Leprosy is an infectious disease that causes severe, disfiguring skin sores and nerve damage in the arms and legs. The disease has been around since ancient times, often surrounded by terrifying, negative stigmas and tales of leprosy patients being shunned as outcasts. Outbreaks of leprosy have affected, and panicked, people on every continent. The oldest civilizations of China, Egypt, and India feared leprosy was an incurable, mutilating, and contagious disease. However, leprosy is actually not that contagious. You can catch it only if you come into close and repeated contact with nose and mouth droplets from someone with untreated leprosy. Children are more likely to get leprosy than adults. Today, about 180,000 people worldwide are infected with leprosy, according to the World Health Organization, most of them in Africa and Asia. About 200 people are diagnosed with leprosy in the U.S. every year, mostly in the South, California, Hawaii, and some U.S. territories. What Causes Leprosy? Leprosy is caused by a slow-growing type of bacteria calledMycobacterium leprae (M. leprae). Leprosy is also known as Hansen's disease, after the scientist who discovered M. leprae in 1873. What Are the Symptoms of Leprosy? Leprosy primarily affects the skin and the nerves outside the brain and spinal cord, called the peripheral nerves. It may also strike the eyes and the thin tissue lining the inside of the nose. The main symptom of leprosy is disfiguring skin sores, lumps, or bumps that do not go away after several weeks or months. The skin sores are pale-colored. Nerve damage can lead to:
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Leprosy is an infectious disease that causes severe, disfiguring skinsores and nerve
damage in the arms and legs. The disease has been around since ancient times, often
surrounded by terrifying, negative stigmas and tales of leprosy patients being shunned
as outcasts. Outbreaks of leprosy have affected, and panicked, people on every
continent. The oldest civilizations of China, Egypt, and India feared leprosy was an
incurable, mutilating, and contagious disease.
However, leprosy is actually not that contagious. You can catch it only if you come into
close and repeated contact with nose and mouth droplets from someone with untreated
leprosy. Children are more likely to get leprosy than adults.
Today, about 180,000 people worldwide are infected with leprosy, according to the
World Health Organization, most of them in Africa and Asia. About 200 people are
diagnosed with leprosy in the U.S. every year, mostly in the South, California, Hawaii,
and some U.S. territories.
What Causes Leprosy?
Leprosy is caused by a slow-growing type of bacteria calledMycobacterium leprae (M.
leprae). Leprosy is also known as Hansen's disease, after the scientist who
discovered M. leprae in 1873.
What Are the Symptoms of Leprosy?
Leprosy primarily affects the skin and the nerves outside the brain and spinal cord,
called the peripheral nerves. It may also strike the eyes and the thin tissue lining the
inside of the nose.
The main symptom of leprosy is disfiguring skin sores, lumps, or bumps that do not go
away after several weeks or months. The skin sores are pale-colored.
Nerve damage can lead to:
Loss of feeling in the arms and legs
Muscle weakness
It usually takes about 3 to 5 years for symptoms to appear after coming into contact with
the leprosy-causing bacteria. Some people do not develop symptoms until 20 years
later. The time between contact with the bacteria and the appearance of symptoms is
called the incubation period. Leprosy's long incubation period makes it very difficult for
doctors to determine when and where a person with leprosy got infected.
Forms of Leprosy
Leprosy is defined by the number and type of skin sores you have. Specific symptoms
and treatment depend on the type of leprosy you have. The types are:
Leprosy Overview(continued)In this article
What Causes Leprosy?
What Are the Symptoms of Leprosy?
Forms of Leprosy
How Is Leprosy Diagnosed?
How Is Leprosy Treated?
Leprosy Complications
Forms of Leprosy continued...
Tuberculoid. A mild, less severe form of leprosy. People with this type have only one or
a few patches of flat, pale-colored skin (paucibacillary leprosy). The affected area of
skin may feel numb because of nerve damage underneath. Tuberculoid leprosy is less
contagious than other forms.
Lepromatous. A more severe form of the disease. It has widespread skin bumps
and rashes (multibacillary leprosy), numbness, and muscle weakness. The
nose, kidneys, and male reproductive organs may also be affected. It is more
contagious than tuberculoid leprosy.
Borderline. People with this type of leprosy have symptoms of both the tuberculoid and
lepromatous forms.
How Is Leprosy Diagnosed?
If you have a suspicious skin sore, your doctor will remove a small sample of the
abnormal skin and send it to a lab to be examined. This is called a skin biopsy. A skin
smear test may also be done. With paucibacillary leprosy, no bacteria will be detected.
In contrast, bacteria are expected to be found on a skin smear test from a person with
multibacillary leprosy.
How Is Leprosy Treated?
Leprosy can be cured. In the last two decades, more than 14 million people with leprosy
have been cured. The World Health Organization provides free treatment for all people
with leprosy.
Treatment depends on the type of leprosy that you have. Antibiotics are used to treat
the infection. Long-term treatment with two or more antibiotics is recommended, usually
from six months to a year. People with severe leprosy may need to take antibiotics
longer. Antibiotics cannot treat the nerve damage.
Anti-inflammatory drugs are used to control swelling related to leprosy. This may include
steroids, such as prednisone.
Patients with leprosy may also be given thalidomide, a potent medication that
suppresses the body's immune system. It helps treat leprosy skin nodules. Thalidomide
is known to cause severe, life-threatening birth defects and should never be taken
by pregnantwomen.
Leprosy Complications
Without treatment, leprosy can permanently damage your skin, nerves, arms, legs, feet,
and eyes.
Complications of leprosy can include:
Blindness or glaucoma.
Disfiguration of the face (including permanent swelling, bumps, and lumps).
Erectile dysfunction and infertility in men.
Kidney failure.
Muscle weakness that leads to claw-like hands or an inability to flex the feet.
Permanent damage to the inside of the nose, which can lead tonosebleeds and a
chronic, stuffy nose.
Permanent damage to the nerves outside the brain and spinal cord, including those in
the arms, legs, and feet.
Nerve damage can lead to a dangerous loss of feeling. A person with leprosy-related
nerve damage may not feel pain when the hands, legs, or feet are cut, burned, or
otherwise injured.
WebMD Medical Reference
View Article Sources Reviewed by Melinda Ratini, DO, MS on April 23, 2013
Leprosy / ̍ l ɛ p r ə s i / ,[1] also known as Hansen's disease (HD), is a chronic infection caused by the bacteria Mycobacterium leprae [2] and Mycobacterium lepromatosis.[3] Initially, infections are without symptoms and typically remain this way for 5 to as long as 20 years. [2] Symptoms that develop include granulomas of the nerves,respiratory tract, skin, and eyes.[2] This may result in a lack of ability to feel pain and thus loss of parts of extremities due to repeated injuries. [4] Weakness and poor eyesight may also be present.[4]
The two main types of disease are based on the number of bacteria present: paucibacillary and multibacillary.[4]The two types are differentiated by the number of poorly pigmented, numb skin patches present, with paucibacillary having five or fewer and multibacillary having more than five.[4] The diagnosis is confirmed by findingacid-fast bacilli in a biopsy of the skin or via detecting the DNA by polymerase chain reaction.[4] It occurs more commonly among those living in poverty and is believed to be transmitted by respiratory droplets.[4] It is not very contagious.[4]
Leprosy is curable with treatment.[2] Treatment for paucibacillary leprosy is with the medications dapsone andrifampicin for 6 months.[4] Treatment for multibacillary leprosy consists of rifampicin, dapsone, and clofazimine for 12 months.[4] These treatments are provided for free by the World Health Organization.[2] A number of other antibiotics may also be used.[4] Globally in 2012, the number of chronic cases of leprosy was 189,000 and the number of new cases was 230,000.[2] The number of chronic cases has decreased from some 5.2 million in the 1980s. [2][5][6] Most new cases occur in 16 countries, with India accounting for more than half. [2][4] In the past 20 years, 16 million people worldwide have been cured of leprosy. [2] About 200 cases are reported per year in the United States.[7]
Leprosy has affected humanity for thousands of years. [4] The disease takes its name from the Latin word lepra, which means "scaly", while the term "Hansen's disease" is named after the physician Gerhard Armauer Hansen.[4]Separating people in leper colonies still occurs in countries like India, with more than a thousand;[8] China, with around hundreds;[9] and in Africa.[10] However, most colonies have closed.[10] Leprosy has been associated withsocial stigma for much of history,[2] which remains a barrier to self-reporting and early treatment. World Leprosy Day was started in 1954 to draw awareness to those affected by leprosy.[11]
o 4.1 Endemic areas o 4.2 United States o 4.3 Classification
5 Prevention 6 Treatment 7 Epidemiology
o 7.1 Disease burden 8 History
o 8.1 The Bible 9 Society and culture
o 9.1 Treatment cost o 9.2 Stigma in India o 9.3 Notable cases
10 References 11 External links
Signs and symptoms[edit]
Hands deformed by leprosy, 1990, India
Lepers in Tahiti, circa 1895
Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external sign. [12] Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs, and eyes. Contrary to folklore, leprosy does not cause body parts to fall off, although they can become numb or diseased as a result of secondary infections; these occur as a result of the body's defenses being compromised by
the primary disease.[13][14] Secondary infections, in turn, can result in tissue loss causing fingers and toes to become shortened and deformed, as cartilage is absorbed into the body.[13][14][15]
Cause[edit]
M. leprae[edit]
M. leprae, one of the causative agents of leprosy: As an acid-fastbacterium, M. leprae appears red when
a Ziehl-Neelsen stain is used.
Main article: Mycobacterium leprae
M. leprae and M. lepromatosis are the causative agents of leprosy. M. lepromatosis is a relatively newly identified mycobacterium isolated from a fatal case of diffuse lepromatous leprosy in 2008. [3][12]
An intracellular, acid-fast bacterium, M. leprae is aerobic and rod-shaped, and is surrounded by the waxy cell membrane coating characteristic of the Mycobacterium genus.[16]
Due to extensive loss of genes necessary for independent growth, M. leprae and M. lepromatosis are obligate pathogens, and unculturable in the laboratory, a factor that leads to difficulty in definitively identifying the organism under a strict interpretation of Koch's postulates.[3]
[17] The use of nonculture-based techniques such as molecular genetics has allowed for alternative establishment of causation.
While the causative organisms have to date been impossible to culture in vitro, it has been possible to grow them in animals.
Naturally occurring infection also has been reported in nonhuman primates, including the African chimpanzee, sooty mangabey, and cynomolgus macaque, as well as in armadillos and red squirrels.[18]
Several genes have been associated with a susceptibility to leprosy. Around 95% of people are believed to be naturally immune.[19]Research suggests a defect in cell-mediated immunity causes susceptibility to leprosy. The region of DNA responsible for this variability is also involved in Parkinson's disease, giving rise to current speculation that the two disorders may be linked in some way at thebiochemical level.[20]
Risk factors[edit]
At highest risk are those living in areas with polluted water and poor diet or people suffering from diseases that compromise immune function. There appears to be little interaction between HIV and the risk of leprosy.[21]
Transmission[edit]
Although the mode of transmission of leprosy remains uncertain, M. leprae is probably spread from person to person in nasal droplets.[6] Leprosy can be transmitted to humans by armadillos.[22]
[23] Leprosy is not known to be either sexually transmitted or highly infectious after treatment. Sufferers are no longer infectious after as few as two weeks of treatment.[19]
Pathophysiology[edit]
The precise mechanism of transmission of leprosy is unknown; however, both prolonged close contact and transmission by nasal droplets are thought to be implicated. [24] In addition to humans, leprosy has been observed in the nine-banded armadillo, (which is among the primary sources of new cases of leprosy in the population of North America), [23] and three species of non-human primates.[25] The bacterium can also be grown in the laboratory by injection into the footpads of mice.[26] Some evidence indicates not all people who are infected with M. leprae develop leprosy, and genetic factors have long been thought to play a role, due to the observation of clustering of leprosy around certain families, and the failure to understand why certain individuals develop lepromatous leprosy while others develop other types of leprosy. [27] Due to genetic factors, an estimated 5% of the population is susceptible to leprosy.[28] This is mostly because the body is naturally immune to the bacteria, and those persons who do become infected experience severe allergic reactions to the disease. However, the role of genetic factors is not entirely clear in determining this clinical expression. In addition, malnutrition and prolonged exposure to infected persons may play a role in development of the overt disease.
The most widely held belief is that the disease is transmitted by contact between infected persons and healthy persons.[29] In general, closeness of contact is related to the dose of infection, which in turn is related to the occurrence of disease. Of the various situations that promote close contact, contact within the household is the only one easily identified, although the incidence among contacts
and the relative risk for them appear to vary considerably in different studies. In incidence studies, infection rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per year in Cebu, Philippines [30] to 53 per 1000 per year in part of western India to 55.8 per 1000 per year in a part of southern India.[31]
Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not clear. Lepromatous cases show large numbers of organisms deep in the dermis, but whether they reach the skin surface in sufficient numbers is doubtful.[32]Although reports have been made of acid-fast bacilli being found in the desquamating epithelium (sloughing of superficial layer of skin) of the skin, researchers reported they could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and contacts.[33] Fairly large numbers of M. leprae were found in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting the organism could exit along with the sebaceous secretions.[34]
The importance of the nasal mucosa was recognized as early as 1898 by Schäffer, in particular that of the ulcerated mucosa.[35] The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy was demonstrated with counts ranging from 10,000 to 10,000,000. [36] The majority of lepromatous patients showed leprosy bacilli in their nasal secretions as collected through blowing the nose.[37] Nasal secretions from lepromatous patients could yield as many as 10 million viable organisms per day.[38]
The entry route of M. leprae into the human body is also not definitively known. The skin and the upper respiratory tract are most likely. While older research dealt with the skin route, recent research has increasingly favored the respiratory route. Experimental transmission of leprosy through aerosols containing M. leprae in immune-suppressed mice was accomplished, suggesting a similar possibility in humans.[39] Successful results have also been reported on experiments with nude mice when M. leprae was introduced into the nasal cavity by topical application. [40] In summary, entry through the respiratory route appears the most probable route, although other routes, particularly broken skin, cannot be ruled out.
In leprosy, both the reference points for measuring the incubation period and the times of infection and onset of disease are difficult to define, the former because of the lack of adequate immunological tools and the latter because of the disease's slow onset. Even so, several investigators have attempted to measure the incubation period for leprosy. The minimum incubation period reported is as short as a few weeks based on the very occasional occurrence of leprosy among young infants.[41] The maximum incubation period reported is as long as 30 years, or over, as observed among war veterans known to have been exposed for short periods in endemic areas, but otherwise living in nonendemic areas. The average incubation period is generally believed to be between three and five years.
SOURCE: http://en.wikipedia.org/wiki/Leprosy
Leprosy (Hansen's disease) facts 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
The Ziehl-Neelsen stain is an example of the special staining techniques used to view the acid-fast
organisms under the microscope.
Currently, the organisms cannot be cultured on artificial media. The bacteria take an extremely long
time to reproduce inside of cells (about 12-14 days as compared to minutes to hours for most
bacteria). The bacteria grow best at 80.9 F-86 F, so cooler areas of the body tend to develop the
infection. The bacteria grow very well in the body's macrophages (a type of immune system cell) and
Schwann cells (cells that cover and protect nerve axons). M. lepraeis genetically related
to M. tuberculosis (the type of bacteria that cause tuberculosis) and other mycobacteria that infect
humans. As with malaria, patients with leprosy produce anti-endothelial antibodies (antibodies
against the lining tissues of blood vessels), but the role of these antibodies in these diseases is still
under investigation.
In 2009, investigators discovered a new Mycobacterium species, M. lepromatosis, which causes
diffuse disease (lepromatous leprosy). This new species (determined by genetic analysis) was found
in patients located in Mexico and the Caribbean islands.
What are the risk factors for leprosy?Comment on thisShare Your Story
People at highest risk are those who live in the areas where leprosy is endemic (parts of India,
China, Japan, Nepal, Egypt, and other areas) and especially those people in constant physical
contact with infected people. In addition, there is some evidence that genetic defects in the immune
system may cause certain people to be more likely to become infected (region q25 on chromosome
6). Additionally, people who handle certain animals that are known to carry the bacteria (for
example, armadillos, African chimpanzee, sooty mangabey, and cynomolgus macaque) are at risk of
getting the bacteria from the animals, especially if they do not wear gloves while handling the
animals.
What are leprosy symptoms and signs?Comment on thisRead 1 Comment Share Your Story
Unfortunately, the early signs and symptoms of leprosy are very subtle and occur slowly (usually
over years). The symptoms are similar to those that may occur with syphilis, tetanus,
andleptospirosis. Numbness and loss of temperature sensation are some of the first symptoms that
patients experience. As the disease progresses, the sensations of touch, then pain, and eventually
deep pressure are decreased or lost. Signs that occur, such as relatively painless ulcers, skin
lesions of hypopigmented macules (flat, pale areas of skin), and eye damage (dryness, reduced
blinking) are experienced before the large ulcerations, loss of digits, and facial disfigurement
develop. This long-term developing sequence of events begins and continues on the cooler areas of
the body (for example, hands, feet, face, and knees).
Are there different forms (classifications) of leprosy?There are multiple forms of leprosy described in the literature. The forms of leprosy are based on the
person's immune response to M. leprae. A good immune response can produce the so-called
tuberculoid form of the disease, with limited skin lesions and some asymmetric nerve involvement. A
BackgroundLeprosy is a chronic infection caused by the acid-fast, rod-shaped bacillusMycobacterium leprae. Leprosy can be considered 2 connected diseases that primarily affect superficial tissues, especially the skin and peripheral nerves. Initially, a mycobacterial infection causes a wide array of cellular immune responses. These immunologic events then elicit the second part of the disease, a peripheral neuropathy with potentially long-term consequences.
The social and psychological effects of leprosy, as well as its highly visible debilities and sequelae (as seen in the image below), have resulted in a historical stigma associated with leprosy. To minimize the
prejudice against those with leprosy, the condition is also known as Hansen disease, named after G.A. Hansen, who is credited with the 1873 discovery of M leprae. This mycobacterium grows extremely slowly and has not been successfully cultured in vitro.
Hands with Z-thumbs, clawing, contractures, and shortening of fingers due to repetitive injury and healing. Ho Chi Minh City, Vietnam. (Courtesy of D. Scott Smith, MD)
In the 1990s, the World Health Organization (WHO) launched a campaign to eliminate leprosy as a public health problem by 2000. Elimination, as defined by the WHO, was defined as a reduction of patients with leprosy requiring multidrug therapy to fewer than 1 per 10,000 population. This goal was achieved in terms of global prevalence by 2002, but 15 of the 122 countries where leprosy was endemic in 1985 still have prevalence rates of greater than 1 per 10,000 population.[1]
Although multidrug regimens have been used globally to cure nearly 14 million patients with leprosy since 1985, the number of new leprosy cases remained relatively unchanged from 1980 to 2000, ranging from 500,000-700,000 worldwide per year.[2] Access and delivery of antibiotics continues to be a problem in the most endemic nations. With the precise transmission mechanism of leprosy still unknown and a lack of an effective vaccine, leprosy will probably continue to pose an ongoing public health problem in the coming decades.
The goal of the WHO by the end of 2015 is to reduce the rate of new cases with grade-2 disabilities worldwide by at least 35%. This will be carried out by enforcing activities to decrease the delay in diagnosing the disease and actuate treatment with multidrug therapy. This will also have the impact of reducing transmission of the disease in the community.[2]
PathophysiologyLeprosy can manifest in different forms, depending on the host response to the organism.
Individuals who have a vigorous cellular immune response to M leprae have the tuberculoid form of the disease that usually involves the skin and peripheral nerves. The number of skin lesions is limited, and they tend to be dry and hypoesthetic. Nerve involvement is usually asymmetric. This form of the disease is also referred to as paucibacillary leprosy because of the low number of bacteria in the skin lesions (ie, < 5 skin lesions, with absence of organisms on smear). Results of skin tests with antigen from killed organisms are positive in these individuals.
Individuals with minimal cellular immune response have the lepromatous form of the disease, which is characterized by extensive skin involvement. Skin lesions are often described as infiltrated nodules and plaques, and nerve involvement tends to be symmetric in distribution. The organism grows best at 27-30°C; therefore, skin lesions tend to develop in the cooler areas of the body, with sparing of the groin, axilla, and scalp. This form of the disease is also referred to as multibacillary leprosy because of the large number of bacteria found in the lesions (ie, >6 lesions, with possible visualization of bacilli on smear). Results of skin tests with antigen from killed organisms are nonreactive.
Patients may also present with features of both categories; however, over time, they usually evolve to one or the other (indeterminate or borderline leprosy). Interestingly, most individuals who are exposed to leprosy never develop the disease.
Classification of leprosy: Leprosy has 2 classification schemas: the 5-category Ridley-Jopling system and the simpler and more commonly used WHO standard.
Ridley-Jopling: Depending on the host response to the organism, leprosy can manifest clinically along a spectrum bounded by the tuberculoid and lepromatous forms of the disease. Most patients fall into the intermediate classifications, which include borderline tuberculoid leprosy, midborderline leprosy, and borderline lepromatous leprosy. The classification of the disease typically changes as it evolves during its progression or management. The Ridley-Jopling system is used globally and forms the basis of
clinical studies of leprosy. It may also be more useful in guiding treatment regimens and assessing risk of acute complications. Physical findings in each subtype are presented in the Clinical section.
WHO system: The WHO recommends classifying leprosy according to the number of lesions and the presence of bacilli on a skin smear. This method is useful in countries where biopsy analysis in unavailable.
o Paucibacillary leprosy is characterized by 5 or fewer lesions with absence of organisms on smear. Paucibacillary leprosy generally includes the tuberculoid and borderline lepromatous categories from the Ridley-Jopling system.
o Multibacillary leprosy is marked by 6 or more lesions with possible visualization of bacilli on smear. Lepromatous leprosy, borderline lepromatous leprosy, and midborderline leprosy on the Ridley-Jopling scale are included in the multibacillary leprosy category.
EpidemiologyFrequency
United StatesAn average of 150-250 cases are diagnosed each year in the United states.[1]
In 2010, according to the Registry of National Hansen’s Disease Programs (NHDP), 205 new cases of leprosy were detected in the United States.[3]
In 2010 WHO reports, 169 new cases of leprosy were detected. The number of new cases of MB leprosy reported was 105. The number of females among the new cases was 53, and 6 cases in children were reported. No cases of relapse were reported in 2010.[2]
Most cases of leprosy in the United States are found in immigrants, although endemic foci exist in parts of Louisiana, Florida, and Texas along the Gulf of Mexico; in Mexican and Asian California populations; and in Spanish Americans in New York City. Around 75% of these detected leprosy cases involve patients who have lived in foreign countries, primarily Asia, Africa, and Latin America.[3]
Some cases among native US citizens can be accounted for by exposure to leprosy overseas. Some cases can be attributed to a contact with a known case of leprosy or exposure to infected armadillos.
Based on genetic analysis studies, wild armadillos and many patients with leprosy in the southern United States are infected with the same strain of M leprae.[4]Leprosy may be a zoonosis in the southern United States because armadillos are a large reservoir for this disease.
Nonetheless, history of exposure cannot be verified in many patients.[3]
InternationalAccording to WHO figures and as reported by 130 countries, the global annual detection rates have declined from 2004-2010, when 407,791 and 228,474 new cases were reported, respectively (see the images below). The prevalence registered worldwide at the beginning of 2010 was 192,246 cases. Of the new cases, 95% were detected worldwide during 2010 in the following countries: Angola, Bangladesh, Brazil, China, Democratic Republic of the Congo, India, Ethiopia, Indonesia, Madagascar, Mozambique, Myanmar, Nepal, Nigeria, Philippines, Sri Lanka, Sudan, and United Republic of Tanzania.[2] These countries still exhibit pockets of high endemicity.
Leprosy prevalence rates, data reported to WHO as of beginning January 2011. Courtesy of WHO, Leprosy: Global
situation, http://www.who.int/lep/situation/en/, accessed March 14, 2013. Leprosy new case detection rates, data reported to WHO as of beginning January 2011. Courtesy of WHO, Leprosy: Global situation, http://www.who.int/lep/situation/en/, accessed March 14, 2013.
Mortality/Morbidity
Leprosy is rarely fatal, and the primary consequence of infection is nerve impairment and debilitating sequelae. According to one study, 33-56% of newly diagnosed patients already displayed signs of impaired nerve function.[5] According to estimates, 3 million people who have completed multidrug therapy for leprosy have sustained disability due to nerve damage. Although both lepromatous leprosy and tuberculoid leprosy involve the skin and peripheral nerves, tuberculoid leprosy has more severe manifestations. Nerve involvement results in loss of sensory and motor function, which may lead to frequent trauma and amputation. The ulnar nerve is most commonly involved.
Damage in the following nerves is associated with characteristic impairments in leprosy:o Ulnar and median - Clawed hando Posterior tibial - Plantar insensitivity and clawed toeso Common peroneal -Foot dropo Radial cutaneous, facial, and greater auricular nerves (may also be involved; as seen in the image
below) Patient with facial nerve palsy and contractures of the hand. Daloa, Ivory Coast. (Courtesy of D. Scott Smith, MD)
Infiltration by bacteria may lead to destruction of nasal cartilage (lepromatous leprosy), ocular involvement, and diffuse thickening of the skin. Advanced cases of leprosy involve the loss of eyebrows and lashes, but these deformities are less common today.
Worldwide, leprosy is considered the most common cause of crippling of the hand, which is caused by ulnar nerve involvement.[6] Peroneal nerve involvement can lead to foot drop, posterior tibial nerve involvement, and clawed toes.
Race
Leprosy was once endemic worldwide, and no racial predilection is known. In the late 1800s, the incidence of leprosy in northern Europe and North America dropped dramatically, and the disease is now reported primarily in tropical areas.
Sex
Leprosy is generally more common in males than in females, with a male-to-female ratio of 1.5:1. In some areas in Africa, the prevalence of leprosy among females is equal to or greater than that in males.[2]
Leprosy can occur at any age, but, in developing countries, the age-specific incidence of leprosy peaks in children younger than 10 years, who account for 20% of leprosy cases. Leprosy is very rare in infants; however, they are at a relatively high risk of acquiring leprosy from the mother, especially in cases of lepromatous leprosy or midborderline leprosy.
Classification of Leprosy and the clinical symptoms
Disease Clinical Features
Indeterminate leprosyThey are the first type of skin lesions characterized by hypo-pigmented spots
The lesions undergo healing spontaneously
Paucibacillary (tuberculoid leprosy)
A large red patch with well-defined raised borders or a large hypo pigmented asymmetrical lesion.
Lesion is dry and hairlessInfectivity is minimal at this stageLoss of sensation is seenNerves become thick followed by loss of functionIt either progresses to the borderline stage or spontaneously get cured
Borderline borderline leprosyCharacterized by small and numerous skin lesions
The disease goes back to the tuberculoid stage or progresses to the next stage
Borderline borderline leprosySeveral small, irregular red lesions are seen
Moderate sensory loss is seenIt either goes back to the previous stage or progresses to the next
Borderline lepromatous leprosySeveral lesions such as plaques, macules, papules, and nodules are seen
Lesions have a characteristic inverted saucer like appearance
Several lesions such as plaques, macules, papules, and nodules are seenNasal congestion, discharge and bleeding is seenInflammation of the leg and anklesProgressive symptoms:Thickening of the dermis (skin) in the forehead and ear lobesLoss of eyebrows and eyelashesEye defects such as glaucoma and blindness are seenNodules in the legs break and form ulcersEnlargement of the breast and sterility occurs in the malesInternal infection results in the enlargement of the liver and lymph nodesLoss of sensation in the peripheral nerves. Deformation of the fingers and toes results due to painless repeated trauma
Leprosy is classified into several types based on the bacterial load present in the lesions, the extent of skin and nerve involvement and based on the presence of deformities. Several types of classification like Madrid classification, Ridley & Jopling classification Indian Classification, WHO classification , Field Worker's Classification etc.
Based on the 2 commonly used classifications, leprosy is classified into six types based
on the clinical features (Ridley & Jopling classification):The type of the disease is a reflection of the immune status of the host.
The first sign of the disease is the feeling of numbness or loss of sensation for temperature (heat) followed by touch and pain which usually begins at the extremities. The skin lesions appear later during the course of the disease.
The Indian classification has an additional type, the neuritic type, which is bacteriologically negative and shows neural involvement without any skin lesions.