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
Discovery revolutionized the treatment of duodenal and gastric
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.
Historical Background (Contd.)
The bacterium lives in the
stomach of about half the people
in the world. Many are apparently
inflammation of the stomach lining,
a condition which is called
condition which causes ulcers and
possibly including cancer of the
Marshall and Warren culture
organism from human gastric
mucosa and show association with
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).
Morphology and structure of H. Pylori
oxidase and catalase-positive
motile bacterium with 4-6 flagella.
Almost all the bacteria have the
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.
Morphology and structure of H.
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
Possible for H. pylori to survive
Not cleared by host immune
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.
Transmission of H.pylori
Transmission — Route by which
infection occurs remains unknown
Humans are major source of
transmission - if not only –
Transmission among persons
Family members often carry same
Person-to-person transmission of
H. pylori through either fecal/oral
or oral/oral exposure seems most
Organism can be cultured from
Infection from environment or from
Defense mechanism of
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.
The reaction of urea hydrolysis is
important for diagnosis of H.pylori
by the breath test.
Site of infection
Highly adapted organism that lives
only on gastric mucosa.
Gastric antrum is the most
Present in the mucus that overlies
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:
Mucinases and phospholipases - disrupt gastric mucus
Vacuolating cytotoxin - induces vacuolation in epithelial cells that results in
epithelial cell damage
Symptoms of H.pylori infection
Abdominal pain with burning
or gnawing sensation.
Pain is often made worse
with empty stomach; night
time pain is common.
Blood in stool.
Diseases associated with
Gastric (Stomach) Ulcer
Weird Syndromes (associated with acne
rosacea, gulf veterans syndrome, chronic
fatigue syndrome and chronic halitosis)
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.
Laboratory diagnosis noninvasive tests
Serology : detect an immune
response by examining a blood
sample for antibodies to the
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
Faecal antigen test : detects H.
(PCR) : can detect HP within a
few hours. Not routine in clinical
Urease Test: Urease activity in
the stomach qualitatively detects
active infection with a sensitivity
and specificity of more than 90
Histological examination of biopsy specimens of
gastric/duodenal mucosa take a endoscopy
Not sensitive then a skilled microscopy histological section
Can be used for antibiotic resistance testing
Requires selected agars and incubation periods
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
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