Monday 6 October 2003
HPC:311 : Follicular gastritis and active chronic gastritis, non-atrophical, Helicobacter pylori-associated.
Helicobacter pylori is a species of epsilon proteobacteria which colonizes the harsh environment of the human stomach (Chalmers et al., 2004). Its name refers to both its spiral shape (Helicobacter) and the area of the lower stomach which it habitually colonizes: the gateway (pylorus) between the stomach and small intestine (Meyers, 2007). This bacterium is thought to be present within up to 50% of the human population and has been linked to the development of a number of different medical conditions (Chalmers et al. 2004).
Coccal forms or circular forms
Studies conducted by Ng et al. (1985) found that within colonies of H. pylori, the circular, or coccoid forms were found at the centre of the colony while the spiral forms were found at the edges and were actively dividing.
It is theorized that the circular form of H. pylori is inactive and represents a survival adaptation which allows the organism to survive unfavourable conditions (Curry & Jones 1990).
It is also theorized that it is the coccal forms that are involved in the transmission of H. pylori.
In prolonged culture the morphology of Helicobacter pylori alters from “the normal” helical form to a spherical cell via U- and V-shaped forms. This morphological transformation may be the result of less than optimal cultural conditions, a reaction to waste products, or it may be a natural phenomenon.
Helicobacter pylori infects the lower regions of the mucus layer of the human stomach and is associated with gastritis and the formation of both gastric and duodenal (upper intestinal) ulcers (Helicobacter Foundation, 2006).
It has also been linked to the formation of gastric lymphoma and other cancers (Helicobacter Foundation, 2006).
Once infected the human host can remain affected for life unless treated with strong antibiotic or antimicrobial therapies (Chalmers et al., 2004).
Infected individuals do not necessarily express symptoms, and it is believed that up to 50% of the human population are infected with the bacteria (Chalmers et al., 2004).
H. pylori can be detected through biopsy of the stomach, through a breath test which looks for exhalation of the excess carbon dioxide produced when the bacteria break down urea, or through a blood test which looks for antibodies created when the body’s immune system responds to the H. pylor infection (Helicobacter Foundation, 2006).
Although the transmission route of H. pylori is unknown, it appears to be related to the lack of access to clean water (Helicobacter Foundation, 2006). The faecal-oral route, which would transmit H. pylori through contaminated food and water sources, is the most commonly supported theory of H. pylori transmission (Chalmers et al. 2004).
polymorphsims in the IFNGR1 coding for interferon-gamma receptor (#12516030#)
coccal forms of Helicobacter pylori
Curry, A., Jones, D.M. (1990). The Genesis of Coccal forms of Helicobacter pylori . p. 29-37 In Ditschuneit, H., Malfertheiner, P. Eds. Helicobacter pylori, Gastritis and Peptic Ulcer . Springer-Verlag, New York.
D’Elios MM, Appelmelk BJ, Amedei A, Bergman MP, Prete GD. Gastric autoimmunity: the role of Helicobacter pylori and molecular mimicry. Trends Mol Med. 2004 Jul;10(7):316-23. PMID: #15242679#
Hatakeyama M. Oncogenic mechanisms of the Helicobacter pylori CagA protein. Nat Rev Cancer. 2004 Sep;4(9):688-94. PMID: #15343275#
Suerbaum S, Michetti P. Helicobacter pylori infection.
N Engl J Med. 2002 Oct 10;347(15):1175-86. PMID: #12374879#