Infectious Endocarditis - Kristich Flashcards Preview

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Flashcards in Infectious Endocarditis - Kristich Deck (14):

Name (4) common bacteria seen in infectious endocarditis, and where they generally come from. How do these gain access to the endocardium?

  • S. aureus - anterior nares
  • Coagulase-negative staphylococci (ex: S. epidermidis) - skin
  • viridians streptococci (ex: S. sanguinis, S. mutans, S. mitis) - oral cavity
  • enterococci (ex: E. faecalis, E. faecium) - GI tract

all gain access to the endocardium via transient bacteremia



  1. dextran
  2. adhesins
  3. fibrinogen-binding adhesins

  1. exopolysaccharide used for adhesion by viridians streptococci
  2. mediates attachment to platelets and fibrin - used by viridians streptococci
  3. used as an adhesion agent by S. aureus


Describe a 'vegetation'

What implications does this have for Abx therapy?

  • heterogenous matrix of bacteria, platelets, fibrin, and other matrix ligans
  • provides protection from immune cells
  • high-density packing of bacteria -> therefore slow growth

Antibiotic therapy requires:

  • bactericidal activity
  • long-term parenteral administration (sustained activity)


Name the likely organism genus: Gram-positive, cocci, clustered



Name the likely organism genus: Gram-positive, cocci, chains



Name the general mechanism of each:

  1. ceftriaxone
  2. gentamicin
  3. daptomycin
  4. penicillin
  5. nafcillin
  6. cefazolin
  7. rifampin
  8. vancomycin

  1. cell wall agent
  2. protein synthesis inhibitor
  3. cell wall agent
  4. cell wall agent
  5. cell wall agent
  6. cell wall agent
  7. RNA synthesis inhibitor
  8. cell wall agent


Name the key side-effect of beta-lactam antibiotics



Name the key resistance mechanism bacteria use against beta-lactams

PBP mutations/alterations to prevent the binding of beta-lactam antibiotics


Mechanism of action: vancomycin

binds D-Ala-D-Ala of the peptide side chain of peptidoglycan precursors, blocking PBP cross-linking action


Why is vancomycin so ineffective on Gram-negative bacteria?

What is the key resistance mechanism?

The Gram-negative outer membrane acts as a permeability barrier against the large vancomycin molecule

Resistance: modification of the peptidoglycan precursor target -> change D-Ala-D-Ala to D-Ala-D-Lac


Mechanism of action: Daptomycin

When is this drug used?

bind and disrupt the cytoplasmic membrane, creating a distruption of cell membrane potential -> cause cell death

Use: highly resistant bacteria. Its novel mechanism helps retain activity against bacteria resistant to other Abx mechanisms


Mechanism of action: Rifampin

Describe a mechanism of resistance

binds and inhibits RNA polymerase to prevent gene expression

resistance: point mutations in RNAP


Mechanism of action: Gentamicin

Name the mechanism of resistance

irreversibly bind 30S subunit, causing misreading and premature release of ribosome from RNA

resistance: enzymatic modification of the drug to prevent ribosome binding


Is gentamicin good for monotherapy against G+ organisms?

What are some major adverse effects?

No. Use synergistically with a cell-wall-active agent to enhance penetration of gentamicin into the target cell

AE: ototoxic and nephrotoxic