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Leprosy SW

Leprosy, or Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae, primarily affecting peripheral nerves and skin. The disease has seen significant decline globally due to effective treatments like multidrug therapy, with a 90% decrease in cases since 1991. Diagnosis is based on clinical signs, and control measures focus on early detection, treatment, and rehabilitation to prevent deformities.

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0% found this document useful (0 votes)
8 views49 pages

Leprosy SW

Leprosy, or Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae, primarily affecting peripheral nerves and skin. The disease has seen significant decline globally due to effective treatments like multidrug therapy, with a 90% decrease in cases since 1991. Diagnosis is based on clinical signs, and control measures focus on early detection, treatment, and rehabilitation to prevent deformities.

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dzn4t4ftw4
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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LEPROSY

Hansen's Disease
 Leprosy is a chronic infectious
disease caused by Myobacterium
leprae.

 It affects mainly the peripheral nerves.


It also affects the skin, muscles, eyes,
bones, testes and internal organs.
HISTORY
Leprosy was discovered by G.A
Hansen in 1873.
It was the 1st bacteria to be
identified as causing disease in man.
Treatment of leprosy only appeared
in the late 1940s with the
introduction of dapsone and it's
derivatives.
Gerhard Armauer
Hansen
• In 1991, WHO stated decrease in leprosy in the world
by 90%.
• 16 million cases are cured over past 20 years.
• Drop in prevalence rate from 21.1 cases per 10,000
population in 1985 to 0.32% at beginning of 2014.
• Elimination of leprosy from 119 out of 122 countries.
Global Burden
• New leprosy cases detected worldwide per year~1.4 to 1.5
lakh (140,000–150,000 cases)
• Countries contributing ~80% of global burden- India, Brazil,
Indonesia
• Global prevalence rate- <1 case per 10,000 population
• Child case proportion globally~6–8%
• Grade 2 disability among new cases~2–4%
Classification
1. Indian classification
2. Madrid classification
3. Ridley Jopling classification
4. WHO classification
 Indian and Madrid classification are
most widely used and are similar
except one additional pure
neuretic type in Indian
classification system
(Based on clinical, bacteriological, immunological &
histopathological findings)
a. Indeterminate type:
• 1 or 2 vague hypopigmented macules.

Indian Classification
• Definite sensory impairment
• Bacteriologically negative lesions

b. Tuberculoid type:
• 1 or 2 well defined lesions, may be flat or raised
• Hypopigmented
• Bacteriologically negative lesions

c. Borderline type:
• 4 or more lesions, may be flat or raised, well or undefined
• Hypopigmented
• Show sensory impairment or loss
• Bacteriologically positive lesions
• If untreated progresses to lepromatous type.
d. Lepromatous type:
• Numerous flat or raised, poorly defined, shiny, smooth,
symmetrically distributed lesions.
• Bacteriologically positive lesions

e. Pure neuretic type:


• Show nerve imnvolvement but no lesion on skin
• Bacteriologically negative
WHO Classification :
Used in NLEP (National Leprosy Eradication
Programme)
🔹 Simple, field-friendly classification
Type Paucibacillar Multibacillary
y
Criteria ≤5 skin lesions >5 skin lesions

Skin lesions Up to 5 More than 5


Nerve One nerve More than one
involvement nerve
Ridley-Jopling Classification

Type TT BT BB BL LL I
(tubercu (borderli (borderli (borderli (leprom (indeter
loid) ne ne ne atous) minate)
tubercul borderli leproma
oid) ne) tous)

Immunit High Moderate Unstable Low Very low Early


immunity immunity immunity immunity immunity immunity
y

Bacilli Few bacilli Few bacilli Moderate Many bacilli Numerous Uncertain
bacilli bacilli features
load
 The disease manifests itself in two forms, namely
the lepromatous leprosy and tuberculoid leprosy
lying at the two ends of a long spectrum of the
disease.

 Between these two polar types occur the borderline


and indeterminate forms depending upon the host
response to infection.
Cardinal features:

a. Hypopigmented patches
b. Partial or total loss of cutaneous
sensation in the affected areas.
c. Presence of thickened nerves
d. Presence of acid fast bacilli in the
skin or nasal smears.
e. Muscle weakness
f. Deformities in advanced cases
Epidemiology

Agent factors

 Agent: leprosy is caused by M.leprae. they are acid fast


and occur in the human host both intracellularly and
extracellularly.

 They have an affinity for Schwann cells and cells of the


reticulo- endothelial system. They remain dormant in
various sites and cause relapse.
Source of infection:

 It is generally agreed that multibacillary cases i.e lepromatous


and borderline lepromatous cases are the most important source
of infection in the community.

 Role of Individuals with tuberculoid forms of the disease as


source of infection is not cleared.

 All patients with active leprosy must be considered infectious.

 There is now evidence that natural infections with M. leprae are


present in wild animals, eg- armadillos, mangabey monkeys and
chimpanzees but it is not know if it is a threat to public health.
Portal of exit:

It is widely accepted that nose is a


major portal of exit. Lepromatous
cases harbour millions of M.leprae in
their nasal mucosa which are
discharged when they sneeze or
blow the nose. The bacilli can also
exit through ulcerated or broken skin
of bacteriologically positive case of
leprosy.
Mode of Transmission of Leprosy
Primary Mode – Droplet Infection
Inhalation of infected nasal secretions from untreated
multibacillary cases.
Most common route.

Direct Skin-to-Skin Contact


Prolonged, close contact with lesions.
Especially in household or repeated exposure settings.

Indirect Transmission (Rare)


Through contaminated clothing, bedding, or utensils.
Bacilli may survive in cool, moist conditions temporarily.
Infectivity:

 Highly infectious disease but if low pathogenesity.

 It is claimed that an infectious patient can be rendered non


infectious by treatment with dapsone for 90 days or with
rifampicin for 3 weeks. Local application of rifampicin (spray or
drops) might destroy all the bacilli in 8 days.

 Among house hold contact of lepromatous case, a varying


proportion -4.4% -12% is expected to show signs within 5 years
 Prolonged close contact with
untreated cases
 Nasal droplets primary source
 Possible skin contact (less
common)
Risk Factors
 Not highly contagious
Host factors

Age:

Not particularly a disease of children


• Infection can take place at any time depending on exposure
opporunities.
• Disease is acquired commonly during childhood in endemic
areas.
• Youngest case: 2½ months old infant in South India.
• Incidence rates generally rise at peak from 10 to 20 years.
• However, it may appear late in areas where leprosy is rare.
Sex:

• Both the incidence and prevalence of leprosy


appear to be higher in males than females.
• Sex difference is found least in children below
15 years.
• More marked among adult and lepromatous
cases than non lepromatous cases.
Migration

In India, Leprosy was considered to be mostly a


rural problem. however, with migration it has also
creating a problem in urban areas.

Genetic factors

There is now evidence that Human lymphocytes


antigen (HLA) linked genes influence the type of
immune response.
Immunity

CMI level Clinical type of Features


• Only a few person leprosy
exposed to
Strong Tuberculoid Localised lesions,
infection develop Leprosy few bacilli, good
the disease. prognosis

• CMI controls the Intermediate Borderline forms Unstable, can shift


towards TT or LL
multiplication of
M. leprae.
Absent/Low Lepromatous Numerous lesions,
leprosy many bacilli, poor
• Humoral immunity resistance
(antibodies) is not
protective
Environmental
Factors
1. Climate
Leprosy is more common in tropical and
subtropical climates. 4. Low Socioeconomic Status
Warm, humid climates support longer survival Poor housing, numultibacillary cases)
of the bacillus in the environment. increases risk.
Dry, cold areas have relatively lower The risk is directly proportional to the
prevalence. duration and closeness of exposure.

2. Overcrowding 7. Occupation
Increases the chances of close contact with Occupations involving close person-to-
infected individuals. person contact, poor hygiene, or
High density in households, slums, or hostels exposure to infected soil/surfaces may
enhances droplet transmission. raise risk.

3. Poor Sanitation and Hygiene


Indirect transmission through contaminated
fomites (clothing, bedding) is possible.
Dirty surroundings promote skin abrasions,
allowing easier entry of bacilli.
Incubation period: Clinical Diagnosis

Average: 3 to 5 years Leprosy is primarily diagnosed clinically,


Range: 6 months to 20 especially in field settings. WHO
years or more recommends that the presence of any one
of the following three cardinal signs is
sufficient for diagnosis:

✅ Three Cardinal Signs of Leprosy:


1.Skin Lesion with Sensory Loss
Hypopigmented, reddish, or copper-colored
patch.
Definite loss or impairment of sensation
(pain, touch, temperature)
May be single or multiple
2. Thickened Peripheral Nerve
Commonly involved nerves: ulnar, radial cutaneous,
posterior auricular, tibial, peroneal
Associated with:
Tingling or numbness
Muscle weakness or paralysis
Loss of sweating or hair in that region.

3. Presence of Acid-Fast Bacilli (AFB)


Seen on slit-skin smear from lesions, ear lobes, or
elbows
Confirms the presence of Mycobacterium leprae
🔹 II. Laboratory Diagnosis
(Supportive Methods)

Used for confirmation, classification, and


treatment decisions. 🔹 III. WHO Field Diagnosis
1. Slit Skin Smear (SSS)
Ziehl-Neelsen (ZN) staining used For practical field use, if any 1 of the 3
cardinal signs is present → Leprosy is
Detects acid-fast bacilli in dermal tissue
diagnosed.
Sample taken from:
Ear lobes No need for lab confirmation if clinical
Lesional skin signs are clear, especially in resource-
limited settings.
Elbows
Used to calculate:
Bacterial Index (BI): Indicates bacilli load
Morphological Index (MI): Indicates viability of
bacilli
🔹 1. Bacterial Index (BI)
BI indicates the number of bacilli present in a slit-skin
smear.
It reflects the density of bacilli and overall bacterial load.

🟡 Purpose:
Helps in classifying cases (MB if BI ≥ 2+)
Useful in monitoring treatment response
🔹 2. Morphological Index (MI)
MI indicates the percentage of viable (living) bacilli among the total
seen in a smear.
It is based on staining pattern using Ziehl-Neelsen stain.

🟢 Purpose:
Indicates activity of disease
High MI → active infection
Falling MI → treatment is woring.
• Solid fragmented granular (SFG) percentage
• The procedures for recording solid, fragmented and granular
bacilli is same as that used for determining MI. Since the
percentages are mentioned seperately it gives better picture
of bacterial morphology than MI. more sensitive indicator of
the patient's treatment response.

• FOOT-PAD culture
• This is considered the only certain method to identify M. leprae by
inoculating material into mouse foot-pads and demonstrating
bacterial multiplication.
• It's ten times more sensitive than slit-skin smears in detecting M.
leprae but is time-consuming (6-9 months for results), cumbersome,
and expensive. Newer in vitro methods like macrophage culture offer
faster results (3-4 weeks).
• It's used for detecting drug resistance, evaluating the potency of anti-
Histamine Test:
A reliable method for early detection of peripheral nerve damage in leprosy
Performed by intradermally injecting histamine phosphate or chlorohydrate
into hypopigmented patches or anesthetic areas.
• In normal individuals, it elicits a Lewis triple response (wheal and
erythematous flare), while in leprosy with nerve damage, the flare
response is absent or diminished.

Biopsy:
Recommended when other examinations fail to yield a diagnosis.
Histopathological examination of tissue samples (skin or nerve) is
necessary for definitive diagnosis and classification of leprosy.

• Lepromin Test,
• an immunological test used in leprosy to assess cell-mediated
immunity (CMI) and aid in disease classification, though it's not a
diagnostic tool for the disease itself.

• Procedure: A small amount (0.1 ml) of lepromin (a suspension of
inactivated Mycobacterium leprae) is injected intradermally into the
forearm.

• Types of Reactions:
• Early Reaction (Fernandez Reaction): Appears within 24-48 hours,
characterized by redness and induration. A diameter over 10mm at
48 hours is considered positive, indicating prior sensitization to
leprosy bacilli.

• Late Reaction (Mitsuda Reaction): Develops later, becoming
apparent in 7-10 days and maximizing in 3-4 weeks. Read at 21
Value in Classification and Prognosis:
• Strongly positive in tuberculoid leprosy and borderline tuberculoid
cases, reflecting robust CMI.
• Negative or weak reactions are seen in lepromatous and near-
lepromatous cases due to a lack of CMI to M. leprae.
• It helps distinguish between the different forms of leprosy,
particularly in classifying borderline cases, aiding in treatment
planning and understanding the patient's immune status.

• Limitations:
• Not a diagnostic test for leprosy; diagnosis relies on clinical signs
and smear tests.
Positive results can occur in individuals without leprosy (non-cases),
and negative results can occur in some lepromatous cases.
LTT and LMIT: These in vitro tests measure cell-mediated immunity but
are sophisticated and not suitable for mass application in field
conditions.

Tests for Humoral Responses:


1. FLA-ABS test: Widely used for detecting subclinical infection, it shows
high sensitivity and specificity for M. leprae specific antibodies.

2. Monoclonal antibodies: Produced against M. leprae antigens, these


can be used to identify M. leprae and are the basis for tests like the
Soluble Antigen Competition Test (SACT)

3. Other sensitive tests: Include radio-immune assay and ELISA tests,


with ELISA often based on phenolic glycolipid (PGL) antigen
LEPROSY CONTROL
Following elements are required for leprosy control programs:
1. Medical measures:
I. Estimation of the problem
II. Early case detection
III. MDT
IV. Surveillance
V. Immunoprophylaxis
2. Social support
VI. Chemoprophylaxis
3. Program management
VII. Deformities
3. Evaluation
VIII. Rehabilitation
IX. Health education
The primary goals are to interrupt transmission, treat patients for cure
and rehabilitation, and prevent deformities.

Estimating the Problem:


1. Leprosy control begins with epidemiological surveys to define the
disease load, including prevalence, age/sex distribution, and
available health care facilities.

Early Case Detection:


2. The aim is to identify and register leprosy cases early, often
involving primary health care workers and community
participation due to the disease's often symptomless early
stages and social stigma.
3. Multidrug Therapy (MDT):
• Aims to interrupt transmission by sterilizing infectious
patients, ensuring early detection and treatment to
prevent deformities, and preventing drug resistance.

• Key Drugs in MDT: The core drugs discussed are Rifampicin
(RMP), Dapsone (DDS), and Clofazimine (CLF) ,Ethionamide
and protionamide, Minocycline, Clarithromycin.
• It varies depending on the type of leprosy:
• Multibacillary leprosy typically requires a longer course than
Paucibacillary leprosy.

• Managing Defaulters: Patients who stop treatment but return with
signs of the disease, such as new or changing skin lesions, nerve
involvement, lepromatous nodules, or signs of leprosy reactions,
should receive a new course of MDT and are not considered newly
detected cases.

• MDT and Special Conditions: MDT can be used in patients with HIV
infection without specific contraindications. It is also considered
safe during pregnancy. While small amounts of anti-leprosy drugs
pass into breast milk, significant adverse reactions in infants are
uncommon, though mild skin discoloration can occur with
clofazimine.
• Lepra Reactions:
• These are acute, immunologically-mediated inflammatory episodes that
can occur before, during, or after MDT.

• Type 1 (Reversal Reaction): A delayed hypersensitivity reaction, common
in BT, BB, BL leprosy, characterized by reddish, swollen, painful skin
lesions and tender nerves, often leading to nerve function impairment if
untreated.

• Type 2 (Erythema Nodosum Leprosum - ENL): Primarily seen in MB cases
(LL, BL), characterized by painful, tender skin nodules (ENL lesions),
fever, malaise, and potential systemic involvement (joints, eyes, testes,
etc.).

• Management of Reactions: Prompt and adequate treatment, typically
with corticosteroids (e.g., prednisolone), is crucial to prevent permanent
deformities and nerve damage. Thalidomide is an alternative for ENL,
Type 1
Type 2
• Contraindications: Steroids should be used with caution or avoided in
patients with certain conditions like tuberculosis, diabetes, deep
ulcers, osteomyelitis, or corneal ulcers unless the underlying
condition is also being treated.

• Pregnant Women: Treatment at a referral level is recommended for
pregnant women to help manage steroid use and minimize potential
adverse effects on the fetus.

• Children: Children under twelve should also be managed at a referral
level to help minimize potential effects on growth, with considerations
for treatment approaches that may reduce growth impact.

• Diabetes: Patients showing symptoms of diabetes or with positive
urine glucose tests should be referred.
4.Surveillance:
• Clinical surveillance after treatment is crucial for long-term
success and early detection of relapses. Paucibacillary cases
require annual examination for at least 2 years, while
multibacillary cases need annual examination for at least 5
years post-treatment.

• 5. Immunoprophylaxis:
• While a definitive tool for detecting leprosy infection is lacking, trials
with BCG vaccine (alone or with other vaccines) have shown
protective efficacy in reducing the disease burden.

6. Chemoprophylaxis:
• This approach, involving preventive medication, is beneficial in chronic
infectious diseases, especially for individuals at higher risk of
developing the disease.
7. Deformities:
Approximately 25%
of untreated
leprosy patients
develop anesthesia
and/or deformities
of the hands and
feet, making
leprosy a leading
cause of deformities
and crippling. These
deformities can
arise from the
disease process
itself or from nerve
damage leading to
muscle paralysis
8. Rehabilitation:
It aims for the physical and mental restoration of treated patients to enable them to
resume normal activity in their home, society, and industry.

Preventive Rehabilitation:
It emphasizes early diagnosis and adequate treatment to prevent physical deformities
and social/vocational disruption, which is considered the cheapest and surest form of
rehabilitation.

Community-Based Rehabilitation (CBR):


Defined by WHO and NGOs, Its a strategy within general community development
focused on rehabilitation, equalizing opportunities, and social inclusion for all people
with disabilities, implemented through collaborative efforts of individuals, families,
organizations, and various services.

Rehabilitation Measures:
These measures involve planned and systematic medical, surgical, social, educational,
and vocational actions, requiring sustained counseling, health education, and
coordinated efforts from various departments and organizations.
9. Health Education:
• Crucial for patient compliance, preventing disabilities, and addressing the
social stigma associated with leprosy by educating both patients/families
and the general public about the curability and non-hereditary nature of the
disease.

• Social Support:
• Essential to address the economic and social problems faced by leprosy
patients and their families, including assistance with travel, basic needs,
education, and job placement, often provided by voluntary agencies and
social welfare departments.

• Programme Management:
• Involves long-term planning and effective management of resources like
infrastructure, trained personnel, drugs, and vehicles to achieve rapid
control of leprosy.. The National Leprosy Eradication Programme incorporates all
these elements.

• Evaluation:
• Requires assessing the impact of control operations using indicators to measure
Anti-leprosy work in India :

• Began in 1874 with the founding of the Mission to Lepers (now


Leprosy Mission) in Chamba, Himachal Pradesh.

• Numerous voluntary organizations, including prominent ones like
Hind Kusht Nivaran Sangh and Gandhi Memorial Leprosy
Foundation, have emerged to combat leprosy in India.

• The National Leprosy Control Programme, initiated in 1954, was
converted into an eradication program in 1983, marking a
significant shift in the national strategy against leprosy.

• The National Leprosy Organization, established in 1965, serves as a
platform for these organizations to collaborate and share
experiences.
Leprosy Vaccines

1. BCG Vaccine
Bacillus Calmette–Guérin (BCG) used mainly for
tuberculosis
Provides partial protection against leprosy
Protection ranges from 20% to 80% depending on
region and population
Used in many countries (including India) as part of
Universal Immunization Programme (UIP)
Also used in contacts of leprosy patients in some
programs
2. MIP Vaccine (Mycobacterium indicus pranii)
(Also called Mw vaccine)
Developed in India (formerly Mycobacterium w)
Boosts cell-mediated immunity against
Mycobacterium leprae

Used for:
Immunotherapy (along with MDT) in MB leprosy.
Prophylaxis in contacts of leprosy cases
Approved for use under National Leprosy
Eradication Programme (NLEP)
THANK YOU
FOR YOUR ATTENTION

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