Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
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.
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
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
Leprosy
From Wikipedia, the free encyclopedia
For the Biblical term and its varied meanings, see Tzaraath. For other uses, see Leprosy
(disambiguation).
Leprosy
A 24-year-old
man from
Norway,
infected
leprosy, 1886.
ICD-10
A30
ICD-9
030
OMIM
246300
DiseasesDB
8478
with
MedlinePlus
001347
eMedicine
med/1281 derm/223neuro/187
NCI
Leprosy
Patient UK
Leprosy
MeSH
D007918
Leprosy /lprsi/,[1] also known as Hansen's disease (HD), is a chronic infection caused by
the bacteriaMycobacterium 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]
Contents
[hide]
2 Cause
o
2.1 M. leprae
2.2 Genetics
2.4 Transmission
3 Pathophysiology
4 Diagnosis
o
4.3 Classification
5 Prevention
6 Treatment
7 Epidemiology
o
10 References
11 External links
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.
Genetics[edit]
Name
Locus
OMIM
Gene
LPRS1
10p13
609888
LPRS2
6q25
607572
PARK2, PACRG
LPRS3
4q32
246300
TLR2
LPRS4
6p21.3
610988
LTA
LPRS5
4p14
613223
TLR1
LPRS6
13q14.11
613407
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 Schffer, 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 is a slowly developing, progressive disease that damages the skin and nervous
system.
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.
What is leprosy?
Leprosy is a disease 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.
Currently, there are several areas (India, East Timor) of the world where the WHO and other
agencies (for example, the Leprosy Mission) are working to decrease the number of clinical cases of
leprosy and other diseases such as rabies and schistosomiasis that occur in remote regions.
Although researchers hope to eliminate leprosy like smallpox, endemic (meaning prevalent or
embedded in a region) leprosy makes complete eradication unlikely. In the U.S., leprosy has
occurred infrequently but is considered endemic in Texas, Louisiana, Hawaii, and the U.S. Virgin
Islands by some investigators.
Leprosy is often termed "Hansen's disease" by many clinicians in an attempt to have patients forgo
the stigmas attached to being diagnosed with leprosy.
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.
Indeterminate leprosy: a few hypopigmented macules; can heal spontaneously, this form
persists or advances to other forms
Tuberculoid leprosy: a few hypopigmented macules, some are large and some become
anesthetic (lose pain sensation); some neural involvement in which nerves become enlarged;
spontaneous resolution in a few years, persists or advances to other forms
Borderline tuberculoid leprosy: lesions like tuberculoid leprosy but smaller and more
numerous with less nerve enlargement; this form may persist, revert to tuberculoid leprosy, or
advance to other forms
Borderline lepromatous leprosy: many skin lesions with macules (flat lesions) papules
(raised bumps), plaques, and nodules, sometimes with or without anesthesia; the form may
persist, regress or progress to lepromatous leprosy
Lepromatous leprosy: Early lesions are pale macules (flat areas) that are diffuse and
symmetric; later many M. leprae organisms can be found in them. Alopecia (hair loss) occurs;
often patients have no eyebrows or eyelashes. As the disease progresses, nerve involvement
leads to anesthetic areas and limb weakness; progression leads toaseptic necrosis (tissue
death from lack of blood to area), lepromas (skin nodules), and disfigurement of many areas,
including the face. The lepromatous form does not regress to the other less severe forms.
Histoid leprosy is a clinical variant of lepromatous leprosy that presents with clusters of
histiocytes (a type of cell involved in the inflammatory response) and a grenz zone (an area of
collagen separating the lesion from normal tissue) seen in microscopic tissue sections.
The Ridley-Jopling classification is used globally in evaluating patients in clinical studies. However,
the WHO classification system is more widely used; it has only two forms or classifications of
leprosy. The 2009 WHO classifications are simply based on the number of skin lesions as follows:
Paucibacillary leprosy: skin lesions with no bacilli (M. leprae) seen in a skin smear
Multibacillary leprosy: skin lesions with bacilli (M. leprae) seen in a skin smear
However, the WHO further modifies these two classifications with clinical criteria because "of the
non-availability or non-dependability of the skin-smear services. The clinical system of classification
for the purpose of treatment includes the use of number of skin lesions and nerves involved as the
basis for grouping leprosy patients into multibacillary (MB) and paucibacillary (PB) leprosy."
Investigators state that up to about four to five skin lesions constitutes paucibacillary leprosy, while
about five or more constitutes multibacillary leprosy.
Multidrug therapy (MDT) with three antibiotics (dapsone, rifampicin, and clofazimine) is used for
multibacillary leprosy, while a modified MDT with two antibiotics (dapsone and rifampicin) is
recommended for paucibacillary leprosy and composes most current treatments today (see
treatment section below). Paucibacillary leprosy usually includes indeterminate, tuberculoid, and
borderline tuberculoid leprosy from the Ridley-Jopling classification, while multibacillary leprosy
usually includes the double (mid-) borderline, borderline lepromatous, and lepromatous leprosy.
The majority of cases of leprosy are diagnosed by clinical findings, especially since most current
cases are diagnosed in areas that have limited or no laboratory equipment available.
Hypopigmented patches of skin or reddish skin patches with loss of sensation, thickened peripheral
nerves, or both clinical findings together often comprise the clinical diagnosis. Skin smears or biopsy
material that show acid-fast bacilli with the Ziehl-Neelsen stain or the Fite stain (biopsy) can
diagnose multibacillary leprosy, or if bacteria are absent, diagnose paucibacillary leprosy. Other tests
can be done, but most of these are done by specialized labs and may help a clinician to place the
patient in the more detailed Ridley-Jopling classification and are not routinely done (lepromin test,
phenolic glycolipid-1 test, PCR, lymphocyte migration inhibition test or LMIT). Other tests such
as CBC test, liver function tests, creatinine test, or a nerve biopsy may be done to help determine if
other organ systems have been affected.
Muscle weakness
Progressive disfigurement (for example, eyebrows lost, disfigurement of the toes, fingers,
and nose)
In addition, the sensory loss causes people to injure body parts without the individual being aware
that there is an injury; this can lead to additional problems such as infections and poor wound
healing.
Clinical Features
Etiologic Agent
Incidence
Sequelae
Transmission
Risk Groups
Surveillance
Trends
Challenges
Opportunities
More information
More Information
Additional Information
Clinical Features
This chronic infectious disease usually affects the skin and peripheral nerves but has a wide range of
possible clinical manifestations. Patients are classified as having paucibacillary or multibacillary
Hansen's disease. Paucibacillary Hansen's disease is milder and characterized by one or more
hypopigmented skin macules. Multibacillary Hansen's disease is associated with symmetric skin
lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting
in nasal congestion and epistaxis.
Etiologic Agent
Mycobacterium leprae, a bacillus that multiplies very slowly and mainly affects the skin, nerves, and
mucous membranes, is the organism responsible for Hansens disease. The organism has never been
grown in bacteriologic media or cell culture, but has been grown in mouse foot pads.
Incidence
In 2008, the number of new cases detected worldwide was 249,007. In 2007, 109 cases occurring in
the United States were reported to CDC. In 2008, Brazil, India, and Indonesia had 77% of all cases
reported to the World Health Organization (WHO). Over 94% of all reported cases are reported from
17 countries.
Sequelae
Worldwide, 1-2 million persons are permanently disabled as a result of Hansen's disease. However,
persons receiving antibiotic treatment or having completed treatment are considered free of active
infection.
Top of Page
Transmission
Although the mode of transmission of Hansen's disease remains uncertain, most investigators think
thatM. leprae is usually spread from person to person in respiratory droplets.
Top of Page
Risk Groups
Close contacts of patients with untreated, active, predominantly multibacillary disease, and persons
living in countries with highly endemic disease are at risk of contracting Hansens disease.
Top of Page
Surveillance
Hansen's disease is nationally notifiable in the United States.
Top of Page
Trends
Prevalence has remained relatively stable in the United States. Cases appear to be predominantly
related to immigration. Worldwide, the number of cases are decreasing, however, there are pockets of
high prevalence in certain countries.
Top of Page
Challenges
Multi-drug therapy has not been implemented in many endemic areas. Early case finding is difficult in
many areas where the disease is most prevalent. Nerve damage must be recognized and managed.
Relapse rate after completion of short course multi-drug therapy may rise.
Top of Page
Opportunities
Opportunities exist for participation in Hansen's disease elimination activities in endemic-disease
countries, and for Mycobacterium research in the Laboratory Research Branch of the National Hansen's
Disease Program.
SOURCE: http://www.cdc.gov/nczved/divisions/dfbmd/diseases/hansens_disease/technical.html#
Background
Leprosy is a chronic infection caused by the acid-fast, rod-shaped bacillus Mycobacterium 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.
Hands with Z-thumbs, clawing, contractures, and shortening of fingers due to repetitive injury and healing. Ho Chi
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]
Pathophysiology
Leprosy 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 2730C; 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.
Epidemiology
Frequency
United States
An average of 150-250 cases are diagnosed each year in the United states. [1]
In 2010, according to the Registry of National Hansens 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]
International
According 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:
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.
o
o
o
o
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]
Age
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.
SOURCE: http://emedicine.medscape.com/article/220455-overview#a0199
Leprosy
Share on facebookShare on twitterBookmark & SharePrinter-friendly version
Leprosy is a disease that has been known since biblical times. This infectious disease causes skin sores,
nerve damage, and muscle weakness that gets worse over time.
Causes
Leprosy is caused by the bacterium Mycobacterium leprae. It is not very contagious and it has a long
incubation period (time before symptoms appear), which makes it hard to know where or when someone
caught the disease. Children are more likely than adults to get the disease.
Leprosy has two common forms: tuberculoid and lepromatous. Both forms produce sores on the skin.
However, the lepromatous form is most severe. It causes large lumps and bumps (nodules).
Leprosy is common in many countries worldwide, and in temperate, tropical, and subtropical climates.
About 100 cases per year are diagnosed in the United States. Most cases are in the South, California,
Hawaii, and U.S. islands.
Effective medications exist. Isolating people with this disease in "leper colonies" is not needed.
Drug-resistant Mycobacterium leprae and an increased numbers of cases worldwide have led to global
concern about this disease.
Symptoms
Symptoms include:
Skin lesions that are lighter than your normal skin color
o
Muscle weakness
Lepromin skin test can be used to tell the two different forms of leprosy apart, but it is not used to
diagnose the disease
Treatment
A number of different antibiotics (including dapsone, rifampin, clofazamine, fluoroquinolones, macrolides,
and minocycline) are used to kill the bacteria that cause the disease. More than one antibiotic is often
given together.
Aspirin, prednisone, or thalidomide is used to control inflammation.
Outlook (Prognosis)
Diagnosing the disease early is important. Early treatment limits damage, prevents a person from
spreading the disease, and allows the person to have a normal lifestyle.
Possible Complications
Disfigurement
Muscle weakness
Sensory loss
People with long-term leprosy may lose the use of their hands or feet due to repeated injury because they
lack feeling in those areas.
Clinical Features
Paucibacillary (tuberculoid
leprosy)
A large red patch with well-defined raised borders or a large hypo pigm
The disease goes back to the tuberculoid stage or progresses to the next stage
Several small, irregular red lesions are seen
Borderline lepromatous
leprosy
Multibacillary Hansens
disease (lepromatous
leprosy)
Loss of sensation in the peripheral nerves. Deformation of the fingers and toes results du
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.