MMI 301: Lecture 19: Campylobacter and Helicobacter

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  1. Campylobacter and Helicobacter first recognized as human pathogens when?
  2. Campy/Helico share what?
    • Gram -
    • Spiral shape
    • Low Guanosine/cytosine content
    • Inability to ferment/oxidize carbohydrates
    • microaerophilic growth
  3. Campylobacter responsible for gastroenteridis
    • C. jejuni and C. coli
    • Jejuni is most common cause in US
    • Coli bigger in africa and asia
  4. Campylobacter responsible for bacteremia, meningitis and septic abortions
    C. fetus
  5. Campylobacter morphology
    • Gram -
    • Curved rods
    • Motile: Polar flagella
    • Often come end to end for Seagull look
    • Thin, hard to visualize, can make it through .45 micro filter, but not .2
  6. Growing Campylobacter in lab
    • Need microaerophillic conditions (low oxygen)
    • Nutritionally fastidious
    • Grow best at 42 degrees C
  7. Campylobacter are one of few organisms that use the flagella for:
    • Virulence, non-flagellated mutants much less virulent
    • Flagellas under go phase and antigenic variation
  8. Campylobacter pathogenesis
    • Destroy mucosal surfaces of lower small intestine/colon
    • Result in diarrhrea from LACK OF ABSORPTION as opposed to excess secretion like most
    • Stools also contain leukocytes and blood
    • Invade sub-epithelial layer
  9. C. jejuni surface structures
    • Many polysaccharides
    • Highly variable capsule (many serotypes)
    • Important for virulence, epithelial cell adherence and cell invasion
    • Lipooligosaccharide (LOS) structures
    •    -serum resistence, adherence and invasion
    •    -mimic neuronal gangliosides
    •           -Guillain-Barre syndrome
    • Flagellum needed for colonization
    •       -secretion
  10. Camplyobacter Reservoirs
    • Considered normal biota for many animals
    • Dogs may be source
    • Poultry products
    • Infective dose is relatively low
  11. Gulliain-Barre syndrome
    • Sequelae of bacterial and viral infections
    • Results in myelin sheath attack in peripheral nerves
    • Paralysis
    • Associate with Campylobacter infection
    • Some antigen resembles nerve tissue
  12. Heliobacter pylori history
    • Discovered to be pathogen 30 years ago
    • Thought to be species of Campylobacter
    • Genetic analysis made it its own species
    • Reservoir for organism is not animals
  13. Pathogenicity of Heliobacter pylori discovery
    • Barry Marshall and Robin Warren
    • Were not beleived, Marshall drank culture
    • Got sick
    • Studied use of antibiotics to treat ulcers
  14. Heliobacter pylori morphology
    • Gram - (hard to visualize by light microscopy)
    • Have unusual membrane covering sheathed flagella which make them highly motile
  15. Culturing Heliobacter pylori
    Needs enriched media, microaerophilic, grows best at 37 degrees C, needs 4-7 days to grow
  16. Heliobacter pylori detection
    Giemsa staining of infected tissue
  17. Most common cause of gastritis is:
    • Heliobacter pylori
    • Originally though to be stress, chemical irritation, bile reflux, ischemia
  18. Heliobacter pylori virulence factor
    • Urease production
    •   -Key diagnostic feature
    • Creation of ammonia from urea breakdown neutralizes and protects from stomach acid.
    • High amounts of CO2 and Ammonia can be dangerous to cells
    • H. pylori is most active urease known among bacteria
  19. Type IV secretion of CagA
    • H. pylori strains with increased pathogenicity 
    • cag pathogenicity island
    •     -Encodes Type IV Secretion System,
    •     -CagA and other proteins
    • CagA is inserted into host cell and causes dramatic morphological changes by phosphorylating tyrosine residue of SRC-kinase family
    •      -Actin rearrangement: hummingbird
  20. T4SS are used for:
    • Secreting DNA or Protein
    • H. pylori uses one T4SS for CagA and one for natural transformation
  21. VacA
    • H. pylori virulence factor
    • Vacuolating cytotoxin
    • Causes production of large vacuoles through host cell cytoplasm
    • Cell damage
    • 1. enter stomach cell, make vacuoles
    • 2. Localization to mitochondria, release cytochrome c
    • 3. get into T cells, proinflammatory
  22. H. pylori virulence factors
    Flagella, Urease, Lipopolysaccharides, Outer proteins, Exotoxins, Secretory enzymes, Type IV secretion system, effectors (cagA)
  23. Molecular mimicry of H. pylori
    LPS antigens are same as human blood
  24. H. pylori used to do what?
    Map human migration
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MMI 301: Lecture 19: Campylobacter and Helicobacter
2013-11-22 20:42:00
MMI 301

MMI 301
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