ANSWERS WITH COMPLETE SOLUTIONS VERIFIED
selective toxicity
A drug that kills harmful microbes without damaging the host
bacterial protein synthesis inhibitors
-initiation: aminoglycosides, oxazolidinones
-elongation: tetracyclines, macrolides, clindamycin, chloramphenicol
bacterial protein synthesis
mRNA binds 30s
Formylmethionyl tRNA and 50s added to form initiation complex
Aminoacyl tRNA adds to ribosome
Forms peptide bond
Translocation, chain extension, and release of completed protein
Enzymes required for all steps
resistance and ribosomal binding sites
-aminoglycosides bind to 30s ribosomal subunit
-oxazolidinones bind to site present in 50s ribosome
, -tetracyclines bind to unique site on 30s ribosome
-clindamycin and macrolides bind to transpeptidase region on 50s
T/F: aminoglycosides are the only bactericidal drugs; the rest are bacteriostatic
True
aminoglycosides
-Gentamicin
-bactericidal
-inhibits protein synthesis in 3 different ways:
-blocks initiation of protein synthesis
-blocks further translation and elicits premature termination
-incorporation of incorrect amino acid
Gentamicin
-aminoglycoside
-extended spectrum = gram + and gram - but ONLY aerobes
-NOT active against anaerobes = don't readily get inside unless there is a transporter and this transporter
is only found in organisms that are growing aerobically
-used to treat serious aerobic gram-negative infections
-NOT absorbed orally, must be given by IV (polycationic)
-synergistic in combination with cell wall drugs (i.e. beta-lactams or vancomycin)
-resistance in gram - aerobes is usually due to expression of drug modifying enzymes
-post-antibiotic effect = even after drugs levels in the body are reduced to below the minimum inhibitory
concentration, it can still inhibit the growth of microbes