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H. pylori

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  • 1. Helicobacter pylorian overview Presented By: Nasir Nazeer
  • 2. Historical Background        Human stomach long considered inhospitable for bacteria. Spiral shaped organisms occasionally visualized in gastric mucous layer, but no evidence of disease association. 1982 - Marshall and Warren identified and subsequently cultured the gastric bacterium, Campylobacter pyloridis, later reclassified as Helicobacter pylori. Discovery revolutionized the treatment of duodenal and gastric ulcers. Earned them the Nobel Prize for Medicine in 2005. Nearly 20 species of Helicobacter are now recognized. The gastric helicobacters colonise the stomachs of animals. The monkey, cat, dog, tiger all harbour their own species.
  • 3. Historical Background (Contd.)    The bacterium lives in the stomach of about half the people in the world. Many are apparently well, and most have an inflammation of the stomach lining, a condition which is called "gastritis". Gastritis is the underlying condition which causes ulcers and other digestive complaints, possibly including cancer of the stomach. Marshall and Warren culture organism from human gastric mucosa and show association with gastric inflammation.
  • 4. A silver stain of H. pylori on gastric mucus-secreting epithelial cells (x1000). From Dr. Marshall's stomach biopsy taken 8 days after he drank a culture of H. pylori (1985).
  • 5. Morphology and structure of H. Pylori     Spiral-shaped Gram-negative, oxidase and catalase-positive motile bacterium with 4-6 flagella. Almost all the bacteria have the same size length:2.5~4.0μm width:0.5~1.0μm Microaerophilic, i.e. it requires oxygen but at lower levels than those contained in the atmosphere With its flagella and its spiral shape, the bacterium drills into the mucus layer of the stomach, and can either be found suspended in the gastric mucosa or attached to epithelial cells.
  • 6. Morphology and structure of H. Pylori Produces adhesins which bind to membrane-associated lipids and carbohydrates and help its adhesion to epithelial cells Breaks down urea (NH2CONH2) to NH4+ and CO2 Stomach acidity  Possible for H. pylori to survive Not cleared by host immune response.
  • 7. Biological properties of H. pylori
  • 8. Epidemiology      The most common chronic bacterial infection in humans. The risk of acquiring H. pylori infection is related to socio-economic status and living conditions early in life. Developing nations: the majority of children are infected before the age of 10, the prevalence in adults peaks at more than 80 percent before age 50. Developed countries: evidence of infection in children is unusual but becomes more common during adulthood. Immigration is responsible for isolated areas of high revalence in some Western countries.
  • 9. Infective ratio all over the world
  • 10. Transmission of H.pylori        Transmission — Route by which infection occurs remains unknown Humans are major source of transmission - if not only – reservoir. Transmission among persons sharing the same living environment. Family members often carry same strain. Person-to-person transmission of H. pylori through either fecal/oral or oral/oral exposure seems most likely. Organism can be cultured from feces. Infection from environment or from animals cannot be totally excluded.
  • 11. Defense mechanism of H.pylori   Once H. pylori is ensconced in the mucus, it is able to fight the stomach acid that does reach it with an enzyme called urease. Urease converts urea, of which there is an abundant supply in the stomach (from saliva and gastric juices), into bicarbonate and ammonia, which are strong bases. This creates a cloud of acid neutralizing chemicals around the H. pylori, protecting it from the acid in the stomach.   The reaction of urea hydrolysis is important for diagnosis of H.pylori by the breath test.
  • 12. Site of infection • • • Highly adapted organism that lives only on gastric mucosa. Gastric antrum is the most favoured site. Present in the mucus that overlies the mucosa.
  • 13. How H.pylori infection progresses?
  • 14. Pathogenesis        Most bacteria are killed in hostile environment of gastric lumen. H. pylori proliferates in mucus layer over epithelium and is not cleared by host immune response. Pathophysiology of H. pylori infection and its eventual clinical outcome is a complex interaction between the host and the bacterium. H. pylori survives and grows there because of a variety of virulence factors that contribute to gastric inflammation, alter gastric acid production, and cause tissue destruction. Flagella - allows penetration of H.pylori into gastric mucous layer. Adhesins - mediate binding to host cells. Localized tissue damage mediated by:   Mucinases and phospholipases - disrupt gastric mucus Vacuolating cytotoxin - induces vacuolation in epithelial cells that results in epithelial cell damage
  • 15. Mechanism of Helicobacter pylori infection
  • 16. Symptoms of H.pylori infection           Abdominal pain with burning or gnawing sensation. Pain is often made worse with empty stomach; night time pain is common. Poor appetite. Weight loss. Heart burn. Indigestion (dyspepsia) Belching. Nausea. Vomiting. Blood in stool.
  • 17. Diseases associated with H. Pylori • • • • • • Duodenal Ulcer Gastric (Stomach) Ulcer Non-Ulcer dyspepsia Weird Syndromes (associated with acne rosacea, gulf veterans syndrome, chronic fatigue syndrome and chronic halitosis) Stomach Cancer MALT Lymphoma
  • 18. Sequence of histological and endoscopic events in H. pylori infected stomach with accompanying transformation of chronic atrophic gastritis to chronic active gastritis with polyp, intestinal metaplasia and dysplasia to cancer.
  • 19. Laboratory diagnosis noninvasive tests • • • •  Serology : detect an immune response by examining a blood sample for antibodies to the organism (ELISA). Urea breath test : a urea solution labelled with C14 isotope is given to pt. The C02 subsequently exhaled by the pt contains the C14 isotope and this is measured. A high reading indicates presence of H. pylori. Faecal antigen test : detects H. pylori antigens in faecal specimens. Polymerase chain reaction (PCR) : can detect HP within a few hours. Not routine in clinical use. Urease Test: Urease activity in the stomach qualitatively detects active infection with a sensitivity and specificity of more than 90 percent.
  • 20. Invasive testing   Histological examination of biopsy specimens of gastric/duodenal mucosa take a endoscopy Culture    Not sensitive then a skilled microscopy histological section Can be used for antibiotic resistance testing Requires selected agars and incubation periods
  • 21. Tests for detecting H.pylori infection
  • 22. Conclusion A characteristic of H. pylori infection in humans is gastritis, which persists for decades without causing serious damage in most cases. The clinical complications of H. pylori infection, such as peptic ulcer disease and gastric cancer, appear to represent an imbalance in gastric homeostasis.
  • 23. Bibliography • • • • • • • • • • Suerbaum S, Michetti P. Helibacter pylori infection. NEnglJMed 2002;347:1175-86 Malfertheiner P, Megraud F et al. Current concepts in the management of Helicobacter pylori infection–The Maastricht 2-2000 Consensus Report. Aliment Pharmacol Ther 2002; 16:167-80 Hjalmarsson S, Sjolund M, Engstrand L. Determining antibiotic resistance in Helicobacter pylori. Expert Rev Mol Diagn. 2(3):267-72, 2002 May. Vaira D, Vakil N, Menegatti M et al. The stool antigen test for detection of Helicobacter pylori after eradication therapy. Ann Intern Med 2002;136:280-7 Qasim A, O’Morain CA. Review article: treatment of Helicobacter pylori and factors influencing eradication. Aliment Pharmacol Ther 2002; 16 (Seppl. 1):24-30. vanZwet AA, Vandenbrouke-Grauls CMJ et al. Stable amoxicillin resistance in Helicobacter pylori. Lancet 1998;352:1595 Perez Aldana et al. The relationship between consumption of antimicrobial agents and the prevalence of primary Helicobacter pylori resistance. Helicobacter 2002;7(5):306309 Xia HX, Buckley M, Keane CT. Clarithromycin resistance in Helicobacter pylori: prevalence in untreated dyspeptic patients and stability in vitro. J Antimicrob Chemother 1996;37:473-81 Jenks PJ. Causes of failure of eradication of Helicobacter pylori. BMJ 2002;325:3-4 Buckley MJ, Xia HX et al. Metronidazole resistance reduces efficacy of triple therapy and leads to secondary clarithromycin resistance. Dig Dis Sci 1997;42:2111-5
  • 24. Bibliography 1. 2. 3. 4. Houben MHM, Van De Beek D. A systematic review of Helicobacter pylori eradication therapy – the impact of antimicrobial resistance on eradication rates. Aliment Pharamcol Ther 1999;13:1047-55 Owen RJ. Molecular testing for antibiotic resitance in Helicobacter pylori. Gut 2002;50:285-9 Meyer JM, Siliman N. Risk factors for Helicobacter pylori resistance in the United States: The Surveillance of H. pylori Antimicrobial resistance partnership (SHARP) study, 1993 – 1999. Ann Intern Med 2002;136:1324 Wen M, Zhang Y et al. An evaluative system for the response of antibacterial therapy: Based on the morphological change of Helicobacter pylori and mucosal infllammation. Pathology International April 99 49:4;332-341

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