Micro 22

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Micro 22

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H Pylori

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morphology of H pylori

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gram negative, helical shaped microbe

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how is H pylori encountered

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acquired through fecal-oral or oral-oral routes

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primary survival mechanism of H pylori in acidic stomach

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urease production

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toxin associated ith H pylori that supresses T cell responses

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VacA

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can cause cell death of gastric epithelium

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VacA

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can disrupt tight junctions between cells

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CagA

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most colonized pt present this way

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asymptomatic chronic gastritis and low level inflammation

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10% of H pylori develop this

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duodenal ulcers

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risk factor for gastric adenocarcinoma

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atrophic gatritis

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triple therapy

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two antibiotics and proton pump inhibitor

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diagnosis methods for H pylori

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rapid urease test, histology, microbial culture on biopsy

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vaccination for H pylori

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there isnt one yet

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spectrum of GI diseases linked to H pylori

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gastric/duodenal ulceration, gastric adenocarcinoma, MALT lymphoma, NHL of stomach

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H pylori inhabits the human stomach for ________

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decades

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inflammatory response to H pylori

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low grade

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describe the progression of normal gastric mucosa to gastric adenocarcinoma due to H pylori (hint: figure 22-2)

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normal mucosa; h pylori colonization ; weeks later superficial gastritis ; years later chronic gastritis ; atrophic gastritis ; intestinal metaplasia; dysplasia ; gastric adenocarcinoma

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H pylori is present in ___________% of world pop

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50%

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risk factors for H pylori infection

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low SES, overcrowding, ethnicity, endemic infection rates in nation of origin, developing countries

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reduces risk of gastric AdenoCA

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eradication of H pylori infection

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to reduce risk the H pylori need be eradicated before development of

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premalignant lesions (intestinal metaplasia)

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urease

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allows H pylori to survive in acidic environment of stomach

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rxn of urease

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urea to ammonia and CO2 (ammonia neutralizes acid)

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how does H pylori overcome gastric peristalsis

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efficient motility (polar flagella) as well as chemotaxis and adherence to gastric epithelium

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percent of H pylori that adhere to epithelium vs free floating

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20% adhere

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polar flagella allow H pylori to do what

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move through gastric mucus layer efficiently

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BabA

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blood group antigen binding adhesin ; binds to Lewis blood group antigens present on gastric mucosal surface

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SabA

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sialic acid binding adhesin ; binds to lewis X antigens present on gastric mucosal surface

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expression of BabA and SabA on H pylori is associated with

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increased gastric cancer risk

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H pylori flagella/LPS have this advantage

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they are less immunogenic than those of other bacteria

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immune defenses of H pylori

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undergoes phase variation and expresses human lewis antigens on its LPS

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VacA (vacuolating cytotoxin A ) can modulate host immune resoinse by

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directly supressing T lymphocyte responses

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inflammatory response to H pylori resulting in loss of epithelal glands

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atrophic gastritis

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atrophic gastritis is a risk factor for

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gastric adenoCA and MALT lymphoma

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virulence factors associated with peptic ulceration and carcinogenesis

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cagA

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genomic location of cagA

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cag pathogenicity island

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cagA is a ______________ toxin

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type 4 secretion system

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what does cagA do after it is introduced to host epithelial cells

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activates host signaling pathways leading to disruption of tight and adherens junctions

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cagA is presint in _______% of duodenal ulcer pt

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90%

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inflammation is higher in strains with cagA , this is displayed by the presense of this potent inflammatory cytokine

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IL8

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VacA induces this in epithelial cells, cagA presense does what to this

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vacA induces apoptosis, cagA inhibits that apoptosis

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additional effects of vacA

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acts as a pore that allows H pylori to become permeable to urea, increases permeabiltiy to key nutrients

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effect of H pylori on endocrine activity in stomach

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downregulate D cells (somatostatin) leading to increased gastrin and increased gastric acid secretion

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what contributes to ulceration specifically in duodenum

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metaplasia to gastric epithelium which results in increased acid production

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basis of progression to carcinoma due to h pylori

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h pylori increases proliferation, decreases apoptosis, resulting in long term exposure of injured cell to inflammatory mediators

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mutation that increases risk of atrophic gastritis

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polymorphism that increases expression of IL-1 and TNF alpha

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role of gastrin in H pylori infection

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hypergastrinemia occurs early, stimulates epithelial cell proliferation and preceeds atrophic gastritis

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inexpensive and sensitive stain for H pylori

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geisma stain

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steiner and warthin starry stain

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sensitive and expensive stains for H pylori

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assays for this can confirm H pylori

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urease, catalase, oxidase

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noninvasive test of choice for h pylori

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urea breath test and stool antigen tests

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serologic test for H pylori

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IgG ELISA

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how does urea breath test work

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radiolabeled urea ingested, if metabolized by H pylori to ammonia the radioactive CO2 will be detected in breath samples

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HpSA

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H pylori stool antigen, test is both sensitive and specific

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stool antigen is no longer present how long after infection clears

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5 days

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limitations of H pylori treatment, what does this mean for when we should diagnose/treat

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rapid developing resistance, reduced efficacy and noncompliance are making treatment less effective, as such we should only test and treat those with present/past hx of PUD, MALT lymphoma, or nonulcer dyspepsia

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definition of sucessful eradication of H pylori

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negative test 4 or more weeks post therapy

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antibiotics of choice for H pylori

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clarithromycin and amoxicillin or metronidazole

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why is it preferable to use amoxicillin instead of metronidazole in first line tx

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2nd line tx involve metronidazole

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quadruple therapy

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PPI, bismuth subsalicylate, metronidazole, tetracycline 14 days

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sequential therapy

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10 days: first 5 are amoxicillin BID, then for 5 more daus use triple therapy of PPI clathriomycin and metronidazole BID