1. HANSEN’S DISEASE
DIPLOMA
IN MEDICAL
SCIENCE
SCHOOL OF
ALLIED
SCIENCE
WINDFIELD
INTERNATIONAL
COLLEGE

2. HANSEN’S
DISEASE
RUTH NAOMI
MANUEL
SARAVANAN
A/L SURESH
SRIRENUKAA A/P
MARIMUTHU

3. INTRODUCTION
Also known as leprosy
Chronic infection
Caused by Mycobacterium Leprae & Mycobacterium
Lepromatosis
Affects skin, nerves & eyes
• Paucibacillary - 5 or less poorly pigmented numb skin
patches present
• Multibacillary - More than 5 poorly pigmented numb skin
patches present
Two main types of disease based on the number of bacteria present-

4. TYPES OF LEPROSY
1-Indeterminate leprosy-
A few hypopigmented macules
can heal spontaneously
2-Tuberculoid leprosy-
A few hypopigmented macules
some are large and some
become anesthetic
(lose pain, tactile and termic
sensation)
nerves become enlarged;
spontaneous resolution

5. Borderline
tuberculoid leprosy-
Lesions like
tuberculoid
leprosy but
smaller and
more numerous
with less nerve
Enlargement
nerves; this
form may
persist, revert to
Mid-borderline
leprosy-
Many reddish
plaques
asymmetrically
distributed,
moderately
anesthetic
regional
adenopathy
(swollen lymph
nodes)

6. Histoid leprosy
lepromatous
leprosy that
presents with
clusters of
histiocytes
(a type of cell
involved in the
inflammatory
response)
A grenz zone
(an area of
collagen
separating the
lesion from
normal tissue)
Lepromatous leprosy
Early lesions are
pale macules
;(flat areas) that
are diffuse and
symmetric
Alopecia (hair
loss) ; often
patients have no
eyebrows
nerve
involvement
leads to
anesthetic areas
& limb weakness;
progression leads
to aseptic
necrosis (tissue
death from lack
of blood to area)
lepromas (skin
nodules)
disfigurement of
many areas
including the face

7. CAUSES
• An intracellular, acid-fast bacterium
• Aerobic & rod-shaped bacterium
• surrounded by the waxy cell
membrane
• does not form capsules, flagella, or
spores
Mycobacterium
leprae &
Mycobacterium
lepromatosis
• Are obligate pathogens
• Are unculturable in laboratory
Due to extensive
loss of genes
necessary for
independent
growth ;

8. Mycobacterium
Leprae
Electron
Micrograph
Acid Fast
Gram
Staining

9. MODE OF TRANSMISSION
Person to person-
leprosy spread
from person to
• through infected
respiratory
droplets
• Through close
contact with the
affected person
Genetics
• Parents of
someone with
leprosy
• Children of
someone with
leprosy
The extent of
exposure
Environmental
conditions
• Poor hygiene
condition

10. PATHOGENECITY (VIRULENCE FACTOR)
Iron
utilization
• Help the pathogen acquire nutrients for growth
• NRAMP proteins
• Allow transportation of iron into the macrophage for
survival
Waxy
exterior
• Allows intake into the macrophage and into
some dendritic cells in which it can survive
Macrophage
invasion
• Prevent phagosome and lysosome fusion to
avoid degradation
• Bacteria are absorbed into the phagolysosome

11. Schwann
cell invasion
Major target of
Mycobacterium leprae
To access the cells,
Mycobacterium leprae gets
into the lymphatic system and
the blood vessels
Mycobacterium leprae binds
to the Schwann cell via
laminin-binding protein
The bacteria will enter
through the vascular
epithelium into the cell
Drug
resistance
Allow it to continue to
survive despite
antimicrobial presence

13. PATHOGENESIS
Mycobacteri
um leprae
has a
difficult time
replicating
outside of
host cells
It is a very
slowly
replicating
bacteria that
can take up
to 13 days
Leprosy -
bacterial
replication inside
intracellular
vesicles
• macrophages,
Schwann cells,
& endothelial
cells

14. CELL BINDING
Bacteria binds to receptors
on the host cell surface
In neural Schwann cells, the phenolic
glycolipid-1 (PGL-1) or LBP21 receptor on M.
leprae binds to the α-2 side chain of laminin-
2 & α-dystroglycan receptor(1)
Presence of the histone-like protein
Hlp, secreted by M. leprae, enhances
Schwann cell binding
Facilitates phagocytosis by the
classical complement pathway

16. Once binding has
occurred, M.
leprae is taken
into the host cell
by phagocytosis
and is
encapsulated by a
phagosome
Survive
phagosome-
lysosome
fusion & live
long enough
to replicate
Replication
will take
place

18. SIGNS & SYMPTOMS
Leprosy symptoms generally appear three to
five years after a person becomes infected with
bacteria
Skin lesions that are lighter than your normal skin color; lesions have
decreased sensation to touch, heat, or pain and lesions do not heal after
several weeks to months
Numbness or absent sensation in the hands,
arms, feet, and legs
Muscle weakness
Eye problems
Skin rash
Skin stiffness

19. Hypopigmented Macule Deformity
Skin Lesions

20. EXAMS AND TESTS

21. Epidemicology Triangle of
Leprosy
Agent-
Mycobacteruim
leprae
Environment-
Transmitted by person
to person contact
Host – Infected
to human

22. Lab
Diagnosis
Skin
lesion
biopsy
CBC
PCR
Liver
blood
Creatinine
blood
Lepromin
skin

23. Incisional
biopsy
Exicisional
biopsy
Punch
biopsy
Shave
biopsy
Types of Skin
biopsy

24. Shave Biopsy
least invasive
method.
Your doctor uses a
small blade to remove
the outermost layers
of skin.
The area removed
includes all or part of
the lesion.
Do not need
stitches.
At the end of the
procedure, medicine
is applied to the area
to stop any bleeding.

26. Excisional Biopsy
usually done
by a surgeon.
During the
procedure, the
entire lesion is
removed.
Numbing
medicine is
injected into
the area.
The entire lesion is
removed, going as
deep as needed to
get the whole area.
The area is
closed with
stitches.
If a large area is
biopsied, a skin graft or
flap of normal skin may
be used to replace the
skin that was removed.

28. Incisional
Biopsy
Only a piece
of a large
lesion for
examination.
Numbing
medicine is
injected
into the
area.
A piece of
the growth is
cut and sent
to the lab for
examination.
You may
have
stitches, if
needed.
The rest of
the growth
can be
treated after
the diagnosis
is made.

30. CBC (
Complete
Blood
Count )
Most
commonly
ordered
blood tests.
The
complete
blood count
is the
calculation
of the
cellular
(formed
elements)
of blood.
Determined
by special
machines
that analyze
the
different
component
s of blood
in less than
a minute.
To measure
of the
concentrati
on of white
blood cells,
red blood
cells, and
platelets in
the blood.

32. PCR (Polymerase
Chain Reaction)
PCR
recombined
DNA
technology
have allowed
for
development
of genes
M.leprae
Used in
biopsy
samples ,
blood and
tissue section

34. Liver
blood
test.
Most
commonly
performed
blood tests.
Can be used
to assess
liver
functions or
liver injury.
An initial step is
a simple blood test
to determine the
level of certain
liver enzymes
(proteins) in the
blood.
But when the
liver is injured for
any reason, these
enzymes are
spilled into the
blood stream.

35. Creatinine
blood test.
If the kidney
become impaired
, the creatinine
level rise due to
poor clearance of
creatinine by the
kidney.
Found to be a
fairly reliable
indicator of
kidney
function.
Elevated
creatinine level
signifies
impaired
kidney
function.

36. Lepromin skin test
Used to determine what type of leprosy a
person has.
A sample of inactivated leprosy-causing bacteria is
injected just under the skin, usually on the forearm,
so that a small lump pushes the skin up.
The lump indicates that the antigen has been
injected at the correct depth.
The injection site is labelled and examined 3 days, and
again 28 days, later to see if there is a reaction.

38. Medication
Surgical
care
Treatment

40. Dapsone
Bactericidal
Mechanism of action
is the prevention of
formation of folic
acid, inhibiting
bacterial growth
Part of a 2-drug regimen
for treatment of
paucibacillary leprosy;
part of a 3-drug regimen
for treatment of
multibacillary leprosy

41. Rifampin
For use in combination
with at least 1 other
antituberculous drug.
Inhibits DNA-
dependent bacterial
RNA polymerase.
Cross-resistance
may occur.
Treat for 6-9 months or
until 6 months have
elapsed from time of
negative sputum test.

42. Clofazimine
Inhibits
mycobacterial
growth, binds
preferentially to
mycobacterial DNA.
Has antimicrobial
properties, but
mechanism of
action is unknown.
Part of 3-
drug regimen
for treatment
of
multibacillary
leprosy.

45. Epidemiology
The number of new
cases of leprosy per
year (incidence) also
fell from
approximately
720,000 in 2000 to
about 300,000 in
2005
Since then this has
stabilised, with an
estimated 230,000 new
cases reported in 2010.
The highest numbers of
new cases in 2010 were
reported from India,
Brazil, Indonesia, the
Democratic Republic of
Congo, and Ethiopia