Antibiotics 1,2,3,4 Flashcards

1
Q

3 classes of antimicrobial agents

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

3 reason to make semi-synthetic drugs

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

2 effects of antimicrobials

A
  1. bacteriostatic

2. bacteriocidal

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4
Q

Tetracycline down sides:

A

had to take 4x/day, short half life

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5
Q

Describe B-lactam ring:

A

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

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6
Q

MRSA is resistant to what?

A

ALL the Beta-lactams

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7
Q

5 targets of antimicrobials:

A
  1. cell wall
  2. cytoplasmic membrane
  3. ribosomes
  4. nucleic acid
  5. folic acid
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8
Q

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

A

N-acetyl glucosamine
N-acetyl muramic acid
Both disaccharides

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9
Q

how are peptidoglycan connected?

A
4 peptide chain
pentapeptide bridge (gly)
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10
Q

T/F Humans can only use L-Glu?

A

Yep, only bacteria can use the D form

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11
Q

Where does vancomysin bind?

A

binds to precursor: D-ala D-ala

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12
Q

what do you treat MRSA with?

A

Vancomycin

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13
Q

Does Vancomycin work on Gram -ve?

A

Nope. Only gram +ve

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14
Q

How did enterococci become resistant to Vanco?

A

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

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15
Q

What is VISA?

A

Vanco intermediate staph aureus: makes thicker peptidoglycan

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16
Q

VSSA?

A

Vanco sensitive staph aureus:

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17
Q

how does penicillin work?

A

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

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18
Q

What’s beta lactamase?

A

bacterial enzyme that hydrolyzes and deactivates penicillin

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19
Q

Altered penicillin-binding proteins

A

form of beta lactam resistance

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20
Q

What’s so special about clavulanic acid?

A

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

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21
Q

Amoxyclav gets around plasmid or chromosomal? which bug?

A

Plasmid. can treat staph aureus

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22
Q

amoxyvclav won’t work on Pseudomonas. why?

A

has chromosomal resistance

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23
Q

Ticarcillin is used for?

A

treating pseudomonas cause it’s not affected by chromosomal resistance

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24
Q

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

A

Ticarcillin plus clavulanic acid = Timentin

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25
Q

tetracylcines and amino glycosides act on what?

A

bacterial protein synthesis

26
Q

Aminoglycosides treat gram what?

A

negative

27
Q

how does amino glycosides interfere with protein synthesis?

A

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

28
Q

Resistance to aminoglycosides: 4 ways

A
  1. modify outer membrane
  2. ribosomal mutation
  3. Efflux (tetracycline)
  4. enzymatic mod in the periplasm
29
Q

What is the story behind metronidazole?

A

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

30
Q

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

A

MDR-TB: resists 2 our of the 4 drugs

XDR-TB: resists 4 our of the 4 drugs

31
Q

I have ecoli, can I use metronidozal? why?

A

Nope. cause ecoli is not a strict anaerobe.

32
Q

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

A

vancomycin

33
Q

What is resistant to all Beta lactams?

A

Pseudomonas cause of chromosomal resistance

34
Q

3 ways for gene transfer in bacteria

A
  1. transformation
  2. phage-mediated
  3. plasmid-mediated
35
Q

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

A

transformation

36
Q

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

A

Your own damn commensals…

37
Q

What’s the two phases in bacteriophage cycle?

A

lysogenic (chillin’)

lytic (bursting)

38
Q

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

A

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

39
Q

What’s transduction

A

gene transfer through a bacteriophage

40
Q

Plasmid-mediated conjugation sucks: why?

A

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

41
Q

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

A

cytoplasmic bridges between bacteria where plasmid transfer occurs

42
Q

is typhoid fever caused by one pathogen?

A

No, multiple

43
Q

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

A

susceptible
resistant
intermediate

44
Q

What are some host factors to consider when choosing antibiotics?

A

pregnancy? allergies?

45
Q

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

A

Nope. It doesn’t work in vivo

46
Q

Do newer quinilones work in chest infections?

A

Yes. older ones couldn’t reach the lungs

47
Q

Why do antimicrobial susceptibility testing?

A

may have acquired resistance

48
Q

Dilution methods involve what?

A

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

49
Q

Why do you need a control for the MIC determination?

A

cause it may be bacteriostatic

50
Q

why disc susceptibility test?

A

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

51
Q

What’s an E-test strip?

A

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

52
Q

When would you treat TB with only one drug.

A

When dont’ have active TB or symptoms

53
Q

3 effects of antibiotic combinations:

A
  1. indifference
  2. antagonism
  3. synergy
54
Q

Penicillin G and streptomycin did what to endocarditis?

A

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

55
Q

Mechanisms of synergy:

A
  1. block sequential steps (eg. synthesis of folic acid)
  2. inhibit enzymatic degradation
  3. enhance antimicrobial uptake by baterial cell
56
Q

example of inhibition of enzymatic degradation

A

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

57
Q

Example of enhance antimicrobial uptake by baterial cell

A

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

58
Q

How does tetracylcine and penicillin G antagonize each other?

A

the bactericidal activity is inhibited by a bacteriostatic agent

59
Q

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

A

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

60
Q

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

A

competition for binding sites

inhibition of target

61
Q

What’s Jawetz’s Laws?

A

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

62
Q

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?

A

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