H pylori resists acidity of gastric content due to -
Urease
Vacuolating cytotoxin
Secretion of alkaline contents
Cagpai
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).
Bacteria