Infectious Endocarditis - Kristich Flashcards
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
define:
- dextran
- adhesins
- fibrinogen-binding adhesins
- exopolysaccharide used for adhesion by viridians streptococci
- mediates attachment to platelets and fibrin - used by viridians streptococci
- 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
Staphylococcus
Name the likely organism genus: Gram-positive, cocci, chains
Streptococcus
Name the general mechanism of each:
- ceftriaxone
- gentamicin
- daptomycin
- penicillin
- nafcillin
- cefazolin
- rifampin
- vancomycin
- cell wall agent
- protein synthesis inhibitor
- cell wall agent
- cell wall agent
- cell wall agent
- cell wall agent
- RNA synthesis inhibitor
- cell wall agent
Name the key side-effect of beta-lactam antibiotics
hypersensitivity
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
