Hansen’s disease (also known as leprosy) is an infection caused by bacteria called Mycobacterium leprae. These bacteria grow very slowly and it may take up to 20 years to develop signs of the infection.

The disease can affect the nerves, skin, eyes, and lining of the nose (nasal mucosa). The bacteria attack the nerves, which can become swollen under the skin. This can cause the affected areas to lose the ability to sense touch and pain, which can lead to injuries, like cuts and burns. Usually, the affected skin changes color and either becomes:

• lighter or darker, often dry or flaky, with loss of feeling, or
• reddish due to inflammation of the skin.

If left untreated, the nerve damage can result in paralysis of hands and feet. In very advanced cases, the person may have multiple injuries due to lack of sensation, and eventually the body may reabsorb the affected digits over time, resulting in the apparent loss of toes and fingers. Corneal ulcers and blindness can also occur if facial nerves are affected. Other signs of advanced Hansen’s disease may include loss of eyebrows and saddle-nose deformity resulting from damage to the nasal septum.

Early diagnosis and treatment usually prevent disability that can result from the disease, and people with Hansen’s disease can continue to work and lead an active life. Once treatment is started, the person is no longer contagious. However, it is very important to finish the entire course of treatment as directed by the doctor.

Each year, about 150 people in the United States and 250,000 around the world get the illness. In the past, Hansen’s disease was feared as a highly contagious, devastating disease, but now we know that it’s hard to spread and it’s easily treatable once recognized. Still, a lot of stigma and prejudice remains about the disease, and those suffering from it are isolated and discriminated against in many places where the disease is seen. Continued commitment to fighting the stigma through education and improving access to treatment will lead to a world free of this completely treatable disease.

Leprosy, also called Hansen disease, is a disorder known since ancient times. It is caused by bacteria called Mycobacterium leprae and is contagious, which means that it can be passed from person to person. It is usually contracted by breathing airborne droplets from affected individuals' coughs and sneezes, or by coming into contact with their nasal fluids. However, it is not highly transmissible, and approximately 95 percent of individuals who are exposed to Mycobacterium leprae never develop leprosy. The infection can be contracted at any age, and signs and symptoms can take anywhere from several months to 20 years to appear.

Leprosy affects the skin and the peripheral nerves, which connect the brain and spinal cord to muscles and to sensory cells that detect sensations such as touch, pain, and heat. Most affected individuals have areas of skin damage (cutaneous lesions) and problems with nerve function (peripheral neuropathy); however, the severity and extent of the problems vary widely. Leprosy occurs on a spectrum, in which the most severe form is called multibacillary or lepromatous, and the least severe form is called paucibacillary or tuberculoid. Patterns of signs and symptoms intermediate between these forms are sometimes called borderline forms.

Multibacillary leprosy usually involves a large number of cutaneous lesions, including both surface damage and lumps under the skin (nodules). The moist tissues that line body openings such as the eyelids and the inside of the nose and mouth (mucous membranes) can also be affected, which can lead to vision loss, destruction of nasal tissue, or impaired speech. Some affected individuals have damage to internal organs and tissues. The nerve damage that occurs in multibacillary leprosy often results in a lack of sensation in the hands and feet. Repeated injuries that go unnoticed and untreated because of this lack of sensation can lead to reabsorption of affected fingers or toes by the body, resulting in the shortening or loss of these digits.

Paucibacillary leprosy typically involves a small number of surface lesions on the skin. There is generally loss of sensation in these areas, but the other signs and symptoms that occur in multibacillary leprosy are less likely to develop in this form of the disorder.

In any form of leprosy, episodes called reactions can occur, and can lead to further nerve damage. These episodes can include reversal reactions, which involve pain and swelling of the skin lesions and the nerves in the hands and feet. People with the more severe forms of leprosy can develop a type of reaction called erythema nodosum leprosum (ENL). These episodes involve fever and painful skin nodules. In addition, painful, swollen nerves can occur. ENL can also lead to inflammation of the joints, eyes, and the testicles in men.

Leprosy has long been stigmatized because of its infectious nature and the disfigurement it can cause. This stigma can cause social and emotional problems for affected individuals. However, modern treatments can prevent leprosy from getting worse and spreading to other people. While the infection is curable, nerve and tissue damage that occurred before treatment is generally permanent.

About 250,000 new cases of leprosy are diagnosed every year. The condition occurs worldwide, but is most common in India, Brazil, and other areas with warm climates. Between 100 and 250 new cases per year occur in the United States.

World Leprosy Day is observed on the last Sunday of January each year. Established in 1954 by French philanthropist Raoul Follereau, it aims to raise awareness about leprosy (now called Hansen’s disease) and teach people about this ancient disease that is easily curable today. While rare in the United States, many people around the world continue to suffer from this curable disease due to lack of access to basic medical care and continued stigma surrounding the illness.

Leprosy was renamed Hansen’s disease after Norwegian scientist Gerhard Henrik Armauer Hansen, who in 1873 discovered the slow-growing bacterium now known as Mycobacterium leprae as the cause of the illness. It is difficult to catch, and it can take many years to develop symptoms of the disease following an infection. However, people who catch the disease can easily be cured with antibiotics.

Together, we can put a stop to discrimination and stigma against people with Hansen’s disease. We can learn to recognize symptoms and know when to see a physician for diagnosis. Educate yourself and your community and separate the facts from the myths about Hansen’s disease.

Burden of Hansen’s Disease

Around the world:

• The number of new cases reported globally to World Health Organization (WHO) in 2019 was more than 200,000.
• Close to 15,000 children were diagnosed with Hansen’s disease in 2019, more than 40 a day.
• An estimated 2 to 3 million people are living with Hansen’s disease-related disabilities globally.
• In 2019, the countries with the highest number of new diagnoses were India, Brazil, and Indonesia.
• Over half of all new cases of Hansen’s disease are diagnosed in India, which remains home to a third of the world’s poor, a group disproportionately affected by the disease.

In the United States:

• About 150 to 250 cases are reported each year.
• In 2018, 185 new cases were reported to the National Hansen’s Disease Program (NHDP), which coordinates care, research, and information about Hansen’s disease in the U.S.
• Most U.S. cases occur in people who have lived in areas of the world where the disease is still common. Most new cases in 2018 were reported from Arkansas, California, Florida, Hawaii, Louisiana, New York, and Texas.
• In some parts of the southern United States, nine-banded armadillos have been found to carry the bacterium that causes Hansen’s disease. Experts think the armadillos may spread it to people when they handle these animals.

Challenges of Hansen’s Disease

Hansen’s disease mainly affects people in resource-limited countries, especially those who live in crowded conditions. Many have difficulty accessing health care due to high costs of going to the doctor and long distances to reach providers and clinics familiar with Hansen’s disease. Because of this, many of those affected don’t complete treatment or don’t receive it at all, even though the WHO has a program that provides free treatment. Due the continued stigma against people with Hansen’s disease, they may not seek help when first symptoms appear, causing delay in diagnosis and development of disabilities.

Girls and women affected by Hansen’s disease face the added issue of gender and social discrimination, which may also delay detection of the disease. In some countries, the law allows a person to legally divorce a spouse because they are affected by the disease. Unfortunately, this may leave many women destitute, homeless, and unable to care for their children.

Many people living with Hansen’s disease are unable to work due to disability caused by the disease or may face stigma that prevents them from working.

The good news is that Hansen’s disease is curable with antibiotics. Education and improving access to basic health services for all are keys to successful elimination of stigma and disability associated with the illness.

Hansen’s Disease FAQ

There are some misconceptions about Hansen’s disease that continue to cause confusion and fuel stigma and discrimination. Here are seven common questions and answers about the disease so you can get the facts.

What You Can Do to Help

Many people think of leprosy as an ancient disease that was eradicated many years ago. But each year, thousands of men, women, and children all over the world develop this disease. Despite effective treatment, leprosy is one of the world’s most stigmatized diseases, and people living with leprosy-related disabilities in many countries are shunned, denied basic human rights, and discriminated against. The stigma of leprosy affects the physical, psychological, social, and economic well-being of those with leprosy, contributing to the cycle of poverty in the affected regions.

During World Leprosy Day, we seek to increase public understanding of Hansen’s disease and tackle the social stigma attached to this completely curable disease.

How can you do your part?

• Educate yourself about Hansen’s disease and share with friends and family that leprosy is a curable illness.
• Help depict a positive image of leprosy and increase awareness about it in your community.
• Promote a positive image of leprosy which helps focus on the abilities of the affected individuals rather than disability.
• Search for World Leprosy Day activities online and see what’s happening in your area.

What is Hansen's disease?

Hansen's disease, also known as leprosy, is a complex infectious disease caused by a bacterium. The disease is often mistakenly identified as the "leprosy of the Old Testament," which has been clearly shown not to be Hansen's disease. Hansen's disease is not highly contagious and 95 percent of the human population has a natural immunity. It responds well to treatment and, if diagnosed and treated early, does not cause disability.

The Hansen's disease bacteria infect skin and sometimes other tissues, including the eye, the mucosa of the upper respiratory tract (nose) and the testes. Hansen's disease always involves the peripheral nerves. If untreated, nerve damage can result in crippling of hands and feet and blindness. Early diagnosis and treatment are the keys to preventing Hansen's disease-related disabilities. A person with HD can continue to work and lead an active life.

Hansen’s disease risk

Those at greatest risk are the family of a person who has the disease, but is not being treated. This could be because they are genetically susceptible and/or because they have prolonged contact with the infected individual. A spouse is the least at-risk family member. At greatest risk are children, brothers or sisters, or parents of an individual with untreated Hansen's disease.

Hansen's disease is not passed on from a mother to her unborn baby during pregnancy. Neither is it transmitted through sexual contact.

Is Hansen’s disease contagious?

Yes. However, it is not acquired from casual contact such as shaking hands, sitting next to someone on a bus, or sitting together at a meal. Hansen’s disease is far less contagious than other infectious diseases. More than 95 percent of the human population has a natural immunity to the disease. Healthcare workers rarely contract Hansen’s disease. Most cases of Hansen’s disease respond to treatment and become non-infectious within a very short time.

Treatment of Hansen’s disease

Hansen’s disease is curable using antibiotics. The three most commonly used are Dapsone, Rifampin and Clofazimine. Other antibiotics, such as Clarithromycin, Ofloxacin, Levofloxacin and Minocycline also work well against M. leprae. Dapsone and other Sulfone drugs were discovered to be effective in treating HD at the National Hansen’s Disease Program in 1941. These medications continue to be an important weapon against this disease.

Treatment regimens differ depending upon the form of the disease (see Treatment Guidelines). The National Hansen’s Disease Programs recommends treatment for 1 or two years, depending on the form of disease.

Treatment rapidly renders the disease non-communicable by killing nearly all the bacilli within a few days. These dead bacilli are then cleared from the body slowly, within a variable number of years, so that these dead bacilli may continue to be found in skin biopsies for several years.

Where on body is Hansen’s disease found?

Because the bacteria that cause Hansen's disease like the cooler parts of the body, the skin and its nerves are affected. This can cause dryness and stiffness of the skin. In some cases affected nerves can swell, causing pain. There can be loss of feeling and weakness in the muscles of the hands or feet.

Identifying Hansen’s disease

Hansen's disease in the U.S. is rare, but between 150 and 200 new cases are reported each year.

The first signs of Hansen's disease are usually pale or slightly red areas or a rash on the trunk or extremities. Frequently, but not always, there is an associated decrease in light touch sensation in the area of the rash. A loss of feeling in the hands or feet may also be the first signs of Hansen's disease. These changes in sensation are a valuable clue to diagnosis. Nasal congestion may be a sign of infection, but infection is more often associated with changes of the skin on the face, such as thinning of the eyebrows or eyelashes.

Your doctor can make the diagnosis by doing a test called a skin biopsy, which reveals a particular pathologic pattern and demonstrates the specific "red" staining bacteria. By far the most important diagnostic tool is the biopsy of the rash. There are no reliable ‘blood tests’ for the diagnosis of Hansen’s disease. Although some blood tests are promoted in some countries, they are not used in the United States.

Hansen’s disease and disfigurement

People with Hansen's disease who are diagnosed and treated early avoid many of the complications associated with the disease and experience no disfigurement or disability. Problems with insensitive fingers or toes can be prevented by avoiding injury and infections to these areas, and by taking the Hansen's disease medicines.

Many patients with the tuberculoid or Paucibacillary form of Hansen's disease can even self-heal without benefit of treatment, but it is the standard of care to treat all patients identified with the disease.

Hansen’s disease transmission

The most commonly accepted theory is that Hansen's disease is transmitted by way of the respiratory tract, since large numbers of bacteria can be found in the nose of some untreated patients. The degree of susceptibility of the person, the extent of exposure and environmental conditions are among factors probably of great importance in transmission.

Exposure to Hansen’s disease

If you think you have been exposed to Hansen's disease, you do not need to take any action. Most people have a natural immunity and there is no need for prophylaxis.

We do not yet have a vaccine or a blood or skin test that will tell if you have been exposed or if you have pre-clinical disease, although both of these are active areas of research at the National Hansen's Disease Programs.

Household contacts of people with Hansen's disease should have a thorough physical examination annually for five years. If they develop a questionable skin rash, they should notify their healthcare providers and have the skin rash biopsied to determine whether or not Hansen's disease is present.

Hansen’s disease in the U.S. and the world

In the U.S., there are approximately 6,500 cases on the National Hansen's Disease Programs Registry. This includes all cases reported since the registry began and who are still living. The number of cases with active disease and requiring drug treatment or management is approximately 3,300.

The NHDP compiles a statistical summary of new cases which present in the United States each year. Between 150 and 200 new U.S. cases are reported to the Registry annually.

The World Health Organization, which compiles global Hansen's disease data, registered a total of 296,499 new cases worldwide in 2008. This data indicates a rapid, drastic reduction of the number of cases seen each year for the previous 12 years and have raised questions. See the World Health Organization report, Global Leprosy Situation 2006 (not a U.S. Government Web site, pdf). Such data is very dependent upon operational factors such as the method of case finding (i.e., active screening of high risk groups, vs ‘passive’ case finding – waiting for patients to come to a clinic).

Delayed Hansen’s disease diagnosis

Unfortunately, the rash caused by Hansen's disease often resembles other skin diseases. Hansen's disease is a slowly developing, chronic, infectious disease and 2 to 10 years may elapse before clinical signs and symptoms appear.

Moreover most private sector physicians in the U.S. lack experience with this disease, and do not consider a diagnosis of Hansen's disease, even in a patient who has lived in or migrated from a country where Hansen's disease is prevalent. Often a patient sees several physicians before the correct diagnosis is made, delaying the initiation of treatment even more.

Forms of Hansen’s disease

Classification of this disease is complex, but overall there are two forms. Tuberculoid (or Paucibacillary – few bacilli) is a limited form of the disease that is contagious.
Lepromatous (or Multibacillary – many bacilli) is a more generalized form. Proper classification requires a skin biopsy. These are evaluated at the National Hansen’s Disease Programs at no charge.

Hansen’s disease and tuberculosis

Mycobacterium leprae, the bacillus that causes Hansen's disease is in the same bacterial family as M. tuberculosis, the bacillus that causes tuberculosis. Because of this relationship, the National Hansen's Disease Program conducts extramurally-funded research on tuberculosis. For more information, please see the National Hansen’s Disease Program Research webpage.

Hansen’s disease reaction

Some patients experience what is called a reaction after treatment has begun. This is a response of the immune system to dead or dying bacteria and can cause worsening of the rash or a painful neuritis which can affect sensation and/or strength. Reactions are NOT caused by the treatment, and are NOT a sign that the treatment is working.

Reaction can be mild or severe. If mild, no treatment or only over the counter anti- inflammatory medication may be sufficient. More severe reactions can be harmful to nerves and should be promptly treated by a physician. If you think you are having a reaction of any type, it is best to notify your physician so that he can decide on appropriate treatment.

Combinations of many variations in genes involved in the immune system affect a person's likelihood of contracting Mycobacterium leprae infection if exposed to the bacteria. Gene variations affecting the immune system also help determine the form of leprosy that individuals develop if the Mycobacterium leprae infection takes hold.

The body's initial, nonspecific response to an invading organism (innate immune response) is its first line of defense against Mycobacterium leprae. If this is followed by an immune system response specific to Mycobacterium leprae infection (adaptive immune response) that restricts the spread of the bacteria, an individual will probably develop the less severe paucibacillary form or not develop leprosy at all. If little or no adaptive immune response occurs, the bacteria can spread widely on the body, traveling through the skin and into the peripheral nerves, and sometimes into deeper tissues, leading to the more severe signs and symptoms of multibacillary leprosy.

Variations in immune system-related genes also affect the likelihood of developing episodes of reaction. Reactions occur when the immune system generates inflammation in response to dead bacteria that are still in the body.

The genes involved in leprosy provide instructions for making proteins that are involved in immune system processes such as recognition of the bacteria, immune system signaling, initiation of inflammation by the innate immune system, and production by the adaptive immune system of immune proteins (antibodies) specific to Mycobacteria leprae. The combined effect of the gene variations, as well as nongenetic factors that are not well understood, determine the effectiveness of these processes and the individual's vulnerability to leprosy.

Normal Function

The PRKN gene, one of the largest human genes, provides instructions for making a protein called parkin. Parkin plays a role in the cell machinery that breaks down (degrades) unneeded proteins by tagging damaged and excess proteins with molecules called ubiquitin. Ubiquitin serves as a signal to move unneeded proteins into specialized cell structures known as proteasomes, where the proteins are degraded. The ubiquitin-proteasome system acts as the cell's quality control system by disposing of damaged, misshapen, and excess proteins. This system also regulates the availability of proteins that are involved in several critical cell activities, such as the timing of cell division and growth. Because of its activity in the ubiquitin-proteasome system, parkin belongs to a group of proteins called E3 ubiquitin ligases.

Parkin appears to be involved in the maintenance of mitochondria, the energy-producing centers in cells. However, little is known about its role in mitochondrial function. Research suggests that parkin may help trigger the destruction of mitochondria that are not working properly.

Studies of the structure and activity of parkin have led researchers to propose several additional activities for this protein. Parkin may act as a tumor suppressor protein, which means it prevents cells from growing and dividing too rapidly or in an uncontrolled way. Parkin may also regulate the supply and release of sacs called synaptic vesicles from nerve cells. Synaptic vesicles contain chemical messengers that transmit signals from one nerve cell to another.

Health Conditions Related to Genetic Changes

Parkinson's disease

Researchers have identified more than 200 PRKN gene mutations that cause Parkinson's disease, a condition characterized by progressive problems with movement and balance. Mutations in this gene are associated with the juvenile form of Parkinson's disease, which appears before age 20, and some cases of the more common, late-onset form that begins after age 50.

Some PRKN gene mutations lead to an abnormally small parkin protein that is nonfunctional and is rapidly broken down (degraded) within cells. Other mutations insert, delete, or change DNA building blocks (nucleotides) in the PRKN gene, leading to a defective version of the parkin protein or preventing the production of this protein. The PRKN gene mutations associated with Parkinson's disease usually lead to a loss of parkin activity.

It is unclear how PRKN gene mutations cause Parkinson's disease. The loss of parkin activity probably disturbs the ubiquitin-proteasome system, which allows unneeded proteins to accumulate. A buildup of these proteins could disrupt normal cell activities such as the supply and release of synaptic vesicles, particularly those that contain a chemical messenger called dopamine. As parkin is normally abundant in the brain, its loss could lead to the impairment or death of nerve cells, including those that produce dopamine. Loss of dopamine-producing nerve cells is a characteristic feature of Parkinson's disease.

Mutations in the PRKN gene may also disrupt the regulation of mitochondria. Researchers speculate that mitochondrial dysfunction in dopamine-producing nerve cells may play an important role in causing the signs and symptoms of Parkinson's disease.

Leprosy

Studies suggest that common variations (polymorphisms) in the PRKN gene (and a neighboring gene called PACRG) can increase the risk of contracting Hansen disease, also known as leprosy. This disease affects the nerves and skin and is caused by the bacterium Mycobacterium leprae. It remains unclear how PRKN polymorphisms increase susceptibility to Hansen disease. Researchers believe that the ubiquitin-proteasome system may play a role in controlling infection. Polymorphisms in the PRKN gene may subtly alter parkin's function, making the ubiquitin-proteasome system less efficient.

Lung cancer

The PRKN gene spans part of a region on chromosome 6 known as FRA6E. This region is known as a fragile area because it is unstable and prone to breakage and rearrangement. Changes involving the FRA6E region have been reported in several forms of human cancer, including lung cancer. In some cancerous tumors, segments of the FRA6E region, including part or all of the PRKN gene, are abnormally deleted or duplicated. These genetic changes are described as somatic because they occur only in tumor cells and are not inherited. As a result of these alterations, parkin activity is reduced or absent in these cells. Because parkin is thought to act as a tumor suppressor, a shortage of this protein's function could allow cells to grow and divide in an uncontrolled manner, leading to tumor formation.

Ovarian cancer

Changes involving the FRA6E region (described above) have also been reported in ovarian cancer. These changes include abnormal deletion or duplication of segments of the FRA6E region, including part or all of the PRKN gene. As a result of these somatic alterations, parkin activity is reduced or absent in affected cells. Because parkin is thought to act as a tumor suppressor, a shortage of this protein's function could allow cells to grow and divide in an uncontrolled manner, leading to tumor formation.

Cancers

Deletion or duplication of segments of the FRA6E region that involve the PRKN gene have also been found in glioblastoma (a form of brain cancer) and colorectal cancer. As a result of these somatic alterations, parkin activity is reduced or absent in tumor cells. Because parkin is thought to act as a tumor suppressor, a shortage of this protein's function could allow cells to grow and divide in an uncontrolled manner, leading to tumor formation.

Other Names for This Gene

• AR-JP
• PARK2
• parkin
• Parkinson disease (autosomal recessive, juvenile) 2, parkin
• parkinson protein 2, E3 ubiquitin protein ligase (parkin)
• PDJ
• PRKN2_HUMAN
• ubiquitin E3 ligase

Genomic Location

Normal Function

The VDR gene provides instructions for making a protein called vitamin D receptor (VDR), which allows the body to respond to vitamin D. This vitamin can be acquired from foods in the diet or made in the body with help from sunlight exposure. Vitamin D is involved in maintaining the proper balance of several minerals in the body, including calcium and phosphate, which are essential for the normal formation of bones and teeth. One of vitamin D's major roles is to control the absorption of calcium and phosphate from the intestines into the bloodstream. Vitamin D is also involved in several processes unrelated to bone and tooth formation.

The VDR protein attaches (binds) to the active form of vitamin D, known as calcitriol. This interaction allows VDR to partner with another protein called retinoid X receptor (RXR). The resulting complex then binds to particular regions of DNA, known as vitamin D response elements, and regulates the activity of vitamin D-responsive genes. By turning these genes on or off, the complex helps control calcium and phosphate absorption and other processes.

Although the mechanism is not completely understood, the VDR protein is also involved in hair growth. Studies suggest that this process does not require calcitriol binding.

Health Conditions Related to Genetic Changes

Vitamin D-dependent rickets

Mutations in the VDR gene cause vitamin D-dependent rickets type 2A (VDDR2A), also known as hereditary vitamin D-resistant rickets (HVDRR). This disorder of bone development is characterized by low levels of calcium (hypocalcemia) and phosphate (hypophosphatemia) in the blood, which lead to soft, weak bones (rickets) that are prone to fracture. A common feature of this condition is abnormally curved (bowed) legs.

The VDR gene mutations that cause this condition prevent the VDR protein from functioning properly. Some changes in the VDR gene lead to an abnormally short version of the VDR protein. Others result in the production of an abnormal receptor that cannot bind to calcitriol, to RXR, or to DNA. Although there is plenty of calcitriol in the body, the altered VDR protein cannot stimulate gene activity important for mineral absorption. The lack of calcium and phosphate absorption in the intestines slows deposition of these minerals into developing bone (bone mineralization), which leads to soft, weak bones and other features of VDDR2A. Hypocalcemia also causes muscle weakness and seizures in some affected individuals. Most VDR gene mutations impair hair growth, leading to hair loss (alopecia); however, mutations that block VDR's ability to interact with calcitriol do not cause alopecia, indicating that calcitriol is not necessary for the receptor's role in hair development.

Alopecia areata

MedlinePlus Genetics provides information about Alopecia areata

Intervertebral disc disease

MedlinePlus Genetics provides information about Intervertebral disc disease

Kidney stones

MedlinePlus Genetics provides information about Kidney stones

Leprosy

MedlinePlus Genetics provides information about Leprosy

Other Names for This Gene

• 1,25-dihydroxyvitamin D3 receptor
• NR1I1
• nuclear receptor subfamily 1 group I member 1
• vitamin D (1,25- dihydroxyvitamin D3) receptor
• vitamin D3 receptor

Genomic Location

Who Is at Risk?

In the U.S., Hansen’s disease is rare. Around the world, as many as 2 million people are permanently disabled as a result of Hansen’s disease.

Overall, the risk of getting Hansen’s disease for any adult around the world is very low. That’s because more than 95% of all people have natural immunity to the disease.

You may be at risk for the disease if you live in a country where the disease is widespread. Countries that reported more than 1,000 new cases of Hansen’s disease to WHO between 2011 and 2015 are:

• Africa: Democratic Republic of Congo, Ethiopia, Madagascar, Mozambique, Nigeria, United Republic of Tanzania
• Asia: Bangladesh, India, Indonesia, Myanmar, Nepal, Philippines, Sri Lanka
• Americas: Brazil

You may also be at risk if you are in prolonged close contact with people who have untreatedHansen’s disease. If they have not been treated, you could get the bacteria that cause Hansen’s disease. However, as soon as patients start treatment, they are no longer able to spread the disease.

It is not known exactly how Hansen’s disease spreads between people. Scientists currently think it may happen when a person with Hansen’s disease coughs or sneezes, and a healthy person breathes in the droplets containing the bacteria. Prolonged, close contact with someone with untreated leprosy over many months is needed to catch the disease.

You cannot get leprosy from a casual contact with a person who has Hansen’s disease like:

• Shaking hands or hugging
• Sitting next to each other on the bus
• Sitting together at a meal

Hansen’s disease is also not passed on from a mother to her unborn baby during pregnancy and it is also not spread through sexual contact.

Due to the slow-growing nature of the bacteria and the long time it takes to develop signs of the disease, it is often very difficult to find the source of infection.

In the southern United States, some armadillos are naturally infected with the bacteria that cause Hansen’s disease in people and it may be possible that they can spread it to people. However, the risk is very low and most people who come into contact with armadillos are unlikely to get Hansen’s disease.

For general health reasons, avoid contact with armadillos whenever possible. If you had a contact with an armadillo and are worried about getting Hansen’s disease, talk to your healthcare provider. Your doctor will follow up with you over time and perform periodic skin examinations to see if you develop the disease. In the unlikely event that you have Hansen’s disease, your doctor can help you get treatment.

Symptoms mainly affect the skin, nerves, and mucous membranes (the soft, moist areas just inside the body’s openings).

The disease can cause skin symptoms such as:

• Discolored patches of skin, usually flat, that may be numb and look faded (lighter than the skin around)
• Growths (nodules) on the skin
• Thick, stiff or dry skin
• Painless ulcers on the soles of feet
• Painless swelling or lumps on the face or earlobes
• Loss of eyebrows or eyelashes

Symptoms caused by damage to the nerves are:

• Numbness of affected areas of the skin
• Muscle weakness or paralysis (especially in the hands and feet)
• Enlarged nerves (especially those around the elbow and knee and in the sides of the neck)
• Eye problems that may lead to blindness (when facial nerves are affected)

Symptoms caused by the disease in the mucous membranes are:

• A stuffy nose
• Nosebleeds

Since Hansen’s disease affects the nerves, loss of feeling or sensation can occur. When loss of sensation occurs, injuries such as burns may go unnoticed. Because you may not feel the pain that can warn you of harm to your body, take extra caution to ensure the affected parts of your body are not injured.

If left untreated, the signs of advanced leprosy can include:

• Paralysis and crippling of hands and feet
• Shortening of toes and fingers due to reabsorption
• Chronic non-healing ulcers on the bottoms of the feet
• Blindness
• Loss of eyebrows
• Nose disfigurement

Other complications that may sometimes occur are:

• Painful or tender nerves
• Redness and pain around the affected area
• Burning sensation in the skin

Hansen’s disease can be recognized by appearance of patches of skin that may look lighter or darker than the normal skin. Sometimes the affected skin areas may be reddish. Loss of feeling in these skin patches is common. You may not feel a light touch or a prick with a needle.

To confirm the diagnosis, your doctor will take a sample of your skin or nerve (through a skin or nerve biopsy) to look for the bacteria under the microscope and may also do tests to rule out other skin diseases.

Hansen’s disease is treated with a combination of antibiotics. Typically, 2 or 3 antibiotics are used at the same time. These are dapsone with rifampicin, and clofazimine is added for some types of the disease. This is called multidrug therapy. This strategy helps prevent the development of antibiotic resistance by the bacteria, which may otherwise occur due to length of the treatment.

Treatment usually lasts between one to two years. The illness can be cured if treatment is completed as prescribed.

If you are treated for Hansen’s disease, it’s important to:

• Tell your doctor if you experience numbness or a loss of feeling in certain parts of the body or in patches on the skin. This may be caused by nerve damage from the infection. If you have numbness and loss of feeling, take extra care to prevent injuries that may occur, like burns and cuts.
• Take the antibiotics until your doctor says your treatment is complete. If you stop earlier, the bacteria may start growing again and you may get sick again.
• Tell your doctor if the affected skin patches become red and painful, nerves become painful or swollen, or you develop a fever as these may be complications of Hansen’s disease that may require more intensive treatment with medicines that can reduce inflammation.

If left untreated, the nerve damage can result in paralysis and crippling of hands and feet. In very advanced cases, the person may have multiple injuries due to lack of sensation, and eventually the body may reabsorb the affected digits over time, resulting in the apparent loss of toes and fingers. Corneal ulcers or blindness can also occur if facial nerves are affected, due to loss of sensation of the cornea (outside) of the eye. Other signs of advanced leprosy may include loss of eyebrows and saddle-nose deformity resulting from damage to the nasal septum.

Antibiotics used during the treatment will kill the bacteria that cause leprosy. But while the treatment can cure the disease and prevent it from getting worse, it does not reverse nerve damage or physical disfiguration that may have occurred before the diagnosis. Thus, it is very important that the disease be diagnosed as early as possible, before any permanent nerve damage occurs.

In the U.S., people with Hansen’s disease may be treated at special clinics run by the National Hansen’s Disease Program. There are several federally supported outpatient clinics throughout the U.S. and Puerto Rico.