ability of drug to kill or inhibit pathogen while damaging host as little as possible
therapeuticdose
drug level required for clinical treatment
toxicdose
drug level at which drug becomes too toxic for patient, produces side effects
therapeuticindex
ration of toxic does to therapeutic dose
narrow-spectrumdrugs
attack only a few different pathogens
broad-spectrumdrugs
attack many different pathogens
minimal inhibitory concentration
lowest concentration of drug that inhibits growth of pathogen
minimal lethal concentration
lowest concentration of drug that kills pathogen
dilutionsusceptibilitytests
inoculating media containing different concentrations of drug to test for MIC and MLC
e test
similar to disc diffusion but with strips that contain a gradient of an antibiotic, for use with anaerobic pathogens
penicillins
inhibit cell wall synthesis by blocking the enzyme that catalyzes the links in peptidoglycan leading to lysis of cell; acts only on growing bacteria, can also bind to PBPs, activate autolysins, or stimulate holins to form holes in the membrane
cephalosporins
broad-spectrum drugs that can be used when a patient is allergic to penicillin
vancomycin and teicoplanin
glycopeptide drugs that inhibit cell wall synthesis, important for treatment in MRSA/E infections
aminoglycosides
inhibit protein synthesis by binding to 30S ribosomal subunit and cause the misreading of the mRNA
tetracyclines
broad-spectrum and bacteriostatic drugs that inhibit protein synthesis by binding to the 30S ribosomal subunit and stops bind of aminoacul-tRNA molecules to the A site of the ribosome
macrolides (erythromycin, clindamycin, zithromax)
broad-spectrum bacteriostatic drugs that inhibit protein synthesis by binding to the 23S and 50S ribosomal subunits to stop peptide chain elongation; used for patients allergic to penicillin
chloramphenicol
inhibits protein synthesis by binding to the 23S and 50S ribosomal subunits and stopping peptidyl transferase reactions; toxic, not used often
sulfonamides
antimetabolites that are structurally similar to PABA, which is used for the synthesis of folic acid which is a precursor to nucleic acids
trimethoprim
broad-spectrum antimetabolite that blocks DHFR in folic acid pathway; has lots of side effects
quinolones
broad-spectrum drugs that inhibit NA synthesis by stopping bacterial DNA-gyrase and topoisomerase II
mycoses
topical and oral treatments like candida that disrupt membrane permeability and inhibit sterol synthesis; may inhibit protein and DNA synthesis by disrupting mitotic spindle
systemicmycoses
difficult to treat and often fatal, amp B binds to sterols in membranes, 5-flucytosine disrupts RNA function, and fluconazol (preventative)
antiprotozoans
antiviral drugs that block steps in NA synthesis, ETC, protein synthesis and folic acid production
mechanisms of drug resistance
prevent entrance of drug, drug efflux, chemical inactivation of drug, modification of target enzyme or organelle, and use of alternative metabolic pathways
immunity genes
resistance genes that exist in nature to protect antibiotic producing microbes from their own antibiotics
horizontal gene transfer
transferred immunity genes from antibiotic producers to non-producers