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55 Cards in this Set
- Front
- Back
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What % of the population is infected with H. pylori? What % of them have symptoms?
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50% are infected
-20-30% of them have symptoms |
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What diseases are associated with H. pylori?
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-Chronic superficial gastritis
-Peptic ulcer disease -Gastric carcinoma/lymphoma |
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What type of stain is used for H. pylori?
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silver stain
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What is the gram stain of H. pylori?
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Curved Gram neg rods
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Is helicobacter motile?
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yes
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What type of flagella does Helicobacter have?
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Multiple unipolar
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What biochemical test helps id helicobacter?
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Urease production
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How does Helicobacter survive the stomach's acidity?
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By living in a little niche in the gastric mucus that overlays the gastric mucosa.
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Why does Helicobacter prefer that little niche?
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It has a much higher pH actually
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When do people typically get colonized with H. pylori?
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In childhood
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Are all people infected by the same helicobacter?
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No there is broad diversity in unrelated individuals.
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What is the natural reservoir for helicobacter?
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Humans
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What is the core unit of H pylori transmission?
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The family
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What is the mode of transmission of H. pylori?
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Unknown
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What happens that H. pylori changes from being normal flora, to a pathogen?
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It adheres to the mucosal epithelium below the mucus layer and replicates
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What are the 2 adherence proteins on H. pylori's surface that mediate attachment to the mucosal epithelium?
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-BabA
-LPS |
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What do BabA and LPS bind to?
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Lewis b antigens on gastric epithelium
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What are the theories as to how H pylori elicits pathogenesis?
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-Antigenic mimicry disruption of toleration of the epithelium
-Autoantibody induction |
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Does H pylori invade gastric tissue?
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no
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What important feature of H. pylori allows it to get below the lumen to a higher pH?
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motility
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What is the gold standard diagnostic test for H pylori?
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Urease breath test
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What does Urease catalyze? What is the purpose of the reation?
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Conversion of Urea to ammonia and carbon dioxide - to buffer the immeiate area around the bug
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What are the predominant histological findings in H pylori infection?
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Inflammatory infiltrates with
-PMNs -Lymphocytes -Eosinophils |
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What are the 3 bacterial products of H pylori that cause inflammation?
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-NAP
-VacA -CagA |
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What is NAP?
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Neutrophil activating protein
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What is VacA?
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A cytotoxin that interferes with intracellular vesicle trafficking and vacuole formation - may cause gastric erosion
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What is CagA?
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Cytotoxin associated gene
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What is CagA always associated with?
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VacA
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What is the Cag locus?
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A pathogenicity island that encodes a type 4 secretion pathway
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What is the difference between type 3 and type 4 secretion systems?
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Type 3 = evolved from flagella
Type 4 = evolved from pili |
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What are type 4 secretion pathways specialized for?
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Exporting macromolecular complexes.
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What are type 3 secretion pathways specialized for?
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Passage of threaded, unfolded proteins.
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What are Cag+ strains of H pylori strongly associated with?
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Peptic ulcers and cancer
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What is the structure of Urease like?
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A double ring of six UreA and six UreB
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What does the ammonia produced from urea breakdown do?
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Neutralizes the cytosol and periplasm and makes a layer around the bacterium
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What does the neutralized layer around H pylori in the gut allow the bug to do?
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-Survive the acid
-Swim through mucus -Adhere to the epithelium by its Lewis blood group antigens |
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How big is the Cag pathogenicity island and how many genes does it contain? Where is it located?
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-40 kb
-30 genes -On H pylori's chromosome |
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What do 12 of the genes on the Cag PAI encode?
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The type 4 secretion system - CagA
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What do 14 of the genes on the Cag PAI encode?
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IL-8 transcription induction
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What does IL-8 activate?
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c-fos protooncogene
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What is protooncogene activation by IL-8 involved in?
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Severe gastrc inflammation and ulceration
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What type of H pylori strains cause mild gastritis?
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Cag PAI negative strains
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What type of H pylori strains cause severe gastritis and ulcers?
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Those that are positive for Cag PAI
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What is the result of CagA being injected into host intestinal cells by the type 4 secretion system?
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-Altered cytoskeleton
-Pedestal formation -IL8 release |
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So what are the steps in the model of H. pylori infection? (4)
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1. Secretes urease
2. Swims thru mucus via flagella 3. Adheres to apical epithelium 4. Injects CagA via type IV system, alters actin, forms pedestal, induces IL8 release |
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So CagA is associated with what again?
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VacA
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And what is VacA's mode of operation?
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-Binds receptors on epithelial cell
-Internalized by endocytosis -Multifunctions as a toxin |
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Is VacA endocytosis clathrin mediated?
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no
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What are the toxic effects of VacA on gastric epithelial cells?
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-Vacuolization
-Tight junction alteration -Gastric erosion |
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When is VacA released during H. pylori infection?
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After CagA injection stimulated release of IL8 and all that..
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What happens after VacA release?
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NAP release and tissue damage via ROI's
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What is the end result of all the pathogenesis of H pylori?
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Gastric ulcers
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How is Helicobacter diagnosed macroscopically?
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Via phase contrast of fresh gastric biopsy and gram stain
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What is the gold standard diagnostic test?
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Urea breath testing
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Why are breath tests the gold standard?
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They're the only way to tell if the bacterium has been cured.
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