Helicobacter-Pseudomonas-Bordetella-Corynebacterium Flashcards
Helicobacter pylori
gram and shape
gram -
vibrio
Helicobacter pylori virulence factos
urease VacA CagA mucinase flagella superoxide dimutase
Helicobacter pylori metabolize what?
AA not carbs
urease of Helicobacter pylori
converts urea to ammonia and raises the pH to neturalize stomach acid
VacA of Helicobacter pylori
acts on gastric mucosa epithelia and promotes urea flow into stomach
CagA of Helicobacter pylori
protien injected into host cells, cells change, prelude to cancer
mucinase of Helicobacter pylori
degrades the mucus for invasion
flagella of Helicobacter pylori
used for colonization
superoxide dimutase of Helicobacter pylori
prevents phago/ intrcell killing
Gastric ulcer
inital infection response to heliobacter pylori
Initial infection induces a low grade immune response with IgM, followed by IgA and IgG production. This suppresses bacterial growth and leads to the typical low-level persistent infection which remains symptom-free for 80-90% of carriers.
prevention/ treatment of helio pylori infection
proton pump inhibitor and Ab
symptoms of heliobacter pylori infection
Symptoms of stomach and upper duodenum infection:
in most people: no symptoms (symptom-free carrier).
in some: gastritis, peptic and duodenal ulcers, Potential for gastric adenocarcinoma
If ulcers/cancer: stomach pain, tenderness and bleeding.
Pseudomonas aeruginosa gram shape flagella O2 use nutrient req temp range
Gram− short rods polar flagella (one or more; high mobility) obligate aerobe simple nutrient requirements (acetate) broad temperature range: 20 to 43 ºC
notable virulence factors of Pseudomonas aeruginosa
pili flagellum siderophores pyocyanin exotoxin A alginate LPS
pili of Pseudomonas aeruginosa
adherence function
flagellum of Pseudomonas aeruginosa
motility and adherence
siderophores of Pseudomonas aeruginosa
scavenge iron