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37 Cards in this Set

  • Front
  • Back
How do bacteria resist Tetracycline?
With antibiotic efflux pumps
How do bacteria resist Vancomycin?
By modifying the target of Vancomycin
How do bacteria resist Aminoglycosides?
By modifying the structure of the antibiotic
How do bacteria resist B-lactams?
By destroying the b-lactam ring with b-lactamase
How many classes of B-lactam Antibiotics are there, and what are their names?
Which 2 classes are almost identical?
Penicillin and Cephalosporin
How many stages are in PG biosynthesis? Where does each occur?
What occurs in the cytoplasm stage?
Assembly of PG units - UDP-NAG converts to UDP-NAM, Peptide added, then dALA-dALA
What happens in the membrane phase?
Shuffling of the PG units from UDP to Bactoprenol, then adding of a NAG
What happens in the Periplasm stage?
Crosslinking of the PG to form stable polymers.
What are the cephalosporins produced by?
The fungus cephalosporium
What is the use of Cephalosporins having a little bit different of a structure?
They can be used as an alternative for patients that are allergic to the penicillins.
What can happen to 5% of patients allergic to Penicillin?
Cross-reactivity to Cephalosporin too
What are the 3 sites for modification of Cephalosporins?
1. B-lactamase for inactivation
2. Amidase for changing R group and synthetic derivatives
3. Esterase site
What are the 2 effects of changing the R group?
-Can change the activity of the drug to be against GP's vs GN's
-Can prevent B-lactamase inactivation for resistance
What is the effect of modifying Cephalosporins at the Esterase site?
It changes the half life of the drug in vivo.
What is the goal of constantly changing the R groups at the amidase and esterase sites?
To always stay one step ahead of the microbes that develop resistance.
What is the target of action of the b-Lactam ring of Cephalosporin?
What happens when the B-lactam of cephalosporin binds the PBPs?
It prevents them from being able to cleave the 5th d-ALA, and crosslink adjacent peptides.
Where on the growth curve do the Cephalosporins work?
Only during the logarithmic growth phase.
What is the Nonspecific mechanism of resistance to b-lactam antibiotics?
Mutations in outer membrane porin proteins to decrease permeability to the drug
What is a more specific mechanism of resistance to b-lactam antibiotics?
Mutations in PBPs - change the carboxypeptidase and transpeptidase so that the drugs won't inactivate them.
What bug is especially associated with mutations in PBPs?
Streptococcus pneumoniae
What is the most important mechanism for resistance to B-lactam antibiotics?
Acquisition of new DNA by conjugation plasmid transfer that encodes for altered Beta lactamases.
What is a Competitive Cell Wall Synthesis inhibitor?
How does Cycloserine appear?
Similar to D-alanine
What step in peptidoglycan synthesis does Cycloserine inhibit?
The formation of D-ala from L-ala (racemase) and the synthesis of D-alyl-D-Alanine (synthetase)
How does Cycloserine inhibit the Alanine racemase and D-alyl-D-alanine synthetase?
It has higher affinity for the enzymes than D-ala, the natural substrate.
What is the structure of Vancomycin like? What type of antimicrobial is it?
-A complex saccharide-peptide
What is the mechanism of action of Vancomycin?
It complexes with D-ala-D-ala on the peptide of the peptidoglycan waiting to be crosslinked.
At what step in PG synthesis does Vancomycin work?
Just before carboxypeptidase has a chance to cleave the 5th aa d-Ala.
What organisms is Vancomycin mostly effective against?
Gram positives
When is Vancomycin use reserved for?
Situations of
-Penicillin resistance or -Cephalosporin hypersensitivity
Against what specific bug is Vancomycin used to treat infections?
What is the mechanism of Bacitracin?
Prevention of the recycling of Bactoprenol in the membrane phase of PG synthesis.
So what are the antimicrobials that are Cell Wall Inhibitors?
So what are the 3 clinically useful highlights of the cell wall inhibitors?
1. Highly selective for proks
2. Low in host toxicity
3. Active in the log growth phase