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3.
INTRODUCTION
Chronic infectious disease
Surface infection
Caused by M leprae
Affects mainly the peripheral nerves
4.
Cardinal features
Hypo-pigmented patches
Loss of cutaneous sensations
Thickened nerves
Presence of acid-fast bacilli in the skin or nasal smear
Signs of advanced disease are:
Lumps in the skin of the face and ears
Plantar ulcers
Loss of fingers or toes
Nasal depression
Foot drop and claw toes
5.
History
Oldest disease known to mankind
Leper - Greek word – scaly
Confused with psoriasis, elephantitis and pellagra
Known as kushta roga
1873 – Hansen of Norway discovered M. leprae
1943 – sulphone drugs used in the treatment
6.
Problem Statement
1991 – WHO Member State resolved to decrease the level
of leprosy by over 90%
Fall in prevalence rate largely is due to
Improvement in management of cases
Low rates of relapse
High cure rate
Absence of drug resistance
Short duration treatment
WHO global strategy for further reducing the leprosy burden
and sustaining leprosy control activities(2006-10)
7.
Main elements of the strategy are
Sustain leprosy control activities in all endemic countries
Use case detection as the main indicator to monitor
progress
Ensure high-quality diagnosis, case management, recording
and reporting and reporting in all endemic communities
Strengthen routine and referral services
Discontinue the campaign approach
Develop tools and procedures that are home/community
based, integrated and locally appropriate for the prevention
of disabilities/impairments and for provision of rehabilitation
services
Promote operational research in order to improve
implementation of a sustainable strategy
Encourage supportive walking arrangements with partners
at all levels
8.
India
Leprosy was widely prevalent in India
Now out of 611 districts,487 are free from leprosy
A total of 0.87 lakh cases are recorded on 1st April 2008
Prevalence rate is 0.74 leprosy cases/10,000 population
9.
Epidemiological determinants
Agent :
Caused by M. leprae
They have affinity for Schwann cells and cells of the
reticulo-endocrine system
The bacterial load is the highest in the lepromatous cases
(2 to 7 billion were estimated in one gram of leproma)
Phenolic glycolipid (PGL) is the specific M. leprae
Source of infection
Multibacillary cases imp source of infection
All patients with “active leprosy” must be considered
infectious
Man is the only source and host
10.
Portal of exit
Nose is a major portal of exit
M. leprae are discharged in the nasal mucosa
Can also exit through ulcerated or broken skin
Infectivity
Highly infectious but of low pathogenicity
Can be rendered non – infectious by treatment of 3 weeks
Local application of rifampicin can destroy bacilli within 8
days
Attack Rate
In households 4.4% to 12% is expected to show signs of
leprosy within 5 years
11.
Host factors
Age
Infection can take place at any time depending upon the
opportunity for exposure
Incidence rates peak between 10 and 20 years of age and
then fall
A high prevalence of infection among children means that
the disease is active and spreading
Sex
Incidence and prevalence higher in males than in females
Migration
Mostly a rural problem
Due to migration it is causing a problem in urban areas also
12.
Genetic factors
Human lymphocyte antigen (HLA) linked genes influence
the type of immune response that develops
13.
Environmental Factors
Humidity favors survival of M.leprae
Can remain viable in dried nasal secretion at least 9 days
In moist soil at room temp. for 46 days
14.
Modes of transmission
Droplet infection
Aerosols containing M. leprae
Contact transmission
Person to person by close contact (direct or indirect)
Other routes
Insect vectors
Tattooing needles
16.
Classification
Three types of classification
Ridly and jopling classification
Madrid classification
Indian Classification
Indian classification
Indeterminate type
Tuberculoid type
Borderline type
Lepromatus type
Pure neuritic type
17.
Ridly and jopling classification
Indeterminate type
Tuberculoid type
Borderline type
Lepromatus type
Pure neuritic type
Madrid classification
Indeterminate type
Tuberculoid type
Borderline type
Lepromatus type
18.
Drugs
Only bactericidal drugs are used
Rifampicin
High bactericidal against M.leprae
Single dose of 1500mg
3-4 consecutive daily doses of 600mg
Side-effects are nausea,abdominal pain,vomiting
Dapsone
Used all over the world for 30years
1-2mg/kg of body weight
Weakly bactericidal effect
19.
Clofazimine
Synthesized for treatment of TB
Found to have greater value against M.leprae
May give darkish coloration to the skin,urine,sweat
Ethionamide and protionamide
Bactericidal drugs killing 98% of M.leprae in 4-5 days
More expensive and toxic
Used as the 3rd durgs in multibacillary leprosy
20.
Quinolones
Inhibiting DNA synthesis during bacterial replication
Ofloxacin is most preferable drug in this group
22 doses of Ofloxacin kill 99.9% of viable M.laprae
21.
WHO Recommeneded
For adults
Multibacillary leprosy
Rifampicin-600mg once monthly
Dapsone-100mg daily
Clofazimine-300mg once monthly
50 mg daily
Paucibacillary leprosy
Rifampicin-600mg once monthly
Dapsone-100mg daily for 6 months
22.
For children 10-14years
Multibacillary leprosy
Rifampicin-450mg once monthly
Dapsone-50mg daily
Clofazimine-150mg once monthly
50 mg daily
Paucibacillary leprosy
Rifampicin-400mg once a day
Dapsone-50mg daily
23.
Estimation of problem
Disease load on the community has to be estimated by
surveys
Prevalence can be determined by examining school –
age children
24.
Diagnosis
Clinical examination
Integration
Collection of bio data
Family history
History of contact with leprosy case
Previous history of treatment
Present complaint
Physical examination
Inspection of skin
Palpation of commonly involved peripheral and
cutaneous nerve
Presence of thickening of nerves
Testing for loss of sensation for heat, cold, pain and
touch in skin patches
25.
Bacteriological examination
Skin smears
Material from the skin obtained from an active
lesion and also from both ear lobes
Nasal smears
Best preparation from early morning mucous
material
Nasal scraping
Nasal mucosal scrapper is used
26.
Biopsy
When the examination do not yield diagnosis histo-
pathological examination may be necessary
It gives an accurate classification of the disease
27.
Immunological tests
Two types of tests
Test for detecting cell mediated immunity
Test for detecting humoral antibodies
28.
Test for CMI
Lepromin test
Injecting 0.1ml of lepromin intradermally
2 types of reaction is seen
Early reaction
Late reaction
29.
Early reaction
Known as fernandez reaction
Inflamatory reaction seen in 24-48hrs
Tends to disappear in 3-4 days
If the redness is more then 10mm at the end of 48hrs then
the test is considered to be positive
Indicates previous sensitisation
Late reaction
Reaction becomes apperent in 7-8 days
Maximum in 3-4weeks
If there is a nodule more then 5mm in diameter then test is
positive
30.
LTT & LMIT
Newer in in vitro tests such as lymphocyte
transformation test and leucocyte migration inhibition
test has been developed
They give a measure of CMI
Used to detect sub clinical infection
31.
Test for humoral response
FLA-ABS test (Fluorescent Leprosy Antibody Absorption
Test)
Used to identify sub clinical infections
It is 92% sensitive and 100% specific in detecting M.leprae
Monoclonal antibodies
These against M. leprae antigens have been produced
If antibodies against specific antigens are found, they will
become reagent of choice for identifying M. leprae
ELISA test
Based on a phenolic glycolipid (PGL) antigen
32.
Surveillance
Paucibacillary leprosy-recomended to be examined
clinically atleast once a year for minimum 2 years
Multibaccilary leprosy-leprosy-recommended to be
examined clinically at least once a year for minimum 5
years
33.
immunoprophylaxis
BCG can provide some protection against leprosy
Several alternative vaccines are under development
Called as candidate vaccines
None of them attained “vaccine hood” yet
34.
deformities
If leprosy not treated at an early stage develops
deformities
It is due to damage of peripheral nerve trunks or injury
from infection to hand and feet's
Paralysis may occur to some muscle
35.
Health Education
Anti-leprosy campaign is incomplete without education
Health education aims at helping people to avoid this
type of diseases
It should be direct towards the patient and his/her
family
It should educate people on the true facts about leprosy
and removes superstation and wrong beliefs and the
social stigma associated with leprosy
36.
Social support
Chemotherapy alone is not likely to solve this problem
It needs social support also
Economic and social problems should be identified
37.
Anti-leprosy activates in India
1874-Mission To Leprosy was found by Baily at Chamba
in the Himachal Pradesh
After that a lot of organizations are established
Hindu Kusth Nivaran Sangha
Gandhi Memorial Leprosy Foundation
National Leprosy organization(1965)
German Leprosy Relief Association
Damien Foundation
Danish save the child foundation
National Leprosy Control Program(1954) was converted
in to Eradication Programme(1983)