Helicobacter pylori Flashcards
When was H.pylori discovered?
Back in 1984 at Royal perth hospital where Dr.Robin and Barry isolated a spiral shaped bacteria from gastric biopsies in patients suffering from gastritis
- Helicobacter pylori stands for
- Helico = helical/spiral structure
- Bacter = bacteria
- Pylori = found in the pylorus of the stomach
What is the epidempiology of h.pylori?
- H.pylori colonizes the gastric mucosa of more than half of the worldwide population and it is the cause of (100% gastritis, 90% of duodenal ulcer, 80% of gastric ulcers, and 70% of gastric cancer)
- In developing countries the prevalence of H.pylori infection is 80% compared to 20-50% in industrialized countries
How is H.pylori transmitted?
- Oral ingestion of the bacterium (contaminated food and not water)
What are the diseases that H.pylori can protect us from?
1) Acid reflux disease
2) Barrett’s esophagus
3) Esophageal cancer
What is the antibody tested to screen if someone has H.pylori?
Using the ELISA technique, IgG is the antibody tested
What are the risk factors for acquiring H.pylori?
1) Infected family member
2) Crowded living conditions
3) Poor hygiene
4) Number of sibling (>2)
5) Poor sanitation
6) Fecal contamination of water supply
7) Health care professionals
What are the characteristic of Helicobacter pylori (v.imp)?
1) Gram-negative
2) Rod curved/spiral in shape (but can appear cocci in culture)
3) Very motile (has a flagella)
4) Microaerophilic (this means that it is a microorganism that requires environments containing lower levels of dioxygen than that are present in the atmosphere for optimal growth)
5) Grows at body temp (37)
What are the virulence factors of H.pylori?
1) Highly motile (corkscrew motility)
- Allows it to move rapidly through the mucus layer and towards a neutral pH (moving from the mucosa to the submucosa to create an alkaline environment)
2) Produces urease a lot (urease can breakdown urea into ammonia and CO2, and ammonia can neutralize the acidic environment of the stomach) in addition to the fact that localized tissue damage is caused by the by-products of urease
3) Outer proteins enables it to adhere to host cells
4) Lipopolysaccharides, which enables it to adhere to the host cell inflammation
5) Exotoxins (vacuolating toxins “vacA” which can induce gastric mucosal injury by producing vacuoles)
6) Secretory enzymes (mucinase, protease and lipase, which can induce gastric mucosal injury)
7) Type 5 secretion system which is a pill like structure that can inject effector like (cagA, which induces IL-8 production, apoptosis inhibition “leads to cancer”, and thus the thigh junctions gets loosen)
What are the main viruelnce factorws of H.pylori?
1) Highly motile
2) Production of urease
3) Injecting effector (like cagA, via the type 4 secretion system
Explain the pathogenesis of H.pylori
1) Attracted by the chemotactic substances (hemin and urea) the H.pylori can penetrate the mucus layer lining the stomach epithelium
2) H.pylori will then recruit active inflammatory cells and it also releases UREASE which cleaves urea producing NH3 which neutralizes the stomach acid
3) H.pylori cytotoxin, and the ammonia produced by its urease causes the destruction of the mucus producing cells exposing the underlying connective tissue to the stomach acid
How can H.pylori lead to cancer?
Due to cagA which inhibits apoptosis
Explain the pathogenesis of gastric cancer
1) Normal mucosa
- Then comes the H.pylori and turns it into
2) Chronic active gastritis/asymptomatic
- The comes the immune response, diet, gastrin, host genetics and makes it turn into
3) Gastric atrophy
- Then comes the carcinogens and achlorhydria and turns it into
4) Intestinal metaplasia
5) Dysplasia
6) Gastric cancer
What are the clinical outcomes of H.pylori infection?
1) >80% is asymptomatic or chronic gastritis
2) Chronic atrophic gastritis, intestinal metaplasia, gastric or duodenal ulcers in 15-20%
3) Gastric cancer, MALT lymphoma in less than 1%
What are the clinical manifestations/symptoms of H.pylori?
1) Bloating
2) Nausea
3) Passing gas
4) Bleching (burp)
5) Bad breath
6) Burning
7) Vomiting
8) Loss of appetite
9) Gnawing pain
What are the ways to diagnose H.pylori?
1) Invasive tests
- Histology is the gold standard
2) Non-invasive tests
What are the invasive tests to diagnose H.pylori?
1) Histology (the gold standard)
2) Blood culture (as a confirmatory test)
3) Rapid urease test (increased pH is detected after placing a biopsy in a cassette changing the color from yellow to red due to the increased pH from ammonia)
4) Molecular (for research)
What are the non-invasive tests to diagnose H.pylori?
1) Serology test (to detect the antibodies)
2) Urea breath test
3) Stool antigen test (best one for the non-invasive category “can be done multiple times and for follow-ups to test drug effectiveness”)
What is the gold standard test to detect H.pylori?
Histology testing
Describe the urea breath test
- Patient must come with an overnight fast
1) A liquid containing C13 (non-radioactive) or C14 (radioactive) is taken as a capsule
2) After 10-20 minutes the subject breaths into a balloon
3) The balloon air is the analyzed in a centralized fascility using scintillation chamber in case of C14, or a Mass-spectrometer in case of C13
4) CO2 production is detected, incase the bacteria is present
- The use of antibiotic or PPI before this test can lead to a false-negative result
How to treat H.pylori?
- The goal of therapy is to eradicate the organism
- Triple, quadruple, and sequential therapy are there combining antibiotics with PPI
