question

where do antibiotics come from?

answer

they are naturally produced by bacteria and fungi, some are modified or entirely synthetic

question

what does it mean that antibiotics are selectively toxic?

answer

that they kill/injure invading organisms w/o harming cells of the host. however, to varying degrees, some antibiotics are toxic or have side effects

question

what does it mean to say that an antibiotic is bacteriostatic?

answer

it reversible inhibits metabolic processes of bacteria, (stops growth)

question

what does it mean to say that an antibiotic is bactericidal? can bacteriostatic antibiotics be bactericidal at higher doses?

answer

this kind of antibiotic kills susceptible bacteria. some bacteriostatic antibiotics can be bactericidal at higher doses.

question

what does it mean to say that a drug has a narrow spectrum of activity? extended? broad?

answer

narrow spectrum antibiotics will only act on a single or limited group of microbes. extended spectrum antibiotics can be modified to be effective against gram + and gram – organisms. broad spectrum antibiotics are active against a wide range of bacteria

question

what is the difference between antibiotic susceptible and resistant bacteria?

answer

susceptible: in vitro and in vivo susceptibility means the growth can be inhibited or killed by antibiotic.
resistant: in presence of antibiotic the organism will continue to grow and live

question

can some antibiotics be static for some organisms and cidal for others? what would be a reason for using specifically bacteriocidal drugs?

answer

some organisms that remain alive at all in the presence of a drug can still make toxin, so bacteriocidals might be needed. also some bacteriocidal drugs like PCN can kill but not at once, while erythromycin stops toxin productin immediately.

question

what do the best antibiotics target?

answer

the best antibiotics target biosynthetic processes that are only in bacteria, and not in eukaryotic cells.

question

what is the first line of antibiotics to be considered?

answer

antibiotics that inhibit cell wall synthesis, b/c peptidoglycan can't be found in eukaryotic cells.

question

what are PCN binding proteins, PBPs?

answer

PBPs bind transpeptidases that are involved in peptidoglycan cross-linking

question

what are beta lactams? what is their degree of toxicity?

answer

antibiotics with a beta lactam ring which bind to PBPs which are transpepsidases. PCN, cephalosporin are examples. they have low toxicity.

question

how do beta lactams work?

answer

beta lactams bind transpeptidases (PBPs) preventing peptidoglycan cross-linking while the organism is growing and cross-linking can no longer occur, causing lysis of the organism. the organism has to be growing however for the drug to work.

question

what is a method of resistance, (MOR) that bacteria can use against beta lactams?

answer

beta lactamases cleave the beta lactam ring, which inactivates antibiotic

question

what is a MOR gram - bacteria can use to keep antibiotics out?

answer

spontaneous mutations of porins where antibiotics cannot enter organism

question

what is a MOR MRSA uses to fight PCN?

answer

alteration of PBPs that keeps PCN from binding

question

how does vancomycin work? what is a MOR against it?

answer

vancomycin interacts with D-ala, D-ala termini preventing cross-linkage of peptidoglycan layers. some organisms change to D-ala, D-lac - which vancomycin doesn't bind to

question

how does bacitracin work?

answer

bacitracin prevents movement of peptidogylcan precursors through the cytoplasmic membrane to the cell wall

question

how does polymyxin work?

answer

polymyxin inserts itself into gram - outer membranes by interacting with LPS and phospholipids, and interrups the membrane

question

what are the cell wall antibiotics?

answer

beta lactams, (PCN, cephalosporin, bind PBPs while organism is growing. vancomycin binds D-ala, D-ala, preventing cross-linkage of peptidoglycan layers. bacitracin, which prevents movement of peptidoglycan precursors through the cytosol. polymyxin which inserts itself into the outer membrane of gram - bacteria.

question

what do antibiotics that inhibit protein synthesis target? are there selective toxicity concerns for these?

answer

these disrupt the ribosomes. prokaryotes have 70s, (total), ribosomes while eukaryotes have 80s,(total), these are techinically different, but some similarities, so there is some effect on eukaryotic cell function, (tetracycline can affect teeth development and cause toxicity to renal tubules and inner ear)

question

what do aminoglycosides do? do they have to do anything first in orde to accomplish this?

answer

aminoglycosides bind to the 30s ribosome and cause premature release of the peptide chains. however to do this they must penetrate the gram - cell wall and associated with the active transport system, (oxidative)

question

what are MORs developed against aminoglycosides?

answer

obligate anaerobes have inactive transport. altered uptake of the drug. modification by addition of adenyl, acetyl or phosphoryl group, (plasmid, transposon encoded), mutation in ribosome -> no binding

question

how do tetracyclines work?

answer

these bind to the aminoacyl-tRNA site on the 30s ribosomal subunit and block its attachment to the acceptor site on mRNA ribosome complex, preventing protein synthesis.

question

what are some MORs against tetracycline?

answer

decreased uptake or active efflux of the drug from the bacteria mediated by a transporter it can aquire a gene for. (keeps antibiotic conc low inside cell)

question

what do macrolides do? what is an example of one?

answer

macrolides prevent polypeptide elongation at the 50S ribosome.

question

what are some MOR developed against macrolides?

answer

decreased cell uptake, enzymatic inactivation, and mutation causing decreased binding to ribosome

question

what are antibiotics that work to inhibit protein synthesis?

answer

aminoglycosides, (bind 30s, produce premature release of mRNA), tetracycline, (bind 30s, blocks aminoacyl-tRNA attachment to acceptor site on mRNA ribosome complex) macrolides, (prevent polypeptide elongation by binding to 50s subunit)

question

what are DNA gyrases? do eukaryotes have these?

answer

a topoisomerase that keeps cells from twisting around itself. eukaryotes do not have these.

question

what do quinolones do?

answer

block activity of DNA gyrase, prevent DNA from being replicated b/c it keeps getting twisted.

question

what is an MOR for quinolone?

answer

mutations in DNA gyrase so that it can no longer bind

question

what is rifampin?

answer

this inhibits DNA dependent RNA polymerase which inhibits initiation of transcription, by binding to the beta subunit

question

is RNA polymerase in prokaryotes different than that in eukaryotes?

answer

yes

question

what is a rifampin MOR?

answer

mutation in RNA polymerase that frequently happens when the anitbiotic is used alone

question

what are antibiotics that inhibit nucleic acid synthesis?

answer

quinolones, rifampin

question

what do sulfonamides do?

answer

inhibit dihydropteroate synthase which inhibits folic acid synthesis in prokaryotes.

question

what does trimethoprin do?

answer

inhibits dihydrofolate reductase, (bacteria need to make their own folic acid, they cannot use the folic acid humans make)

question

what antibiotics inhibit the metabolism?

answer

sulfonamides and trimethoprin

question

what some considerations in terms of selecing antimicrobial therapy?

answer

ID organism and susceptibility patterns, site of infection, pt factors, (age, liver/kidney disfunction, pregnant, immune status), pharmacologic factors, (delivery, distrobution, elimination, toxicity, interactions with other drugs)

question

what are the two ways of approaching antibiotic prescription?

answer

empirical theory or selection of therapy with known etiology

question

what is empirical theory?

answer

presumtive prescription of antibiotics, assuming you know the organism, susceptibility pattern, etc. justification is improvement of morbidity, mortality, or public health. (writing a rx for a pt you think has chlamydia/gonhorra, or for a pt you think has spinal menigitis)

question

what are considerations for empirical theory?

answer

knowledge of association between pathogen and disease: (streptococcus pneumonia = number 1 cause of pneumonia and meningitis, so you know what rx to write. pt hx: including age, immune status, disease state, pregnancy?, travel? broader spectrum of therapy: may be required to cover possible organisms that may be causing the infection

question

what is selection of therapy with known etiology? what should be considered in terms of what organism it is, what it will respond to, continuing conditions, and local environment?

answer

when you need to know what the organism is, ex if the bacteria has a hx of resistance to antibiotics, you may want a narrower, more efficient spectrum antibiotic. a cx can give definite ID of organism within 24 hrs, which helps with initial therapy and antibiotic susceptibility tests can be done within 48 hrs as well. microbiological assessment can be continued for duration of tx, our own normal flora may carry antibiotic resistance genes that can be passed on to the pathogen. local epidemiology on certain species' incidence is also helpful

question

what is an minimal INHIBITORY concentration, (MIC)? how is it done? how is the minimal bacteriCIDAL concentration done?

answer

the organism is grown in broth culture, and serial dilutions of an antibiotic are added to different test tubes. the tube where the least antibiotic and still lack of bacterial growth exist is the minimal inhibitory concentration. minimal bactericidal concentration testing will be done on a plate,
when organism doesn’t grow even in removal of antibiotic, this is the minimal bacteriCIDAL concentration.

question

what is the agar disk diffusion method? how is it done? what does it tell you?

answer

bacteria are plated and little discs of differing antibiotic conc. are placed on it. it is incubated overnight and zones of inhibition are looked for and measured. this will tell you if the organism is sensitive or resistant to the antibiotic, in a QUALITATIVE "antibiogram"

question

what is the gradient elution test? what information does it provide?

answer

tries to make the agar disk diffusion method a little more quantitative, (mix between broth culture and agar disk test).

question

what are pharmacodynamic considerations? for bacteriostatic, bacteriocidal drugs?

answer

consideration of the relationship between antibiotic conc. and antimicrobial effect. (in vitro vs what is reasonable in vivo). bacteriostatic agents arrest the growth or replication of bacteria at serum levels achievable in the pt. bacteriocidal agents kill bacterial at serum levels achievable in the pt, should be used when defenses are impaired.

question

what are the two kinds of bacteriocidal agents?

answer

those that effect conc. dependent killing and those that effect time dependent killing.

question

how does the action of drugs that enact concentration dependent killing look?

answer

the rate and extent increases with increasing concentration, (single dose antibiotics)

question

how does the action of drugs that enact time dependent killing look?

answer

activity continues as long as serum concentrations are at a certain level.

question

what is the post antibiotic effect, (PAE)? what are considerations for drugs that lack this?

answer

some antibiotics bind to a target in the organism and even after the conc of the antibiotic gets to be low, they remain stuck to the target and it still has its effect. drugs without a PAE should remain above the MIC serum concentration for intervals between dosing. this plays a part in the efficacy of some one-daily dose regimes

question

what are pharmacokinetic considerations? how does this affect route of administration?

answer

absorption, distrobution, and elimination of the drug from the body. this includes oral administration and parenteral (IV) administration.

question

why might oral routes of administration be chosen?

answer

less costly and few complications?

question

why might paraenteral, (IV) administration be considered?

answer

if the drug is poorly adsorbed from the intestinal tract, if the pt has disease that would impair absorption, or if the pt is critically ill/suffers from menigitis,(to get through the blood brain barrier) or endocarditis

question

what are some conditions that can alter antimicrobial kinetics? (dosage vs state of vascular availability)

answer

impaired renal/hepatic function leads to reduced elimination, and dosage needs to be decreased. pts with burns, CF, or trauma, dosage should be increased. dosage should also be altered in elderly, neonates, and in pregnancy.

question

when might conc. of bodily fluids need to be taken into account? what organs or areas of the body have special consideration for this?

answer

CSF concentration is limited due to blood/brain barrier. the prostate and eye have limited distrobution as well.

question

what are some considerations in terms of antimicrobial safety? in terms of pt hx?

answer

some anti-microbials are toxic to eukaryotic cells and are thus reserved for life-threatening conditions. an allergy, drug and medical hx should be obtained. groups with frequent adverse rxns include: neonates, elderly, renal failure, and AIDs pts

question

what are some advantages in terms of combining antimicrobial drugs, synergism?

answer

this makes the antibiotic more broad spectrum, can treat polymicrobial infections more effectively, decrease the emergence of antibiotic resistance, (harder to generate resistance against 2 drugs), and reduce dose-related toxicity, (smaller dose of 2 drugs w/different side effects)

question

to obtain rationale for synergistic antibiotic rx, what increase in inhibition or killing should be seen in MIC or MBC vs used alone?

answer

4x

question

what is an example of synergism leading to enhancement of antimicrobial uptake?

answer

aminoglycosides can have a difficult time getting into a cell, but given with penicillin to break up the cell wall, aminoglycosides can enter

question

what are other mechanisms of synergism in terms of metabolic sequences or enzyme inhibition?

answer

blockade of sequential steps in a metabolic sequence or inhibition of enzymatic inactivation, (ex. inhibition of B-lactamase by B lactamase inhibitor drugs)

question

what is an example of antagonism between antibiotics if taken at the same time?

answer

inhibition of cidal activity by static agents, (cidals can require growth to function)

question

can one antibiotic enzymatically inactivate another?

answer

yes

question

what things must an antibiotic do to be effective?

answer

it must associate with the bacteria and penetrate the envelope. it must be transported to an intracellular site of action. it must bind to its target

question

what are mechanisms of antibiotic resistance?

answer

prevention of access to the target, alteration of the target or aquisition of the ability to destroy or modify the antibiotic

question

how can various bacteria prevent access of antibiotics to their targets? how is the action of PCN and ceph affected? aminoglycosides? vancomycin? can mutations in porins prevent entrance of more than one antibiotic into the cell, (cross resistance)?

answer

PCN and cephalosporin can be blocked by mutations in the outer membrane where porins, (OMP f), shrink and the drugs can't get in. outer membrane protein expression can be decreased for aminoglycosides so they can't enter either. porins on gram - bacteria are normally too small for vancomycin even without development of resistance. and cross resistance does happen.

question

what is another way that antibiotic access to the target can be prevented?

answer

active efflux of the antibiotic, bacteria can aquire the "tet" gene which expresses a transporter that flushes tetracycline out of the cell

question

what are examples of antibiotic targets in bacteria being altered for PCN, aminoglycosides, and vancomycin?

answer

with PCN, transpeptidase, (PBP), can be altered. with vancomycin, the termini can be altered. with aminoglycosides, the 30s subunit can be altered

question

how did staphylococcus aureus become methicillin resistant, (MRSA)?

answer

staphylococcus aureus produce PBP2a', which has a low affinity for beta-lactam antibiotics, which allowed cell wall synthesis to continue in their presence. They also produced betalactamases which reduced the efficacy of PCN/cephalosporin. Methicillin was then developed b/c it couldn't be affected by betalactamase. staphylococcus aureus then developed another transpepdidase that did not bind to methicillin. staphylococcus aureus then became methicillin resistant, (MRSA)

question

what is PBP2a'? what encodes it? how is it tested for?

answer

PBP2a' is the altered transpeptidase which as a low affinity for beta-lactam antibiotics. it is encoded by the mecA gene. it is tested for using PCR and antibody test for PBP2a. the organism can express this gene at really low level, so you can look for this gene using PCR instead of looking directly at resistance.

question

what strains of bacteria can develop vancomycin resistance?

answer

strains with VanA,B and D genes can replace the last ala with lac so vancomycin can't bind.

question

what is used as the last resort for MRSA and enterococci?

answer

vancomycin, but VRE have emerged since the late 1980s

question

what are some examples of enzymes that cleave antibiotics in defense of the bacteria? are there ones for specific antibiotics? what is ESBL?

answer

beta lactamases. penicillinase only affects PCN, cephalosporinase only effects cephalosporins. ESBL are extended spectrum beta lactamases these can affect PCN and cephalosporin for ex.

question

how are antibiotics like aminoglycasides be modified by bacterial enzymes?

answer

aminoglycasides be modified via N-acetylation, phosphorylation, and 0-adenylation

question

what are some reasons for phenotypic resistance, (therapeutic resistance despite susceptibility in vitro), in terms of beta-lactams? abcesses? intracellular growth?

answer

bacteria may not be dividing and beta-lactams cannot work b/c they require growth. bacteria could be walled off inside an abcess and then antibiotic can't get to it. the organism could also be growing intracellularly, and again, out of antibiotic range.

question

what is an example of genetically originated resistance in chromosomes? plasmids? transposons?

answer

chromosomal point mutations, low frequency, usually resistance to a single antibiotic. plasmids, frequently mediate resistance to multiple antibiotics (through R factors), most common in gram -. transposons have potential for widespread dissemination of resistance genes, (through R-determinants), can't replicate independent of a plasmid/chromosome, but translocates within a chromosome, plasmid, or phage DNA.

question

what is the epidemiology of resistance?

answer

clinical use of antibiotics is followed by resistance, increase use -> increase resistance. preexisting resistance strains can be selected for by antibiotic usage

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