occurring, and molecular epidemiology. Leprosy Pictures, Symptoms, History & Treatment Medical Author: Charles Patrick Davis, MD, PhD Charles Patrick Davis, MD, PhD Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications. Medical Editor: Melissa Conrad Stöppler, MD Melissa Conrad Stöppler, MD Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr.

Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology. Leprosy is a slowly developing, progressive disease that damages the skin and nervous system. Leprosy is caused by an infection with Mycobacterium leprae or M. lepromatosis bacteria. Early symptoms begin in cooler areas of the body and include loss of sensation. Signs of leprosy are painless ulcers, skin lesions of hypopigmented macules (flat, pale areas of skin), and eye damage (dryness, reduced blinking). Later, large ulcerations, loss of digits, skin nodules, and facial disfigurement may develop. The infection is thought to be spread person to person by nasal secretions or droplets. Leprosy is rarely transmitted from chimpanzees, mangabey monkeys, and nine-banded armadillos to humans by droplets or direct contact. Susceptibility to getting leprosy may be due to certain human genes. Antibiotics are used in the treatment of leprosy.

What is leprosy? Leprosy is a disease mainly caused by the bacteria Mycobacterium leprae, which causes damage to the skin and the peripheral nervous system. The disease develops slowly (from six months to 40 years) and results in skin lesions and deformities, most often affecting the cooler places on the body (for example, eyes, nose, earlobes, hands, feet , and testicles). The skin lesions and deformities can be very disfiguring and are the reason that infected individuals historically were considered outcasts in many cultures. Although human-to-human transmission is the primary source of infection, three other species can carry and (rarely) transfer M. leprae to humans: chimpanzees, mangabey monkeys, and nine-banded armadillos. The disease is termed a chronic granulomatous disease, similar to tuberculosis , because it produces inflammatory nodules (granulomas) in the skin and nerves over time. Medically Reviewed by a Doctor on 8/12/2016 What is Hansen's Disease? (with picture) What is Hansen's Disease?

Last Modified Date: 23 December 2016 Copyright Protected: These 10 facts about space will blow your mind Hansen's Disease is another name for leprosy , a disease which has haunted human civilization for thousands of years. Many people prefer to use the term “Hansen's Disease” to refer to this condition because “leprosy” has many negative associations, many of which are undeserved. Historically, people with Hansen's Disease were isolated from society in leper colonies, shunned because people did not understand how the disease was transmitted, and because of widespread fear of physical disabilities. Because diagnostics was an imperfect science, people with syphilis and a range of other diseases were often isolated along with lepers, thanks to mistaken diagnoses of leprosy. Clear evidence of leprosy has been uncovered in research dating to 600 BCE, and historical records suggests that the disease is much older. It is caused by an infection with Mycobacterium leprae. The bacteria colonizes the nervous system, especially in the extremities, and the mucous membranes.

Classically, distinctive skin lesions known as granulomas appear in the extremities, and the patient often experiences a loss of feeling in the extremities as the bacteria attacks the body. Ad Contrary to popular belief, Hansen's Disease does not make the limbs fall off. However, people are more prone to extremity damage because of the loss of feeling, so they may lose fingers and toes to damage and infections which went unnoticed. Lepers are also not typically covered in rotting sores, but if they do get skin infections, the infections may not be identified immediately, again due to the loss of feeling; Hansen's Disease also impedes the sense of smell by attacking the membranes of the nose, so patients don't recognize the characteristic odors of infection and decay. Hansen's Disease is named for Norwegian researcher Gerhard Henrik Armauer Hansen, who discovered the bacterium behind the disease in 1873. His discovery reshaped the way people thought about leprosy; previously, people thought the disease was used to punish the wicked, and that it was highly infectious.

Later research uncovered the fact that around 95% of the population is actually naturally immune to Hansen's Disease, and that prolonged close personal contact with a patient who has an active form of the disease is required in order to be at risk of developing it. Two forms of Hansen's Disease are recognized today: tuberculoid, a less serious form, and leprotomaus. Both can be treated with the assistance of antibiotics, although the sooner the treatment is administered, the better, because Hansen's Disease can cause permanent disability and damage. Hansen's Disease is primarily present in the tropics today, with treatment taking place in the community, rather than in isolated facilities. Ad Leprosy: History, Symptoms and Treatment Read more on Leprosy from Healthwise What is Leprosy? Leprosy, also called Hansen's disease, is a chronic infectious disease that primarily affects the skin, the peripheral nerves, the mucosa of the upper respiratory tract, and the eyes. Leprosy can lead to progressive permanent damage of these structures, and the resulting devastating disfigurement and disability has led to the historical social stigma and isolation (leper colonies) of those affected by the disease.

Historically speaking, leprosy has existed since at least 4000 BC, and the disease was present and described in the ancient civilizations of China, India, and Egypt. The first known written reference to the disease on Egyptian papyrus dates from about 1550 BC. It is believed that leprosy was brought to Europe by the Romans and the Crusaders and that later the Europeans brought it to the Americas. For centuries, leprosy remained a poorly understood disease characterized by human suffering and social isolation. In 1873, G.A. Hansen discovered the bacterial cause of this infectious disease. The first medication breakthrough occurred in the 1940s with the development of the drug dapsone , and later it was discovered that the bacteria which caused leprosy was more effectively killed by using multiple medications. Leprosy is a curable disease with the use of multidrug therapy (MDT). In 1991, the World Health Assembly passed a resolution to eliminate leprosy as a public-health problem by the year 2000.

The elimination of leprosy was defined as a prevalence rate of less than one case per 10,000 people in all countries, focused primarily on those where leprosy was commonly found. In the year 2000, the global elimination of leprosy, according to the prevalence rate, was achieved. With assistance from the World Health Organization (WHO), MDT has been distributed free to all patients with leprosy since 1995. Though leprosy is still endemic in a few developing countries (primarily in the tropics), there has been a dramatic worldwide decrease in the prevalence of the disease due to this successful public-health initiative. Over the past 20 years, close to 16 million leprosy patients have been cured, and the prevalence rate of the disease has decreased by 90%. Leprosy has been eliminated from 119 countries out of the 122 countries where previously leprosy had previously been deemed a public-health concern in 1985.

Official reports from 115 countries around the world reported 232,857 new cases of leprosy in 2012, with about 95% of these cases occurring in only 16 different countries. Countries in which leprosy is more commonly found include Angola, Bangladesh, Brazil, China, Central African Republic, Ethiopia, India, Indonesia, Madagascar, Myanmar, Nepal, Nigeria, Philippines, Sudan, South Sudan, Sri Lanka, United Republic of Tanzania, Democratic Republic of the Congo, and Mozambique. In the United States, according to the National Hansen's Disease Registry, 294 new cases were reported in 2010, with 65% of these cases occurring in California, Florida, Hawaii, Louisiana, New York, Texas, and Massachusetts. On average, 150-250 new cases of leprosy are diagnosed each year in the United States, with most cases occurring in immigrants. However, because the bacteria can be found in wild animals (for example, armadillos and chimpanzees), it is unlikely that leprosy will be totally eliminated like smallpox .

Medically Reviewed by a Doctor on 12/17/2015 Medical Author: Transmission | Hansen's Disease (Leprosy) | CDC Hansen's Disease (Leprosy) ShareCompartir Hansen’s disease is caused by infection with bacteria. Evidence suggests that the bacteria that cause Hansen’s disease can spread from person to person. This might happen when someone with the disease coughs or sneezes. This can release droplets into the air. It might also happen if you are exposed to other nasal fluids (also known as secretions). Droplets and other secretions can contain the bacteria that cause Hansen’s disease. If you breathe these in, you can become sick with the disease. File Formats Help: National Hansen's Disease (Leprosy) Program Caring and Curing Since 1894 Google Bookmarks National Hansen's Disease (Leprosy) Program Caring and Curing Since 1894 A genetic study at the National Hansen’s Disease Program reports that armadillos may be a source of infection in the southern United States.

The National Hansen's Disease Program advises: The risk of transmission from animals to humans is low, but armadillos are wild animals and should be treated as such, with all proper precautions. Individuals should decide for themselves whether or not to interact with these animals and, if so, what precautions to take. Learn more: Interview with Dr. Richard Truman, Chief, Laboratory Research Branch Hansen's disease, also known as leprosy, is a chronic bacterial disease that primarily affects the skin, peripheral nerves and upper airway. Feared as a highly contagious and devastating disease, it is well established that Hansen's disease (leprosy) is not highly transmissible, is very treatable, and, with early diagnosis and treatment, is not disabling. Compiled statistics reveal that Hansen's disease (leprosy) is rare in the U.S. There are currently approximately 6,500 cases; about 3,300 require active medical management. People with Hansen's disease (leprosy) can generally continue their normal work and other activities uninterrupted while they are under treatment, which may last several years. Yet Hansen's disease (leprosy) remains a misunderstood human infectious disease.

The stigma long associated with the disease still exists in most of the world and the psychological and social effects may be more difficult to deal with than the actual physical illness. Hansen's Disease (Leprosy) Facts Most (95%) of the human population is not susceptible to infection with M. leprae, the bacteria that causes Hansen's disease (leprosy). Treatment with standard antibiotic drugs is very effective. Patients become noninfectious after taking only a few doses of medication and need not be isolated from family and friends. Diagnosis in the U.S. is often delayed because health care providers are unaware of Hansen's disease (leprosy) and its symptoms. Early diagnosis and treatment prevents nerve involvement, the hallmark of Hansen's disease (leprosy), and the disability it causes. Without nerve involvement, Hansen's disease (leprosy) is a minor skin disease. 178 new cases were reported in the U.S. in 2015 (the most recent year for which data are available).

Most (129 or 72%) of these new cases were reported in Arkansas Texas The National Hansen's Disease (Leprosy) Program The National Hansen's Disease Program is the epicenter of Hansen's disease (leprosy) care, research and information in the U.S. Cares for patients at its facility at the Ochsner Medical Center in Baton Rouge. Oversees an ambulatory care network with clinics throughout the United States and Puerto Rico and makes referrals for treatment. Consults with private sector physicians and accepts referrals for patients with Hansen's disease (leprosy)-related complications. Advances treatment and educates medical professionals about Hansen's disease (leprosy). Conducts research intramural Hansen's disease (leprosy) biomedical research. Reaches out to medical professionals with a comprehensive Hansen's disease (leprosy) training program. The U.S. Government established the predecessor of the National Hansen's Disease (Leprosy) Program, the National Leprosarium in Carville, Louisiana, in 1917. Outpatient clinics were established in 1981.

Contact Information Leprosy Leprosy Aka: Leprosy, Mycobacterium leprae, Hansen's Disease, Hansen's Bacillus Epidemiology Children more vulnerable to infection than adults Immunity in 95% of patients Endemic areas United States (rare except in a few states) Texas Mycobacterium leprae (acid fast bacilli) Pathophysiology Incubation: 3 to 20 years Growth best in cooler parts of body at 35.6C (96.0F) Transmission Nasal secretions from untreated patients Low risk from casual and household contact Types Tuberculoid Leprosy (intact cellular immunity) Nerve changes predominate Lepromatous Leprosy (defective cellular immunity) Skin changes predominate Extensive bilateral symmetric Macule s and Papule s High Bacteria l load Macule s or Papule s, Nodule s or Plaque s Hypopigmented in dark skinned individuals May be hyperpigmented in other patients Sensation may be dulled in these areas Loss of lateral eyebrows Crippling of hand (Worldwide most frequent cause) Differential Diagnosis Acid-fast stain (Fite method) for acid-fast bacilli

 Skin smears, or skin or nerve biopsy Bacteria abundant in Lepromatous Leprosy Skin lesion biopsy Macrophage s with foamy cytoplasm Serology Dapsone 50-100 mg qd for 24-30 months AND Rifampin 600 mg qd for 6-12 month Borderline Lepromatous Dapsone 50-100 mg qd for 24 months AND Rifampin 600 mg qd for 24 months Lepromatous (may require indefinate treatment) Dapsone 50-100 mg qd for 24 months AND Rifampin 600 mg qd for 24 months AND Clofrazamine 50-200 mg qd for 24 months References Leprosy ( C0023343 ) Definition (MSHCZE) Chronická granulomatózní infekce vyvolaná MYCOBACTERIUM LEPRAE.

Granulomatózní léze se projevují na kůži, sliznici a periferních nervech. Lepra má dvě základní formy - lepromatózní (nervová) a tuberkuloidní (kožní neboli uzlová). Definition (NCI) A bacterial granulomatous infection caused by Mycobacterium leprae. It is a progressive disease affecting the skin, peripheral nerves, and limbs. If untreated, it causes permanent tissue damage leading to autoamputations. Definition (MSH) A chronic granulomatous infection caused by MYCOBACTERIUM LEPRAE. The granulomatous lesions are manifested in the skin, the mucous membranes, and the peripheral nerves. Two polar or principal types are lepromatous and tuberculoid. Definition (CSP) chronic granulomatous infection caused by Mycobacterium leprae; granulomatous lesions are manifested in the skin, the mucous membranes, and the peripheral nerves; two polar or principal types are lepromatous and tuberculoid.

Concepts 187316006, 186339006, 154298007, 266184007, 81004002 English Disease, Hansen, Hansen Disease, Hansen's Disease, Hansens Disease, Leprosies, Disease, Hansen's, Leprosy NOS, Leprosy, unspecified, [X]Leprosy, unspecified, HANSEN DIS, HANSENS DIS, leprosy, leprosy (diagnosis), Mycobacterium leprae infection NOS, infection due to Mycobacterium leprae, Leprosy [Hansen's disease], Leprosy [Disease/Finding], hansen disease, hansen's disease, Disease;Hansens (Leprosy), hansens disease, leprosy nos, Leprous infections, Leprosy NOS (disorder), [X]Leprosy, unspecified (disorder), Hansen's disease, Infection due to Mycobacterium leprae, Mycobacterium leprae infection, Leprosy (dis

order), Hansen, Leprosy, NOS, Leprosy, Hansens (leprosy) disease Italian Infezioni leprose, Malattia di Hansen, Lebbra, non specificata, Lebbra NAS, Infezione da Mycobacterium leprae NAS, Morbo di Hansen, Lebbra Dutch lepra, niet-gespecificeerd, Mycobacterium leprae-infectie NAO, ziekte van Hansen, lepra NAO, Lepra, niet gespecificeerd, lepra-infecties, lepra, Lepra [ziekte van Hansen], Hansen-ziekte, Lepra, Ziekte van Hansen French Lèpre, non précisée, Lèpre SAI, Infection à Mycobacterium leprae SAI, Infections lépreuses, Lèpre, Maladie de Hansen German Mycobacterium leprae Infektion NNB, Lepra NNB, Lepra, unspezifisch, Lepra [Aussatz], Lepra, nicht naeher bezeichnet, Leprainfektionen, Aussatz, Hansen-Krankheit, Lepra Portuguese Lepra NE

, Infecção a Mycobacterium leprae NE, Lepra, Infecções leprosas, Doença de Hansen, Hanseníase Spanish Lepra NEOM, Infección por Mycobacterium leprae NEOM, Lepra no especificada, lepra, SAI, lepra, SAI (trastorno), [X]lepra, no especificada (trastorno), [X]lepra, no especificada, Mal de Hansen, enfermedad de Hansen, infección por Mycobacterium leprae, lepra (trastorno), lepra, Infecciones por Mycobacterium leprae, Lepra, Enfermedad de Hansen Japanese ハンセン病、詳細不明, ハンセン病ＮＯＳ, らい菌感染ＮＯＳ, らい菌感染, ﾗｲｷﾝｶﾝｾﾝ, ﾗｲｷﾝｶﾝｾﾝNOS, ﾊﾝｾﾝﾋﾞｮｳｼｮｳｻｲﾌﾒｲ, ﾊﾝｾﾝﾋﾞｮｳ, ﾊﾝｾﾝﾋﾞｮｳNOS, Hansen病, �

�い, らい病, ハンセン病, レプラ, 癩, 癩病, ハンセン氏病 Swedish Spetälska Czech lepra, Lepra NOS, Lepra, Hansenova nemoc, Infekce Mycobacterium leprae NOS, Lepra, blíže neurčená, Infekce způsobené Mycobacterium leprae Finnish Hansens Etiologic agent: Mycobacterium leprae Transmission: The most frequently hypothesized method for the spread of M.

leprae is by droplet transmission from person to person (1). This hypothesis is supported by the finding the nasal mucosa of a leprosy patient may be a source of more than 10 million viable cells per day (6). An extended period of close contact is required for infection; M. lepraeï¿½s portal of entry may be by contact with intact skin or through the mucous membranes (3). With suitable conditions, as in tropical environments, the organism may remain viable for up to nine days; this suggests the possibility of transmission by indirect contact with the penetration of a wound (6). Additionally, armadillos in the southern United States carry the disease and matching strains have been identified in human cases. Leprosy may be a zoonosis spread by contact transmission or possibly by vehicle transmission with the consumption of an infected armadillo (4). Investigators have not determined the mode of transmission concretely, thus mechanical or biological insect vector transmission cannot be ruled out (6). Reservoirs: Humans are thought to be the natural reservoir of leprosy (6). More specifically persons with untreated, severe forms of the disease, coming from areas with endemic occurrences are more likely sources (1).

Scientists have sequenced the genomes of M. leprae from domestic cases and from wild armadillos, and they have found the strains to be identical (4). This new evidence identifies armadillos as an additional reservoir of the disease (id.). Chimpanzees, cynomolgus macaques, and sooty mangabey monkeys have also been reported to carry the disease; however transmission from these sources is highly unlikely (6). General characteristics: The organism is taxonomically classified as follows: kingdom Bacteria, phylum Actinobacteria, class Actinobacteria, subclass Actinobacteridae, order Actinomycetales, suborder Corynebacterineae, family Mycobacteriaceae, genus Mycobacterium, and species leprae (15). As M. leprae is of the phylum Actinobacteria, it is a high G + C, gram-positive bacteria (16). M. leprae may show filamentous growth of aerobic, non-endospore forming rods with unique cell walls containing mycolic acids (id.).

The gram-negative like cell wall defers in composition of the outermost layer which determines the bacteriumï¿½s waxy and water-resistant characteristics (id.). M. leprae is an obligate, intracellular parasite (6). The bacterium also has unique temperature requirements, as it grows best at the relatively low temperature of 30 degrees Celsius (16). The bacteriumï¿½s optimum growth temperature, host requirement, and lengthy doubling time of 12 days in vivo causes difficulty in cultivation; M. leprae has not been successfully grown in vitro (3). Growth in mouse foot pads and armadillos have been used to overcome the bacteriumï¿½s requirements (1). Identification tests: At present serological tests have not yet been developed for the diagnosis of leprosy, thus biopsy is the standard test performed (16). The tissue sample is taken from the spreading edges of the patientï¿½s lesions or from nodules and plaques (12). Acid-fast bacillus smears may be performed to detect the presence of bacteria from the genus Mycobacterium (11).

The procedure involves applying special stain to a slide thinly smeared with sampled cells followed by microscopic examination (id.). This test can determine the presence of acid fast bacilli of the genus within several hours (id.) A negative AFB smear indicates that the pathogen is not M. leprae, however the possibility of insufficient numbers cannot be excluded (id.). The positive AFB smear indicates infection, but does not definitively identify the species and thus drug sensitivity of the organism or the certainty of its absence (id.). An AFB culture must be performed to confirm leprosy diagnosis with results taking days to weeks (id.). In culturing, tissue is used to allow growth of the organism (16). With the results of the culture, a negative test may then rule out a leprosy diagnosis; positive test cultures may lead to the refinement of treatment (11). Another test, called the lepromin skin test is sometimes also used (7). The lepromin skin test is similar to the PPD test for tuberculosis with a reaction at the antigen injection site indicating a positive result (10).

Reactions only occur in patients with the most severe form of leprosy; a positive result may only be used to classify the type of leprosy (id.). It must also be noted that prior immunization with the bacillus Calmette-Guï¿½rin (BCG) vaccine will cause a false positive result (10). Improved testing time and specificity remain in the future, however advances in the field of genomics are promising (6). Signs and symptoms: Leprosy is also called Hansenï¿½s Disease. After infection, signs and symptoms generally appear 5 to 7 years later, then progress slowly (9). There are many forms of leprosy; the 2 poles are the less severe tuberculoid leprosy and more severe lepromatous leprosy (id.). In the tuberculoid form, cell-mediated immunity remains intact and fewer organisms are present (7). This form is paucibacillary, with patients presenting only one or few skin lesions (12).

The skin lesion(s) are characterized as ï¿½centrally hypopigmented macules with sharp, raised borders,ï¿½ with numbness due to underlying nerve damage accompanying the rash (id.). The tuberculoid form is ï¿½milder, less common, and less contagiousï¿½ (id.). In the lepromatous form, immunosuppression by the pathogen leads to higher organism numbers as cell-mediated defenses do not function properly (7). This form is multibacillary, with patients presenting with many lesions that may be on the skin, kidneys, nose, or testes (12). The skin lesions are characterized as ï¿½macules, papules, nodules, or plaques [that are] often symmetricï¿½ (id.). When on the face, papules and nodules may cause significant disfiguration (id.). Nerve damage is more severe in this form with a greater number of numb areas and muscle group weakness (id.). These symptoms may lead to inadvertent self injury and deformities (id.). Male breast enlargement, loss of eyelashes, eyebrows, fingers, or toes may occur in patients (id.).

The lepromatous form is the most contagious (id.). Complications of leprosy may be deadly, as with the development of plantar ulcers that are particularly vulnerable to secondary infection (id.). Between the two poles is a form called borderline leprosy, with patients displaying various ratios of tuberculoid and lepromatous presentations that may vary with time (id.). The borderline form is also very contagious (id.). Inflammatory reactions may occur in leprosy patients leading to skin swelling, vasodilation, skin redness, tenderness, progressively worse nerve function, destruction of blood vessels, liver inflammation, anemia, arthritis, fever, enlarged lymph nodes, and testicular swelling (id.). Other complications of the systemic disease include: chronic nasal congestion and bleeds, nasal septum damage, glaucoma, corneal scarring, blindness, erectile dysfunction, male infertility, and renal failure (id.). History: The written record of leprosy begins in India with the first widely accepted description in 600 BC (6). The disease then spread eastward to China by 500 BC, then on to Japan (id.).

Traders and conquering armies facilitated leprosyï¿½s travel to the Middle East and Greece (id.). The disease is thought to have arrived in the Mediterranean and Western Europe first by the Romans, and more so during the Crusades (id.). During the Middle Ages, leprosy spread rapidly throughout Europe, which was then followed by a rapid decline in cases (id.). ï¿½The factors involved in the near self-elimination of the disease in Europe remain unknownï¿½ (id.). Within the past 500 years, it is thought that leprosy was introduced to Western Africa and the Western Hemisphere by European explorers and the slave trade (id.). The impact of leprosy on cultures past and present is far reaching. In Mesopotamian and Jewish tradition, skin disease was thought to require ceremonial quarantine and purification (id.). Leprosy and sin are synonymous in Japanese Shintoism (id.). In China, it was believed that spread of the disease could only be thwarted by the live burial of individuals with leprosy (id.). The Hindu belief once attributed the disease to divine punishment (id.).

The Western view of leprosy has been detrimentally skewed by an inaccurate translation of the bible into Greek using the word ï¿½lepraï¿½ for unclean acts, which actually refers to ï¿½a scaly skin conditionï¿½ (id.). The mid-1800ï¿½s ushered in the modern scientific era and began the path toward freedom from persecution, stigmatization, and fear for leprosy sufferers (id.). In 1847, On Leprosy was published by Dr. Daniel Danielssen and Dr. Carl Boeck; their book clearly defined leprosy with the two main forms described and illustrated (id.). Then in 1873, Dr. Gerhard Amauer Hansen observed rod-shaped bacilli in a leprosy patientï¿½s nasal biopsy; he had discovered the etiological agent of the disease, Mycobacterium leprae (id.). In the 1940s, Dr. Guy Faget achieved great improvement in patients with Promin treatment, until then the ineffective use of chaulmoogra oil had been the only treatment available (id.).

Further leprosy drug research in the late 1940s led to the development of dapsone, which was used exclusively until the 1970s when drug resistance became apparent (id.). With advances in treatment in 1945, the American Public Health Association repealed recommendations for quarantine and isolation (5). Finally in 1960, the last compulsory isolation was enforced in the United States (id.). Virulence factors: M. leprae grows best at 30 degrees Celsius; the outer, cooler portions of the body provide a suitable environment for the pathogen (16). An important contribution to M. leprae virulence is the presence of mycolic acids in the outermost layer of the bacteriaï¿½s cell wall (id.). This characteristic allows the bacterium to resist penetration by antimicrobial drugs and prevents drying (id.). The bacterium also has the ability to survive within macrophages and the Schwann cells of peripheral nerves (6). The ability of the pathogen to remain inside cells provides protection from immune forces, provided antigens do not form on the host cell surface, and enables bacterial multiplication (13). Immune system responses to M.

leprae involve the lysis of infected cells (3). When the immune system responds to bacterial antigens, damage to infected nerves and tissues in the area ensues (6). Control and treatment: Control of Hansenï¿½s disease complications and outbreaks can be accomplished by provider and population awareness of early signs and symptoms (14). The Centers for Disease Control and Prevention along with the National Hansenï¿½s Disease Program offer surveillance and advice; cases should be reported to them (1). Approximately 95% of the human population is naturally insusceptible to the development of the disease, and only severe cases are considered contagious (14). Precautions such as hand hygiene and awareness of possible fomite contamination should be observed (1). Patient isolation is not necessary, as patients become noninfectious after only a few doses of medication (14). Treatment of Hansenï¿½s disease requires the use of multidrug therapy; which drugs are chosen and how they are used depend upon the form of the disease, the degree of progression, and cost (12).

For multibacillary patients the World Health Organization recommends the oral administration of rifampin 600 mg and clofazimine 300 mg once a month, and dapsone 100 mg with clofazimine 50 mg once per day (id.). With consideration of disease severity, treatment in this manner should be continued for 1 to 2 years (id.). Healthcare providers in the United States treat with oral rifampin 600 mg and oral dapsone 100 mg once per day for 3 years (id.). In borderline cases the dapsone is taken for 10 years, and in lepromatous leprosy it is taken indefinitely (id.). In paucibacillary cases the WHO regimen is oral rifampin 600 mg once a month and oral dapsone 100 mg once a day for 6 months (id.). If a patient only has one skin lesion one dose of rifampin 600 mg, oflaxacin 400 mg, and minocycline 100 mg are administered.

In the United States, oral rifampin 600 mg and oral dapsone 100 mg are both taken once a day for 6 months (id.) With tuberculoid leprosy dapsone treatment continues for 3 years, and for borderline tuberculoid leprosy dapsone treatment continues for 5 years (id.) Prevention: Avoiding skin to skin contact and contact with bodily fluids of infected persons ï¿½is the best preventionï¿½ (12). With the recent observance of possible zoonotic cases of leprosy, contact and consumption of armadillos should also be avoided (4). The BCG vaccine is sometimes used to protect against leprosy, although it is more commonly used to confer tuberculosis immunity (12). The BCG vaccineï¿½s effectiveness is not well studied; however positive results have been observed in areas with endemic disease (3). Investigators at the National Hansenï¿½s Disease Program are working toward an improved vaccine for Hansenï¿½s disease (14). Tom Gillis, Jim Krahenbuhl and Linda Adams aim to develop a DNA vaccination against M.

leprae (id.) Local cases: From 1985 to 2006, reported cases in the United States decreased (17). In 2002, 96 new cases were reported nationwide (1). By 2006, the number of national cases reported declined to 66 with 9 from Texas (20). Then in 2007, an increase in reported cases was observed in the United States (17). That year the CDC received 101 reports of new cases with 23 cases coming from Texas (19). By 2008, the decreasing trend returned with reported cases declining by 26.6%; that year California, Florida, Hawaii, and New York City accounted for 70% of new cases with 80 cases reported in total, and surprisingly none in Texas (17). Interestingly, the southern region of the United States reports cases of leprosy in Americans having had no foreign exposure; this is likely linked to the infection of wild armadillos in the south (4).

Global cases: In 1985, the prevalence of leprosy worldwide was estimated to be between 10 and 12 million people with 122 countries reporting an endemic presence of the disease (6). By 1994, the global burden of the disease had decreased dramatically to 2.7 million people (id.) Endemic disease decreased as well, with only 12 countries reporting such numbers in 2002 (id.) Also in 2002, global incidence was reported to be 763,917 with Brazil, Madagascar, Mozambique, Tanzania, and Nepal contributing to 90% of the cases (1). By 2003, new cases declined to 515,000 and endemic countries dropped from 12 to 9; these counties were India, Brazil, Nepal, Mozambique, Madagascar, Angola, Central African Republic, Democratic Republic of Congo, and United Republic of Tanzania (6). These same nine countries accounted for 88% of the global incidence and 84% of the global prevalence (id.).

By 2007 global incidence had decreased to 213,373 cases: 31,037 from the African Region, 2,854 from the Americas, 169,528 from South-East Asia, none from the European Region, 4,089 from the Eastern Mediterranean, and 5,865 from the Western Pacific (21). In 2008 global incidence remained fairly constant with 248,983 new reported cases: 29,814 from the African Region, 41,891 from the Americas, 167,505 from South-East Asia, none from the European Region, 3,938 from the Eastern Mediterranean, and 5,835 from the Western Pacific (18). Current global impact remains significant with between 1 and 2 million people disabled by the disease, however there is hope in that the number of cases reported each year generally decreases (1). Works cited: National Center for Zoonotic, Vector-Borne, and Enteric Diseases. Centers for Disease Control and Prevention.

ï¿½Hansenï¿½s Disease (Leprosy).ï¿½ Last updated: May 3, 2011. Accessed: May 3, 2011. Immigrant and Refugee Health. Centers for Disease Control and Prevention. ï¿½Required Evaluation Components: Hansenï¿½s disease (leprosy).ï¿½ Last Updated: May 3, 2011. Accessed: May 3, 2011. McMurray, David N. ï¿½Medical Microbiology.ï¿½ Published: 1996. Accessed: May 3, 2011. #A1834 Truman, Richard W., et al. ï¿½Probable zoonotic leprosy in the southern United States.ï¿½ Published: April 28, 2011. Accessed: May 3, 2011. Sato, Hajime and Janet E. Frantz.

ï¿½Termination of the leprosy isolation policy in the US and Japan: Science, policy changes, and the garbage can model.ï¿½ Published: March 16, 2005. Accessed: May 3, 2011. Bennett, Brian H., David L. Parker and Mark Robson. ï¿½Leprosy: Steps Along the Journey of Eradication.ï¿½ Published: March 2008. Accessed: May 3, 2011. Fox, Alvin. University of South Carolina School of Medicine. ï¿½Bacteriology: Mycobacteria and Corynebacteria.ï¿½ Last updated: June 28, 2010. Accessed: May 3, 2011. Spencer, John, et al. The American Association of Immunologists. ï¿½Identification of Specific Proteins and Peptides in Mycobacterium leprae Suitable for Selective Diagnosis of Leprosy.ï¿½ Published: December 15, 2005. Accessed: May 3, 2011. American Academy of Family Physicians.

ï¿½Leprosy.ï¿½ Last updated: February 2011. Accessed: May 3, 2011. U.S. National Library of Medicine. National Institutes of Health. ï¿½Lepromin skin test.ï¿½ Last updated: August 28, 2009. Accessed: May 3, 2011. American Association for Clinical Chemistry. ï¿½AFB Smear and Culture.ï¿½ Last updated: March 22, 2011. Accessed: May 3, 2011. Merck Sharp & Dohme Corp. ï¿½The Merck Manual for Healthcare Professionals.ï¿½ Last updated: September 2009. Accessed: May 3, 2011. Todar, Kenneth. ï¿½Bacterial Defense against Specific Immune Responses.ï¿½ Last updated: 2011. Accessed: May 4, 2011. Health Resources and Services Administration. U.S. Department of Health and Human Services.

ï¿½National Hansenï¿½s Disease (Leprosy) Program.ï¿½ Last updated: May 4, 2011. Accessed: May 4, 2011. The UniProt Consortium. ï¿½Taxonomy: Mycobacterium leprae.ï¿½ Last updated: May 4, 2011. Accessed: May 4, 2011. Tortora, Gerard J., Berdell R. Funke and Christine L. Case. ï¿½Microbiology: An Introduction.ï¿½ Published: January 9, 2009. Accessed: May 4, 2011 and May 5, 2011. Centers for Disease Control and Prevention. ï¿½Morbidity and Mortality Weekly Report: Summary of Notifiable Diseases.ï¿½ Published: June 25, 2010. Accessed: May 5, 2011. World Health Organization. ï¿½World Health Statistics: 2010.ï¿½ Published: 2010.

Accessed: May 5, 2011. Centers for Disease Control and Prevention. ï¿½Morbidity and Mortality Weekly Report: Summary of Notifiable Diseases 2007.ï¿½ Published: July 9, 2009. Accessed: May 5, 2011. Centers for Disease Control and Prevention. ï¿½Morbidity and Mortality Weekly Report: Summary of Notifiable Diseases 2006.ï¿½ Published: March 21, 2008. Accessed: May 5, 2011. World Health Organization. ï¿½World Health Statistics: 2009.ï¿½ Published: 2009. Accessed: May 5, 2011.

Question: Hansen's disease is another name for which bacterial infection ?
Answer: LEPROSY