Although the human stomach is usually regarded as a hostile habitat, an unusual vibrio, Helicobacter pylori, has found its own special niche there. Not only does it thrive in the acidic environment, but evidence has clearly linked it to a variety of gastrointestinal ailments. It is known to cause an inflammatory condition of the stomach lining called gastritis and is implicated in 90% of stomach and duodenal ulcers. It is also an apparent cofactor in the development of a common type of stomach cancer called adenocarcinoma. The curved cells were first detected by J. Robin Warren in 1979 in stomach biopsies from ulcer patients. He and an assistant, Barry J. Mar- shall, isolated the microbe in culture and even served as guinea pigs by swallowing a good-sized inoculum to test its effects. Both developed transient gastritis. Studies have revealed that the pathogen is present in a large pro- portion of people. It occurs in the stomachs of 25% of healthy middle- aged adults and in more than 60% of adults over 60 years of age.
Helicobacter pylori is probably transmitted from person to person by the oral-oral or oral-fecal route. It seems to be acquired early in life and carried asymptomatically until its activities begin to damage the digestive mucosa. Because other animals are also susceptible to H. pylori and even develop chronic gastritis, it has been proposed that the disease is a zoonosis transmitted from an animal reservoir. Reports on its high frequency in cats suggest that they may be a significant reservoir source. It can also be spread by houseflies acting as mechanical vectors. Other studies have helped to explain how the vibrio takes up residence in the gastrointestinal tract. First, it bores through the outermost mucus that lines the epithelial tissue. Then it attaches to specific binding sites on the cells and entrenches itself. It turns out that one receptor specific for Helicobacter is the same receptor as type O blood, which accounts for the higher rate of ulcers in people with this blood type (1.5 2 times). An- other protective adaptation is the formation of urease, an enzyme that converts urea into ammonium and bicarbonate, both alkaline compounds that can neutralize stomach acid. As the immune system recognizes and attacks the pathogen, infiltrating white blood cells damage the epithelium to some degree, leading to chronic active gastritis. In some people, these lesions lead to deeper erosions and ulcers and, eventually, can lay the groundwork for a cancer to develop. Helicobacter pylori is isolated primarily from biopsy specimens. Because it gives off large amounts of urease, it can be initially identified by inoculating a urease test. A less invasive technique is the urea breath test. This test involves swallowing labeled urea that gives off radioactive CO2 in exhaled air if H. pylori is present.
A PCR test for microbial DNA in biopsies and feces is also being marketed. Understanding the underlying pathology has useful applications in treatment. Gastritis and ulcers have traditionally been treated with drugs(Tagamet, Zantac) that suppress symptoms by slowing the secretion of acid in the stomach and must be taken continuously for indefinite periods, and relapses are common. The newest recommended therapy is 2 to 4 weeks of clarithromycin to eliminate the bacterial infection, and Zantac, which inhibits the formation of stomach acid. This regimen can actually cure the infection and eliminate symptoms.
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