Helicobacter pylori is a spiral-shaped bacteria that lives in the stomach. It was originally considered that bacteria could not survive in the acidic stomach. Marshall and Warren first cultured H. pylori from human stomachs and showed it was associated with gastric inflammation. H. pylori infection can cause dyspepsia, peptic ulcers, gastric cancer, and other diseases. Testing and treating H. pylori infections can help prevent future illness.

2. Helicobacter Pylori
Related gastroenterology
Prepared & Presented By:
Dr.Usman ul Haq
BEMS,RMP,UOP,

3. HELICOBACTER PYLORI
Background
Human stomach long considered inhospitable for
bacteria.
Spiral shaped organisms occasionally visualized in
gastric mucous layer, but no evidence of disease
association.
Organism classified first as Campylobacter pylori And
Now Helicobacter pylori.
Other species of Helicobacter isolated from stomach,
intestine of other animals.
Marshall and Warren culture organism from human
gastric mucosa and show association with gastric
inflammation.

4. Helicobacter pylori

5. A silver stain
of H. pylori
on gastric
mucus-
secreting
epithelial cells
(x1000).
From Dr.
Marshall's
stomach
biopsy taken 8
days after he
drank a
culture of H.
pylori (1985).

6. MORPHOLOGY
Gram negative
Spiral rod
 Flagellated
Microaerophilic

7. H. Pylori Bacteria
 Urease positive*
 Present in gastric
antrum
 Proliferates in
mucus overlying
gastric type
mucosa
 Not cleared by
host immune
response
*Scanning microscopic view of H. pylori

8. TRANSMISSION
Humans are major - if not only - reservoir
Transmission believed to be by fecal-oral
route.
Organism can be cultured from feces.
Family members often carry same strain
Prevalence of infection likely related to
inferior hygienic conditions and poor
sanitation.
Infection from environment or from
animals cannot be totally excluded.

9. EPIDEMIOLOGY
1. Gastric colonization rate in developing countries is
about 80%
2. Gastric colonization rate in US and other developed
countries is about 30%
3. Prevalence of infection increases with age
Age 10 = ~5%
Age 30 = ~ 25%
Age 60 = ~ 50%
4. In US, prevalence rates are higher in African-Americans
and Hispanics
Age and low income = main risk factors for H. pylori infection

10. H. pylori Infection Risk Factors
Low socioeconomic status
Crowded or unsanitary living conditions
Born in a developing country
Exposure to gastric contents
– Nurses
– Endoscopists

11. PATHOGENESIS
 Colonization
Most bacteria killed in hostile environment of
gastric lumen.
H. pylori proliferates in mucus layer over
epithelium and is not cleared by host immune
response.
H. pylori survives and grows there because of a
variety of virulence factors that contribute to
gastric inflammation, alter gastric acid production,
and cause tissue destruction.

12. VIRULENCE FACTORS
 Initial colonization facilitated by:
 Acid inhibitory protein - blocks acid secretion from
parietal cells during acute infection
 Urease - neutralizes gastric acids due to ammonia
production. [also stimulates monocytes and neutrophils
chemotaxis; stimulates production of inflammatory
cytokines]
 Heat shock protein: Enhances urease expression; co-
expressed with urease on bacterial surface

13. Flagella - allows penetration into gastric
mucous layer and help in movement.
Adhesins - mediate binding to host cells
Localized tissue damage mediated by:
Mucinases and phospholipases - disrupt
gastric mucus
Vacuolating cytotoxin - induces vacuolation in
epithelial cells that results in epithelial cell
damage

14. All these factors plus LPS stimulate
inflammatory response
Catalase - prevent from phagocytosis and
intracellular killing
Plus other poorly defined factors that
stimulate
IL-8 secretion by epithelial cells, that induce
nitric oxide synthase which mediates tissue
injury, and that induce programmed death of
gastric epithelial cells.
Cag pathogenicity island - includes genes that
confer enhanced pathogenicity, in part by
inducing epithelial cells to produce inflammatory
cytokines.

15. Pathogenesis of H. pylori infection
The Flagellae make
it motile, allowing it
to live deep beneath
the mucosal layer.
It uses an adhesin
molecule(BabA) to
bind to epithelial
cells Where the pH
there is close to

16. Any acidity is buffered
by the organism's
production of the
enzyme urease,
which catalyzes the
production of
ammonia (NH3) from
urea & raises the pH
there.
The bacterium
stimulates chronic
gastritis by provoking
a local
proinflammatory
response.

17. In the cellular level:
H. pylori express
cagA & vacA
genes
cagA gene 
signals to the
epithelial cells
involving: -
Cell replication,
-
Apoptosis, &
-
Morphological
changes.

18. In the cellular level:
vacA gene 
producing a
pore-forming protein,
which has many
destructing effect to
the epithelium like:
-↑Cell
permeability & efflux
of micronutrients,
-
Induction of
apoptosis, & -
Suppression of local
cell immunity

19. H.pylori as a cause of PUD
Studies show
that about 95%
of patients with
85% 95% DU DU
GU & 85% with GU
are infected
with H. pylori

20. Evidence supporting H. pylori as
major cause of peptic ulcer disease
H. pylori is found in almost all cases of PUD,
(80%)while the use of NSAIDs (20%) .
When H. pylori is treated and eradicated, the rate
of ulcer recurrence is dramatically reduced.
H. pylori induced changes in acid secretion and
mucosal resistance provide a plausible path
physiologic explanation.

21. Pathogenesis of H. pylori infection
Effects of H. pylori on gastric Hormones
- ↓ Somatostatin production from antral D-cells due to antral
gastritis
This effect is exaggerated among smokers!
- Low somatostatin will ↑Gastrin release from G-cell 
hypergastrinemia
- This will stimulate acid production by the parietal cells 
leading to further duodenal ulceration.

22. H Pylori Disease Associations
other than GIT
Migraine
Headache
Glaucoma
Stroke
Morning Sickness

23. Outcomes of H.Pylori Infection
Nearly all H. pylori colonized persons
have gastric inflammation - but this - by
itself is asymptomatic.
Symptoms are due to illness - such as
peptic ulceration or gastric malignancy.
Develop in <10% individuals colonized
with H. pylori.

24. Outcomes of H. pylori Infection
Often asymptomatic (latent), but not benign,
with progressive gastric damage1
Dyspepsia
Gastritis
Gastric tumors
PUD2: duodenal and gastric ulcers (17%)
– Life-threatening complications occur in 1%-2%
of patients with peptic ulcer disease per year
Gastric cancer3
Mucosa-associated lymphoid tissue
(MALT)/primary gastric B-cell lymphoma3

25. Outcomes of H. pylori Infection
Latest research suggests
~45% of babies with Colic have H.
pylori.
Eradication of H. pylori in Glaucoma
improved eyesight significantly.
H. pylori is involved in some cardiac
conditions.

26. Natural History of Helicobacter pylori Infection

27. H. pylori Infection
The bad news
High morbidity
– Chronic and acute gastritis
– Peptic ulcers
– Gastric cancer
Classified by WHO as a Class I carcinogen

28. H. pylori Infection
The best news is:
It is curable

29. Indications for H. pylori testing
Dyspepsia in primary care setting.
Documented gastric and duodenal ulcer.
History of peptic ulcer.
Gastric Mucosa-Associated Lymphoma.
After resection of early gastric
adenocarcinoma.
First-degree relative of a patient with gastric
cancer.

30. Problems with Current
Management of Dyspepsia
Many patients with dyspepsia are infected
with H. pylori .
PPIs mask the symptoms of H. pylori ; they
do not cure the underlying disease.
Cure reduces healthcare costs by avoiding
further morbidity and mortality.
– 90% of patients with PUD do not experience a
recurrence after H. pylori eradication

31. Current Trends in Management of
Dyspepsia
Undifferentiated dyspepsia
Empiric trial of H2 blocker or
Proton Pump Inhibitor (PPI)
Symptoms persist?
Yes
Positive Test for H. pylori Negative
Eradication GI referral
therapy or long-term
PPI therapy

32. Recommended Management of
Dyspepsia
Undifferentiated dyspepsia
Empiric trial of H2 blocker or
Proton Pump Inhibitor (PPI)
Symptoms persist?
Yes No Routine follow-up
Positive Test for H. pylori Negative
Eradication GI referral
therapy or long-term
PPI therapy

33. Diagnosis of H. pylori
 Non-invasive
C13 or C14 Urea Breath Test
Stool antigen test
H. pylori IgG titer (serology)
 Invasive
Gastric mucosal biopsy
Rapid Urease test

34. Indications for Noninvasive Testing for
H. pylori *
Strongly Recommended
– Dyspepsia
– History of/active peptic ulcer disease
– Gastric MALT lymphoma
– Following gastric cancer resection
– Following peptic ulcer surgery
– First-degree relative with gastric cancer
– Long-term Non-steroidal anti-inflamatory
drugs (NSAID) therapy

35. Indications Noninvasive Testing for H.
pylori *(cont.)
Advisable
– Family history of duodenal ulcer
– Family members with H. pylori infection
– GERD requiring long-term PPI therapy

36. Diagnosis of H. pylori
Non-invasive
1. C13 or C14 Urea Breath Test
The best test for the detection
of an active infection

37. Diagnosis of H. pylori
Invasive
Upper GI endoscopy
– Highly sensitive test
– Patient needs sedation
– Has both diagnostic & therapeutic role

38. Diagnosis of H. pylori
Invasive (endoscopy)
– Diagnostic:
– Detect the site and the size of the ulcer, even
small and superficial ulcer can be detected
– Detect source of bleeding
– Biopsies can be taken for rapid urease test,
histopathology & culture

39. Diagnosis of H. pylori
Invasive (endoscopy)
Rapid urease test ( RUT)
o Considered the endoscopic diagnostic test of
choice
o Gastric biopsy specimens are placed in the
rapid urease test kit. If H pylori are present,
bacterial urease converts urea to ammonia,
which changes pH and produces a COLOR
change

40. Diagnosis of H. pylori
Invasive (endoscopy)
* Histopathology
o Done if the rapid urease test result is
negative
* Culture
o Used in research studies and is not available
routinely for clinical use

41. H. Pylori: Gastric biopsy
H & E stain H. pylori immunostain

42. Diagnostic Tests for Helicobacter pylori
Invasive
Test Sensitivity Specificity Usefulness
(%) (%)
Endoscopy with Diagnostic strategy of choice
biopsy in children with persistent or
severe upper abdominal
symptoms
Histology > 95 100 Sensitivity reduced by PPIs,
antibiotics, & bismuth-
containing compounds
Urease activity 93 to 97 > 95 Sensitivity reduced by PPIs,
antibiotics, bismuth-
containing compounds, &
active bleeding
Culture 70 to 80 100 Technically demanding

43. Diagnostic Tests for Helicobacter pylori
Noninvasive
Test Sensitivity Specificity Usefulness
(%) (%)
Serology for IgG 85 79 Sensitivity & specificity vary
widely; positive result may
persist for months after
eradication.
Reliability in children not
adequately validated; not
recommended

44. Diagnostic Tests for Helicobacter pylori
Noninvasive
Test Sensitivity Specificity Usefulness
(%) (%)
Urea breath test 95 to 100 91 to 98 Requires separate
appointments; sensitivity
reduced by PPIs, antibiotics, &
bismuth-containing compounds;
reliable test for cure.
Best available noninvasive test
in children but higher false +ve
rates in infants & children
younger than six years
compared with school-age
children & adolescents

45. Diagnostic Tests for Helicobacter pylori
Noninvasive
Test Sensitivity Specificity Usefulness
(%) (%)
H. pylori stool 91 to 98 94 to 99 Test for cure 7 days after
antigen therapy is accurate;
sensitivity reduced by
PPIs, antibiotics, &
bismuth-containing
compounds.
Easy to perform
independent of age;
possible alternative to urea
test; monoclonal antibody-
based test most reliable

46. Why Test Patients with GERD?
Reflux symptoms have been shown to
improve when H. pylori is eradicated.
Patients with GERD and H. pylori
infection experience decreased
frequency of hospital visits and use of
antiacid medications when H. pylori is
eradicated-

47. Suggested Guidelines for
Treatment of Patients with GI or
Ulcer Disease
History & Physical Exam
Peptic ulcer Undifferentiated Symptoms Use of NSAIDs
disease dyspepsia of GERD or aspirin
Positive Test for H. pylori
Eradication
therapy
Confirmation of cure

48. Suggested Guidelines for
Treatment of Patients with GI or
Ulcer Disease
History & Physical Exam
Peptic ulcer Undifferentiated Symptoms Use of NSAIDs
disease dyspepsia of GERD or aspirin
Positive Test for H. pylori Negative
Eradication Treat for PUD,
therapy Initiate PPI therapy,
or discontinue NSAIDs
Confirmation of cure
.

49. Confirmation of Cure of
H. pylori Infection
Active tests must be used
–Cannot use serology
Risks of not testing
–Recurrent ulcer
–Ulcer complications, gastric
cancer
–Transmission to others

50. Conclusions
H. pylori is a transmissible, infectious disease
with potentially serious outcomes.
H. pylori infection may be asymptomatic or
cause dyspepsia.
Eradication therapy can cure H. pylori
infection and prevent morbidity and
downstream events such as PUD and gastric
cancer.
Patients with symptoms of upper-GI disease,
and who use aspirin or NSAIDs should be
tested for H. pylori infection.

51. Conclusions (cont.)
Several noninvasive tests to detect H.
pylori infection are available.
– Categorized as detecting active infection or
identifying the presence of antibodies
against H. pylori
Active tests of infection are required for
post-treatment confirmation of cure of
H. pylori infection

52. Thank U

H. pylori