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1. Welcome
to
my
presenta/on,
Here
I
will
be
discussing
how
helicobacter
pylori
causes
gastric
ulcera/ons
and
how
this
can
be
linked
to
cancers
of
the
stomach.
I
hope
you
enjoy
the
following
slides
1

2. It
affects
around
50%
of
the
world’s
popula/on.
It’s
one
of
the
most
common
infec/ons
in
the
U.K.
Unless
it
is
treated,
the
infec/on
will
stay
for
the
rest
of
an
individuals
life.
Now
this
is
due
to
the
fact
that
H.pylori
will
not
show
any
symptoms
or
problems
caused
by
H.pylori
and
so
will
not
even
know
that
they
are
affected.
However,
further
complica/ons
may
indicate
the
presents
of
H.pylori
in
the
gut
and
will
then
allow
individuals
to
seek
medical
help.
Helicobacter
Pylori
is
a
gram-­‐nega/ve
spiral
shaped
bacterium
that
grows
in
mucus
layer
that
coats
the
inside
of
the
human
stomach.
Gram-­‐nega/ve
refers
to
the
thin
layer
of
pep/doglycan
and
presents
of
a
outer
membrane
in
the
helicobacter
cell
wall
Helicobacter
was
detected
by
Robin
Warren
who
was
a
pathologist
and
a
physician
named
Barry
Marshall
in
Australia.
Although
many
individuals
did
not
believe
Warren
&
Marshall
as
H.pylori
did
not
show
symptoms.
Barry
Marshall
had
decided
to
do
something
dras/c
and
drank
a
solu/on
of
H.pylori
and
within
2
weeks
developed
acute
symptoms
which
we
will
discuss
later
on
2

3. The
prevalence
of
H.Pylori
infected
varies
widely
by
geographic
area
it
can
be
seen
that
countries
such
as
South
America
and
Africa
have
the
highest
prevalence.
This
is
due
to
the
transmission
of
H.pylori.
It
is
mostly
transmiSed
through
contamina/on
of
water
and
food
which
is
much
more
likely
to
occur
in
3rd
world
countries
and
when
we
compare
these
percentages
with
those
such
as
The
united
states
or
united
kingdom
or
even
Australia,
we
can
see
here
that
the
sani/za/on
are
much
beSer
and
therefore
the
prevalence
is
much
more
lower.
Next
Slide
3

4. There
are
4
different
steps
that
helicobacter
pylori
does
in
order
to
affect
the
human
host.
1.
Firstly
there
is
the
addi/on
of
Helicobacter
Pylori
to
the
host
cell
2.
Secondly,
and
most
importantly
helicobacter
pylori
minimizes
the
content
of
the
acid
in
the
stomach
3.
it
colonizes
4.
and
finally
the
degrades
the
epithelial
cells
1à
The
addi/on
of
helicobacter
pylori
is
enabled
by
the
flagella
which
allows
the
bacterium
to
be
mo/le
and
also
permits
the
bacteria
to
propel
itself
through
the
gastric
fluid,
mucus
layer
and
finally
adheres
itself
to
the
epithelial
lipopolysaccharides
and
membrane
proteins,
using
this
it
interacts
with
epithelial
cells
of
stomach
2à
The
hydrochloric
acid
keeps
the
pH
of
the
stomach
strongly
acidic,
between
a
pH
of
one
and
two,
H.pylori
is
able
to
survive
in
acidic
condi/ons
but
as
the
stomach
pH
is
a
liSle
too
acidic
for
the
bacteria
it
uses
an
enzyme
to
raise
the
pH
around
the
bacteria
to
a
more
survivable
level.
Urease
enzyme
is
used
where
it
will
breakdown
urea
and
water
to
produce
carbon
dioxide
and
ammonia.
As
we
know
that
ammonia
is
a
base
and
HCl
is
an
acid
this
allows
a
neutralizing
reac/on
making
the
pH
of
the
stomach
increase.
3àThis
creates
a
microenvironment
for
the
bacterium
to
survive
this
allows
the
coloniza/on
of
more
and
more
H.Pylori
to
thrive
in
this
environment
4

5. Now
the
degrada/on
of
the
epithelial
cells
occurs
in
many
different
ways:
The
Vac
A
exotoxin
causes
injury
to
the
mucosal
membrane
by
inducing
altera/ons
in
mitochondrial
membrane
permeability
and
apoptosis,
it
also
s/mulates
pro-­‐inflammatory
signaling
and
increases
the
permeability
of
the
plasma
membrane.
Type
IV
secre/on
system
uses
a
pillus
to
inject
effectors
such
as
Cytotoxin-­‐associated
gene
A
-­‐
cagA
is
a
needle-­‐like
appendage
that
injects
a
toxin
which
remodels
ac/n
the
cytoskeleton
of
the
cell
thereby
disrup/ng
the
epithelial
barrier
and
facilita/ng
the
passage
of
Vac
A,
it
is
also
found
to
inhibit
apoptosis.
These
responses
altogether
inhibits
immune
response
by
T
cell
ac/va/on
and
prolifera/on
so
the
body
cannot
produce
an
immune
response
against
Helicobacter
pylori
and
this
is
the
development
of
gastric
ulcera/ons
Next
Slide
5

6. So
this
image
shows
the
propor/ons
of
individuals
with
differing
disease
severity
The
50%
of
the
worlds
popula/on
who
has
helicobacter
pylori
is
more
suscep/ble
in
developing
duodenal
ulcers
about
90%
compared
to
the
unaffected
popula/on.
The
development
of
gastri/s
is
more
likely
when
affected
with
the
bacterium.
There
is
a
nine
fold
risk
of
developing
precancerous
gastric
condi/ons
when
compared
with
individuals
with
and
without
the
bacterium.
Also
almost
all
cases
of
gastric
lymphoma
is
linked
to
helicobacter
pylori
being
present
in
the
human
host.
As
discussed
before
the
prevalence
of
helicobacter
pylori
in
individuals
and
country
is
strongly
associated
with
poor
socioeconomic
condi/ons.
Next
slide
6

7. How
helicobacter
pylori
leads
to
gastric
cancer
is
not
well
understood
but
some
ideas
are
put
forward
by
scien/st,
it
is
unclear
whether
it
is
one
specific
cause
or
a
collec/on
of
all
of
these
effects
of
helicobacter
pylori
which
increases
the
chance
of
gastric
cancer.
Long-­‐term
exposure
to
cagA
toxin
causes
chronic
inflamma/on
and
can
induce
oncogenesis,
this
inflamma/on
leads
to
a
damaged
mucosal
membrane
and
can
increase
the
carcinogenic
effect
of
risk
factors
leading
to
gastric
cancer
such
as
high
salt
intake
and
smoking.
Recent
research
suggest
that
cagA
may
lead
to
inac/va/on
and
altera/on
of
tumor
suppressor
proteins
such
as
p53
which
normally
leads
to
apoptosis
and
therefore
inac/va/on
can
promote
the
development
and
progression
of
gastric
cancer
Next
Slide
7

8. 80%
of
individuals
who
suffer
with
helicobacter
pylori
will
experience
chronic
gastri/s
which
is
characterized
by
chronic
inflamma/on
of
the
stomach
mucosa
which
is
caused
by
injury
to
the
gastric
mucosa
resul/ng
from
reflux
of
bile
and
pancrea/c
secre/ons
into
the
stomach
acer
adhesion
of
helicobacter
pylori.15-­‐20%
of
theses
individuals
will
further
develop
chronic
atrophic
gastri/s
known
as
Type
A
or
B
gastri/s
is
a
process
of
chronic
inflamma/on
of
the
stomach
mucosa
leading
to
loss
of
gastric
glandular
cells
and
their
eventual
replacement
by
intes/nal
and
fibrous
/ssues.
A
duodenal
ulcer
can
also
develop
due
to
the
corrosive
HCl
in
the
stomach
causing
inflamma/on
and
ulcers
to
area
of
epithelial
cells
that
are
infected
with
helicobacter
pylori.
Furthermore
1%
of
these
individuals
can
finally
be
presented
with
gastric
carcinoma
Next
Slide
8

9. Indiges/on
is
the
main
symptom
of
helicobacter
pylori
due
to
a
induced
ulcer
however
this
symptom
is
common
among
many
types
of
disorders,
so
can
be
difficult
to
link
to
helicobacter
induced
disorder.
Indiges/on
can
further
be
accompanied
by
dull
and
burning
pain
which
is
worse
on
an
empty
stomach
and
can
be
relieved
by
antacids
very
briefly.
This
burning
pain
can
last
for
minutes
to
hours
and
comes
and
goes
over
days
an
weeks.
Gastric
carcinoma
can
present
itself
as
weight
loss,
vomi/ng,
dysphagia
and
anemia.
Next
Slide
9

10. Blood
tests
are
used
to
measure
an/bodies
to
Helicobacter
pylori.
An/bodies
are
proteins
made
by
the
body’s
immune
system
when
it
detects
harmful
substances
such
as
bacteria.
Blood
tests
for
Helicobacter
pylori
can
only
tell
if
your
body
has
Helicobacter
pylori
an/bodies.
It
cannot
however
tell
if
you
have
a
current
infec/on
or
how
long
you
have
had
it,
this
is
because
the
test
can
be
posi/ve
for
years
even
if
the
infec/on
is
cured.
As
a
result
blood
tests
cannot
be
used
to
see
if
the
infec/on
has
been
cured
acer
treatment.
During
breath
tests
the
pa/ent
is
asked
to
swallow
a
special
substance
that
has
urea
labeled
with
carbon
14.
Urea
is
a
waste
product
the
body
produces
as
it
breaks
down
protein.
The
urea
used
in
the
test
has
been
made
harmlessly
radioac/ve.
If
Helicobacter
pylori
is
present,
the
bacteria
convert
the
urea
into
CO2,
which
is
detected
and
recorded
in
your
exhaled
breath
acer
10
minutes.
This
test
can
iden/fy
almost
all
people
who
have
Helicobacter
pylori.
A
biopsy
may
also
be
taken
from
the
stomach
lining
which
is
the
most
accurate
way
to
tell
if
an
individual
has
Helicobacter
pylori..
To
remove
the
/ssue
sample
the
pa/ent
undergoes
an
endoscopy.
Common
complica/ons
of
helicobacter
pylori
infec/on
are
gastri/s
and
ulcers.
To
check
for
ulcers,
you
may
have
a
special
stomach
x-­‐ray
examina/on
acer
a
barium
meal
which
becomes
visible
on
x-­‐rays.
Next
Slide
10

11. I
found
it
interes/ng
when
doing
my
research
about
helicobacter
pylori
the
origins
and
geographic
distribu/on
worldwide
affec/ng
50%
of
the
worlds
popula/on
and
genomic
interac/ons
universally.
Helicobacter
pylori
was
first
originated
in
the
African
content
and
mutated
across
the
world
and
has
undergone
gene/c
muta/ons
along
this
spread.
Where
the
old
world
met
the
new
world
the
co-­‐evolu/on
was
disrupted
and
helicobacter
pylori
was
not
dependent
on
infec/ng
host
cells
in
the
African
content.
Individuals
started
to
become
infec/on
with
helicobacter
pylori.
Helicobacter
pylori
encountered
new
gene/c
material
and
evolved
differently
than
compared
to
its
origin.
If
an
individual
did
not
contain
the
resistant
genomic
sequence
to
helicobacter
pylori
it
could
become
cancerous.
Scien/sts
in
Tumaco
Colombia
had
found
the
majority
of
their
DNA
ancestry
and
helicobacter
pylori
strains
come
from
Africa.
The
mountain
popula/on
from
Tuquerres
is
67%
American/Indian
and
31%
European.
Their
helicobacter
pylori
are
mostly
from
European
which
replaced
the
na/ve
strains.
If
the
H.pylori
strains
have
a
different
origin
to
their
hosts,
they
are
more
likely
to
cause
cancer.
Strains
origina/ng
in
Africa
are
mostly
harmless
to
Africans,
but
caused
cancer
in
people
with
a
largely
American/Indian
background
Next
Slide
11

12. Helicobacter
pylori
is
treated
with
a
double-­‐dose
Proton
pump
inhibitors
such
as
omeprazole,
lansoprazole
and
pantoprazole
which
decreases
the
stomach’s
produc/on
of
acid
allowing
damaged
/ssue
to
heal,
this
is
accompanied
with
2
an/bio/cs
which
increases
treatment
success
and
an/bio/c
resistance.
These
two
an/bio/cs
can
either
be
metronidazole,
clarithromycin
and
amoxicillin
Next
Slide
12

13. 13

14. 14