Epidemiology of leprosy

1. Prepared By:
Mrs. Namita Batra Guin
Associate Professor
Department of Community Health Nursing

2. Hansen’s disease
Chronic infection caused by Mycobacterium leprae.
Affects peripheral nerves.
Manifests in two polar forms: lepromatous and tuberculoid
leprosy
Between the polar forms borderline and intermediate
forms occur depending upon the host response to
infection.

3. Oldest disease known to mankind
Known as “kushtha roga” in India since ancient times.
During middle ages it was widespread in almost all the
countries.
It declined in European nations.
Only way to handle patient was to isolate them.
Introduction of sulphone drugs in 1943 helped in the
treatment of disease.

4. Widely prevalent in India.
Distribution is uneven.
Total of 1.38 lakh new cases were detected during 2007-
2008.
29 states have achieved the levels of elimination (report:
2007-08)

5. Agent factors:
• Agent: M.leprae. Acid fast bacilli. Occurs in
clumps (globi). Have affinity to Schwann cells and
cells of reticulo-endothelial system.
• Source of infection: multi-bacillary cases. All cases
of active leprosy (current view).
• Portal of exit: nasal discharge, broken or
ulcerated skin of positive cases.
• Infectivity: highly infectious but low pathogenicity.
Local application of rifampicin might destroy all
bacilli within 8 days.

7. Host factors:
• Age: not a disease of childhood. But in endemic
areas, disease is commonly acquired during
childhood. Youngest case was 2.5 month old
infant. Incidence is usually seen between 10-
20years. High prevalence in of infection in children
means disease is spreading and active.
• Sex: higher in males. Sex difference is least in
children below 15years.
• Migration: considered rural. But now it has
become urban problem also.

8. Host factors:
• Inactivation of disease: it is important mode of
elimination of cases from the prevalence pool.
Some of the cases particularly tuberculoid and
indeterminate types tends to get cured
spontaneously.
• Immunity: Only few persons exposed to infection
develop disease. Early lesions heal spontaneously
in large proportions of people exposed. Immunity
can develop through infections with other related
mycobacteria.

9. Host factors:
• Genetic factors: HLA (human lymphocyte antigen)
linked genes influence the type of immune
response that develops in the disease.

10. Environmental factors:
• Presence of infectious cases in that environment.
• M.leprae remain viable in dried nasal secretions
for 9 days and in moist room for 46days.
• Overcrowding and lack of ventilation within
household.

11. Droplet infection: by nasal discharges.
Contact transmission: transmitted from
person to person by close contact between
infected and healthy person. The contact
may be direct or indirect.
Other routes: it may also spread by insect
vectors or tattooing needles.
INCUBATION PERIOD: has long
incubation period- 3 to 5years. Tuberculoid
has shorter I.P.

12. There are many classification given for the
disease. The classifications are based on
clinical, bacteriological, immunological and
histological status of the patients.
Indian and Madrid classification system
are most widely used in field of leprosy
programs

13. Indeterminate type: denotes early cases
with one or two hypopigmented macules
and definite sensory impairement. Lesions
are bacteriologically negative.
Tuberculoid type: cases with one or two
well defined lesions, which may be flat or
raised, hypopigmented or erythematous
and are anesthetic. Bacterilogically
negative lesions.

16.  Borderline type: cases with four or more lesions
which may be flat or raised, well or ill-defined,
hypo-pigmented or erythematous and show
sensory impairment or loss. Bacteriological
positivity is variable. Without treatment it may
progress to lepromatous.
 Lepromatous type: cases with diffuse infiltration
or numerous flat raised, poorly defined shiny,
smooth symmetrically distributed lesions.
Bacterilogically positive

17.  Pure neuritic type: cases which shows nerve
involvement but do not have lesions in the skin.
Bacteriologically negative.

18. Clinically characterized by one or more
cardinal features
• Hypopigmented patches.
• Partial or total loss of cutaneous sensation in
affected areas.
• Presence of thickened nerves and
• Presence of acid-fast bacilli in skin and nasal
smears.
signs of advanced stages : presence of nodules or
lumps especially on face and ears, planter ulcers,
loss of fingers or toes, nasal depression foot drop
and deformities etc.

20. Clinical examination: procedure is called
case taking.
• Interrogation:
 Collection of biodata- name,age, sex, occupation etc.
 Family history of leprosy
 History of contact with leprosy cases.
 Details of previous history of treatment for leprosy.
 Presenting complaints or symptoms.

21. Clinical examination:
• Physical examination:
 A thorough inspection of body surface to the extent
permissible
 Palpation of the commonly involved peripheral and
cutaneous nerves for the presence of thickening and
tenderness.
 Testing for loss of sensation for heat, cold, pain and
light touch in skin patches. Paralysis of muscles of
hands and feet leading to disabilities or deformities.

23. Stage I
 Thickening of nerve trunk
 Pain & tingling along
the nerve trunk
 Tenderness along the
course of nerve trunk
 No evidence of loss of
nerve function
Stage II
•Incomplete / complete
paralysis of recent origin
•Loss of sweating
•Loss of sensibility
•Muscle weakness/ Paralysis
Stage III
•Complete Nerve Paralysis for
1 year/ more
•Recovery of Nerve function
not possible

24. Bacteriological examination: skin smears
and nasal smears.
• Skin smears: from active skin lesions and ear
lobe by “slit and scrape” method .
• Skin is nipped between thumb and forefinger.
• A tiny incision is made 5mm in length, the incision
is scraped 2-3 times and tissue pulp is obtained.
• On glass slide it is spread over an area of 5-7mm
diameter.
• Same site can be used to assess the effect of
treatment.

25. Sites for smears
• Multibacillary: smears are taken from 3-6 sites- earlobe (atleast one)
and 2-4 clinically active skin sites. For previously treated patients,
smears to be taken from previously found to be positive sites.
• Paucibacillary: clinically more active lesions are preferred. Minimum
3 sites- including earlobe and two representative active skin lesions.
If single lesion two smears can be taken.

26. • Nasal smears or blows: smears prepared from early
morning mucous material.
• Nose is blown on clean cellophane or plastic sheet.
Smear should be immediately made and fixed.
• In lepromatous leprosy, it shows higher % of solid
staining bacilli.
• Nasal scrapings: after going in 4.5cm, blade is
rotated towards septum and scraped few times and
withdrawn.
• Leprosy bacilli are not found in scrapings if they are
absent in lesions.
• During treatment they may disappear from nasal
mucosa before they disappear from skin lesions.

27. Foot-pad culture: Material is inoculated
into foot-pads of mice. It is 10 times more
sensitive at detecting M. leprae. It is very
time consuming method.
Used for detecting drug resistance,
evaluating potency of drugs, detecting
viability of bacilli during treatment.
Other methods include: Histamine test,
biopsy, immunological tests

28. Lepromin test: 0.1ml of lepromin is
inoculated in the forearm of the individual.
Two types of positive reaction:
• Early reaction: also known as Fernandez reaction.
Inflammatory response within 24-48hrs.
Evidenced by redness and induration at the site of
inoculation. If the red area is more than 10mm –
test is positive.
• Late reaction: Mitsuda reaction. Becomes
apparent in 7-10days. It is read at 21days at end
of 21 day, if there is nodule more than 5mm at the
site- test is positive.

30. Estimation of problem: by means of
random sample surveys.
Early case detection: aim is to identify
cases and register them.
Multidrug therapy: drugs included in
regimen are:
• Rifampicin: 1500mg or 3-4 consecutive doses of
600mg.
• Dapsone: 1-2mg/kg body weight. Commom
adverse effects include- hemolytic anemia,
hepatitis, peripheral neuropathy.

31. • Clofazimine: has both anti-leprosy and anti-
inflammatory. Though less effective than dapsone
but has less toxic effects.
• Ethionamide and Protionamide: bactericidal drug.
Can be used in place of Clofazimine.
• Quinolones: ofloxacine is most preferred drug
from the group.
• Minocycline: standard doe of 100mg daily.
• Clarithromycin: daily administration of 500mg kills
99% bacilli within 28days.

32. • Recommended WHO Treatment regimen:
• Multibacillary: duration 12 months
 Rifampicin: 600mg once monthly, under supervision.
 Dapsone: 100mg daily self administered.
 Clofazimine: 300mg once monthly supervised, 50mg
daily self administered.
• Paucibacillary: for 6months
 Rifampicin: 600mg once monthly, for 6 months
supervised.
 Dapsone: 100mg(1-2mg/kg body wt.) daily for 6 moths,
self administered.

33. Surveillance:
• Paucibacilary: examined clinically at least once a
year for minimum of 2 years after completion of
the treatment
• Multibacilary: examined clinically at least once a
year for a minimum period of 5years after
completion of therapy.
Immunoprophylaxis: BCG provide some
protection against clinical leprosy.
Chemoprophylaxis: dapsone 1-4mg/kg body
wt. in children given for atleast 3 years

34.  Deformities: classified into 3 grades:
• Hands and feet-
 Grade 0 (no anesthesia and no visible disability)
 Grade 1 (anesthesia but no visible disability)
 Grade 2 (visible deformity/damage)
• Eye:
 Grade 0 (no eye problem, no evidence of loss of vision)
 Grade 1 (eye problem due to leprosy but vision not
affected)
 Grade 2 (severe visual impairment, lagophthalmos)
 Rehabilitation: integral part of leprosy control
 Health education: to patient, family, general
public

35. Each hand and foot should be assessed anion, graded
separately. Damage in this context include ulceration,
shortening, disorganization, stiffness and loss of part or all
of the hand or foot.
OVERALL GRADING OF PATIENT:
• Highest value of the leprosy disability grade for any part should be
taken as overall disability grading of the patient

36.  1874- mission to Lepers now known as leprosy
Mission was founded by Baily at Chamba in H.P.
 Hind Kusht Nivaran sangh
 Gandhi Memorial leprosy foundation,
Sevagram, Wardha.
 National Leprosy Control Program in 1954
which was converted to eradication program
in 1983.