Antibiotics 1,2,3,4

Question 1

3 classes of antimicrobial agents

Answer 1

1. natural
2. synthetic (chemotherapeutic)
3. semi-synthetic

Question 2

3 reason to make semi-synthetic drugs

Answer 2

1. reduce toxicity
2. change kinetics
3. modify spectrum

Question 3

2 effects of antimicrobials

Answer 3

1. bacteriostatic

2. bacteriocidal

Question 4

Tetracycline down sides:

Answer 4

had to take 4x/day, short half life

Question 5

Describe B-lactam ring:

Answer 5

house (5 ring) and garage(4 ring): S for chimney, N for door, O for car near garage

Question 6

MRSA is resistant to what?

Answer 6

ALL the Beta-lactams

Question 7

5 targets of antimicrobials:

Answer 7

1. cell wall
2. cytoplasmic membrane
3. ribosomes
4. nucleic acid
5. folic acid

Question 8

structure of peptidoglycan has 2 main blocks M and G, they are:

Answer 8

N-acetyl glucosamine
N-acetyl muramic acid
Both disaccharides

Question 9

how are peptidoglycan connected?

Answer 9

4 peptide chain
pentapeptide bridge (gly)

Question 10

T/F Humans can only use L-Glu?

Answer 10

Yep, only bacteria can use the D form

Question 11

Where does vancomysin bind?

Answer 11

binds to precursor: D-ala D-ala

Question 12

what do you treat MRSA with?

Answer 12

Vancomycin

Question 13

Does Vancomycin work on Gram -ve?

Answer 13

Nope. Only gram +ve

Question 14

How did enterococci become resistant to Vanco?

Answer 14

found a new ways to make cell wall: put a D-Lac instead of D-ala D-ala

Question 15

What is VISA?

Answer 15

Vanco intermediate staph aureus: makes thicker peptidoglycan

Question 16

VSSA?

Answer 16

Vanco sensitive staph aureus:

Question 17

how does penicillin work?

Answer 17

blocks the enzymes needed to catalyze Gly - D-ala D-ala reaction

Question 18

What’s beta lactamase?

Answer 18

bacterial enzyme that hydrolyzes and deactivates penicillin

Question 19

Altered penicillin-binding proteins

Answer 19

form of beta lactam resistance

Question 20

What’s so special about clavulanic acid?

Answer 20

inhibits beta-lactamase, irreversibly binds to it. then allows amoxycillin to do it’s work. Amoxyclav

Question 21

Amoxyclav gets around plasmid or chromosomal? which bug?

Answer 21

Plasmid. can treat staph aureus

Question 22

amoxyvclav won’t work on Pseudomonas. why?

Answer 22

has chromosomal resistance

Question 23

Ticarcillin is used for?

Answer 23

treating pseudomonas cause it’s not affected by chromosomal resistance

Question 24

How would you treat pseudomonas aeruginosum that acquired a plasmid encoded resistance gene?

Answer 24

Ticarcillin plus clavulanic acid = Timentin

Question 25

tetracylcines and amino glycosides act on what?

Answer 25

bacterial protein synthesis

Question 26

Aminoglycosides treat gram what?

Answer 26

negative

Question 27

how does amino glycosides interfere with protein synthesis?

Answer 27

bind to 30S and messes with codons, mutating the protein, low concentration initially, then becomes leaky and then high concentration and stops protein synthesis

Question 28

Resistance to aminoglycosides: 4 ways

Answer 28

1. modify outer membrane 2. ribosomal mutation 3. Efflux (tetracycline) 4. enzymatic mod in the periplasm

Question 29

What is the story behind metronidazole?

Answer 29

only works on strict anaerobes, is a prodrug which is activated by bacteria's own metabolism

Question 30

difference between multi-drug resistant and extensively drug-resistant TB?

Answer 30

MDR-TB: resists 2 our of the 4 drugs | XDR-TB: resists 4 our of the 4 drugs

Question 31

I have ecoli, can I use metronidozal? why?

Answer 31

Nope. cause ecoli is not a strict anaerobe.

Question 32

Which drug can't get through gram -ve cell wall?

Answer 32

vancomycin

Question 33

What is resistant to all Beta lactams?

Answer 33

Pseudomonas cause of chromosomal resistance

Question 34

3 ways for gene transfer in bacteria

Answer 34

1. transformation 2. phage-mediated 3. plasmid-mediated

Question 35

bacteria just sucks up some fragment DNA in the environment, what's that called?

Answer 35

transformation

Question 36

What's the source of antibiotic resistance in horizontal gene transfer?

Answer 36

Your own damn commensals...

Question 37

What's the two phases in bacteriophage cycle?

Answer 37

lysogenic (chillin') | lytic (bursting)

Question 38

How can you tell that a bacteria got new DNA in the genome?

Answer 38

change in phenotype. eg. Germany group got ecoli that made shiga toxin

Question 39

What's transduction

Answer 39

gene transfer through a bacteriophage

Question 40

Plasmid-mediated conjugation sucks: why?

Answer 40

one bacteria can transfer mutilresistance plasmid and knock out 5 classes of antibiotics we can use

Question 41

what are sex-pili? (besides being an awesome band name.)

Answer 41

cytoplasmic bridges between bacteria where plasmid transfer occurs

Question 42

is typhoid fever caused by one pathogen?

Answer 42

No, multiple

Question 43

What does S, R, I, mean wrt in vitro susceptibility

Answer 43

susceptible resistant intermediate

Question 44

What are some host factors to consider when choosing antibiotics?

Answer 44

pregnancy? allergies?

Question 45

streptomycin kills salmonella typhae in vitro, so LOAD up the patient now right?

Answer 45

Nope. It doesn't work in vivo

Question 46

Do newer quinilones work in chest infections?

Answer 46

Yes. older ones couldn't reach the lungs

Question 47

Why do antimicrobial susceptibility testing?

Answer 47

may have acquired resistance

Question 48

Dilution methods involve what?

Answer 48

test tubes and two-fold dilutions to see the MIC (minimum inhibitory concentration)

Question 49

Why do you need a control for the MIC determination?

Answer 49

cause it may be bacteriostatic

Question 50

why disc susceptibility test?

Answer 50

multiple drugs get tested and can related to MIC via disc diameter

Question 51

What's an E-test strip?

Answer 51

one strip, one antibiotic, many many many concentrations for reading disc edge to determine MIC

Question 52

When would you treat TB with only one drug.

Answer 52

When dont' have active TB or symptoms

Question 53

3 effects of antibiotic combinations:

Answer 53

1. indifference 2. antagonism 3. synergy

Question 54

Penicillin G and streptomycin did what to endocarditis?

Answer 54

synergized and killed all the bacteria within 30 hours of injection!

Question 55

Mechanisms of synergy:

Answer 55

1. block sequential steps (eg. synthesis of folic acid) 2. inhibit enzymatic degradation 3. enhance antimicrobial uptake by baterial cell

Question 56

example of inhibition of enzymatic degradation

Answer 56

co-amoxyclav (clav knocks out plasmid resistance, amoxycillin goes in for the kill

Question 57

Example of enhance antimicrobial uptake by baterial cell

Answer 57

penicillin to start poking holes in the cell wall and let the aminoglycosides rush in to inhibit protein synthesis

Question 58

How does tetracylcine and penicillin G antagonize each other?

Answer 58

the bactericidal activity is inhibited by a bacteriostatic agent

Question 59

what's an example of enzymatic degradation induction re: antibiotic antagonism?

Answer 59

Ampicillin induces more beta lactamase and then piperacillin get inhibited and can't do work when normally piperacillin wouldn't induce it as much

Question 60

How else does antibiotic antagonism happen? 1. inhibition of bacteriocidal via static 2. induction of degradation 3. 4.

Answer 60

competition for binding sites | inhibition of target

Question 61

What's Jawetz's Laws?

Answer 61

Bacteriostaticx2 = additive/indifferent bacteriostatic + bacteriocidal = antagonistic bactericidal x 2 = synergistic

Question 62

With grid formation of antibiotic combinations in vitro, what does it mean when you draw a line between the MIC of both antibiotics? What does the line tell you?

Answer 62

If there are vials below the line: you have synergism If there are vials at the line: additive If vials above the line then it's antagonistic