Helicobacter pylori is a gram-negative microaerophilic organism approximately 2.5 to 3.5 micrometers long and 0.5 to 1 micrometer wide. It has four to six unipolar flagelli and has a spiral shape. These attributes are important to motility. It can also transform from a helical form to a cocci form.
H. pylori can be transferred from person to person and there is a tendency of identical strains to infect family members. Outbreaks are associated with large family size, lower economic class, and overcrowding in childhood. "Infection is prevalent in developing countries, where up to 75% of individuals under age 20 are infected" (Buckley 1). Do to more healthy living conditions, H pylori infection has declined.
It is thought that if H. pylori are acquired during the childhood that the infection will eventually lead to pangastritis, which will further lead to gastric ulceration or gastric cancer. If one is infected in adulthood, most likely infection will result in an antral-predominant gastritis, which is associated with peptic ulceration.
H. pylori are also thought to be transmitted through water. It can remain metabolically active in water for around a week. Cocci forms can survive up to a year in river water. There have not been many recognized reports of animal reservoirs culturing H. pylori.
Most people who are infected with H. pylori have chronic active gastritis and remain asymptomatic. "Worldwide studies have consistently shown that the prevalence of H. pylori in duodenal ulceration is approximately 95% while in gastric ulceration it is approximately 70% to 80%" (Buckley 2). Once the H. pylori infection has been removed from the body, both types of ulcer relapses decrease.
H. pylori are considered a grade 1 carcinogen. H. pylori are responsible for reduction in gastric juice vitamin C levels which is considered to increase the risk of gastric cancer. H. pylori block the active secretion of vitamin C into the gastric juice. It has also been proved that H. pylori significantly increase the gastric epithelial cell proliferation. This may cause an increased risk of developing adenocarcinoma. There is also a risk of developing gastric MALT lymphoma. H. pylori infection produces mucosa-associated lymphoid tissue which produce MALT lymphoma.
H. pylori can infect by using cell surface receptors. These receptors contain fucose residues, which is a constituent of blood group antigens. Type O blood is more likely to develop ulcers than those with A or B because O has higher levels of receptor sites.
This organism reaches the stomach, most likely through an oral route. It is well adapted for the acidic environment of the stomach. The infection grows in the gastric mucous and congregates around intracellular junctions. H. pylori also produce a lot of the enzyme urease, which is critical for colonization of gastric mucosa. Once H. pylori have resisted the stomach acid, the motile flagelli enable initial colonization. There are two ways the organism adheres to the gastric epithelium: loose adherence, which involves multiple low affinity adhesions, and close adherence. Lipopolysaccharides could also play a role in adhering to the epithelium.
Sources:
http://www.cag.ucalgary.ca/sponsers/abbott/symposium/buckley.html
http://www.cag.ucalgary.ca/sponsers/abbott/symposium/logan.html<
*Disclaimer - This report was written by a student participaring in a microbiology course at the Missouri University of Science and Technology. The accuracy of the contents of this report is not guaranteed and it is recommended that you seek additional sources of information to verify the contents.
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