Helicobacter pylori, which was formerly known as Campylobacter pyloridis, is a microaerophilic, Gram-negative bacterium present in the stomach. In 1982, Robin Warren and Barry Marshall discovered that it was found in persons who were suffering from chronic gastric ulcers and gastritis, diseases that were not formerly thought to have been caused by microbes. It is also associated with the development of duodenal ulcers and stomach cancer. Nevertheless, more than 80 percent of persons infected with the bacterium show no symptoms, and it has been contended that it may have a crucial role in the natural ecology of the stomach (Blaser, 2006).
/>
Over 50% of the global population has H. pylori in their upper side of the gastrointestinal tract. Infection is more dominant in growing nations, and occurrence is lessening in Western nations. The helix shape of H. pylori's is believed to have evolved to perforate the stomach’s mucoid lining (Brown, 2000).
In order to survive in the stomach, H. pylori secrete large volumes of the enzyme urease whose molecules are located inside as well as outside of the bacterium. This enzyme degrades urea to give ammonia and carbon dioxide. The ammonia is turned into ammonium through acceptance of a proton (H+) that neutralizes gastric acid. The H. pylori survival in the acidic stomach relies on urease. The ammonia released is toxic to the cells in the epithelium, and, along with the other H. pylori products including vacuolating cytotoxin A, proteases, and some phospholipases, cause destructions to those cells (Stark, Gerwig, & Pitman, 1999).
At least half of the global inhabitants is infected with the bacterium, and this makes it the most prevalent infection worldwide (Pounder, 1995). Actual rates of infection differ from one country to another. The developing countries have higher infection rates than the developed countries, where rates are approximated to be about 25%. The age at which H. pylori is acquired appears to affect the possible pathologic result of the infection. Persons infected with H. pylori during their early stages are likely to have more severe inflammation, which might be accompanied by atrophic gastritis with a higher succeeding risk of gastric cancer, gastric ulcer or the two. Acquisition at a later stage imparts different gastric modifications more likely to result in duodenal ulcer (Brown, 2000). Infections are normally acquired in infancy in all nations (Kusters, van Vliet, & Kuipers, 2006). However, the rate of infection in children, in developing countries, is more than in developed nations, most likely because of poor conditions of sanitation.
H. pylori have the ability to endure in stomach acid since they secrete enzymes, which neutralize the acid. This permits H. pylori to get into the stomach and enter the safe area, the protective stomach wall mucous lining. While the bacterium is in the stomach mucous lining, the natural defenses of the body cannot access it. The immune system will react to an infection caused by H. pylori but will not have the ability to cause death to the bacteria as they are concealed in the lining of the stomach. The immune system will continue sending fighters of infection to the site of infection and H. pylori will get nourishment from the nutrients offered by the body, enabling the bacteria to endure in the harsh stomach conditions. H. pylori weaken the mucous coating that offers protection to the stomach and duodenum, permitting the stomach acid to penetrate to the sensitive lining under. The acid and the bacteria cause irritation on the lining leading to gastritis and possibly the ulcer formation within a few days of the early infection. Satirically, it might not be the H. pylori, but the response of inflammation to the bacteria that causes the ulcer formation (Baldwin, Shepherd, & Kraemer, 2007).
Several diseases are associated with the H. pylori. These include, gastric or stomach ulcers, which are sores in the duodenum or stomach lining, duodenal peptic ulcers, which are ulcers in the duodenum. Stomach cancer is also associated with H. pylori and it affects any part of the stomach. Non-ulcer dyspepsia Non-ulcer dyspepsia is a disease where patients do not suffer from ulcers, but do vomit and experience nausea.
There are several ways used in diagnosis of H. pylori. The tests that are commonly used include blood tests, which can detect specific antibodies produced as a response to H. pylori by the immune system. Breath tests require that a person drink a solution that is specialized containing a substance that is degraded by H. pylori. The products of breakdown are then detected in the person’s breath. Stool tests are also usually done to detect H. pylori. These detect proteins of H. pylori in stool (Logan & Walker, 2001).
In the present society, nicotine, stress, an unhealthy diet, and caffeine can be the main causes of ulcers. If given immediate care, ulcers can be put under control. Changing lifestyle can as well control H. pylori. This means taking less carbonated and alcoholic drinks, citric juices, nicotine, as well as caffeine. These are among the specific causes of ulcers and ought to be reduced at all costs (Hsu, Wu, & Chen, 2008).
Reference List
Baldwin, D. N., Shepherd, B., & K. P. (2007). Identification of Helicobacter pylori Genes That Contribute to Stomach Colonization. Infect Immun, 75(2), 1005–1016.
Blaser, M. J. (2006). Who are we? Indigenous microbes and the ecology of human diseases. EMBO Reports, 7(10), 956–960.
Brown, L. M. (2000). Helicobacter pylori: epidemiology and routes of transmission. Epidemiol Rev, 22(2), 283–297.
Hsu, P. I., Wu, D. C., & Chen, A. (2008). Quadruple rescue therapy for Helicobacter pylori infection after two treatment failures. Eur. J. Clin. Invest., 38(6), 404–409.
Kusters, J. G., van Vliet, A. H., & Kuipers, E. J. (2006). Pathogenesis of Helicobacter pylori Infection. Clin Microbiol Rev, 19(3), 449–490.
Logan, R. P., & Walker, M. M. (2001). Epidemiology and diagnosis of Helicobacter pylori infection. BMJ, 323 (7318), 920–922.
Pounder, R. E. (1995). The prevalence of Helicobacter pylori infection in different countries. Aliment. Pharmacol. Ther., 9(2), 33–39.
Stark, R. M., Gerwig, G. J., & Pitman, R. S. (1999). Biofilm formation by Helicobacter pylori. Lett Appl Microbiol, 28(2), 121–126.
