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Category: Microbial Genetics and Molecular Biology
Distinguishing Pathovars from Nonpathovars: Helicobacter pylori, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817688/9781555812683_Chap09-1.gif /docserver/preview/fulltext/10.1128/9781555817688/9781555812683_Chap09-2.gifAbstract:
Pneumococcal organisms cause disease, most often outside its normal colonization site (the nasopharynx), and the colonization can be prolonged in many individuals. The chronic nature of the carriage and disease occurrence at the same nonsterile site of carriage render such a group of organisms even more difficult to classify as true pathovars. In this chapter, Helicobacter pylori is discussed as an example of such a group. The prevalence of chronic gastric colonization with H. pylori in human populations is high, but only about 10% of infected persons will progress to develop a gastric disease in their lifetime. Most of the H. pylori strain-typing approaches have relied on genotypic methods, which have been generally applied to demonstrate a relationship between gastroduodenal disease and strain type. The most common strain-typing method appears to be the PCR-restriction fragment length polymorphism (RFLP) analysis of selected H. pylori genes, usually vacA, cagA, and the urease genes. The genomic sequence data have provided a better understanding of the population structure of this organism in the stomach, which is important in addressing whether or not H. pylori isolates can be differentiated into pathovars and nonpathovars. With H. pylori infections, environmental exposures—including diet, antibiotics, food preservatives, and other chemicals that alter stomach pH, release of reactive nitrogen and oxygen intermediates, and inflammatory response in the stomach—could contribute to selective pressures on colonizing populations of H. pylori.
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