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Year 2 > Antibiotics Symposium > Flashcards

Antibiotics Symposium Flashcards

1
Q

Define antibiotic

A

Agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms in high-dilution

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2
Q

Why are antibiotics more correctly called antimicrobials

A

Because most agents are semi-synthetic derivative of antibiotics

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3
Q

How do antibiotics work

A

They are molecules that bind a target site on a bacteria which are crucial to the survival of the bacterium

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4
Q

What does penicillin binding protein bind to

A

Cell was to inhibit cell wall synthesis

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5
Q

Role of beta lactams

A

Bind to the transpeptidase active site

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6
Q

Examples of beta lactams

A
  1. Penicillins
    Cephalosporins
    Carbapenems

GLYCOPEPTIDES

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7
Q

Mechanism of beta-lactams in the body

A

Block transpeptidase activity and interrupts cross-linking and cell wall synthesis

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8
Q

What antibiotics interfere with nucleic acid synthesis or function

A
  1. METRONIDAZOLE

2. RIFAMPICIN

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9
Q

How does Fluroquinolones inhibit DNA synthesis

A

Inhibit DNA Gyrase

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10
Q

5 antibiotics that inhibit ribosomal activity and protein synthesis

A
  1. Aminoglycosides
  2. Tetracyclines
  3. Lincosamides
  4. Macrolides
  5. Chloramphenicol
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11
Q

Two antibiotics that inhibit folate synthesis and carbon unit metabolism

A

SULPHONAMIDES

TRIMETHOPRIM

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12
Q

What drug effects bacterium cell membranes

A

Polymyxins

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13
Q

What part of the ribosome do tetracycline and ahminoglycosides inhibit

A

30S subunit

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14
Q

What part of the ribosome do macrocodes, Clindamycin, Linezolid, Chloramphenicol, Streptogramins inhibit

A

50S subunits

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15
Q

What is the role of bacteriostatic antibiotics

A

Prevent growth of bacteria (stop multiplication)

Reduce exotoxin production

Exotoxin surge is less likely from Gram negative bacteria

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16
Q

How long does it take for bacteriostatic antibiotics to kill 90% of bacteria

A

18-24 hours

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17
Q

What do we do with bacteriostatic antibiotics before giving them to patients

A

Produce a minimum inhibitory concentration

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18
Q

How do we carry out a minimum inhibitory concentration

A
  1. Tube dilution with antimicrobial agent
  2. Incubate for 24 hours
  3. Determine MIC based on turbidity
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19
Q

Define turbidity

A

Cloudiness of fluid caused by presence of bacteria

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20
Q

Three reasons why bactericidal antibiotics are useful

A
  1. Good during poor tissue penetration
  2. Good when difficult to read infections (TB)
  3. Eradicates infections quickly
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21
Q

Bacteriostatic vs Bactericidal antibiotics in mechanism

A
  1. Bacteriostatic - prevents growth of bacteria
    Bactericidal - agent skill bacteria
  2. Bacteriostatic - kill more than 90% in 18-24 hours
    Bactericidal - Kill more than 99.9% in 18-24 hours
  3. Bacteriostatic - inhibit protein synthesis, DNA replication, metabolism
    Bactericidal - inhibits cell wall synthesis
  4. Bacteriostatic - Reduces toxin production, endotoxin surge less likely, reduced bacterial component release
    Bactericidal - Useful if poor penetration, difficult to treat infections or need to treat quickly
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22
Q

Does a low MIC mean its a better antibiotic than those that are higher

A

No, drugs have to also occupy enough binding sites (high conc/ in microorganism) + STAY there for a sufficient period of time in order for metabolic processes of bacteria to be inhibited

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23
Q

What are two major determinants of anti-bacterial effects

A
  1. Concentration

2. Time

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24
Q

Define ‘concentration-dependant killing’

A

Key parameters how high the concentration is above MIC

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25
Q

Define ‘time-dependant killing’

A

Key parameter is the time that serum concentrations remain above MIC during dosing interval

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26
Q

How is the value of concentration-dependant killing calculated

A

Peak conc. / MIC ratio

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27
Q

How is the value of time-dependant killing calculated

A

t>MIC

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28
Q

What does the antibiotics ability to reach and remain at the site of bacterial infection rely on

A

Pharmacokinetics

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29
Q

Define pharmacokinetics

A

The movement of a drug from its administration site to the place of its pharmacological activity and elimination from the body

RELEASE
ABSOPTION
DISTRIBUTION
ELIMINATION

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30
Q

What three factors effect the distribution of an antibiotic

A
  1. Which antibiotic will penetrate that site
  2. pH of the site
  3. Is the antibiotic lipid-soluble
31
Q

What other key consideration is there when deciding what antibiotic to use

A

WHAT IS SAFE FOR THE PATIENT

32
Q

How do bacteria resist antibiotics

A
  1. Change antibiotic target
  2. Destroy antibiotic
  3. Prevent antibiotic access
  4. Remove antibiotic from bacteria
33
Q

How do bacteria change antibiotic target

A

Change molecular configuration of antibiotic binding site or masks it

34
Q

How has Methicillin (Flucloxacillin) been affected by a change in antibiotic target

A

Can’t bind to PBP of staphylococci (MRSA)

35
Q

How has Vancomycin been effected by a change in antibiotic target site

A
  1. Wall components change in enterococci and reduces binding
36
Q

How has rifampicin activity been effected by a change in antibiotic target site

A

Reduced by changes to RNA polymerase in MTP

37
Q

How have bacteria been able to disable the effect of penicillin

A

Hydrolysis by the bacterial enzyme beta lactase of beta lactic ring in penicillin and cephalosporins

38
Q

What is the product of penicillin destruction after B-lactam is removed

A

Penicilloic acid

39
Q

Does penicillinase produced by staphylococci inactivate flucloxacillin

A

No

40
Q

How do Gram negative bacteria effect ahminoglycosides

A

Phosphorylate and acetylate them

41
Q

How do bacteria prevent antibiotic access

A

Modify the bacterial membrane prone channel, size, number and selectivity

42
Q

Give an example of prevention of antibiotic access

A
  1. Pseudomonas aeruginosa against imipenem

2. Gram negative bacteria against aminoglycosides

43
Q

How can proteins in bacterial membrane reduce effects of antibiotics

A
  1. Proteins in bacterial membranes act as an export or efflux pumps
44
Q

Example of efflux pumps for antibiotics in S.aureus and s. pneumonia

A
  1. Fluoroquinolones
45
Q

What are Enterbacteriacae resistant to

A

Tetracyclines

46
Q

Three ways horizontal gene transfer can take place

A
  1. Conjugation
  2. Transduction
  3. Transformation
47
Q

What three ways can bacteria develop resistance

A
  1. Naturally
  2. Spontaneous gene mutation
  3. Horizontal gene transfer
48
Q

Define intrinsic resistance

A

All subpopulations of a species will be equally resistant

49
Q

Effect of Vancomycin on gram negative bacteria

A

Can’t penetrate outer membrane

50
Q

Effect of cephalosporins on enterococci

A
  1. PBP not effectively bound
51
Q

Define acquired resistance

A

A bacterium which was previously susceptible obtains the ability to resist the activity of a particular antibiotic

52
Q

What is spontaneous gene mutation

A

New nucleotide base pair in AA sequence change to enzyme or cell structure reduced affinity or activity of antibiotic

53
Q

Define conjugation

A

Sharing extra-chromosomal DNA plasmids

54
Q

Define transduction

A

Insertion of DNA by bacteriophages

55
Q

Define transformation

A

Picking up naked DNA

56
Q

In what way has MRSA developed resistance

A

Transduction of mecA genes

57
Q

What species is MRSA

A

S. Aureus

58
Q

Why is MRSA resistant

A

Chromosome me contains mecA

mecA encodes penicillin-binding protein 2a

Resistance to all Beta lactic antibiotics + methicillin

59
Q

How are Vancomycin-resistant enterococci formed

A
  1. Plasmid mediated acquisition of gene encoding altered AA on peptide chain preventing vancomycin binding
60
Q

What increases the resistance of Vancomycin by enterococci

A

Cephalosporin

61
Q

How has gram-negative bacteria developed resistance

A
  1. Beta-lactamase hydrolyses penicillin

2. Typically remain sensitive to beta-lactamase inhibitors

62
Q

Describe how resistance has developed ESBL (extended spectrum beta lactase)

A

Mutation at active site of extended range of antimicrobial resistance inhibits ESBL and allows oxyamino beta-lactam and monobactam inhibition so more extended beta-lactam resistance

63
Q

When is beta-lactam most sensitive

A

In vitro NOT in vivo

64
Q

How is ESBL spread

A

Plasmid

65
Q

How has AmpC beta-lactamase resistance developed

A
  1. Beta-lactamas inhibitor resistant in vitro and in vivo
66
Q

What bacteria express AmpC beta-lactamase resistance

A

Enterobacter and citrobacter

67
Q

What are bacteria with AmpC Beta-lactamase resistant to

A

Penicillin

68
Q

When is AmpC beta-lactamase resistance expressed

A

Only in the presence of the antibiotic

69
Q

What are carbapenems

A

Antimicrobials of last resort to treat infection s due to ESBL or plasmid-mediated AmpC-producing organisms of the enterobacteriaceae family s

70
Q

What property do carbapenems have

A

Highly resistant to degradation by beta-lactamases or cephalosporinases

71
Q

What bacteria developed carbapenemases

A

Gram-Negative bacteria

72
Q

How do we test for resistance

A
  1. Amount of antibacterial that inhibits visible growth of the microorganism - MIC
73
Q

What are breakpoint plates

A

Plates with a specific breakpoint conc. of antibiotic to see if a given inoculum grows or not

74
Q

Formula for breakpoint conc.

A

(Cmax/et) x f x s

Max = maximum serum conc. following a state dose at steady state

s = shift factor

t= factor to allow for serum elimination half-life

e = factor by which the Cmax should exceed MIC

Year 2 (155 decks)

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