Flashcards in Clinical Uses of Antibiotics & Resistance Deck (100)
other 3rd gen cephs do, but ceftriaxone does not.
Why are we reluctant to use Aminoglycosides?
Do aminoglycosides work on pseudomonas?
What are the 4 big considerations for empirical therapy?
1. Infectious syndrome (site)
2. Pathogens that cause this syndrome?
3. Antibiotic resistance of the possible bugs?
4. Most appropriate AntiB to use...?
Why are E. Coli more likely to undergo R-factor plasmid transfer via conjugation than Pseudomonas?
Both are Gram ? C or R?
E. Coli are enteric so they hang out and conjugate with one another. Pseudomonas are non-enteric, less likely to conjugate.
Both are GNR
What are the Bactericidal Drugs (by class) drugs and the exceptions.
1. Cell Wall Synth. Inhibitors
PCN, Ceph, Vanc.
2. Aminoglycoside (protein synth. inhib, exception)
3. DNA gyrase fn. inhibitors
What are the Bacteriostatic (by class) durgs and what are the exceptions?
Protein Synthesis Inhibitors are bacteriostatic
...with the exception of aminoglycosides which are bacteriocidal.
Aminoglycosides don't work well at _______ pH.
Breakpoints for whether an antimicrobial will be effective against a given bug...
1. Susceptible - likely to get a response
2. Intermediate - intermediate or uncertain response. Higher dose may work.
3. Resistant - probably no response.
The labratory-defined in vitro susceptibility testing breakpoints do not take into account ...
1. infection site (penetrate?)
2. # of bugs (abscess needs to be drained first)
3. host conditions (pH at infection site)
4. patients host defenses (immuno-compromised?)
The minimum requirement for considering a bug to be resistant to an anti-bug...
Cp > MIC
maximal serum concentration should be greater than the minimum inhibitory concentration
Why is E. Coli resistant to penicillin?
What sort of resistance is this?
What drug (in the same class) is effective on E. coli and why?
PCN can't get thru the PORINS in the outer membrane of E. coli (gram neg).
Ampicillin is able (more hydrophobic side chain) to enter thru the porin to reach the PBP and inhibit c.w. synth.
Why is Mycoplasma resistant to beta lactams?
No cell wall --> no effect from the c.w. synth inhibitors.
Why is pseudomonas resistant to multiple agents?
3 types of resistance
Give 4 _tolerance_ resistance mechanisms
Metabolic bypass (sulfonamides example)
3 acquired resistance mechanisms
1. Inactivate or modify the drug
2. Alter the antibacterial target
3. Prevent the drug & target from meeting (efflux)
Pseudomonas resistance mechanism(s) to Fluoroquinolones
2. Altered bacterial target site
Pseudomonas resistance mechanism(s) to beta lactams?
MRSA resistance mechanism(s) to beta lactams?
1. Altered bacterial site (alter PBP)
2. Enzymatic degradation (beta lactamase)
Streptococci resistance mechanism to sulfonamides?
Bypass pathway (metabolic)
Porin channels exist on which bugs?
gram negative only
Role of porin channels in gram negative bacteria?
Selective uptake of nutrients etc.
Conduit for hydrophillic antiB's to get inside cells
How can porins contribute to antiB resistance
Can be intrinsic: prevent antiB entry
Can be acquired...alter structure or # or porins
Efflux pumps exist on which bugs?
Gram (+) and Gram (-)
What is the normal function of efflux pumps?
get rid of substrates from bacterial cytoplasm
efflux pumps are plasmid or chromosomally encoded?
how do efflux pumps contribute to antiB resistance?
can pump antiB out of cell preventing drug from reaching target
are efflux pumps drug specific or multi-drug?
can be both.
pseudomonas - multi drug resistance via efflux pumps