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