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