micro test3 5th

  1. What are basic characteristics of Pseudomonas aeruginosa?
    • Gram negative bacillus in singles
    • Thick slime layer with capsules
    • Oxidase positive – does not ferment but can respire anaerobically using nitrates
    • Fruity odor
    • Pigments common
    • Single flagellum, sometimes two
    • Type IV pili for adherance
  2. Explain the pili found in Pseudomonas aeruginosa, Gonnococcus, and Vibrio
    • Type IV pili with N-methyl-phenylalanine
    • Binds to asialo-GM1 and triggers IL-8 production
    • (neuraminidase converts regular GM1 into asialo-GM1 for better bacterial binding)
  3. What do the pigments in pseudomonas aeruginosa mean?
    • Green-yellow = fluorescein (chelates iron)
    • Blue = pyocyanin (convert O2 to O2-)
    • Red and black are also possible, but we didn’t learn what they meant
  4. When pseudomonas is put on TSI agar what properties are seen?
    • No growth in butt (not anaerobic)
    • Red slant (more basic due to use of amino acids
  5. Pneumococcus and Pseudomonas have a virulence factor called Neuraminidase, what does it do?
    Makes more receptor sites for pili to bind to (converts GM1 to asialo-GM1)
  6. What is the difference in toxic exoprotein regulation between Staph aureus and pseudomonas aeruginosa?
    • Staph aureus relies on the buildup of octapeptide to switch to making exoprotein
    • Pseudomonas aeruginosa relies on the buildup of homoserine lactone
    • Both bind early and poison late in growth
  7. How does exotoxin A function? (Produced by Pseudomonas aeruginosa)
    • Enters cell and is activated by furin (cleaved into two pieces)
    • Enzymatically ribosylates EF2 – this inhibits protein synthesis causing cell death (swaps EF2 for NAD)
    • Low iron content favors toxin A production by Pseudomonas aeruginosa
  8. What is the difference between a strain of Pseudomonas aeruginosa producing Exo S vs Exo U?
    • Exotoxin S: invasive strain – intracellular growth then apoptosis (also T and Y)
    • Exotoxin U: cytotoxic strain – cell lysis (also T)
  9. What do the four toxins produced by pseudomonas do? (S, T, U, Y)
    • S: GTPase that causes cytoskeletal disruptions (reduced phagocytosis) plus ribosylation decreasing DNA replication and apoptosis
    • T: GTPase causes cytoskeletal disruptions (reduced phagocytosis) plus ribosylation causing less cell adhesion
    • U: Phospholipase that quickly kills cells (found in cytotoxic strains only)
    • Y: adenyl cyclase activity that disrupts actin (reduced phagocytosis) – Favors toxin production
  10. Explain how Pseudomonas aeruginosa regulates virulence factor production
    • cAMP -> vfr -> las R -> las I -> homoserine lactone -> expression of virulence factors (also -> las R again)
    • Exo Y starts process by increasing cAMP
    • Low levels of Pseudomonas have low levels of exoprotein; high levels have high so it is similar to the ACR of staph
  11. What are furanones?
    • Compounds that inhibit las R of pseudomonas
    • Not yet used for drugs but possible
    • Found by Australian divers
    • ** cAMP -> vfr -> las R -> las I -> homoserine lactone -> expression of virulence factors
  12. What drugs can be used to treat pseudomonas?
    • Pseudomonas is very resistant to many drugs, the following may work
    • Carbenicillin
    • Beta-Lactam + Aminoglycoside (eg. Ticarcillin + tobramycin)
    • Fluoroquinolones (Cipro)
  13. What percent of pseudomonas infections that spread to blood are lethal?
  14. What are the leading outpatient and hospitalized patient infections associate with pseudomonas?
    • Outpatient:
    • #1 otitis externa (swimmers ear)
    • Keratitis (contact lens)
    • Folliculitis (hot tub infection)
    • Wound/burn/nail
    • CNS
    • Osteomyelitis
    • Endocarditis
    • Inpatient:
    • #1 Burn infections
    • #1 lower respiratory tract infection
    • #3 UTI
    • Wound infection
  15. What is the leading cause of burn infection?
    Pseudomonas aeruginosa
  16. What is the leading cause of Pneumonia?
    Pseudomonas aeruginosa
  17. Why is Pseudomonas nearly impossible to remove in cystic fibrosis patients?
    • The high salt environment induces mutation that produces copious amounts of mucoid Alginate by removing the inhibition of the repression pathway that builds sugars of alginate
    • This biofilm is very protective
  18. What are the basics of Burkholderia pseudomallei?
    • Gram negative rod
    • Transmitted by dust from Southeast Asia or Australia
    • Skin/soft tissue abcesses
    • Treat like pseudomonas (beta lactam + aminoglycoside or Cipro)
  19. What are the basics of Burkholderia cepacia?
    • Gram negative rod
    • Nosocomial in immunocompromised or CF patients
    • Bacteremia/septicemia
    • Treat like pseudomonas (beta lactam + aminoglycoside or Cipro)
  20. What are the basics of Stenotrophomonas maltophilia?
    • Gram negative rod
    • Protects other bacteria by secreting broad spectrum Bla
    • Often on lines or catheters
    • Treat with Timentin or sulfa-trimethoprim
Card Set
micro test3 5th
micro test3 5th