The (from saliva and gastric juice) into ammonia and

The presence of bacteria in
the gastric mucosa of people with stomach disease was observed more than 100
years ago. However, further investigations were not carried out until the late
1970s. John Warren, an Australian pathologist, noted the link between the
presence of spiral-shaped bacteria and inflamed gastric mucosa. In 1982, Warren
and physician Barry Marshall performed large-scale research on the
microorganism and successfully isolated and cultured it. The bacterium was
named Campylobacter pyloridis, and
later reclassified as Helicobacter pylori
(H. pylori). Both Warren and Marshall received the 2005 Nobel Prize in
medicine for proving that peptic ulcers are caused by bacteria and not by
stress.

H. pylori is a Gram-negative, spiral shaped (sometimes
straight), microaerophilic bacterium. Each bacillus measures about 3 microns in
length and about 0.5 microns in width. H. pylori is highly motile owing to each
bacterium possessing 4-6 flagella that are all located at the same end
(lophotrichous). In vitro, H. pylori can be cultivated on blood or chocolate
agar or in Skirrow’s media at 37ºC in a 5% oxygen atmosphere. As it is a slow
growing microorganism, the colonies are usually visible up to 5 to 7 days after
incubation. H. pylori colonies are small, translucent and uniform.

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Figure 1: H. pylori colonies on a Colombia blood agar plate.
Colonies are 0.5 – 2 mm in diameter and water droplet-like. (Guner, 2011)

Under unfavourable conditions, coccoid forms of H. pylori
occasionally emerge in the culture. These coccoid forms may indicate dormant
state of the bacteria as a way of adaptation to hostile environments. Coccoid
forms are more resistant than the regular spiral-shaped bacteria and contribute
to the organism’s survival outside the host, e.g., in drinking water or in
faeces.

H. pylori bacteria can be characterized as catalase, oxidase, phosphatase,
and urease positive. Urease appears to be especially important for the survival
of bacteria and colonization process and makes up about 5% of H. pylori total
protein weight. Urease protects H.pylori from hydrochloric acid component of
gastric juice in that it converts urea (from saliva and gastric juice) into
ammonia and bicarbonate, which neutralizes the acidity.

H. pylori inhabits gastric and duodenal mucosa and is thought to
affect nearly half of the world’s population, making it one of the most
frequent and persistent bacterial infections globally. In developing countries,
up to 90% of the population might be infected, whereas in developed countries,
up to 40% can be affected. The microorganism is adept at surviving in the
acidic environment of the stomach and is able to change its membrane potential
at external pH levels from 3-7 to maintain a neutral internal pH. Some people
colonized by H. pylori never have any signs of infection. However, in some
cases, the affected experience acute gastritis that usually proceeds to chronic
active gastritis. H. pylori infection is also associated with the development
of peptic ulcers, duodenal ulcers, mucosa-associated lymphoid tissue lymphoma
and stomach cancer. As such, H. pylori is the first carcinogen of bacterial
origin to be formally recognized.

H. pylori is believed to be transmitted via the oral route through
food or water and the bacterium is usually acquired in childhood, with the
natural acquisition of H. pylori in adults being rare. About 10% of children
aged 2-8 get infected. Risk factors include poor socio-economic status, poor
sanitation and hygiene and genetic predisposition. 

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