Helicobacter pylori
Helicobacter pylori was previously known as Campylobacter pylori because of its resemblance to campylobacter (Lee & Marks, 2012). It is a motile helical spiral gram-negative bacterium. It is microaerophilic, as it requires oxygen for its survival. It is a flagellated organism, possessing multiple unipolar flagella, which allows it to move from one location to another. It measures between 2.4 - 4.0 m in length and it is an S-shaped, spiral rod (Santacrose, 2011)
Enzymes that the organism produces include oxidase, vacuolating cytotoxin, catalase, lipopolysaccharide and urease (Santacrose, 2011). Urease, produced by the organism, converts urea to ammonium and bicarbonate thereby neutralizing the effect of gastric acid on the organism and providing protection for the organism against the hostile environment which the stomach posses as a result of production of gastric acid. Urease is a potent antigen that induces the production of immunoglobulin G and immunoglobulin A. Vacuolating cytotoxin induces inflammatory cytokines and causes inflammation. Catalase aids the survival of Helicobacter pylori by preventing the formation of oxygen metabolites from hydrogen peroxide in neutrophils. The outer membrane is composed of lipopolysaccharide enhances the organism to colonize the stomach. The organism also produces muccin, which enables it to digest the mucus lining of the stomach epithelium so that it can anchor itself well to the mucosal surface (Santacrose, 2011).
The worldwide prevalence of helicobacter pylori infection is estimated at to be at least 50%. H pylori infection is found in about 90% of people suffering from peptic ulcer disease, although less than 15% of people infected with helicobacter pylori have peptic ulcer disease.
Most cases of helicobacter pylori infection is found in the developing countries, adducing to the fact that income and socioeconomic status is directly linked to the incidence of helicobacter pylori infection (Wong, 2004). The incidence of infection is said to be higher in Hispanics, African Americans and the elderly. The incidence rate in the United States is put at between 20 and 30% of the population (Brown, 2000).
Transmission of infection is most commonly through either mouth-to-mouth transmission or through the fecal-oral route (Lee & Marks, 2012). Helicobacter pylori is able to anchor itself into the mucous layer of the stomach by producing muccin, which digests the mucus lining of the stomach (Santacrose, 2011). It also produces urease, which forms bicarbonate that neutralizes the gastric acid. In addition, helicobacter pylori has a direct cytopathic effect on the epithelium of the stomach. It causes a chronic inflammation by the release of cytokines that mediate the aggregation of inflammatory cells at the site (Lee & Marks, 2012). Ulcers form due to the contact of the mucosal surface of the stomach with the gastric acid because the mucous layer, which normally protects the stomach against this, has been digested by the muccin (Santacrose, 2011).
Helicobacter pylori is associated with peptic ulcer disease, which includes gastric ulcer and duodenal ulcers. Diseases such as gastro-esophageal reflux disease, iron deficiency anemia and mucosa-associated lymphoid tissue lymphomas have all been associated with helicobacter pylori infection.
Diagnosis includes the fecal antigen test, which detects the antigens of helicobacter pylori in stool. The urea breath test detects the products of the reaction, which splits urea. Urea, which contains radiolabelled carbon, is given to the patient to drink. After some time, the level of the radiolabelled carbon is estimated in the breath. A high concentration of the rediolabelled carbon is only high in breath in a case of helicobacter pylori infection. This is because the stomach does not produce urease; therefore, any breakdown of urea is definitely as a result of the urease produced by helicobacter pylori. However, the test can also be falsely negative in cases of helicobacter pylori that does not produce urease (Santacrose, 2011). The cocoid form of helicobacter pylori does not produce urease. A serology test determines the quantity of immunoglobulin G antibodies in the blood. This test us useful in diagnosing a new patient. However, it is not ideal to use this test as a follow-up tool because the result does not specifically confirm the presence of helicobacter pylori infection. The antibody titre of the immunoglobulin G may remain elevated for a long time even after the eradication of helicobacter pylori (Santacrose, 2011).
Lifestyle modification to patients with peptic ulcer include avoiding spicy, acidic and fatty meals. The patient is also advised to eat small frequent meals as against the traditional three-square meal. The patient is also advised to look out for foods that are precipitants and avoid them. Cessation of smoking and consumption of alcohol is also advocated (Santacrose, 2011). The patient is also encouraged to take a lot of fruits and vegetables as they contain Vitamin A that speeds up the rate of ulcer healing. In addition, fruits contain fibers that are protective of the gastric mucosa. The patient can also be advised to cut down on the amount of caffeinated and carbonated drinks as they may increase the susceptibility to helicobacter pylori infection. Olive oil has also been used to manage peptic ulcer disease as it has been shown to be effective against helicobacter pylori, especially some strains that are drug resistant. Non-steroidal anti-inflammatory drugs like aspirin are also to be avoided.
REFERENCES
Luigi Santacroce (2011). Helicobacter Pylori Infection. Medscape reference: Drugs, Diseases & Procedures.
Dennis, Lee & Jay, Marks (2012). Helicobacter Pylori. Medicinenet.
B, Wong et al (2004). Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial. Journal of Americal Medical Association. 291(2):187-94.
Brown (2000). Helicobacter pylori: epidemiology and routes of transmission. Epidemiologic Reviews. 22(2):283-97.
