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Helicobacter Pylori: The Organism, the Disease, the Clinical Picture, the Current Research

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No definite evidence demonstrates a clear relationship between the symptoms of the H pylori-associated gastritis and abdominal pain or dyspeptic symptoms from other conditions, although H pylori gastritis is the cause of dyspepsia in a subset of patients (as when successful H pylori eradication results in sustained symptomatic remission) and is considered a distinct entity

In infected patients, 30%-35% have no symptoms.

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Diseases associated with this bacterium were highly prevalent during the 19th century and gradually have declined. Most diseases associated with H. pylori occurred in individuals older than 40 years of age. However, acquisition of H. pylori occurs mainly in young children inside the family setting. Prevalence and incidence of H. pylori has had a dramatic change in the last part of the 20th century and beginning of the 21th century. In developed countries there is a clear interruption of transmission and the lowest prevalence is observed in children younger than 10 years in these countries. A similar decline is observed but not at the same level in developing countries.Looking back at the history of medical bacteriology, during the last 20 years of the 19th century and for most of the first half of the 20th century, bacteriologists and infectious disease specialists have isolated and identified most of the pathogenic bacteria affecting humans. Helicobacter pylori probably represented one of the latest infectious bacteria isolated from humans. There are two different theories regarding the role of H. pylori in peptic ulcer diseases. One theory proposes the role of H. pylori as the etiological agent of a modern disease: peptic ulcer disease and as a major risk factor for the development of distal gastric cancer. A series of studies suggested that peptic ulcer disease and gastric cancer are diseases related to modern times. The prevalence and incidence of these diseases rose at the end of the 18th century and peaked by the 19th century. There is a potential explanation that may account for both conflicting points of view of H. pylori’s etiological role in peptic ulcer disease and as the major risk factor for the development of gastric cancer

Peptic ulcer disease and gastric cancer are indeed very ancient diseases, but because the number of cases related to these diseases was insignificant until the second half of the 18th century they have been suggested to be modern diseases. However, increased life expectancy in new industrialized countries, specifically the UK and US, may explain the escalation of peptic ulcer disease and gastric cancer cases. Several studies indicated major changes in life expectancy, from less than 45 years in the 18th century to more than 60 years by the 19th century in the same countries.

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Helicobacter pylori is a bacterium that colonizes human stomach and is an established cause of chronic superficial gastritis, chronic active gastritis, peptic ulcer disease and gastric adenocarcinoma. The infection is on a fast decline in most of the western countries, mainly due to the success of therapeutic regimens and improved personal and community hygiene that prevents re-infection. The eradication in some of the countries has been quite promising and the pathogen was declared as an endangered bacterial species. However, the situation is exactly opposite in many of the developing countries due to failure of treatment and emergence of drug resistance. At that time when Warren and Marshall announced their findings, it was a long-standing belief in medical teaching and practice that stress and lifestyle factors were the major causes of peptic ulcer disease. Warren and Marshall rebutted that dogma, and it was soon clear that H. pylori, causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers (Graham DY., 1999). The clinical community, however, met their findings, with skepticism and a lot of criticism and that's why it took quite a remarkable length of time for their discovery to become widely accepted. They had to just push it harder and harder with all experimental and clinical evidences

In 1985, for example, Marshall underwent gastric biopsy to put evidence that he didn't carry the bacterium, then deliberately infected himself to show that it in fact caused acute gastric illness. How long humans carried H. pylori is still a debatable issue. However, it is accepted that this organism has colonized humans possibly for many thousands of years, and the successful persistence of H. pylori in human stomach for such a long period may be a case to conceive that this organism is advantageous to its host (Chow WH, Blaser MJ, 1998).

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On balance, recent studies recommend enhancing the number of biopsy fragments for the rapid urease test. Bacterial culture from the gastric biopsy is the gold standard technique, and is recommended for antibiotic susceptibility test. Serology is used for initial screening and the stool antigen test is particularly used when the urea breath test is not available, while molecular methods have gained attention mostly for detecting antibiotic resistance.

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de Martel C, Llosa AE, Farr SM, Friedman GD, Vogelman JH, Orentreich N, Corley DA, Parsonnet J. Helicobacter pylori infection and the risk of development of esophageal adenocarcinoma. J Infect Dis. 2005

Chow WH, Blaser MJ, Blot WJ, Gammon MD, Vaughan TL, Risch HA, Perez-Perez GI, Schoenberg JB, Stanford JL, Rotterdam H, West AB, Fraumeni JF., Jr An Inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma. Cancer Res. 1998

Graham DY. Helicobacter pylori, GERD, NSAIDs, and cancer: where we really stand. Am J Gastroenterol. 1999

Warburton-Timms VJ, Charlett A, Valori RM, Uff JS, Shepherd NA, Barr H, McNulty CA. The significance of cagA (+) Helicobacter pylori in reflux oesophagitis. Gut. 2001

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