Helicobacter pylori (Microbiology CS3) Case Study

Helicobacter pylori (Microbiology CS3) - Case Study Example It is also believed to be the etiologic agent for peptic ulcers, gastritis and other gastric disorders (Mobley, Mendz and Hazell, 2001). H. 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). 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). The 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). The 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,