Helicobacter pylori

Question 1

Helicobacter pylori

Morphology

Answer 1

Gr- rods, non-spore forming, spiral/curved/ridged
Highly motile

Question 2

Helicobacter pylori

Antigenic structure

Answer 2

Highly motile
LOS - O, Capsular polysaccharide - K & flagella - H

Question 3

Helicobacter pylori

Transmission

Answer 3

human-human, fecal-oral & saliva

Question 4

Helicobacter pylori

Pathogenicity

Answer 4

Urease (urea –> CO2, H2O & NH3), NH3 –> neutralize gastric acid –> corkscrew motion –> dig into gastric mucosa with pH 5-7 = optimal for growth –> colonialization of gastric epithelial cells –> inflammation.
Digging is done by:
- mucinase
- phospholipase
- neutrophil-activting lipoprotein A
- Cytotoxin-associated gene A (CagA): interferes with ep. cells cytoskeletal structures (cytotoxic) –> IL-8 production = chemoatttractant –> neutrophil attraction –> pro-inflammatory
- Vacuolating cytotoxin A (VacA): damages ep. cells by creating vacuoles inside & induce IL-8 production –> acute inflammation mediation
- Urease: a chemoattractant & activator of host phagycytic & inflammatory cells –> inflammation of stomach lining

Question 5

Helicobacter pylori

Symptoms (acute, chronic, ulcer, cancer)

Answer 5

Acute gastritis: feeling full, nausea, vomiting & heartburn (CagA)
Chronic gastritis: similar to above but less acute, some develop: gastric or duodenal peptic ulcers
Ulcer: due to gastric acid, from the enterocytes being exposed due to H. pylori (CagA)
Gastric cancer: from chronic gastritis festering (CagA)

Question 6

Helicobacter pylori

Complications/prophylaxis/ treatment

Answer 6

Complication: MALT lymphoma (infiltrated lympoid tissue)
Prophylaxis: non-specific (avoid sharing water bottles - saliva)
treatment: antibiotics and proton pump inhibitor (if symptomatic)