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Leprosy
Lucileia Johnson, MD, William Harper, MD, Steven M. Opal, MD, and Eleftherios E. Mylonakis, MD
Revised: 20 Oct 2011
Last Updated: 19 Oct 2011
Copyright Elsevier BV. All rights reserved.
Key points
Leprosy is caused by Mycobacterium leprae , a slow-growing bacillus that is an obligate parasite with a
tropism for peripheral nerves, skin, and mucous membranes in the cooler parts of the body, such as the
upper respiratory tract, anterior chamber of the eye, and the testes
Up to 300 cases are reported in the U.S. every year, with the majority in states with the largest
immigrant populations
Persons of all ages and both sexes are affected
Transmission occurs via droplets from the nose and mouth of persons with untreated, severe disease
Once the diagnosis has been established, all household contacts of the patient also should be
assessed, as the risk of infection among family members is substantially higher than for other contacts
Multidrug therapy, namely with dapsone, rifampin, and clofazimine, is the only effective treatment
Long-term follow-up and regular monitoring for the development of lepra reactions are required, as
spontaneous reactions may occur even after curative therapy and, if left untreated, are a major cause of
neuronal and other complications
Background
Description
M. leprae was discovered by the Norwegian Gerhard Henrik Armauer Hansen in 1873, making it the first
bacillus and the second bacterium known to be associated with a human disease
Owing to the extremely slow dividing time of M. leprae (once every 2 weeks), the incubation period
ranges from 6 months to more than 40 years and averages 2 to 5 years
The cardinal features of leprosy are a skin patch with sensory loss, nerve enlargement, and acid-fast
bacilli in the skin; nerve enlargement is the most important feature, as 30% of patients, including many
of those with lepromatous leprosy, may not present with a skin patch with sensory loss, and some
patients simply have a neural form of leprosy, known as neuritic leprosy
The manifestations of the disease are determined by the host's immunopathologic responses to M.
leprae , resulting in a wide clinical spectrum with five distinct forms characterized by Ridley and Jopling
in 1966
The polar forms of leprosy, tuberculoid leprosy and lepromatous leprosy, are immunologically stable,
whereas the intermediate forms, including borderline tuberculoid leprosy, borderline leprosy, and
borderline lepromatous leprosy, are immunologically unstable and lead to either a gradual decline
toward the lepromatous pole or upgrading 'reversal reactions' toward the tuberculoid pole
Tuberculoid leprosy is characterized by a vigorous cellular immune response and limited humoral
immune responses to M. leprae , usually involving the skin and nerves and resulting in few skin lesions.
Lepromatous leprosy, on the other hand, is characterized by a minimal cellular immune response and a
vigorous humoral immune response and, consequently, extensive skin involvement
Indeterminate leprosy, an additional type, is an early form of the disease that features only a small
number skin lesions and no nerve involvement
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Leprosy also may be divided into paucibacillary and multibacillary forms, depending on the number of
bacilli present in skin lesions. Indeterminate leprosy, tuberculoid leprosy, and borderline tuberculoid
leprosy are categorized as paucibacillary forms (characterized by a low number of bacilli), whereas
borderline leprosy, borderline lepromatous leprosy, and lepromatous leprosy are considered
multibacillary. This classification has a significant bearing on the choice of therapy
The introduction of multidrug therapy in 1981 led to a dramatic decline in prevalence and disease
burden; of 122 countries where leprosy is considered to be endemic, the prevalence of the disease has
decreased to less than 1 case per 10,000 persons in 119 countries
A 6- to 12-month course of multidrug therapy is highly effective in treating leprosy and is associated
with few adverse effects and low relapse rates; if left untreated, leprosy can cause nerve damage,
leading to muscle weakness and atrophy with permanent disability
Although emergence of resistance to individual medications ( eg , dapsone) has been reported with
monotherapy in the past, no resistance has been reported with the use of newer multidrug regimens
The dynamic immunopathologic host response to M. leprae during the course of leprosy may result in
spontaneous lepra reactions; these are more common in patients with borderline forms of the disease
and may be precipitated by treatment
Lepra type 1 reactions involve either a downgrading or upgrading reaction, with patients developing
inflammation, neuritis, and potentially fever, and are a major cause of nerve damage. Lepra type 2
reactions or erythema nodosum leprosum affect approximately half of all patients and consist of an
immune complexmediated reaction to M. leprae that has widespread, systemic effects in addition to
causing the development of new skin lesions
Systemic corticosteroids are the mainstay of treatment for lepra reactions
Epidemiology
Incidence and prevalence:
The true incidence of leprosy is difficult to measure, as, unlike tuberculosis, the annual rate of infection
cannot be quantified using the equivalent of the tuberculin skin test reactivity survey. However, it is clear
that the disease burden and prevalence of leprosy have decreased dramatically over the past 20 years,
largely due to the widespread use of multidrug therapy
The most recent case detection rate for leprosy is approximately 250,000 cases per year worldwide,
which represents a significant decline in the last decade, as more than 700,000 new cases were
reported in 2001
Between 100 and 300 cases of leprosy are diagnosed each year in the U.S., 95% of which are acquired
in developing countries; the majority of cases are in states with the largest immigrant populations, such
as the southern states, California, Hawaii, and island possessions
Since 1985, the reported prevalence of leprosy has been reduced by more than 90%, and cure has
been achieved in more than 15 million patients. In 2006, the total number of active cases worldwide was
259,017
The World Health Organization (WHO) reports that the current prevalence of leprosy is less than 1 case
per 10,000 persons in all countries except for Brazil, Mozambique, Madagascar, Tanzania, and Nepal,
where the prevalence exceeds 2 cases per 10,000 persons
Demographics:
Leprosy has a bimodal age distribution, with peaks observed at ages 10 to 14 years and 35 to 44 years
Children seem to be more susceptible to developing leprosy than adults and tend to have the
tuberculoid form rather than the lepromatous form
Although leprosy is rare in infants, those born to mothers with the disease have slow growth and
decreased birth weight; infants whose mothers have lepromatous leprosy are at increased risk of
contracting the disease
Leprosy is more common in men than in women, with a male-to-female ratio of 1.5 to 2.0:1; however,
when the disease occurs in children, both genders are affected equally
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Although leprosy occurs in all races, Africans have a higher incidence of the tuberculoid form than other
groups, and the lepromatous form is more common in light-skinned and Chinese persons
Genetic factors influence both the development of leprosy and the pattern of disease. Whole-genome
screening has revealed susceptibility loci on chromosome 10p13, close to the gene for the mannose
receptor C type 1, and on chromosome 6 within the major histocompatibility complex, where linkage
has been shown to the human leukocyte antigen (HLA) class II and tumor necrosis factor (TNF) genes
in Indian and Brazilian patients, respectively. Polymorphisms in the promoters of both TNF and IL10
genes have been associated with the development of leprosy, particularly multibacillary leprosy in the
case of TNF . The HLA locus also has been shown to affect the pattern of disease, with HLA-DR2 and
HLA-DR3 associated with tuberculoid disease and HLA-DQ1 linked to the lepromatous form
Of the 122 countries that were classified as endemic for leprosy in 1985, 119 reached the elimination
target in 2009
Cases of leprosy are highly concentrated, with 83% of patients located in only six countries: India,
Brazil, Myanmar (Burma), Indonesia, Madagascar, and Nepal. India alone accounts for 64% of all
leprosy cases worldwide
Leprosy has virtually disappeared from Europe, and the majority of cases in North America are among
immigrants from endemic areas. However, cases of leprosy among patients with severe
immunosuppression, such as organ transplant recipients, have been reported
Leprosy is associated with poverty and overcrowding, with improved socioeconomic conditions being a
major contributor to the decline of the disease in Europe and North America
The disease is more common in rural as opposed to urban areas
Causes and risk factors
Causes:
Leprosy is caused by chronic infection with M. leprae , an acid-fast, gram-positive bacillus that is an
obligate intracellular parasite with tropism for macrophages and Schwann cells
M. leprae cannot be cultivated in vitro but is capable of limited multiplication in the mouse footpad, with
a doubling time of 12 to 13 days, allowing drug sensitivity studies to be conducted
Genomic studies have shown that many of the functional genes for energy metabolism in M. leprae are
absent, having been replaced by inactivated genes or pseudogenes. This has resulted in the removal of
entire metabolic pathways and regulatory genes and may make the bacillus dependent on host
metabolic pathways, possibly explaining the long generation time and inability to grow in culture
M. leprae is transmitted via droplets from the nose and mouth of patients with untreated disease during
frequent and close contact. It is estimated that approximately 50% of patients have a history of intimate
contact with an infected person, usually a household member
Although leprosy is not highly infectious, patients with untreated lepromatous leprosy harbor large
numbers of M. leprae in their nasal mucosa and secretions
Risk factors:
Although the majority of cases of leprosy are sporadic, the greatest risk factor for leprosy is household
contact with patients with untreated disease. The relative risk of infection is 8- to 10-fold higher among
household contacts of patients with lepromatous leprosy and 2- to 4-fold higher for contacts of patients
with tuberculoid leprosy
Animal reservoirs of leprosy include nine-banded armadillos (15% of which are thought be to infected in
the wild in Louisiana and Texas), chimpanzees, and mangabey monkeys
Exposure to insect vectors and soil containing M. leprae also have been suggested as possible modes
of transmission
Associated disorders
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Unlike tuberculosis, there is no definitive evidence of an association between human immunodeficiency virus
(HIV) disease and clinical leprosy, although one study conducted in Tanzania suggested that there was an
increase in HIV prevalence among patients with leprosy.
Screening
Not applicable.
Primary prevention
Summary approach
Prevention primarily consists of avoiding close physical contact with patients with untreated disease.
Patients receiving long-term therapy are no longer contagious and, therefore, do not represent a risk
In 1991, the World Health Assembly of the WHO passed a resolution to eliminate leprosy as a public
health problem, defined as a prevalence rate of less than 1 case per 10,000 persons, by 2000. Largely
owing to the widespread use of multidrug therapy, this has resulted in a dramatic decrease in the global
disease burden and the elimination of leprosy from 119 of the 122 countries in which leprosy was
considered to be a public health problem as of 2009
In order to maintain the momentum and ensure that leprosy is contained and eliminated from all
countries, the WHO states:
Political commitment needs to be sustained in countries where leprosy remains a public health
problem
In order to reach all patients, leprosy treatment needs to be integrated into general health
services
Partners in leprosy elimination need to continue to ensure that human and financial resources
are made available for the elimination of leprosy
Because the stigma of leprosy is an obstacle to self-reporting and early treatment, the image of
the disease must be changed at the global, national, and local levels, and a new environment, in
which patients will not hesitate to seek diagnosis and treatment, must be fostered
The WHO recommends the following to contain and eliminate leprosy:
Accessible and uninterrupted multidrug therapy services for all patients through flexible and
patient-friendly drug delivery systems
Sustainability of multidrug therapy services by integration of leprosy services into general health
services and training general health workers to treat leprosy
Encouragement of self-reporting and early treatment by promoting community awareness and
changing the image of leprosy
Monitoring the performance of multidrug therapy services, the quality of patient care, and the
progress made toward elimination via national disease surveillance systems
Population at risk
Household contacts of patients with untreated leprosy.
Preventive measures
Household contacts of patients with lepromatous leprosy, especially children, should be monitored
annually for 5 years following diagnosis
Various attempts have been made to develop a vaccine against leprosy, with the bacille Calmette-
Gurin (BCG) vaccine having mixed results; other vaccines under development or being explored are the
Mycobacterium w, Mycobacterium ICRC, and BCG plus heat-killed Mycobacterium species vaccines
Chemoprophylaxis with dapsone is no longer recommended
Evidence
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A meta-analysis of 7 experimental studies and 19 observational studies found that the overall protective
effect of the BCG vaccine was 26% in the experimental studies and 61% in the observational studies.
There was significant heterogeneity among the trials but few significant differences between the
protective effects of BCG vaccination against paucibacillary or multibacillary disease or between
household contacts and other contacts. However, it was noted that an additional dose of BCG vaccine
was more protective than a single dose in the prevention of leprosy, leading the authors to recommend
that an additional dose may be warranted in contacts of patients with leprosy in areas where the
disease remains a public health problem. [1] Level of evidence: 1
References
Diagnosis
Summary approach
According to the WHO, the diagnosis of leprosy is based on the presence of characteristic clinical
features, consisting of a skin patch with sensory loss and nerve enlargement, supported when possible
by the demonstration of acid-fast bacilli from slit-skin preparations or a biopsy
The presence of a skin patch with sensory loss, nerve enlargement, and/or acid-fast bacilli in the skin
establishes the diagnosis, which should be confirmed if possible with a full-thickness biopsy. The
diagnosis of leprosy can be established solely based on the presence of a skin patch with sensory loss
in approximately 70% of patients; however, 30% of patients, including many of those with lepromatous
leprosy, may not present with this sign, emphasizing the importance of clinical suspicion and nerve
enlargement as an additional sign
In order to maximize the accuracy of the diagnosis based on clinical signs, physicians should look for a
thickened nerve and typical hypopigmented or erythematous skin, with or without sensory loss, and/or
typical nerve function impairment, such as loss of sensation on the palms of the hands or the soles of
the feet
Leprosy also may present purely as a neural disease, without skin lesions, which is known as neuritic
leprosy and is seen in 0.5% of patients with leprosy in Ethiopia, 4.6% of patients in India, and 8.7% of
patients in Nepal; the diagnosis is confirmed by nerve biopsy
Clinical presentation
Patients with leprosy classically present with inflamed skin lesions and/or sensorimotor neuropathy, with nerve
enlargement in those with tuberculoid leprosy. However, it is important to note that symptoms and signs may
take decades to appear due to the long incubation period of M. leprae . Furthermore, the clinical presentation
differs depending on the form of leprosy.
Symptoms
Typical symptoms are as follows:
One or more hypopigmented skin lesions with decreased sensation to touch, heat, or pain
Skin lesions that do not heal after several weeks or months
Numbness or absent sensation in the hands and arms or feet and legs
Muscle weakness due to nerve damage, resulting in, for example, foot drop, in which damage to
the peroneal nerve causes the toe to drag when the foot is lifted to take a step
Prodromal symptoms are often so minor that the disease is not recognized until a cutaneous eruption
occurs. Approximately 90% of patients present with numbness first, potentially years before the
appearance of skin lesions
The first sensation to be lost is temperature, with patients unable to sense extremes of hot or cold. This
is followed by light touch, then pain, and, finally, deep pressure, with the losses especially apparent in
the hands and feet. Patients with long-term leprosy may lose the use of their hands or feet due to
repeated injury resulting from lack of sensation
Signs
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The signs of leprosy vary widely, depending on the form of leprosy.
Indeterminate leprosy:
One to a few hypopigmented or sometimes erythematous macules are present
Sensory loss is unusual
Tuberculoid leprosy:
Cutaneous lesions are few in number, and there is usually one large, erythematous plaque with
well-defined borders that are elevated and slope down to an atrophic center; the lesions can
become arciform or annular and can be found on the face, limbs, or areas other than the scalp
and intertriginous areas
Patients also may have a large, asymmetric, hypopigmented macule with lesional hypesthesia
and involving local alopecia
Neural involvement is common, causing tender, thickened nerves with loss of function; the
greater auricular nerve and superficial peroneal nerves are affected most commonly
A single hypopigmented anesthetic plaque with a raised border and dry surface
Borderline tuberculoid leprosy:
Cutaneous lesions are similar to those seen in patients with tuberculoid leprosy but are smaller
and more numerous
The nerves are less enlarged and alopecia is less common and pronounced than in patients with
tuberculoid leprosy
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Three large, well-defined, erythematous patches with reduced sensation, spreading borders, and
satellite lesions
Erythema and edema in the facial lesions of a patient with borderline tuberculoid leprosy
experiencing an upgrading reversal reaction
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Borderline leprosy:
Cutaneous lesions consist of numerous erythematous, irregular plaques that are less well
defined than those seen in patients with tuberculoid leprosy; the distribution may be the same
as in patients with lepromatous leprosy, but the lesions are more asymmetric
Hypesthesia is only moderate
Regional adenopathy may be present
Borderline lepromatous leprosy:
Cutaneous lesions are numerous and consist of macules, papules, plaques, and nodules;
annular punched-out lesions resembling inverted saucers are common
Hypesthesia is often absent
Characteristic target lesion with an erythematous annular border, punched-out central area, and
impaired sensation
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Lepromatous leprosy:
Early cutaneous lesions may consist mainly of pale, small, diffuse, symmetric macules. Later in
the disease course, lepromatous infiltrations, which contain numerous bacilli and can be diffuse
or in the form of nodules or plaques, occur; diffuse infiltration results in leonine (lion-like) facies,
characterized by heavily furrowed, thickened skin folds on the forehead with prominent
supraorbital ridges and loss of eyebrows
Neuritic lesions are symmetric and slow to develop
There is little or no loss of sensation and no change in skin texture
No thickened nerves are seen, and sweating is normal
Alopecia affects the lateral eyebrows (known as madarosis), which spreads to the eyelashes
and then the trunk; the scalp hair remains intact
Eye involvement may occur and causes pain, photophobia, decreased visual acuity, glaucoma,
and blindness
Stridor and hoarseness result from laryngeal involvement and saddle-nose deformity caused by
nasal infiltration
Testicular involvement may result in sterility and gynecomastia
Lymphadenopathy and hepatomegaly may result from organ infiltration
Aseptic necrosis and osteomyelitis result from repeated trauma after joint invasion
Brawny edema of the lower extremities occurs late in the disease course
Multiple, small, slightly erythematous macules with intact sensation and symmetric distribution; the
skin smear results for both the lesions and intervening skin were positive for acid-fast bacilli
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Diffuse infiltration of the skin by multiple nodules of varying size, each teeming with bacilli
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Tender papules associated with fever, arthralgia, and acute neuritis in a patient with lepromatous
leprosy
Physical examination
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Patients with a history of living in or traveling to areas endemic for leprosy who present with
hypopigmented or erythematous macules should undergo a thorough examination, focusing specifically
on the distribution of any macules and the presence of enlarged, tender nerves. Skin lesions associated
with leprosy are present in the cooler areas of the body and are not found in the scalp, groin, or axilla
A careful sensory and motor examination, including tactile and temperature sensations, also should be
conducted, with a wisp of cotton used to test for lesional hypesthesia
Questions to ask
Presenting condition:
Do you have any areas of skin that are especially pale or particularly red? Hypopigmented or
erythematous macules are common in patients with leprosy, with the number and characteristics
indicative of particular forms of the disease
If so, where are the skin patches located? Skin lesions associated with leprosy typically are confined
to the cooler parts of the body, sparing areas such as the groin, axilla, and scalp
Do you have any patches of skin that are numb or where you no longer feel sensations such as hot or
cold? Sensory loss is common in patients with leprosy, particularly in those with paucibacillary forms
Have you noticed any thickened, tender lines on your skin? Thickened nerves are a common feature of
paucibacillary leprosy
Do you have any patches of skin with hair loss? Alopecia of macules is common in patients with
paucibacillary leprosy, and alopecia of the lateral eyebrows is seen in patients with multibacillary
disease. Scalp hair remains unaffected
Have you noticed any lumps under the skin, such as around the groin, armpit, or neck, that have not
gone away? Adenopathy is sometimes seen in patients with multibacillary leprosy
Contributory or predisposing factors:
Do you come from or have you lived in Asia, Africa, or South America? Leprosy is endemic in a number
of countries in these regions and should be suspected in any patient from these areas with the
characteristic signs
Has leprosy been diagnosed in anyone in your household or in someone with whom you have close
contact? The risk of contracting leprosy is significantly increased in household and close contacts of
patients with leprosy
Has anyone in your household or someone with whom you have close contact spent a lot of time in
Asia, Africa, or South America? Due to the extremely long incubation period, it is possible that leprosy
may have been transmitted before it was diagnosed in the contact
Have you had close contact with wild animals, such as armadillos, chimpanzees, or monkeys? Nine-
banded armadillos, chimpanzees, and mangabey monkeys are all recognized animal reservoirs of
leprosy
Do you live in overcrowded conditions? Overcrowding and poverty are associated with leprosy
Diagnostic testing
The presence of acid-fast bacilli in the skin is best demonstrated by slit-skin smears , which should be
taken from the edges of at least two lesions and both ear lobes. If this is not possible, a skin biopsy
specimen should be stained for acid-fast bacilli using a modified Wade-Fite stain. The extent of
bacillary load may be quantified as a bacterial index on a logarithmic scale of 1+ to 6+. The
morphologic index, which is the number of viable bacilli per 100 bacilli detected, also may be
calculated. Histologic findings vary but can include dermatitis, giant cells, infiltration of nerve bundles
with mononuclear cells, and granulomas. Lepromatous lesions typically contain numerous acid-fast
bacilli and fat-laden macrophages, with a paucity of lymphocytes. In contrast, tuberculoid lesions
contain few, if any, acid-fast bacilli but show granulomatous changes
In patients with neuritic leprosy, a nerve biopsy from a sensory nerve such as the superficial radial nerve
may be diagnostic
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The lepromin skin test does not confirm the diagnosis of leprosy but is useful in distinguishing
lepromatous leprosy from tuberculoid leprosy
Histamine testing allows detection of postganglionic nerve damage
Polymerase chain reaction (PCR) testing for M. leprae deoxyribonucleic acid (DNA) and antibody tests
for antibodies to M. leprae specific phenolic glycolipid (PGL)-1 and other M. leprae specific proteins
present in patients with lepromatous leprosy also may be conducted, but these tests are expensive and
are more commonly confined to epidemiologic studies
Slit-skin smears
Skin biopsy
Nerve biopsy
Lepromin skin test
Histamine test
PCR
PGL-1 antibody testing
Differential diagnosis
Other skin diseases may be differentiated from tuberculoid leprosy by the absence of lesional
hypesthesia and the presence of nerve involvement elsewhere
In contrast, lepromatous leprosy lesions are not hypesthetic, and a biopsy may be necessary in order
to distinguish them from lesions due to other systemic infections, such as leishmaniasis and
secondary or tertiary syphilis, as well as other nodular or infiltrative skin conditions
Other causes of nerve enlargement, such as primary amyloidosis and familial polyneuropathy, are
excluded by biopsy and family history
Cryptococcosis
Blastomycosis
Sporotrichosis
Nocardiosis
Leishmaniasis
Amyloidosis
Neurofibromatosis
Sarcoidosis
Syphilis
Psoriasis
Vitiligo
Contact dermatitis
Treatment
Summary approach
In the early stages of leprosy, treatment is aimed at preventing disability, but the ultimate goal is to
achieve a cure. According to the WHO, early detection and treatment of leprosy with multidrug therapy
has prevented disability in approximately 4 million patients, and leprosy has been cured in more than
14 million patients over the past 20 years, with cure achieved in approximately 4 million patients since
2000
Urgent treatment is necessary in patients experiencing lepra reactions or spontaneous fluctuations in
their clinical status, with the goals being to stabilize the patient's condition and minimize any
complications; if left untreated, lepra reactions represent a major cause of neuronal and other
complications
The WHO recommends multidrug therapy regimens for adults with leprosy consisting of combinations
of dapsone, rifampin, and clofazimine; treatment is the same in pediatric patients but with reduced
doses. After the first dose of multidrug therapy, the disease is no longer contagious, due to interrupted
transmission, and very few relapses occur after completion of the treatment course
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Multidrug therapy was first introduced in 1982, without formal clinical trials, when reported rates of
primary and secondary dapsone resistance reached 30%. Since then, multidrug-resistant strains of M.
leprae have not emerged, although there is no widespread monitoring of clinical outcomes and relapse
rates
Dapsone , an inhibitor of folic acid synthesis derived from sulfonamides, is the mainstay of treatment for
both lepromatous leprosy and tuberculoid leprosy, although lepromatous leprosy requires more
intensive treatment for a longer duration. The bactericidal effects against M. leprae at full dose, low
cost, and low toxicity of dapsone make it an important antileprosy medication. When used alone,
stepwise dapsone resistance emerges as a major problem, but this is prevented with the use of
combination therapy.
Rifampin is the most effective bactericidal agent against M. leprae and, thus, is a key component of
multidrug therapy, although it is too expensive for use at the recommended dosage in many developing
countries. The WHO states that rifampin should be administered once a month in conjunction with at
least one other effective medication in order to prevent resistance. Dosage recommendations in the
U.S. differ from those of the WHO, largely due to the absence of cost considerations applicable to
developing countries; the National Hansen's Disease Program (NHDP) recommends daily
administration of rifampin (600 mg/d) for 12 months in patients with paucibacillary leprosy and for 24
months in patients with multibacillary leprosy
Clofazimine , a fat-soluble phenazine dye that is deposited within the skin, fat stores, and
macrophages, is administered daily and has similar activity against M. leprae as dapsone, as well as
anti-inflammatory activity that makes it moderately effective against lepra type 2 reactions and,
possibly, lepra type 1 reactions
The standard WHO multidrug regimen for adults with multibacillary leprosy is rifampin, 600 mg once a
month; dapsone, 100 mg/d; and clofazimine, 300 mg once a month and 50 mg/d, for 24 months. The
standard regimen for adults with paucibacillary leprosy is rifampin, 600 mg once a month, and dapsone,
100 mg/d, for 6 months
In the U.S., the NHDP regimen for adults with multibacillary leprosy is dapsone, 100 mg/d; rifampin,
600 mg/d; and clofazamine, 50 mg/d, for 24 months. The NHDP regimen for adults with paucibacillary
leprosy is dapsone, 100 mg/d, and rifampin, 600 mg/d, for 12 months
More recently, clinical trials have found that ofloxacin and minocycline rapidly kill M. leprae and
effectively reduce dermal infiltration in patients with lepromatous leprosy. The two drugs currently are
recommended for treatment of single-lesion paucibacillary leprosy; the treatment regimen
recommended by the WHO for adults is ofloxacin, 400 mg; minocycline, 100 mg; and rifampin, 600 mg
Ethionamide is an effective alternative antileprosy agent that is used primarily in patients who cannot
tolerate first-line antileprosy medications or when medication resistance is recognized during treatment
of multibacillary disease. However, ethionamide may cause gastrointestinal problems and liver
dysfunction, especially when used in combination with rifampin, and, therefore, is not recommended
unless liver function can be monitored regularly
Treatment of lepra reactions:
The only effective treatment for lepra type 1 reactions is the addition of a corticosteroid, such as
prednisone , to the antimicrobial treatment regimen. Corticosteroid therapy generally should not
be initiated unless there is neuritis, skin inflammation that may become ulcerated, or
involvement of cosmetically important areas; treatment of minor inflammation is not indicated
First and second lepra type 2 reactions, or erythema nodosum leprosum, may be treated with
aspirin, if mild, or with short courses of prednisone for several days to a week, with withdrawal
over 2 to 3 months. Clofazimine at higher daily doses suppresses erythema nodosum leprosum
after 4 to 6 weeks and can be used to prevent additional episodes
Thalidomide is the medication of choice for recurrent or poorly controlled, severe type 2 lepra
reactions, as it inhibits the release of tumor necrosis factor from macrophages and offers prompt
relief, but should only be used in men and postmenopausal women under strict supervision due
to its teratogenicity. Thalidomide is relatively contraindicated in patients with lepra type 1
reactions as it may upregulate T-helper cell type 1 responses and worsen neuronal damage
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Surgery may be necessary in patients with profound nerve inflammation presenting with a nerve
abscess or loss of nerve function secondary to compression; prompt drainage often can restore nerve
function. Lagophthalmos, or the inability to close the upper eyelid, may require elective surgery, and
patients with lepromatous leprosy may need nasal reconstruction and other cosmetic procedures.
Tendon transfers may correct functional disabilities in the extremities but should not be done until 6
months after initiation of therapy or the occurrence of a significant reaction, particularly in the affected
nerve distribution
Physical therapy should be offered to patients with muscle weakness
Medications
Dapsone
Rifampin
Clofazimine
Minocycline
Ofloxacin
Prednisone
Thalidomide
Ethionamide
Special circumstances
Pregnancy ideally should be planned when leprosy is well controlled, but rifampin, dapsone, and
clofazimine are all safe for use during pregnancy; rifampin should be administered only as a single
monthly dose, but dapsone and clofazimine doses do not need to be altered
In pregnant women with lepra type 1 or lepra type 2 reactions, prednisone and clofazimine can be
administered, but thalidomide should be avoided. It is advisable to postpone pregnancy temporarily
during the posttreatment period if there is evidence of a reaction, relapse, or neuritis
Infants are at relatively high risk of contracting leprosy from untreated mothers, especially those with
borderline leprosy or lepromatous leprosy
Surgical therapy is sometimes appropriate for patients with sustained nerve damage or other
complications
Consultation
Consultation with an ophthalmologist, plastic surgeon, orthopedic surgeon, otolaryngologist, neurosurgeon,
and/or neurologist may be required due to the various complications that may arise in patients with leprosy.
Follow-up
Plan for review:
The WHO recommends that patients with paucibacillary leprosy be monitored for 2 years and patients
with multibacillary leprosy be monitored for 5 years
The patient's eyes, nose, and nerves should be examined at follow-up visits to ensure timely recognition
of reactive disease; sensation and muscle strength in the hands and feet also should be checked
regularly
A complete blood count should be obtained at frequent intervals during treatment with dapsone and less
frequently after completion of the treatment course
Prognosis:
If left untreated, leprosy leads to progressive and permanent damage to the skin, nerves, limbs, and
eyes; thus, early recognition is important, as it limits the damage caused by the disease, eliminates
the risk of transmission, and allows for a normal lifestyle
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Although both lepromatous leprosy and tuberculoid leprosy are associated with skin and peripheral
nerve involvement, the tuberculoid form has more severe manifestations; for example, nerve involvement
results in loss of sensory and motor function, which may lead to frequent trauma and, ultimately,
amputation
In patients with lepromatous leprosy, infiltration by bacteria may lead to destruction of nasal cartilage,
ocular involvement, and thickening of the skin
The main factors affecting prognosis are access to therapy, compliance, and early initiation of
treatment
Most cases of indeterminate leprosy evolve into tuberculoid leprosy or lepromatous leprosy, depending
on the patient's immunity to the disease; spontaneous resolution may occur in patients with strong
immunity, and the disease may remain in the indeterminate stage in some patients
Patients with tuberculoid leprosy may experience spontaneous resolution within a few years, leaving
pigmentary disturbances or scars, or progression of disease, leading to borderline lepromatous leprosy
or, rarely and in untreated cases, to lepromatous leprosy
Borderline tuberculoid leprosy can remain in the same stage, convert back to the tuberculoid form, or
progress. Borderline leprosy may remain in the same stage, convert back through borderline tuberculoid
leprosy to tuberculoid leprosy, or progress. Likewise, borderline lepromatous leprosy may remain in the
same stage, improve, or progress
Unlike other forms of leprosy, lepromatous leprosy cannot convert back to the less severe borderline or
tuberculoid forms of the disease
Patients with leprosy may experience recurrence, with the greatest risk in those who do not
successfully complete a course of multidrug therapy. Although comprehensive monitoring is lacking,
there have been very few reports of resistance to multidrug therapy since its introduction
Occurrence of lepra type 1 and type 2 reactions is associated with a poor prognosis
Complications:
The most common complications in patients with leprosy are reactional states, which can result in
permanent neurologic sequelae and, hence, disability and deformity
Lepra type 1 reactions affect patients with borderline disease. A downgrading reaction
represents a shift toward the lepromatous pole before initiation of treatment, and a reversal
reaction represents a shift toward the tuberculoid pole after initiation of treatment; both are
believed to be associated with a change in cellular immunity and may result in inflammation,
neuritis, and, possibly, fever. In reversal reactions, T-helper cell dermal infiltration increases
significantly, with an associated increase in local cytokines, especially interferon-. If not treated
early, lepra type 1 reactions can lead to irreversible motor and sensory loss
Lepra type 2 reactions ( erythema nodosum leprosum) occur in the first few years of disease in
approximately half of all patients with lepromatous leprosy and may precede initiation of
treatment, thereby precipitating the diagnosis, or may occur up to 10 years after initiation of
treatment, when patients have negative slit-skin smear results. Erythema nodosum leprosum is
characterized by the presence of erythematous and painful papules or subcutaneous nodules
that may pustulate and ulcerate, along with fever, neuritis, lymphadenitis, orchitis, arthritis
(particularly in large joints, such as the knees), and glomerulonephritis. Histologically, erythema
nodosum leprosum appears to be a polymorphonuclear vasculitis or panniculitis and is believed
to be due to circulating immune complexes or events associated with increased T-helper cell
function; levels of circulating tumor necrosis factor also may increase. Patients may develop
anemia from erythrocyte destruction or bone marrow suppression and hepatic inflammation, with
abnormalities in liver function test results. An unusual lepra type 2 reaction (sometimes
designated a lepra type 1 reaction) characterized by cutaneous hemorrhagic infarcts, known as
the Lucio phenomenon, occurs in patients with diffuse lepromatous leprosy and is common in
Mexico and Central America
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Peripheral nerve involvement, specifically nerve trunks and microscopic dermal nerves, as a
consequence of the infection and the host inflammatory response or neuritis associated with lepra
reactions accounts for the majority of complications. The ulnar nerve at the elbow is affected most
commonly, leading to distal hypoesthesia and clawing of the fourth and fifth digits in patients with
severe disease. The perineal, median, and zygomatic branches of the facial nerves and the posterior
auricular nerves also may be involved. Small nerve fibers that respond to hot and cold, fine touch, and
pain are particularly affected, whereas larger nerve fibers responsible for position and vibration sensation
generally are spared
Plantar ulcers with secondary infection are a major cause of morbidity and should be treated with
debridement and appropriate antibiotics. More complicated ulcers require surgical removal, and wide
exploration and good drainage are needed if dead tissue is present
Ocular involvement may be severe. In patients with lepromatous leprosy, M. leprae invades the anterior
chamber, whereas erythema nodosum leprosum may cause iritis, leading to glaucoma. Corneal
insensitivity and involvement of the zygomatic branch of the facial nerve, causing lagophthalmos, may
lead to corneal trauma, scarring, and blindness. Routine use of lubricating eye drops is indicated in
patients with corneal involvement
The nasal mucosa and cartilage are affected in patients with lepromatous leprosy, with untreated
disease often resulting in chronic nasal congestion and, at times, epistaxis, as well as nasal cartilage
perforation and collapse in rare cases
Impotence is sometimes seen in men with lepromatous leprosy due to decreased serum testosterone
levels and increased follicle-stimulating hormone and luteinizing hormone levels, resulting in
hypospermia, aspermia, and infertility. Treatment consists of monthly intramuscular injections of
testosterone enanthate, 200 mg, or liberal application of 5% testosterone cream to the scrotum twice
daily
Amyloidosis and renal failure occasionally are seen in patients with lepromatous leprosy and are
associated with severe, recurrent erythema nodosum leprosum
There is no evidence that pregnancy causes new disease or relapse, but there is a temporal
association between the development of lepra type 1 reactions and neuritis and parturition, when cell-
mediated immunity returns to prepregnancy intensity. Women with lepromatous leprosy may
experience erythema nodosum leprosum throughout pregnancy and lactation, which is linked to earlier
loss of nerve function than in nonpregnant patients
Patient education
Patients in whom leprosy is diagnosed should be given an explanation of the diagnosis, treatment, and
prognosis. It is also important to address any fears resulting from the cultural stigma of leprosy;
psychological counseling may be necessary, as patients may have difficulty coming to terms with the
diagnosis or may feel rejected by society
Patients should be reassured that leprosy, even advanced leprosy with many sores, is curable if they
adhere to and complete the prescribed multidrug therapy regimen
Patients should be made aware that damage to the extremities, including clawing of the fingers in
severe cases, is caused largely by neuropathy, which results in the inability to feel trauma. Patients
who have lost sensation in their feet or hands should be advised to inspect their extremities regularly for
trauma and to wear protective clothing and footwear, consisting simply of canvas shoes with protective
insoles
Patients should be taught how to identify the onset of anesthesia or weakness in the limbs and eyes
and how to recognize the onset of lepra reactions, which require immediate medical attention
Patients with bone or joint destruction should be instructed to minimize weight bearing
Patients with plantar ulceration should be advised of the importance of rest and avoidance of weight
bearing to promote healing
Patients with weakness or paralysis should be encouraged to participate in a regular physical therapy
regimen
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Online information for patients
American Academy of Family Physicians: Leprosy
International Federation of Anti-Leprosy Associations (ILEP): Facts About Leprosy
LEPRA Health in Action
National Institute of Allergy and Infectious Diseases: Leprosy (Hansen's Disease)
U.S. Department of Health and Human Services: National Hansen's Disease (Leprosy) Program
WHO: Leprosy
Resources
Summary of evidence
Evidence
Primary prevention
A meta-analysis of 7 experimental studies and 19 observational studies found that the overall protective
effect of the BCG vaccine was 26% in the experimental studies and 61% in the observational studies.
There was significant heterogeneity among the trials but few significant differences between the
protective effects of BCG vaccination against paucibacillary or multibacillary disease or between
household contacts and other contacts. However, it was noted that an additional dose of BCG vaccine
was more protective than a single dose in the prevention of leprosy, leading the authors to recommend
that an additional dose may be warranted in contacts of patients with leprosy in areas where the
disease remains a public health problem. [1] Level of evidence: 1
Treatment
Dapsone:
An RCT comparing the efficacy of standard multidrug therapy with dapsone and rifampin versus a 4-
week regimen of ofloxacin plus rifampin in 124 patients with paucibacillary leprosy found that, after 10
years of follow-up, one relapse occurred in the group receiving ofloxacin plus rifampin and two relapses
occurred in the group receiving standard therapy, leading the investigators to conclude that both
treatment regimens were effective. [2] Level of evidence: 1
Rifampin:
An RCT comparing the efficacy of standard multidrug therapy with dapsone and rifampin versus a 4-
week regimen of ofloxacin plus rifampin in 124 patients with paucibacillary leprosy found that, after 10
years of follow-up, one relapse occurred in the group receiving ofloxacin plus rifampin and two relapses
occurred in the group receiving standard therapy, leading the investigators to conclude that both
treatment regimens were effective. [2] Level of evidence: 1
An observational study of 105 patients receiving rifampin and clofazimine after withdrawal of dapsone
due to toxicity found that dual therapy produced negative slit-skin smear results in all 36 patients with
positive results at onset. [3] Level of evidence: 2
Clofazimine:
An RCT comparing the efficacy of standard multidrug therapy with dapsone and rifampin versus a 4-
week regimen of ofloxacin plus rifampin in 124 patients with paucibacillary leprosy found that, after 10
years of follow-up, one relapse occurred in the group receiving ofloxacin plus rifampin and two relapses
occurred in the group receiving standard therapy, leading the investigators to conclude that both
treatment regimens were effective. [2] Level of evidence: 1
An observational study of 105 patients receiving rifampin and clofazimine after withdrawal of dapsone
due to toxicity found that dual therapy produced negative slit-skin smear results in all 36 patients with
positive results at onset. [3] Level of evidence: 2
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A systematic review evaluating the efficacy of interventions for erythema nodosum leprosum (lepra type
2 reactions), including aspirin, prednisolone, betamethasone, thalidomide, clofazimine, and others,
identified 13 RCTs involving a total of 445 patients. The reviewers concluded that the sample sizes were
small and the heterogeneity of treatments precluded pooling of data, but clofazimine appeared to be
superior to thalidomide and prednisolone, and thalidomide was superior to aspirin. [4] Level of evidence:
1
Minocycline:
A multicenter RCT comparing the efficacy of a combination of rifampin, ofloxacin, and minocycline
administered as single dose with that of the standard 6-month WHO multidrug therapy regimen for
paucibacillary leprosy in 1,483 patients with single-lesion paucibacillary leprosy (1,381 of whom
completed the study) found that combination therapy with rifampin, ofloxacin, and minocycline was
almost as effective as the standard WHO multidrug therapy regimen. Mild adverse effects and leprosy
reactions were minimal in both groups, occurring in less than 1% of patients. [5] Level of evidence: 1
Ofloxacin:
A multicenter RCT comparing the efficacy of a combination of rifampin, ofloxacin, and minocycline
administered as single dose with that of the standard 6-month WHO multidrug therapy regimen for
paucibacillary leprosy in 1,483 patients with single-lesion paucibacillary leprosy (1,381 of whom
completed the study) found that combination therapy with rifampin, ofloxacin, and minocycline was
almost as effective as the standard WHO multidrug therapy regimen. Mild adverse effects and leprosy
reactions were minimal in both groups, occurring in less than 1% of patients. [5] Level of evidence: 1
An RCT comparing the efficacy of standard multidrug therapy with dapsone and rifampin versus a 4-
week regimen of ofloxacin plus rifampin in 124 patients with paucibacillary leprosy found that, after 10
years of follow-up, one relapse occurred in the group receiving ofloxacin plus rifampin and two relapses
occurred in the group receiving standard therapy, leading the investigators to conclude that both
treatment regimens were effective. [2] Level of evidence: 1
Prednisone:
An RCT evaluating the efficacy of adding low-dose prednisolone to multidrug therapy in preventing lepra
reactions and nerve function impairment in 636 patients with newly diagnosed multibacillary leprosy
found that low-dose prophylactic prednisolone administered during the first 4 months of multidrug
therapy reduced the incidence of new reactions and nerve function impairment in the short term.
However, the effect was not sustained at 1 year. The investigators suggested that the presence of nerve
function impairment at diagnosis may influence the response to low-dose prednisolone. [6] Level of
evidence: 1
A systematic review examining the efficacy of steroids for the treatment of nerve damage due to leprosy
identified three RCTs differing in design and patient parameters. Two trials compared prednisolone
versus placebo and found no significant difference in outcome between groups after 12 months of follow-
up. The third study evaluated three different prednisolone regimens, including high- and low-dose
therapy for 3 and 5 months. Patients assigned to the 3-month course required supplemental steroids
more often than those receiving treatment for 5 months. The reviewers concluded that additional trials
are needed to establish efficacy and optimal regimens. [7] Level of evidence: 1
A prospective, randomized trial comparing the efficacy of prednisolone versus thalidomide in 60 patients
with erythema nodosum leprosum found that patients receiving thalidomide experienced more rapid
improvement and remained free of relapse longer than those receiving prednisolone. [8] Level of
evidence: 2
Thalidomide:
A systematic review evaluating the efficacy of interventions for erythema nodosum leprosum (lepra type
2 reactions), including aspirin, prednisolone, betamethasone, thalidomide, clofazimine, and others,
identified 13 RCTs involving a total of 445 patients. The reviewers concluded that the sample sizes were
small and the heterogeneity of treatments precluded pooling of data, but clofazimine appeared to be
superior to thalidomide and prednisolone, and thalidomide was superior to aspirin. [4] Level of evidence:
1
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A prospective, randomized trial comparing the efficacy of prednisolone versus thalidomide in 60 patients
with erythema nodosum leprosum found that patients receiving thalidomide experienced more rapid
improvement and remained free of relapse longer than those receiving prednisolone. [8] Level of
evidence: 2
Ethionamide:
A 6-month observational study randomly assigned 50 patients with untreated lepromatous leprosy to
directly observed monotherapy with ethionamide or prothionamide. Clinical improvement was noted in
74% of the patients receiving ethionamide and 83% of those receiving prothionamide. Because of the
small sample size, however, the results must be interpreted with caution. The WHO has not endorsed
the routine use of thioamides in the treatment of leprosy. [9] Level of evidence: 2
References
References
Evidence references
[1] Setia MS, Steinmaus C, Ho CS, Rutherford GW. The role of BCG in prevention of leprosy: a meta-analysis.
Lancet Infect Dis. 2006;6:162-70
CrossRef
[2] Balagon MF, Cellona RV, Abalos RM, Gelber RH, Saunderson PR. The efficacy of a four-week, ofloxacin-
containing regimen compared with standard WHO-MDT in PB leprosy. Lepr Rev. 2010;81:27-33
[3] Sapkota BR, Shrestha K, Pandey B, Walker SL. A retrospective study of the effect of modified multi-drug
therapy in Nepali leprosy patients following the development of adverse effects due to dapsone. Lepr Rev.
2008;79:425-8
[4] Van Veen NH, Lockwood DN, van Brakel WH, Ramirez J Jr, Richardus JH. Interventions for erythema
nodosum leprosum. Cochrane Database Syst Rev. 2009:CD006949
CrossRef
[5] Efficacy of single dose multidrug therapy for the treatment of single-lesion paucibacillary leprosy. Single-
lesion Multicentre Trial Group. Indian J Lepr. 1997;69:121-9
[6] Smith WC, Anderson AM, Withington SG, et al. Steroid prophylaxis for prevention of nerve function
impairment in leprosy: randomised placebo controlled trial (TRIPOD 1). BMJ. 2004;328:1459
CrossRef
[7] Van Veen NH, Nicholls PG, Smith WC, Richardus JH. Corticosteroids for treating nerve damage in leprosy.
Cochrane Database Syst Rev. 2007:CD005491
CrossRef
[8] Kaur I, Dogra S, Narang T, De D. Comparative efficacy of thalidomide and prednisolone in the treatment of
moderate to severe erythema nodosum leprosum: a randomized study. Australas J Dermatol. 2009;50:181-5
CrossRef
[9] Fajardo TT, Guinto RS, Cellona RV, Abalos RM, Dela Cruz EC, Gelber RH. A clinical trial of ethionamide
and prothionamide for treatment of lepromatous leprosy. Am J Trop Med Hyg. 2006;74:457-61
Guidelines
The WHO has produced the following:
Regional Office for South-East Asia, WHO. Global Strategy for Further Reducing the Leprosy Burden
and Sustaining Leprosy Control Activities (2006-2010): Operational Guidelines . New Delhi: WHO; 2006
Leprosy Elimination Group, WHO. Guide to Eliminate Leprosy as a Public Health Problem . Geneva:
WHO; 2000
The NHDP , a division of the U.S. Department of Health and Human Services, has produced the following:
Recommended Treatment Regimens . Baton Rouge, LA: NHDP
The Centre for Disease Control , a division of the Northern Territory Department of Health (Australia), has
produced the following:
Guidelines for the Control of Leprosy in the Northern Territory, 2010 . Casuarina, Australia: Centre for
Disease Control; 2010
The International Council of Ophthalmology has produced the following:
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Eye Disease in Leprosy (Initial Evaluation and Management) . San Francisco, CA: International Council
of Ophthalmology; 2011
Further reading
Boggild AK, Keystone JS, Kain KC. Leprosy: a primer for Canadian physicians. CMAJ. 2004;170:71-8
Britton WJ, Lockwood DN. Leprosy. Lancet. 2004;363:1209-19
Randomised controlled trial of single BCG, repeated BCG, or combined BCG and killed Mycobacterium
leprae vaccine for prevention of leprosy and tuberculosis in Malawi. Karonga Prevention Trial Group.
Lancet. 1996;348:17-24
Tejasvi T, Khaitan BK, Khanna N, Pandhi RK, Singh MK. Evaluation of a new fixed duration (12 weeks)
multi-drug regimen of bactericidal drugs in multibacillary leprosy. Indian J Lepr. 2006;78:329-37
Matthews SJ, McCoy C. Thalidomide: a review of approved and investigational uses. Clin Ther.
2003;25:342-95
Van Veen NH, Schreuders TA, Theuvenet WJ, Agrawal A, Richardus JH. Decompressive surgery for
treating nerve damage in leprosy. Cochrane Database Syst Rev. 2009:CD006983
Reinar LM, Forsetlund L, Bjrndal A, Lockwood D. Interventions for skin changes caused by nerve
damage in leprosy. Cochrane Database Syst Rev. 2008:CD004833
Codes
ICD-9 codes
030 Leprosy, including Hansen disease, infection with M. leprae
030.0 Lepromatous [type L]; lepromatous leprosy (macular, diffuse, infiltrated, nodular, neuritic)
030.1 Tuberculoid [type T]; tuberculoid leprosy (macular, maculoanesthetic, major, minor, neuritic)
030.2 Indeterminate [group I]; indeterminate [uncharacteristic] leprosy (macular, neuritic)
030.3 Borderline [group B]; borderline or dimorphous leprosy (infiltrated, neuritic)
030.8 Other specified leprosy
030.9 Leprosy, unspecified
373.4 Infective dermatitis of eyelid of types resulting in deformity. Code first underlying disease as
leprosy (030.0-030.9), lupus vulgaris (tuberculous) (017.0), yaws (102.0-102.9)
711.4 Arthropathy associated with other bacterial diseases [0-9]. Code first underlying disease as
diseases classifiable to 010-040, 090-099, except as in 711.1, 711.3, and 713.5, leprosy (030.0-030.9),
tuberculosis (015.0-015.9). Excludes: gonococcal arthritis (098.50), meningococcal arthritis (036.82)
FAQ
How often should patients with leprosy be monitored?Monthly follow-up is recommended
How long after treatment can relapse occur?Relapse can occur 10 years or more after completion
of treatment; thus, long-term follow-up is needed
Why is the incubation period so long? M. leprae divides very slowly (approximately once every 2
weeks)
Why hasn't M. leprae ever been cultured in vitro ? M. leprae is an obligate mammalian pathogen
that has lost the metabolic gene products necessary for growth on artificial media, such as
mycobacterial culture plates
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Who should manage patients with leprosy todayspecialized treatment centers or general
internal medicine clinicians and family practice physicians?If at all possible, patients with leprosy
should be managed locally by infectious disease specialists or dermatologists familiar with the
diagnostic methods and standard treatment protocols. Treating the disease locally removes the still
extant social stigma associated with leprosy and facilitates access to family and social support. Expert
assistance and advice is readily available from local or regional leprosy centers linked with public health
facilities
Contributors
Lucileia Johnson, MD
William Harper, MD
Steven M. Opal, MD
Eleftherios E. Mylonakis, MD