H pylori resists acidity of gastric content due to -
Ans. is 'a' i.e., Urease * H. pylori produces an exceptionally powerful urease, almost 100 times more active than that of proteus vulgaris, which is vital to its survival in the stomach.* Urease acts on urea to generate ammonia, which neutralizes acid around bacteria.Virulence and pathogenesis* Most H. Pylori colonized persons do not develop clinical sequelae. H. pylori is noninvasive, living in gastric mucus. Gastric antrum is the most common site of colonization.* H Pylori colonises stomach of half of human population in world: 30% in developed countries, and > 80% in developing countries (more prevalent in developing countries).* Following virulence factors have been identified1) Vacuolating cytotoxin (Vac A): It is associated with peptic ulcer.2) Cag Pal (cytotoxic associated gene or Cagpathogenicity island) : It encodes Cag A which is associated with peptic ulcer and gastric adenocarcinoma.3) Bab A: It is an adhesin and associated with increased gastric inflammation.4) Urease: H pylori splits urea rapidly to produce ammonia to survive.* Colonization of gastric antrum leads to depletion of somatostatin producing 'D' cells. This results in loss of inhibition of gastrin release and hypergastrinemia (normally somatostatin inhibits gastrin secretion).
Urease
Vacuolating cytotoxin
Secretion of alkaline contents
Cagpai
Bacteria