Drugs
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| drugs that alter the bacteria cell wall | fosfomycin, cycloserine, vancomycin, bacitracin, B lactams
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| how does fosfomycin work | binds covalently to muramic acid synthesizing enzyme to inhibit synthesis of Muramic
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| how are bacteria developing fosfomycin resistance | decreased uptake
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| how does cycloserine work? | inhibits synthesis of D-ala D-ala
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| how are bacteria becoming resistant to cycloserine | decreased uptake
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| how does vancomycin work | binds D-ala D-ala and prevents transglycosylation
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| how are bacteria becoming resistant to vancomycin | they alter D-ala D-ala to make it D-ala-D lactate
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| who is especially resitant to vancomycin | enterococcus
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| how does bacitracin work | blocks dephosphyorylation of lipid carriers
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| what does bacitracin and vancomycin work against | Gram +
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| how does b lactams work | inhibits PBP which carry out crosslinking, it inhibits transpeptidation
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| are B-lactams bacteriocidal or bacteriostatic | cidal
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| what does the b lactam ring mimic | the D-ala D-ala of the peptidoglycan precursor
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| how do b lactams differ | different side chains same nucleus
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| who are two b-lactamase inhibitors | clavulanic acid and sulbactam
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| What drugs work on cell membrane | polymyxin
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| how does polymyxin work | cationic detergent that binds LPS
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| how is polymyxin applied | topical kills even non-dividing gram neg bacteria
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| what drugs work on the DNA structure | nitrofuantoin adn metronidazole
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| how do drugs that work on the DNA structure function | the nitro group is reduced by a nitroreductase and makes a reactive species that cleaves DNA
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| nitrofurantoin and metroniadazole are only effective against? | anaerobes
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| what drugs alter DNA synthesis | quinolones, fluoroquinolones
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| how do drugs that alter DNA synthesis work? | inhibits DNA gyrase, topoisomerase II blocks DNA supercoiling
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| how are bacteria resistant to quinolones | alter target
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| what drugs alter RNA synthesis | Rifamycins
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| how does rifamycin work | blocks RNA polmerase
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| how does resistance to rifamycin work | alter B subunit of RNA polymerase
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| drugs that alter protein synthesis are static or cidal | static
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| what drugs affect the 50S ribosomal unit | chloramphenicol, macrolides (azithromycin, erythromycin, clarithromycin), lincosamides
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| how do choramphenicols work | bind reversibly to exit tunnel of 50s
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| how do the macrolides work (erythro, azithro, clarithro) | block translocation and elongation
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| how does resistance develope to macrolides | alter target
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| how do lincosamides work | binds 50S and blocks peptide bond formation
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| how does tetracyclin work | stops tRNA from binding
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| who should not get tetracyclin | pregnant women and children (bone seeking)
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| how have bacteria become resistant to tetracyclin | decreased uptake increased efflux
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| how do aminoglycosides work | bind irreversibly to 30S
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| what is special about aminoglycosides | they are bacteriocidal
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| when are aminoglycosides useful | anerobic conditions
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| how are bacteria becoming resistant to aminoglycosides | alter target, inactivate the drug, decrease uptake
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| how does bactrim work | inhibits thymine synth via blockage of dihydropteroate synthetase
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| is bactrim static or cidal | static
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| how has resistance developed to bactrim | alter target, decrease uptake, increase level of target enzymes
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| how does trimethoprim work | inhibits thymine synth
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| how are bacteria becoming resistant to trimethoprim | increase level of targer or alter target
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| what does isoniazid do | inhibits mycolic acid synthesis
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| when is mycolic acid important | M. Tb
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| prblem with isoniazid | hepatotoxic
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