Helicobacter pylori (Microbiology CS3) - Case Study Example

Helicobacter pylori (Microbiology CS3) Schools Number and of (e.g., May 18, 2012)Helicobacter pylori (Microbiology CS3)Introduction Helicobacter pylori, a gram-negative, spiral shaped, flagellated, microaerophilic bacterium is found in the lining of the stomach and the duodenum (Mobley, Mendz and Hazell, 2001; Helicobacter Foundation, 2006). It has been widely studied for its ability to survive in the harsh, acidic and uninhabitable stomach environment. The bacterium lives in the mucus lining where it resists the action of the hydrochloric acid produced by the stomach.

It is believed to be transmitted via the oral route by the ingestion of food and water contaminated with fecal matter, or through oral contact (Helicobacter Foundation, 2006). It is also believed to be the etiologic agent for peptic ulcers, gastritis and other gastric disorders (Mobley, Mendz and Hazell, 2001). Major Enzymes enabling Survival in HostH. pylori produces several key enzymes that enable it to survive in the host. The enzyme, urease, catalyses the breakdown of urea, which is abundantly available in the stomach, into ammonia and bicarbonate (Helicobacter Foundation, 2006).

The resulting ammonia surrounds the bacteria, proving a basic (low pH) environment that protects the bacteria from stomach acid. Another enzyme, superoxide dismutase, protects the bacteria from being killed by macrophages and polymorhonuclear leukocytes by breaking down the dismutase produced by them (Mobley, Mendz and Hazell, 2001). Catalase protects the bacteria from hydrogen peroxide produced by phagocytes (Mobley, Mendz and Hazell).How common is H. pylori Infection?According to the Centers for Disease Control and Prevention, H.

pylori infection afflicts almost two-thirds of the entire population of the world (CDC, 2005). Developing countries have a higher incidence of H. pylori infection than developed countries (Mobley, Mendz and Hazell, 2001).Age and Social Distribution of People Infected by H. pyloriThe infection is more prevalent among lower socio-economic groups and in older adults (CDC, 2005). In the US, Hispanics and African Americans are found to be the most affected (CDC, 2005). The rate of acquisition of the infection differs greatly, both within and across countries (Mobley, Mendz and Hazell, 2001).

Mechanism of PathogenicityThe bacteria first adhere to the mucin in the epithelial cells of the gastric mucosa (Mobley, Mendz and Hazell, 2001). By altering the rheological properties of the mucus gel, the bacteria coats the lining of the stomach wall (Celli et al. 2009). It then generates a cloud of ammonia around itself to achieve low pH for protection from stomach acid. The ammonia is produced by the hydrolysis of urea. The bacteria also produces phospholipase A that degrades cell membranes by breaking down phospholipids (Mobley, Mendz and Hazell, 2001). H. pylori also produces a toxin called Vac A that is responsible for the production of vacuoles in the epithelial cells (Mobley, Mendz and Hazell, 2001).

This toxin is associated with the development of peptic ulcers. Peptic ulcer is not caused directly by H. pylori but rather it is the degradation and inflammation of the stomach lining in response to the H. pylori infection, which causes peptic ulcer.Gastrointestinal Disorders Associated with H. pylori Infection H. pylori causes duodenal ulcers, gastric (Stomach) ulcers, stomach cancer and non-ulcer dyspepsia (Helicobacter Foundation, 2006).Diagnosis The infection is diagnosed through several methods.

Serological tests are used to measure IgG antibodies and the assay specificity ranges from 80-90% (CDC, 2005). The Breath-test is also used for diagnostic purposes. In this test, the patient is made to drink urea labeled with 13C or 14C. The urea is then metabolized. Labeled carbon in the patient’s breath is then measured. Another diagnostic procedure is the upper esophagogastroduodenal endoscopy, in which biopsy samples of the duodenum and stomach are collected and then cultured and subjected to the biopsy urease test and other histologic tests (CDC, 2005).

Drug Treatment and Lifestyle Advice for Patients with Peptic Ulcers Antibiotics such as tetracycline, metronidazole, amoxicillin, or clarithromycin are given. A proton pump inhibitor or a H2 blocker is given to reduce ulcer-related symptoms and also to heal the damaged gastric mucosa (CDC, 2005). Those suffering from peptic ulcers can make lifestyle modifications, which include healthy diet and other measures for coping with the disease. Bland foods along with milk are recommended and it is advised that small amounts of food should be consumed with every meal.

The diet should be rich in fiber and flavonoids. Recommended foods include fruits such as apples and cranberries, vegetables, onions, tea, and celery (Ehrlich, 2011). Spicy foods need to be avoided. Smoking and alcohol abuse has to be minimized or totally avoided. It is also important to reduce coffee and carbonated beverage consumption. Meditation and yoga are also recommended (Ehrlich, 2011).ReferencesCDC. (2005, September 23). Helicobacter pylori and Peptic Ulcer Disease. Retrieved 18 May, 2012 from http://www.cdc.gov/ulcer/Celli, J. P., Turner, B. S., Afdhal, N. H., Keates, S.

, Ghiran, I., Kelly, C. P., Ewoldt, R. H., McKinley, G. H., So, P., Erramilli, S., and Bansil, R. (2009). Helicobacter pylori moves through mucus by reducing mucin viscoelasticity. Proceedings of the National Academy of Sciences of the United States of America, 106 (34), 14321-14326. Ehrlich, S. D. (2011, October 13). Peptic ulcer. Retrieved 18 May, 2012 from http://www.umm.edu/altmed/articles/peptic-ulcer-000125.htmHelicobacter Foundation. (2006). Helicobacter pylori. Retrieved 18 May, 2012 from http://www.helico.com/h_general.

htmlMobley, H. L. T., Mendz, G. L., and Hazell, S. T. (2001). Helicobacter Pylori: Physiology and Genetics. Washington DC: ASM Press.