Professional Documents
Culture Documents
Learning Objectives
On completion of this seminar, students will be able to: Recognize the typical clinical presentation and risk factors for peptic ulcer disease
Case Presentation
Mr. Jones, a 45 year old male presents to your hospital with epigastric abdominal pain x 2 weeks.
Case Symptoms
He describes it as a burning pain which is non-radiating and is worse after he eats. He has frequent belching with bloating sensation but denies nausea, vomiting, diarrhea, constipation, or weight loss. He has tried rolaids (antacids) which do help a little.
http://www.medicinenet.com/peptic_ulcer/
Risk Factors
Aggressive Factors
Acid/Pepsin H. pylori infection NSAIDs Smoking
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Defensive Factors
Mucus-bicarbonate barrier Barrier of apical membrane Mucosal blood flow Prostaglandins Epithelial cell restitution
Aggressive Factors
Defensive Factors
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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).
H.pylori
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Helicobacter Pylori
Most common cause of PUD Gram negative Spiral shaped Microaerophilic Corkscrew motility by 4-6 polar flagella. Unable to ferment or oxidize carbohydrates Slow-growing
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Epidemiology
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Mode of transmission
Humans are principal reservoir Possible environmental reservoirs include contaminated water sources. Oral-oral - Saliva or vomit
Fecal-oral
- Water contaminated with human wastes - Factors linked to poor hygiene
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Virulence Factors
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Sequence of histological and endoscopic events in H. pylori infected stomach Transformation of chronic atrophic gastritis to chronic active gastritis with polyp, intestinal metaplasia and dysplasia to cancer.
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Diagnosis
Invasive tests
Non-invasive tests
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Non-invasive tests
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anti-H.
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Serological Techniques
Techniques : Complement fixation test Latex agglutination test ELISA Antigens used for diagnosis : Urease and flagellar proteins Several Virulence factors
Antibodies detected : IgG is the predominant class even in children IgM rarely observed IgA elevated in majority of infected cases but not all
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Invasive tests
Specimens Endoscopic biopsy Gastric juice Blood Rarely used Liver biopsy
Culture
Urease
Molecular Tests
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Endoscopy
Duodenal ulcer
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Molecular methods
PCR for detection of H. pylori PCR for detection of pathogenic factors Genes involved in adherence Genes involved in pathogenicity Real Time PCR using SYBR green dye or fluorescence resonance energy transfer (FRET) principle
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Histopathological diagnosis
Stains Grams stain Giemsa stain Warthin silver starry stain Hematoxylin & Eosin stain Acridine orange stain Immunostaining (Dako,Denmark)
Helicobacter pylori observed on a gastric biopsy smear after acridine orange staining. Magnification, x1,000
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A silver stain (Warthin Starry) of Helicobacter pylori on gastric mucus-secreting epithelial cells (x1000).
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E-test
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The presence of urease is an indicator of the presence of H. pylori and results in a color change from yellow to pink Urea in substrate pad reacts with urease
NH3 NH3 passes through the semi-porous membrane dark blue or purple color on the yellow pH paper directly above an H. pylori-infected biopsy
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Case Study
H. pylori
Gastric biopsy photomicrograph from J Natl Med Assoc. 2007 January; 99(1): 3134.
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Results
Mr. Jones is suffering from Chronic gastritis The causative organism is Helicobacter pylori Confirmed by histopathologic examination of biopsy specimen
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Treatment
PPI (H2 blocker) or Bismuth
Colloidal Bismuth Subcitrate (CBS)
Two Antibiotics
Clarithromycin Amoxicillin Tetracycline Metronidazole Furazolidone
Triple Therapy
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Future Development
Currently : Vaccine using urease and HspB are on trial in animal models
Prevention
Probiotics may prevent infection Reduction of risk factors such as poor socioeconomic status Improving living conditions and hygiene
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Lets review.
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In Summary
H. pylori is the most common cause of PUD and is a risk factor for gastric cancer Clean and hygienic living conditions help prevent infections Transmission is via person to person Threat is prevalent, about half of the worlds population is infected. Severity of symptoms depend on region, age, and lifestyle. Disease involves chronic gastritis, gastric and duodenal ulcers. H. pylori infection increases risk of PUD, gastric CA, and MALT lymphoma Typical symptoms are nausea, epigastric pain, vomiting, anorexia Diagnostic tests include biopsy, urea breath test, histopathology etc.
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References
Algood HMS, Cover TL. Helicobacter pylori persistence: an overview of interactions between H. pylori and host immune defenses. Clin Microbiol Rev 2006;19:597-613. Dunn BE, Cohen H, Blaser MJ. Helicobacter pylori. Clin Microbiol Rev 1997;10:720-41. Kusters JG, van Vliet AHM, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev 2006;19:449-90. Malfertheiner P, Megraud F, O'moraina C, Hungin APS, Jones R, Axon A et al. Current concepts in the management of Helicobacter pylori infection. The Maastricht 2-2000 Consensus Report. Aliment Pharmacol Ther 2002;16:167-80. Mgraud F, Lehours P. Helicobacter pylori detection and antimicrobial susceptibility testing. Clin Microbiol Rev 2007;20:280-322. Polk DB, Peek RM Jr. Helicobacter pylori: gastric cancer and beyond. Nat Rev Cancer 2010;10:40314. Schmidt H, Hensel M. Pathogenicity islands in bacterial pathogenesis. Clin Microbiol Rev 2004;17:14-56. Singh V, Trikha B, Nain CK, Singh K, Vaiphei K. Epidemiology of Helicobacter pylori and peptic ulcer in India. J Gastroenterol Hepatol 2002;17:659-65. Studies on Helicobacter pylori. National Institute of Cholera And Enteric Diseases (NICED) Annual Report 2004-2005. Wroblewski LE, Peek RM Jr, Wilson KT. Helicobacter pylori and gastric cancer: factors that modulate disease risk. Clin Microbiol Rev 2010;23:713-39.
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Thank You !