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  1. 1. Helicobacter Pylori<br />Lidia Benedict <br /> Angelique Leminger<br />
  2. 2. What is Helicobacter pylori ?<br /><ul><li>Extracellular bacteria that is ingested and colonizes the mucosal lining of the gastric epithelial cells in the antrum of the stomach and the duodenum (first part of small intestine).
  3. 3. “Prefers” the location of the antrum (base of the stomach) due to the lower levels of acidity. Mucous pH 7, acid in lumen pH 1.
  4. 4. Present in about half of the worlds population.
  5. 5. Approximately 80% of the infected population are asymptomatic.
  6. 6. World Heath Organization has classified it as a Class 1 carcinogen (carcinogenic to humans). </li></ul><br />
  7. 7. What is Helicobacter pylori ?<br /><ul><li>Bacteria classified as Helicobacteraceae Helicobacter pylori.
  8. 8. Helical / spiral shaped Gram negative prokaryote with flagella that infects the stomach and duodenum causing stomach ulcers, gastritis and if left untreated, can lead to stomach cancer and MALT lymphoma.
  9. 9. Microaerophile measuring 3.5 microns in length and 0.5 microns in width. If conditions are unsuitable, such as nutritional deficiencies, can be come coccoid in shape.
  10. 10. Grown best at 30-37°C on complex media supplemented with antibiotics, blood and serum and has an affinity for low pH (1.0), very acidic conditions.</li></ul><br />
  11. 11. H. pylori related disorders<br /><ul><li>Gastritis - inflammation of the stomach's lining. Chronic inflammation can damage the lining /tissues of the stomach over time and can result in the loss of acid-producing glands in the stomach. This can lead to the development of stomach cancer.
  12. 12. Peptic stomach (PUD) and duodenal ulcers – open sores in the lining of the stomach and/or duodenum. If the ulcer penetrates deep enough in the lamina propria, can cause perforation to the lining and blood vessels beneath, causing bleeding.
  13. 13. Stomach cancer – rapidly dividing abnormal cells creating a tumor.
  14. 14. Gastric MALT (mucosa-associated lymphoid tissue) lymphoma - a form of a cancerous tumor from lymphocytes (B cells).</li></li></ul><li>H. pylori<br />
  15. 15. H. pylori<br />http://me010/07/06/<br />
  16. 16. Who Discovered H. pylori ?<br /><br />Discovered in 1982 by a pathologist named Robin Warren (born in 1937) and a physician named Barry Marshall (born 1951), both from Perth, Australia.<br />
  17. 17. The Discovery of H. pylori<br /><ul><li>They both won the Nobel prize in Physiology and Medicine in 2005.
  18. 18. Medical community believed stress and spicy foods were the culprits of ulcers and gastritis. They criticized Dr. Marshall for his findings and wouldn’t believe that a single organism could cause these problems and survive an acidic environment as the stomach. Patients were usually told to cut back on spicy foods and seek psychiatric help for their stress.
  19. 19. “Everyone was against me but I knew I was right” (Marshall,2005) – had success treating patients with bismuth subsalicylateand antibiotics but couldn’t test on humans to prove his hypothesis that H. pylori was the cause.
  20. 20. Wanted to fulfill one of Koch’s postulates (introduce organism into healthy individual) by ingesting a turbid solution of H. pylori and shortly after developed acute symptoms. After an examination by endoscopy, found he had developed gastritis (inflammation of the stomach lining). </li></li></ul><li>Laboratory Diagnosis<br /><ul><li>Carbon-14 Urea Breath Test
  21. 21. Patients swallow a capsule containing urea made from an isotope of carbon. (Isotopes of carbon occur in minuscule amounts in nature, and can be measured with special testing machines.)
  22. 22. If H. pylori is present in the stomach, the urea is broken up and turned into carbon dioxide and ammonia. The carbon dioxide is absorbed across the lining of the stomach and into the blood. It then travels in the blood to the lungs where it is excreted in the breath.
  23. 23. If isotope is detected in breath, H. pylori is present. Test is usually repeated after eradication of bacteria.</li></li></ul><li>Laboratory Diagnosis<br /><ul><li>Blood Antibody Test
  24. 24. Checks to see if your body has made antibodies to the H. pylori bacteria. If antibodies are present, then you are either currently infected with the bacteria or you have been infected with the bacteria in the past.</li></ul><br />
  25. 25. Laboratory Diagnosis<br /><ul><li>Endoscopy
  26. 26. Doctor inserts an endoscope which is a flexible viewing tube through the mouth and down the esophagus, into the stomach and duodenum.
  27. 27. During the procedure, small biopsies (samples of tissues) from the stomach lining and duodenum are removed and sent to the lab for testing.</li></ul><br />
  28. 28. A look into the stomach…<br /><br />
  29. 29. What H. pylori causes<br />Ulcer<br /><br />
  30. 30. What H. pylori causes<br />Gastritis<br /><br />
  31. 31. Gram Stain<br /><ul><li>Staining procedures – Gram stain</li></ul><br />
  32. 32. Tissue sample<br />Picture of Dr. Marshalls tissue sample after ingesting H. pylori<br /><br />
  33. 33. How does one get infected?<br /><ul><li>Believed to be transmitted orally by means of fecal matter through ingestion of contaminated food and water and is contagious.
  34. 34. Can be transmitted person to person (oral contact) from belching (symptom of gastritis) or gastro-esophageal reflux in which a small amount of stomach contents are forced back up the esophagus. (GERD).</li></ul><br />
  35. 35. How does H. pylori work?<br />
  36. 36. How does H. pylori work?<br /><ul><li>H. Pylori use flagella with terminal end bulbs to help swim through mucus to colonize in the antrum which is further away from the parietal hydrochloric acid secreting cells. Corkscrew shape helps to drill into mucus layer above gastric epithelial cells.
  37. 37. Able to sense pH gradient in mucus layer by chemotaxis and swims towards more neutral pH area.
  38. 38. Does not invade the gastric epithelial cells.
  39. 39. Produces proteolytic enzymes lipase and phospholipase which help get into mucus layer.
  40. 40. Within the mucus layer, produces urease to help break down urea which is normally secreted in the stomach, into ammonia and CO2. Ammonia neutralizes stomach acid creating a cloud around the bacteria for protection from the acid.
  41. 41. Produces adhesins to help adhere to the epithelial cells.</li></li></ul><li>How does H. pylori work?<br /><ul><li>Secretes proteases and cytotoxinVacA (vacuolating A) which breaks down the protective mucin layer exposing the gastric lining, allowing stomach acid to damage the stomach lining.
  42. 42. Bacteria cause an inflammatory response - causing G cells to secrete gastrin which stimulates parietal cells to secrete more hydrochloric acid. Due to the increase in acid production, ulceration and perforation can occur.
  43. 43. Damaged epithelial tissues produce chemokines that attract neutrophils and macrophages to the lamina propria to fight the bacteria causing more inflammation.
  44. 44. Neutrophils and macrophages are unable to penetrate the mucus layer to get to the bacteria.
  45. 45. In chronic conditions, body continues to send white blood cells to site of infection but unable to reach the bacteria. Eventually causes further tissue damage.</li></li></ul><li>How does H. pylori work?<br />
  46. 46. How does H. pylori work?<br />
  47. 47. Virulence Factors<br /><ul><li>Urease – the breakdown of urea into CO2 and ammonia raises the pH in mucus causing a “cloud” to surround and protect the bacteria. Excess ammonia causes cell death.
  48. 48. Flagella with terminal bulb end – help to reach and remain in the mucus layer above the epithelial cells.
  49. 49. Endotoxin – LPS (lipopolysaccharide) causing inflammatory reaction and cell apoptosis.
  50. 50. Cag-A protein, which seems to stimulate the production of chemotactic factors for the neutrophils by the gastric epithelium. Strains are genetically diverse. CagA + strains enhance the risk of disease and are more virulent than CagA – strains.
  51. 51. Vac-A cytotoxin – causes epithelial tissue damage
  52. 52. Secretory enzymes – protease, lipase, oxidase, catalase
  53. 53. Ability to convert from spiral to coccoid shape in harsh conditions. </li></li></ul><li>Virulence Factors<br />
  54. 54. Symptoms of Infection<br /><ul><li>Signs/symptoms:
  55. 55. An ache or burning pain in your abdomen
  56. 56. A change in appetite with weight loss
  57. 57. Nausea
  58. 58. Vomiting
  59. 59. Frequent burping
  60. 60. Bloating
  61. 61. Bloody vomit or vomit that looks like coffee grounds
  62. 62. Bloody or black tarry stools</li></li></ul><li>Treatment of Infection<br /><ul><li>Hard to eliminate from the stomach because of resistance with commonly used antibiotics. Usual treatment involves two or more antibiotics given together with a PPI (proton pump inhibitor) or H2 blocker and bismuth subsalicylate (Pepto-Bismol). Examples of antibiotics – amoxycillin, clarithromycin, tetracyline.
  63. 63. PPI (proton pump inhibitors) – medication that decreases the production of stomach acid which allow the tissues to heal. Examples include lansoprazole (Prevacid), omeprazole (Priolosec), and esomeprazole (Nexium).
  64. 64. H2 Blocker – block histamine which stimulates acid secretion. Ranitidine - Zantac
  65. 65. Bismuth subsalicylate (Pepto-Bismol) – helps with upset stomach, heartburn, coats ulcers, helps with inflammation.
  66. 66. Treatment involves taking several medications for 7 to 14 days.</li></li></ul><li>Treatment of Infection<br /><ul><li>After initial treatment, it will be followed up with the Carbon C14 Urea Breath Test to make sure that the bacteria has been eradicated.
  67. 67. If not, second round of treatment for an additional 7-14 days with either same round of medication or a change in the antibiotics.</li></ul><br /><br />
  68. 68. Presence in U.S. and the World<br />
  69. 69. Epidemiological Factors<br /><ul><li>Prevalence of H. pylori is higher in third world countries – more than 80% - especially children due to socioeconomic status, poor hygiene and living conditions.
  70. 70. In industrialized countries – less than 40% and lower in children – higher in adults and the elderly.
  71. 71. Rapidly declining in industrialized countries.
  72. 72. Incidence of new H. pylori infections is less than 0.5% per year among adults in the Western world.</li></li></ul><li>Future Vaccine?<br />No current vaccination available.<br />Ondek, private Australian biotechnology company lead by Dr. Marshall – hopes to find a vaccine for H. pylori.<br />Homeopathic remedies that may help surpressH. pylori:<br /><ul><li>Eating yogurt w/ lactobacillus probiotics – helps to supress the H. pylori bacteria colonization and reduce metabolic activity.
  73. 73. Also helps manage the side effect of the antibiotic therapy.
  74. 74. Broccoli sprouts contain sulforaphane - a potent antibiotic.</li></li></ul><li>Preventative Measures<br /><ul><li>The source of H. pylori is not exactly known, so recommendations </li></ul>for avoiding infection have not been made. Always practice good hand washing techniques, eat food that has been properly prepared, and drink water from a safe, clean source. <br />
  75. 75.
  76. 76. References<br />Abourjaily, P. Urease Breath Test for H. pylori. (2007) Retrieved on July 28, 2010 from<br />Academy of Achievement, a Museum of Living History. Retrieved on July 26, 2010 from<br />Amoxicillin and tetracycline. Retrieved July 26, 2010, from Revolution Health:<br />Andersen, L.P., & Wadstrom, T. Basic Bacteriology and Culture. (2001) Retrieved on July 26, 2010 from<br />Agarwal, Z. (n.d.). Helicobacter Pylori. Retrieved July 26, 2010, from Stanford University:<br /> <br />Endoscopy photograph. Retrieved on July 26, 2010 from<br />Gastric Ulcer Bacteria Turn Immune Defense Inwards. (January 27, 2010) Retrieved on July 26, 2010 from<br />Gastrointestinal Disease, H. Pylori. Retrieved on July 26, 2010 from<br />Giardielli MD, Frank & Linkinhoker M,C., Michael. (2009, September 2). Helicobacter Pylori and Gastric Pathology Animation. Retrieved July 26, 2010, from Kuwait-MD:<br />Helicobacter Pylori. Retrieved on July 26, 2010 from<br />Helicobacter Pylori and Peptic Ulcer Disease. The Key to Cure. Retrieved on July 26, 2010 from<br />
  77. 77. References<br />Helicobacter pylori Bacteria. An International Journal of Gastroenterology and Hepatology. Retrieved on July 26, 2010 from<br />Helicobacter Pylori Tests. (2008). Retrieved on July 26, 2010 from<br />Innate Immunity Against Helicobacter Pylori. June 7, 2010. Retrieved on July 26, 2010 from <br /><br />Lopes Jr, J.E. Helicobacter pylori infection: An update on diagnosis and management. (July 6, 2010) Retrieved on July 26, 2010 from<br />MariAnne. Helicobacter Pylori: The Bacteria that causes ulcers. (May 7, 2006) Retrieved on July 28, 2010 from<br />Meet the Microbes. Retrieved on July 28, 2010 from<br />Patient Education Photographs. Retrieved on July 26, 2010 from<br />Patient Eduction Photographs. Retrieved on July 26, 2010 from<br />"Press Release: The 2005 Nobel Prize in Physiology or Medicine". 26 Jul 2010<br />Szczepanik, M. (n.d.). Retrieved July 26, 2010, from Department of Human Developmental Biology:<br />