Helicobacter pylori is a
Gram-negative, curved S-shaped bacterium, which
also has a non-cultural coccoid form with
rounded ends (Figure 1). The species name stems from: Helico, meaning
helical or spiral shape, bacter,
meaning bacteria, and pylori, refering
to pylorus region of the stomach. This pathogen
possesses five to seven distinct flagella and
grows best when cultured at 37°C
(Figure 2). Interestingly, in resting
individuals, 37°C is the
stomach's temperature - the targeted organ; however, the
bacteria is able to withstand temperatures as
low as 25°C.
Figure 1. A
computer-generated image depicting a
Helicobacter pylori bacterium.
S-shaped Helicobacter pylori with five
to seven sheathed polar flagella [bar = 0.5 μm].
Colonies are non-pigmented
(possess no particular colour), translucent, and
about one to two millimeters in diameter. H.
pylori is also microaerophilic (requiring
low oxygen levels to survive) and can be
identified metabolically since this species is
catalase positive, oxidase positive, and urease
positive. H. pylori adapts to the
acidic environment of the stomach by hydrolyzing
(chemically breaking down a molecule with H2O)
urea rapidly, buffering the acidic environment,
which can lead to
peptic ulcers. Prior to its
discovery, people believed that stress was the
main cause of ulcers. Although stress is capable
of potentially decreasing one's energy level and
immune response, stress should only be consider
a contributing factor to a particular problem
and not the main cause.
H. pylori can be
transmitted by fecal-oral spread and is rarely
found in children, but increases in persistency
with age. It is found in the human gastric
mucosa of the stomach, especially in the antrum
(Figure 2). As previously mention, H. pylori
has the ability to hydrolyze urea,
consequently leading to peptic ulcers and
which has been found to increase the risk of
developing duodenal, stomach cancer. In fact,
H. pylori is the major cause of stomach
ulcers, accounting for approximately 80% to 90%
of all infections. H. pylori have
specialized proteins to increase its virulence.
One of these virulence factors is a
vacuolating cytoxin protein or
VacA, which causes vacuoles and pores to form in
certain cells. In fact, epidemiological and
experimental evidence has clearly demonstrated
the association between VacA production and the
occurrence of tissue damage (Figure 3).
Moreover, H. pylori also produces a
cytotoxin-associated gene antigen (CagA). The
CagA protein may be delivered from attached
bacteria into the host cytoplasm by an H.
pylori-specific type IV secretion system.
Once CagA enters the host cell, it becomes
tyrosine phosphorylated via tyrosine residues,
which initiates changes in cell signaling.
Finally, the BabA gene encodes an outer membrane
protein that binds to fucosylated Lewis b
blood group antigen present on the
surface of stomach epithelial cells. The term
fucosylated means a molecule (typically
a glycan) that has been covalently appended with
a fucose residue (an aldohexose
Regions of the stomach affected by
Intracytoplasmatic vacuoles (V) in gastric
epithelial cells induced in vivo by
Helicobacter pylori [bar = 0.5 μm].
Individuals infected with
H. pylori never experience clinical
symptoms other than chronic gastritis. However,
symptoms of H. pylori infection include
dyspeptic symptoms, such as inflammation
(gastritis), weight loss, cramps, bad breath,
burping, nausea, vomiting, flatulence (farting),
black and tarry stools with foul odour, and loss
of appetite. Diagnostic tests utilized to
characterize H. pylori infection
include a urease enzyme test where the infected
person drinks a carbon labeled urea solution in
which the bacteria can metabolize. The labeled
carbon dioxide can then be detected in the
breath. Another test includes a biopsy through
endoscopy. The histology of the biopsy sample is
analyzed for the pathogen' presence and to
determine the degree of infection and damage.
Other non-invasive tests include a
non-quantitative enzyme-linked immunosorbent
assay (ELISA) which detects H. pylori
antibodies in blood serum, and by a fecal
Treatment includes antibiotics to kill the
bacteria, H2 receptor antagonists (reduce
stomach acid to prevent irritation), and
proton-pump inhibitors to reduce the amount of
stomach acid, and surgery to treat developing
ulcers. Risk factors that have been shown to be
related with H. pylori infection
include smoking, those who are occupationally
exposed to wastewater, poor hygiene practices,
density or crowding in a population, and family
history of gastric disease.
Blaser, M., & Atherton, J.
(2004). Helicobacter pylori
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Brown, L. (2000). Helicobacter pylori:
Epidemiology and Routes of Transmission.
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Malfertheiner, P., Bornschein, J., & Selgrad, M.
(2010). Role of Helicobacter pylori
infection in gastric cancer pathogenesis: A
chance for prevention. Digestive Diseases,