This document provides an overview of Helicobacter pylori, including its historical discovery in 1982 by Marshall and Warren which revolutionized ulcer treatment. It describes H. pylori's morphology as a spiral-shaped, flagellated, gram-negative bacterium that lives in the stomach mucus layer. The document discusses H. pylori's worldwide prevalence, routes of transmission, virulence factors, mechanisms of infection, associated diseases like ulcers and stomach cancer, and laboratory tests for diagnosis. In conclusion, H. pylori infection typically causes long-term gastritis in most cases, while clinical complications represent an imbalance in gastric homeostasis.

1. Helicobacter pylorian overview
Presented By:
Nasir Nazeer

2. Historical Background
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Human stomach long considered inhospitable for bacteria.
Spiral shaped organisms occasionally visualized in gastric mucous
layer, but no evidence of disease association.
1982 - Marshall and Warren identified and subsequently cultured
the gastric bacterium, Campylobacter pyloridis, later reclassified as
Helicobacter pylori.
Discovery revolutionized the treatment of duodenal and gastric
ulcers.
Earned them the Nobel Prize for Medicine in 2005.
Nearly 20 species of Helicobacter are now recognized.
The gastric helicobacters colonise the stomachs of animals. The
monkey, cat, dog, tiger all harbour their own species.

3. Historical Background (Contd.)
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The bacterium lives in the
stomach of about half the people
in the world. Many are apparently
well,
and
most
have
an
inflammation of the stomach lining,
a condition which is called
"gastritis".
Gastritis
is
the
underlying
condition which causes ulcers and
other
digestive
complaints,
possibly including cancer of the
stomach.
Marshall and Warren culture
organism from human gastric
mucosa and show association with
gastric inflammation.

4. 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).

5. Morphology and structure of H. Pylori
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Spiral-shaped
Gram-negative,
oxidase and catalase-positive
motile bacterium with 4-6 flagella.
Almost all the bacteria have the
same size
length:2.5~4.0μm
width:0.5~1.0μm
Microaerophilic, i.e. it requires
oxygen but at lower levels than
those contained in the atmosphere
With its flagella and its spiral
shape, the bacterium drills into
the mucus layer of the stomach,
and can either be found
suspended in the gastric mucosa
or attached to epithelial cells.

6. Morphology and structure of H.
Pylori
Produces adhesins which bind to
membrane-associated lipids and
carbohydrates and help its
adhesion to epithelial cells
Breaks down urea (NH2CONH2)
to NH4+ and CO2
Stomach acidity 
Possible for H. pylori to survive
Not cleared by host immune
response.

7. Biological properties of
H. pylori

8. Epidemiology
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The most common chronic bacterial infection in humans.
The risk of acquiring H. pylori infection is related to socio-economic
status and living conditions early in life.
Developing nations: the majority of children are infected before the
age of 10, the prevalence in adults peaks at more than 80 percent
before age 50.
Developed countries: evidence of infection in children is unusual but
becomes more common during adulthood.
Immigration is responsible for isolated areas of high revalence in
some Western countries.

9. Infective ratio all over the
world

10. Transmission of H.pylori
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Transmission — Route by which
infection occurs remains unknown
Humans are major source of
transmission - if not only –
reservoir.
Transmission among persons
sharing
the
same
living
environment.
Family members often carry same
strain.
Person-to-person transmission of
H. pylori through either fecal/oral
or oral/oral exposure seems most
likely.
Organism can be cultured from
feces.
Infection from environment or from
animals
cannot
be
totally
excluded.

11. Defense mechanism of
H.pylori
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Once H. pylori is ensconced in the
mucus, it is able to fight the
stomach acid that does reach it
with an enzyme called urease.
Urease converts urea, of which
there is an abundant supply in the
stomach (from saliva and gastric
juices), into bicarbonate and
ammonia, which are strong bases.
This creates a cloud of acid
neutralizing chemicals around the
H. pylori, protecting it from the
acid in the stomach.
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The reaction of urea hydrolysis is
important for diagnosis of H.pylori
by the breath test.

12. Site of infection
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Highly adapted organism that lives
only on gastric mucosa.
Gastric antrum is the most
favoured site.
Present in the mucus that overlies
the mucosa.

13. How H.pylori infection
progresses?

14. Pathogenesis
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Most bacteria are killed in hostile environment of gastric lumen.
H. pylori proliferates in mucus layer over epithelium and is not cleared by
host immune response.
Pathophysiology of H. pylori infection and its eventual clinical outcome is
a complex interaction between the host and the bacterium.
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.
Flagella - allows penetration of H.pylori into gastric mucous layer.
Adhesins - mediate binding to host cells.
Localized tissue damage mediated by:
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Mucinases and phospholipases - disrupt gastric mucus
Vacuolating cytotoxin - induces vacuolation in epithelial cells that results in
epithelial cell damage

15. Mechanism of Helicobacter pylori
infection

16. Symptoms of H.pylori infection
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Abdominal pain with burning
or gnawing sensation.
Pain is often made worse
with empty stomach; night
time pain is common.
Poor appetite.
Weight loss.
Heart burn.
Indigestion (dyspepsia)
Belching.
Nausea.
Vomiting.
Blood in stool.

17. Diseases associated with
H. Pylori
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Duodenal Ulcer
Gastric (Stomach) Ulcer
Non-Ulcer dyspepsia
Weird Syndromes (associated with acne
rosacea, gulf veterans syndrome, chronic
fatigue syndrome and chronic halitosis)
Stomach Cancer
MALT Lymphoma

20. Sequence of histological and endoscopic events in H. pylori infected stomach
with accompanying transformation of chronic atrophic gastritis to chronic
active gastritis with polyp, intestinal metaplasia and dysplasia to cancer.

21. Laboratory diagnosis noninvasive tests
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Serology : detect an immune
response by examining a blood
sample for antibodies to the
organism (ELISA).
Urea breath test : a urea solution
labelled with C14 isotope is given
to pt. The C02 subsequently
exhaled by the pt contains the C14
isotope and this is measured. A
high reading indicates presence of
H. pylori.
Faecal antigen test : detects H.
pylori
antigens
in
faecal
specimens.
Polymerase
chain
reaction
(PCR) : can detect HP within a
few hours. Not routine in clinical
use.
Urease Test: Urease activity in
the stomach qualitatively detects
active infection with a sensitivity
and specificity of more than 90
percent.

22. Invasive testing
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Histological examination of biopsy specimens of
gastric/duodenal mucosa take a endoscopy
Culture
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Not sensitive then a skilled microscopy histological section
Can be used for antibiotic resistance testing
Requires selected agars and incubation periods

23. Tests for detecting H.pylori
infection

24. Conclusion
A characteristic of H. pylori infection in humans is gastritis, which persists
for decades without causing serious damage in most cases.
The clinical complications of H. pylori infection, such as peptic ulcer
disease and gastric cancer, appear to represent an imbalance in gastric
homeostasis.

25. Bibliography
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Suerbaum S, Michetti P. Helibacter pylori infection. NEnglJMed 2002;347:1175-86
Malfertheiner P, Megraud F et al. Current concepts in the management of Helicobacter
pylori infection–The Maastricht 2-2000 Consensus Report. Aliment Pharmacol Ther
2002; 16:167-80
Hjalmarsson S, Sjolund M, Engstrand L. Determining antibiotic resistance in
Helicobacter pylori. Expert Rev Mol Diagn. 2(3):267-72, 2002 May.
Vaira D, Vakil N, Menegatti M et al. The stool antigen test for detection of Helicobacter
pylori after eradication therapy. Ann Intern Med 2002;136:280-7
Qasim A, O’Morain CA. Review article: treatment of Helicobacter pylori and factors
influencing eradication. Aliment Pharmacol Ther 2002; 16 (Seppl. 1):24-30.
vanZwet AA, Vandenbrouke-Grauls CMJ et al. Stable amoxicillin resistance in
Helicobacter pylori. Lancet 1998;352:1595
Perez Aldana et al. The relationship between consumption of antimicrobial agents and
the prevalence of primary Helicobacter pylori resistance. Helicobacter 2002;7(5):306309
Xia HX, Buckley M, Keane CT. Clarithromycin resistance in Helicobacter pylori:
prevalence in untreated dyspeptic patients and stability in vitro. J Antimicrob Chemother
1996;37:473-81
Jenks PJ. Causes of failure of eradication of Helicobacter pylori. BMJ 2002;325:3-4
Buckley MJ, Xia HX et al. Metronidazole resistance reduces efficacy of triple therapy
and leads to secondary clarithromycin resistance. Dig Dis Sci 1997;42:2111-5

26. Bibliography
1.
2.
3.
4.
Houben MHM, Van De Beek D. A systematic review of Helicobacter pylori
eradication therapy – the impact of antimicrobial resistance on eradication
rates. Aliment Pharamcol Ther 1999;13:1047-55
Owen RJ. Molecular testing for antibiotic resitance in Helicobacter pylori.
Gut 2002;50:285-9
Meyer JM, Siliman N. Risk factors for Helicobacter pylori resistance in the
United States: The Surveillance of H. pylori Antimicrobial resistance
partnership (SHARP) study, 1993 – 1999. Ann Intern Med 2002;136:1324
Wen M, Zhang Y et al. An evaluative system for the response of
antibacterial therapy: Based on the morphological change of Helicobacter
pylori and mucosal infllammation. Pathology International April 99
49:4;332-341