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147 Cards in this Set
- Front
- Back
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whats the deal with AB divelopment
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its slowed down bc there isnt money in it. we are getting resistance and tehre are some bugs we cant treat with AB
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whts the key word in AB
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it kills BACTERIA
-only helps infections that are caused by bacteria |
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what is bactericidal?
what is bacteriostatic? |
1. Bactericidal- kills target organism
2. Bacterostatic- inhibits growth of bacteria and assumes the immune system will clear up the rest. DONT use with immunocomprimised ppl or in privledged areas **sometimes the terms are not as clear. ie a deep infection treated with bactericidal agent may not be totally killed bc the AB cant get as deep as the bug is |
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what kind of drug inhibits growth of bacteria
what kind of drug kills bacteria |
1. Bacteriostatic- it assumes immune system will clean up the rest. dont use in privledged areas or with immunocomprimised ppl
2. Bactericidal |
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what is a narrow and wide range spectrum AB?
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1. Narrow: effective for the identified pathogen, wont kill our flora
2. Wide: kills lots so the pathogen doesnt need to be ID, can be bad bc all bugs lyse including normal flora, also bugs die and spill DNA, this can lead to increased resistance |
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whats kind of AB? tell me some positives and negatives about this class/
Erythromyocin, Vancomyosin, Clindamycin |
Narro Spectrum
**good bc they only kill the pathogen and less resistance is developed but you MUST ID the pathogen |
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whats kind of AB? tell me some positives and negatives about this class/
amoxicillin tetracycline, streptomycin, chloramphenicol |
Broad Spectrum
**you dont need to have the pathogen ID, but it kills all the bugs and can lead to increased resistance. **if given several times in kids under 1 year it can increase incidence of asthma |
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what is selective toxicity?
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it means that AB are more harmful to bug than us
Exploit differences 1. Cell wall proteoglycans 2. Protein synthesis machinery (70s ribosome) |
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by targeting 70s ribosomes what are we doing
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taking advantage of differences!
**selective toxicity **just be careful that there is some structural simliiarity btwn bug 70s and our 80s so there can be some overlap killing |
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what cmpd do many antifungals target? is it selectively toxic
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Ergosterol in the fungi are targeted
**looks a lot like our chcolesterol so we get killing of our cells. it is selectiveyl toxic but its not great |
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what are like 7 key things for a GERAT AB
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1. soluble in body
2. selectively toxic 3. Toxicitiy not easily altered (our metabolism doesnt convert it) 4. Non Allergic 5. Stable, excreted slowely 6. Resistnace isnt easily acquired 7. Cheap |
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what is Emperical therapy? Rational therapy? Prophylactic treatment?
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1. Emperical- predict the sensitivity of the organism adn treat based on predition
2. Rational- find out exactly what the organism is and then treat 3. Prophylatic- treat before you even get an infection. Done before surgery or in HIV pts |
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what are the 5 classes of AB
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1. Inhibit cell wall
2. Disturb Cell membrane 3. Inhibit protein synthesis 4. Inhibit nucleic acid synthesis 5. action as antimetabolites |
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what is the major class of AB and what are 3 examples
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Cell wall inhibitors
1. Penicilin 2. bacitracin 3. cephalosporin |
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how do these kill bugs
b lactam AB bacitracin Vancomyin Cycloserine Fosfomycin |
cell wall inhibitors
**vancomysin tx mrsa |
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so the main mech of killing for B lactam AB is______
the 2 main b lactam AB are _______ |
Cell wall inhibitor
1. Penicillins 2. Cephalosporins **all have the b lactam ring **block transpeptidation |
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what drugs have a b lactam ring? what mech do they use to kill
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b lactam AB:
- Penicillin -cyclosporin **cell wall inhibitor,block transpeptidation. bacteriacidal |
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what class of drugs inhibits transpeptidation of cell wall synthesis
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b lactans
**penicillin and cephalosporin |
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are cell wall inhibitors bactericidal or bacteriostatic
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bacteriacital
**block transpeptidation, cell wall lysis and contents spill out **there is a massive release of new bugs the immune system hasnt seen so we can get a huge immune response |
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are all cell wall inhibitors bacteriacidal
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yep
b lactam bacterican vancomysin cycloserine fosfomycin |
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what is B lactamase
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an enzyme found in bugs that attacks the B lactam ring in the b lactam cell wall inhibitors (like penicilin) and render the bug R to the drug
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why is R to penicilin pretty prevalent
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penicilin is a b lactam and can be inhibited by the b lactamase enzyme in bugs. tihs destroys the b lactam ring in the AB and makes the bug R to the AB
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what is penicilin G?
what is penicilin V? |
G
narrow spectrum drug that is inactivated by b lactamase, and is sensitive to acid hydrolysis. often combined with probenecin ti increase half life V - more acid stable but there is SO much resistance its rarely used. also not very available and has a short half life |
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is pen G or V used more
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G its more bioavailable and less R is made against it (still inactivated by b lactamase)
Narrow spectrum |
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why are penicilin V adn G not the only ones? ie why make synthetics?
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1. Increase acid stability (oral administration)
2. B lactamase Resistance 3. Broaden spectrum |
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what are the 3 groups of synthetic penicillians
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1. penicillnase resistant: b lactamase R, gram +
2. Extended spectrum: works best on gram -, acid stable, sensitive to B lactamase 3. Anti Pseudomonal **the synthetics were developed in order to increase acid stability, prevent B lactamaze degradation, and to expand spectrum |
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tell me about the penicillinase resistant penicillins
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B lactamase Resistant
Used for gram + **always remeber penicilin is a cell wall inhibitor that blocks transpeptidation **methicillin (replaced by fluxlozacillin and dicoxacillin), Nafcillin, Oxacillin |
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what type of penicilin is effective against gram + and is resistance to B lactamase
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penicillinase resistant synthetic
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tell me about the expanded spectrum penicillin
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more effective on gram - (does do some gram +)
acid stable sensitive to B lactamase Ampicillin, amoxacillin |
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what penicillin is acid stable, works on gram - best, and is sensitive to B lactamase degradation
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expanded spectrum synthetic
Ampicillin, amoxicillin **recall penicillin is a cell wall inhibitor that blocks transpeptidation |
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tell me about the antipseudomonal penicillins
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1. super effective on gram neg (more than extended spectrum) not really on gram +
2. fights pseudomonas aeruginosa 3. Not acid stable (not orally abs) 4. sensitive to B lactamase **piperacillin, ticarcillin, carbenicillin |
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what is the penicillin that is really good for pseudomonas aeruginosa
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anti-pseudomonal
**effective on gram neg rods (not as good on gram +) **not acid stable, paraenteral administration **sensitive to b lactamase |
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what is the penicillin that is sensitive to b lactamase adn needs to be given paraenterically
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anti-pseudomonal
**fights gram neg rods like Pseudomonas aeruginosa |
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what is a combination product
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penicillin and penicillin analogue
**the analogue has a b lactam ring that we let b lactamase attack so that the drug isnt harmed **the analogue is a competetive inhibitor for b lactamase, lets drug live **clavulanic acid analogue is paired with amoxicillinq |
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what is clavulanic acid
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penicillin analogue that is given in combination therapies. this is attackes by b lactamase adn the drug is sparred.
**the analogue is a competetive inhibitor |
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tell me about cephalosporins
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bactericidal, its a cell wall inhibitor so of course its bactericidal
**more B lactamase R than penicillin **poor oral abs 1st: gram + cocci, some gram - enterics. (not 1st drug of choice) 2nd: gram -, some gram + 3rd: gram -, R to b lactamase, cross BBB 4th: P aeruginosa, some gram + cocci. Meningitis- cross BBB, |
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when we refer to something being bactericidal what are we referring to
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it kills ACTIVELY dividing cells, an established culture wont really be affected
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you id the cause of pts infection as gram +. while you wait for sensitivities you initiate tx with whick drug?
1. pipercillin 2. ampicillin 3. amoxacilin 4. dicoloxicillin |
1. pipercillin (works on gram -, its antipseudomonal penicillin)
2. ampicillin (sensitive to b lactamase, works on gram -, extended spectrum penicilin) 3. amoxacilin (also extended spectrum, gram -, sensitive to b lactamase) 4. dicoloxicillin*** (Penicillinase resistane synthetic penicilin, used in gram +, resistant to b lactamase. this drug replaces mesithillin) |
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tell me about 1st generation Cephalosporins
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broad: gram + cocci (not MRSA or enterococci)
some gram - enterics **not usually drug of choice |
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tell me about a 2nd generation cephalosporin
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1. gram - more than gram +
**b lactams are a broad category of cell wall inhibitors, within this category are the penecillins and the cephalosporins |
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tell me about 3rd generation cephalosporins
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1. gram -
2. B lactamase Resistance 3. Can cross BBB **recall the cephalosporins are a cell wall . one of the b lactams (b lactams are penecillin and cephalosporin) |
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what generation of cephalosporins cross BBB
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3 generation
**works on gram - **b lactamase resistance **recall the cephalosporins are a cell wall inhibitor |
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what are 2 drugs that work on Pseudomonas aeruginosa
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1. Anti pseudomonal penicillins
2. 4th generation cephalosporins |
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tell me about 4th generation cephalosporins
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1. fight pseudomonas aeruginosa (so does antipsuedomonal penicillin- both are cell wall inhibitors)
2. works on some gram + cocci 3. fight meningitis (cross BBB, so does 3 generation) 4. B lactamase Resistance 5. paraenteral administration (same as antipsuedomonal penicillins) |
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greatest hits 1-4 generation cephalosporins
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FIRST GENERATION
gram + cocci, gram - enterics. not first drug of choice SECOND GENERATION gram - THIRD GENERATION gram - B lactamase R can cross BBB FOURTH GENERATION gram + effective for P aeruginosa and meningitis (BBB cross) B lactamase Resistance Paraenteral administration |
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whats the mech?
bacitracin vancomycin cycloserine fosfomycin |
all cell wall inhibitors
Also penicillin (b lactams) and cephlosporins |
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tell me about bacitracin
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cell wall inhibitors that blocks mvmt of precursors throgh cell wall. bactericidal
gram + and gram - cocci Topical |
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what is the topical that prevents cell wall precursors from going to surface of membrane
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bacitracin
**fights gram + and gram - cocci |
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what works first penicillin or bactracin
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bactracin, this wont even let precursors to the surface of the membrane. the penicillin blocks transpeptidation (this is AFTER the precursors have made it to the surface)
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tell me about vancomycin
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narrow, gram + cocci that are methicillin resistanct
**used for pts allergic to b lactamase AB **can cause toxicity in the ear and kidney, red man |
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whats the drug that is super specific for gram + cocci (especially those Resistant to mesithellin) and is good for ppl who are allergive to B lactamase AB
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vancomyosin
**only prob is its toxic to ears and kidney, causes red man syndrome from increased histamine release |
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what is a good alternative AB for ppl allergive to the B lactams AB
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vancomyosin
Good for gram + cocci (especially those tht are mesithellin resistnace) |
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what the example if a cell membrane disturber
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polymixin
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what are the 2 cell membrane inhibitors
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1. polymyxin: gram - , causes cell to lyse bc it open pores in membranes
2. Daptomycin: gram +, messes with cell membrane polarization |
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what lyses the cell membrane of gram neg
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polymyxins
**cationic detergent **gram + cell walls are disturbed by Daptomycin |
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whats polymyxin
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cell membrane inhibiotr
gram neg **causes lysis by making pores in membrane (cationic detergent) its also toxic to use so its used mainly in neosporin topicals |
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whats daptomycin
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its a cell membrane inhibitor for gram + (polymyxin does gram -)
**messes with membrane polarization **not used with respiratory things like pnemonia bc its inactivated **not used in elderly ppl bc they get eosinophiles that build up in the lungs and cause pnemonia |
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what is the toxicity of daptomycin
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this is a gram + cell membrane inhibiotr (not the lysis but changes in membrane polarization)
**dont use for old folks bc they can get eisonophiles in teh lungs and cause pnemonia |
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what are the examples of AB that inhibit protein synthesis
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1. tetracycline
2. erythromycin (type of macrolide) 3. streptomycin (type of aminoglycoside) 4. chloramphenicol |
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what are the 30s ribisome inhibitors
what are the 50s ribisome inhibitors |
30s
aminoglycosides tetracyclines 50s chloramphenicol macrolids clindamycin streptogramins linezolid |
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what is aminoglycosides
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inhibits 30s ribosome via irreversible binding (bactericidal)
**used for the guts **synergist with b lactams **streptomycin, amikacin, gentamicin |
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what are 3 aminoglycosides that can be used synergystically with b lactames
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streptomycin
amikacin gentamicin **aminoglycosides inhibit 30s robosome via irreversible binding. bactericidal **used in the guts lots |
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what are the 3 ways that aminoglycosides irreversibly bind to the 30s subunit and make it bactericidal
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1. interfere with initiation complex
2. Misread mRNA, make abberent protein 3. Prematrure release of mRNA from ribosome, incomplete protein made **in cases 2 and 3 thre is no good protein made so its immediatly degraded. if the bug cant make protein it wont live |
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what class of drugs both bind 30s? what is the differnce
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1. Tetracyclines: reversible (dont give to kids), bacterialstatic
2. aminioglycosides: irreversible (bactericidal). gut bugs. used with b lactames |
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tell me about tetracyclines
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they reversibly bind to 30s ribsome
**broad spectrum, used for intracellular bugs, protosoa and UTI **dont use in kids bc it penetrates bones ex tetracycline, doxycycline, minocycline, demeclocycline |
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what is the drug that can be used for intracellular bugs, protozoa or UTI?
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tetracyclines, reversible bind to 30s ribisome
**dont give to kids, it penetrates bone **tetracycline, doxycycline, minocycline, demeclocycline |
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what does a tetracycline do?
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reversibly binds to 30s to block the aminoacyl tRNA to the acceptor site on the mRNA ribosome complex
**used in UTI, protozoa, and intracellular bugs (the aminoglycosides were the ones who bound irreversibly and were good for enteric bugs) |
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what is chloramphenicol
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50s blocker
bacteriostatic **broad but only used for a few things bc its toxic: -RMSF -meningococcal infection -typhoid |
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what is the drug that is only used for RMSP, meningitis, and typhoid. how does it work
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chloramphenicol
**50s inhibitor, bacteriostatic (reversible binding) **toxic so its only used on these few **prevents elongation of peptide chain |
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what is the drug with poor selective toxicity that prevents elongation of peptide chain
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chloramphenicol
**its a 50s reversible, bacterostatic **used in RMSF, meningitis, and thyphoid bc its so toxic |
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what is a macrolides
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broad spectrum
inhibit 50s, bacterostatic. blocks formation of initiation complex and translocation during elongation Erythromycin, clarithromycin, azithromycin, telithromycin |
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what mech does erythromycon do
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one of the macrolides
its a reversible 50s inhibitor. blocks protein synthesis **bacterostatic **broad spectrum |
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what is clindamycin
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used for MRSA, anerobes and protozoa (maleria)
**reversible 50s inhibitor (simliar to macrolides). blocks formation of initiation complex and translocation step in protein elongation **topical for acne **cheap for 3rd world |
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what is the 50s inhibitor that is good for MRSA
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clindomycin
**similr mech to macrolides **reversible bind, bacterostatic **also used for anerobes nad protozoa like maleria |
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tell me about streptogramins
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combination drug for 50s inhibition. one binds to change conformation adn let the other bind to make it bacterostatic
gram + resistnt E faecium some MRSA |
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what drug inhibits 50s by binding at 2 dif sites?
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streptogramins
**its a combination drug **fights gram +, resistant E faecium, some MRSA |
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what is linezolid?
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50s inhibitor
gram + or bugs with vancomycin R pretty safe binds A side and blocks initiation |
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what is the 50s inhibitor that can be usd with R to vancomycon
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linezolid
*used for gram + **recall vancomycin is used for MRSA and is a cell wall inhibitor for gram +. also good for ppl with b lactam allergy |
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what are some examples of drugs that inhibit nucleis acid synthesis
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1. rifamycin
2. quinolones |
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what is Rifamycin
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DNA inhibitor. inhibits DNA dependent RNA polymerase
**bactericidal **gram + and M. tuberculosis |
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what is the drug that kills gram + by inhibiting DNA dependent RNA polymerase
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Rifamycin
**also killd TB |
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what are floroquinolnes
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1. synthetic AB for UTI
2. DNA inhibitor, inhibits DNA gyrase 3. Bactericidal 4. kills lots of gram - **ciprofloxacin, norfloxacin |
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what are the 2 floroquinolones, what bugs do they kill. how
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ciprofloxacin and norfloxacin
**kill gram - by inhibiting DNA gyrase |
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what is metronidazole
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makes toxic things that DISRUPT DNA
**kills anerobes and protozoas **bactericidal |
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what bactericidal DNA inhibitor is used for anerobes and protozoa
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metronidazole
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what are some examples of drugs that act as antimetabolites
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1. Sulfonamide
2. Trimethoprim (inhibits duhydrofolate reductase) 3. Dapsone (same mech as sulfa, tx for PCP and leprocy. STATIC) 4. Isoniazid (interferes with mycolic acid synthesis, TB tx. CIDAL) |
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what are the 3 DNA inhibitors
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1. Metronidazole: used on anerobes nad protozoa (makes toxins that disrupts DNA)
2. Rifamycin: used on TB and some gram + (inhibits DNA dependent RNA polymerase) 3. Floroquinolones: kill gram - (inhibits DNA gyrase) |
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what is a sulfonamide
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antimetabolite
**PABA analogue, broad spectrum bacteriostatic. indirectly inhibit DNA synthesis by inhibiting first step in folic acid synthesis **block Dihydropteroate synthase **sulfisoxazole, sulfamerazine, sulfamethoxazole |
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what blocks dihydropteroate synthase?
what inhibits dihydrofolate reductase |
1. sulfonamides, upstream
2. Trimethoprim, downstream **BUGS MUST make thieir folic acid, they have no way to get it from environment. needed for DNA **both are antimetabolites that inhibit folic acid synthesis |
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what inhibits the more upstream folic acid enzyme. what is the name of the enzyme
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Sulfonamides blocl dihydropteroate synthase
**the more downstream enzyme, dihydrofolate reducatase, is blocked by trimethoprim |
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what is trimethoprim
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blocks dihydrofolate reductase (downstream) so that no folic acid is made
**bacteriostatic, used with sulfa drugs **folic acid needed for nucleic acid synthesis |
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what drugs when used in combination to inhibit folic acid synthesis are BACTERICIDAL when used together but bacterostatic on their own
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1. Sulfaonamides
2. Trimethoprin **block duhydropteronate synthase and dihydrofolate reducatse respectively **needed for nucleic acid synthesis |
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what is dapsome
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same mech as the sulfas (block folic acid synthesis via upstream dihydropteronate synthase)
**tx of leprocy and pneumocystic carinii pnemonia (PCP) **can be hepatotoxic |
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what is an antimetabolite drug that is similar to the sulfa drugs? what is it used for
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dapsone, its used for a fungan pnemonia called PCP and leprocy
**hepatotoxic **bacteriostatic |
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what drug is used to treat fungal pnemonia (PCP) nad leprocy
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dapsone
same mech as sulfa drugs (inhibit upstream folic acid synthesis) **hepatotoxic |
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what is isoniazid
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tx of TB, interferes with mycolic acid
**antimetabolite **bactericidal **nicotinamide/pyridoxamine analog |
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waht is teh drug that interfered with mycolic acids
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isoniazid
**mycobacteria have mycolic acid. ex Mycobacterium tuberculosis **its one of the antimetabolite drugs |
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what are the 2 main categories of antifungals
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1. Polyenes: insert into cell membrane
2. Azoles **differ from AB bc AB dont work on fungus and lots of antifungals are toxic to us |
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what is amphoterticin
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antifungal for systemic and opprotunistic bugs
**polyene group (inserts into cell membrane) **can be used IV for systemic, but can stll be toxix |
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what is Nystatin
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antifungal to tx candida
**in the polyene group **targets the ergosterol in fungal cell membranes, (also gets cholesterol bc it looks simliar- toxic!!) and creates pores and things leak out **too toxic for systemic |
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azole group
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antifungal for candida and dermatophytes
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what is the antifungal that can be used IV to tx systemic infections
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amphotericin
**its from the polyene goup. inserts into membrane |
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what do the Azoles do?
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antifungal that inhibits the cell membrane formation- blocks synthesis of erfosterol
**also gets some gram + cocci **resistance is NOT common at all |
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what kill fungus by creating a hole?
what kills fungus by inhibiting cell membrane formation via blocking ergosterol fomration |
polyene
azole |
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what is fluconazole
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its an Azole antifungal used to prevent candida in HIV pts
**remember azoles work by inhibiting cell membrane formation by inhibiting synthesis of ergosterol *wide spectrum for yeast and fungi **itraconazole is simliar but has a broader spectrum, and can cause CHF |
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what drug is given to HIV pts to prevent candida
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fluconazole
**its an azole that inhibits fungus by blocking synthesis of ergosterol so that the cell membrane cant properly form |
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what is itraconazole
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its like fluconazole (antifungal) but has a broader spectrum
**MAY CAUES CHF **inhibits fungal cyto P450 oxidase mediated synthesis of ergosterol |
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what drug may cause CHF
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antifungal called itraconazole
**it prevents cyto P450 from making ergostterol |
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whats terbinafine
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antifungal
**blocks ergosterol synthesis, used in things like athletes foot **can be used in pill but with risk of hepatotoxicity |
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whats the athletes foot med
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terbinafine
**antifungal that blocks synthesis of ergosterol **can also be used as tablet (increased hepatotoxicity) |
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wht is the penicillin of antifungals
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echinocandins
**its the only one that doesnt target ergsterol, it inhibits glucan in the cell wall **used in systemic candida and aspergillosis |
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whats echinocandins
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the penicillin of antifungals
**it inhibits glucan in cell wall (all others do ergrsterol in the cell membrane) **used in systemic candidases and apsergillosis |
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what other chemotherapys are there
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1. Anti Viral
2. Anti Parasites (protozoa and helminths- worms 3. Anti Arthropods |
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is AB resistance created by the AB
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nope, its created bc of the environment it is in
**bugs are Rapidly developing R to all of our AB |
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how doe sthe use of AB create selection for AB R bugs
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they are the only ones who survive,
**use of AB promotes darwinian selection of Resistant bugs |
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whats adding to the R of bugs
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1. there are more of them
2. we use AB to select for them 3. bugs do LOTS of genetic exchange 4. bugs double FAST 5. there is no money in making new AB **the guy who discovered penicillin even saw it coming 60 years ago! |
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what are 2 ways bugs develop AB resistnace
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1. Chromosomal Resistance- random mutation in DNA that confers R
2. Get new chromosomal or plasmid DNA from another bug that has R genes on it. |
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whats RTF or R factor
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resistance transfer factor
**its how bugs can get R- get it from antoher bugs DNA (chromosomal or plasmid) **one plasmid can have SEVERAL R genes |
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do bugs need AB R genes from a frined to get R
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nope, they make so many mistakes with DNA that random mutations can lead to R
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resistance gene transfer and random mutations both allow a bug to.....?
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be AB resistance
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do plasmids have just 1 R gene
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nope, they can have LOTS
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what are 4 mechs of bacterial R
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1. Alteration of drug targets like Ribosomal mutation
2. Alter membrane perm/increased drug transport 3. make enzymes that inactivate AB 4. Alteration of a metabolic path |
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what happens when a bug alters a drug target
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RESISTANCE
**the bug changes the protein that is the target for the drug so the drug can no longer bind **seen in erythromycin and rifamycin resistance |
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what is a common way bugs get R to erythromycin and rifamycin
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by altering the drug target
**they alter their ribosome so the drug no longer binds |
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how do bugs commonly get streptomycin R
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by altering the drug target
the drug can no longer bind where it needs to **also seen in R to erythromycin and rifamycin |
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wht AB get R bc the bug alters its membrane perm so that the drug is just shot right out
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1. erythromycin (also alters drug target)
2. Tetracycline |
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what is it called when an AB cant kill a bug bc the bug shoots the AB right out of its PM
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R due to alteration of membrane perm and or increased drug transport- biofilm development, efflux
**seen with erythromycin and tetracycline **erythromycin is a type of macrolide (50s inhibitor) adn tetracycline is a 30s inhibitor |
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what are some examples of enzymes that bugs make to inhibit AB (one mech for AB R). what is the drug that the enzyme targets
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1. b lactams
2. chloramphenicol 3. aminoglycosides 4. tetracycline |
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how is R agianst these made?
1, b lactames 2. chloramphenicol 3. aminoglycosides 4. tetracycline |
the bug makes an enzyme that kills the AB
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what AB are killed bc bugs alter metabolic pahts (conversion to stationary phase)
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1. sulfonamides
2. trimethoprim **these were involved in folic acid inhibition |
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why dont you want to overuse AB with the "best guess" method and use a wide spectrum AB
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you kill all the normal flora
**the normal flora protect against pathogens from calling your body home. this means when normal flora is gone a pathogen that was AB R can not infect you really easily |
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what are the consequences of AB R
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1. Increased morbidity and mortality
2. increased health care costs |
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AB drugs are too expensive now? why
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poor ppl cant get them bc we have thyphoid and TB resitance that require dif $$$ drugs. cant contain outbreaks
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wat are 3 notoriously resistant bugs
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1. Enterococcus Faecalis (R to vancomyocin)
2. Mycobacterium tuberculosis 3. Pseudomonas Aeruginosa |
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what are the drugs that are used to treat the notoriously R ones
1. Enterococcus faecalis 2. Mycobacterium tuberculosis 3. Pseudomonas aeruginosa |
1.
2. 3. |
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in what parrt of the hospital do we see more R happening
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in teh ICU
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whats a superbug
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its a bug that is resistant to most AB bc of AB overuse
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what are some other things that contribute to AB R
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1. AB in food animals
2. Social things 3. Pts not using them right/docs not prescribing them right 4. Colleteral damage of killing natural flora 5. other transmission (not washing hands btwn pts) |
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does eating AB treated cows cause AB R
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yep
the eat and excrete the AB and them we eat them up. Resistant bugs can spread this way |
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do we get AB R from over prescribing/ prescribing them wo reason
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sure thign
they dont work for virus, dont try!! |
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if an AB doesnt work is it due to AB R
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mainly but can also be...
1. the AB just cant reach teh bug, ie if infection is too deep (abcess) or BBB 2. the drug would need to be given at a super high dose that is toxic |
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what is not a mech of AB resistance?
1. bugs recognice resistnace genes and dont express 2. AB altered or degraded 3. change cell membrane perm to pump out AB 4. target (in streptomycin) enxyme develops decreased affinity for the AB |
1 bugs recognize R genes and dont express them****
bugs dont care they get DNA and express it always |
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which if the following is classified as an anti fungal?
1. bacitracin 2. Amphitericin B 3. Pilymixin B 4. neomycin |
1. bacitracin- cell wall
2. Amphitericin B*** (engosterol) 3. Pilymixin B- cell membrane 4. neomycin |
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what are my 50s inhibitors?
30s |
CCELLS
Chloramphenicol: reversible Clindamycin: bacteriostatic, MRSA Erythromycin (macrolides): reversible Linezolid: prevents initiation complex Streptogramins: bactericidal when used in combination 30s Aminoglycosides (streptomycin, amikacin, gentamicin) irreversible Tetracycline: reversible, bacteriostatic (-cycline, all end in cycline) |
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what are the 4 specific mechs bugs get resistance
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1. alter the drug target
2. shoot the drug out the membrane 3. make enzymes to kill the AB 4. Alter metabolic pathway |
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other thatn the b lactames, who else it killed by enzymes the bug makes
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chloramphenicol
aminoglycosides tetracycline |
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whats a superbug, ex
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its a bug that is R to most AB
ex TB |
