Biology of Helicobacter pylori
Helicobacter are Gram-negative, aerobic or microaerophilic, spiral-shaped bacilli that are motile by way of flagella at one end of the cell. Closely related to Helicobacter are species of the genera Aquaspirillum, Azospirillum, Spirillum, and Camplyobacter. The genetics of Helicobacter pylori are complex; there are many strains of H . pylori which are distinguished by the human disease with which they are associated. Once Helicobacter pylori colonizes its host, it lives in the interface between the surface of gastric epithelial cells and the overlying mucus gel layer, often clustering at the junctions of epithelial cells. In addition H. pylori can also be found on top of the gastric epithelium in the duodenum and esophagus. It was not until 1983 that H. pylori was recognized as having any medical importance. Now, it has been proven that H. pylori infection is the main cause of 
chronic superficial gastritis and it is associated with both gastric and duodenal ulcers.
Human Disease
Peptic ulcer disease is a common clinical ailment, once thought to be caused by oversecretion of acid and pepsin, an enzyme of the stomach that promotes digestion by breaking down proteins. Researchers have found, however, that although the injury caused by acid and pepsin is necessary for the formation of ulcers, acid secretion levels of the majority of patients with gastric or duodenal ulcers are normal. An ulcer is now known to be the result of an imbalance between aggressive and defensive mechanisms in the stomach and duodenum. Part of that imbalance can be attributed to infection by H. pylori.
Humans are the only known host of Helicobacter pylori. Its prevalence in healthy people increases with age to over 50% in people over the age of 60. Studies have shown that Blacks are more susceptible to infection than are Whites, and incidents of infection increase with decreasing socioeconomic status. Evidence of H. pylori infection in families, prisons, and nursing homes suggest that H. pylori is spread by close personal contact. However, the exact mechanism for transmission of the bacteria is not well understood.
Pathogenicity of Helicobacter pylori
Once acquired, Helicobacter pylori infection persists in its host indefinitely, apparently for life. Its persistence can be attributed to features that allow it to colonize the stomach. H. pylori is motile by polar flagella, allowing it to access susceptible areas. In addition, it is able to withstand the acidic environment of the stomach, because it produces urease, which increases the local pH.
Still, researchers are not sure how H. pylori escapes the bactericidal effects of gastric acid, or how it colonizes the gastric mucosa and damages the gastric epithelial cells. H. pylori produces urease, which leads to the formation of ammonia on the gastric mucosa, thereby increasing the pH of its environment. The organism also releases cytotoxins, toxic proteins, platelet activating factor, and lipopolysaccharide. the latter is overproduced in its outer membrane. Colonization of the stomach by H. pylori leads to an inflammatory response that is mediated by several of the bacterium's virulence determinants, which ultimately cause injury to the stomach tissues.
Diagnosis of H. pylori Infection
Several diagnostic tests are used to detect Helicobacter pylori infection (Table 1). These tests, including invasive and noninvasive techniques, have high sensitivity and specificity. The advantages of the various techniques are described below.
Invasive Techniques
Culture.Because of fastidious nature of H. pylori, culturing the bacterium is often tedious and is no more sensitive or specific than simple histologic analyses. Culturing H. pylori also involves the cost of endoscopy, making the method even less practical.
Histologic analysis of biopsy. Routine histologic analysis of biopsy samples is common and practical. This technique is helpful, because one can visualize the mucosa, permitting detection of histologic gastritis and lesions such as MALT-type lymphomas, which are tumors of lymphoid tissues. There are, however, clear drawbacks that should be considered. First, the organism may have a patchy distribution, especially at the base of the stomach, so more than two biopsy specimens are necessary for accurate results. Also, standard staining techniques (i.e., eosin staining) are usually unreliable for detection of H. pylori by microscopy. Adding to the impracticality of this method is that it requires endoscopy and diagnosis cannot be obtained until several days after the procedure.
Camplyobacter-like organism (CLO) test. This test is based on the fact that mucosal biopsy specimens can be inoculated into a medium containing urea and phenol red, a dye that turns pink in a pH of 6.0 or greater. The pH will rise above 6.0 when H. pylori, the Campylobacter-like organism, ----bolizes urea to ammonia by way of its urease activity. This test is commercially available and therefore quite inexpensive. Only one-half hour is required for diagnosis of infection, and the test has shown 98% sensitivity and 100% specificity. These qualities have made the CLO test the invasive technique of choice for diagnosing H. pylori infection.