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1. CP - Core Microbiology > (1) Intro to antibacterial agents > Flashcards

(1) Intro to antibacterial agents Flashcards

1
Q

What is the ‘spectrum’ of an antibiotic?

A

The organisms against which they are active

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2
Q

What is an antimicrobial agent?

A

Umbrella term - can be antibacterial, anti fungal, antiviral agents etc.

Includes antibiotics, synthetic compounds and semi-synthetic compounds

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3
Q

Define antibiotic

A

Chemical products of microbes that inhibit or kill other organisms

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4
Q

What is a semi-synthetic antimicrobial agent?

A

Modified from antibiotics

May have a different antimicrobial activity/spectrum or different pharmacological properties or toxicity

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5
Q

The term ‘antibiotic’ is often used interchangeably with which other term?

A

Antibacterial agent

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6
Q

In which 2 general ways do antibacterial agents act to stop bacteria?

A
  • inhibit bacterial growth (= bacteristatic)

- kill bacteria (=bactericidal)

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7
Q

What is the minimum inhibitory concentration (MIC)?

A

The minimum concentration of antibiotic at which visible growth is inhibited

The smaller the MIC, the more active the antibiotic

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8
Q

Can antibiotics be both bacteristatic and bactericidal?

A

Some antibiotics are bacteristatic at low concentrations and bactericidal at high concentrations

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9
Q

What are the 3 types of antimicrobial interactions?

A
  • synergism
  • antagonism
  • indifference
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10
Q

Synergism is a type of antimicrobial interaction. What does it mean?

A

The activity of 2 antimicrobials given together is greater than the sum of their activity if given separately

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11
Q

Antagonism is a type of antimicrobial interaction. What does it mean?

A

One agent diminishes the activity of another

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12
Q

Indifference is a type of antimicrobial interaction. What does it mean?

A

Activity unaffected by the addition of another agent

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13
Q

Give a clinical example of synergism

A

B-lactam/aminoglycoside therapy of streptococcal endocarditis

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14
Q

What is selective toxicity?

A

The target of the antibacterial is not present in human host or is significantly different in the human host

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15
Q

Give some examples of targets of antibiotics

A
  • cell wall
  • protein synthesis
  • DNA synthesis
  • RNA synthesis
  • plasma membrane
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16
Q

What does the bacterial cell wall consist of?

A

Peptidoglycan

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17
Q

Peptidoglycan is the major component of cell walls in which type of bacteria?

A

Both Gram-positive and Gram-negative bacteria

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18
Q

What is peptidoglycan a polymer of?

A

It is a polymer of glucose-derivatives, N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)

(NAMs joined together by NAGs, forms a network)

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19
Q

Why is targeting the bacterial cell wall good in terms of selective toxicity?

A

There is no cell wall in animal cells

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20
Q

Which classes of antibiotics are cell wall synthesis inhibitors?

A
  • B-lactams

- glycopeptides

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21
Q

What do B-lactams (a cell wall synthesis inhibitor) all contain?

A

The b-lactam ring

Four-membrered ring structure (C-C-C-N)

Structural analogue of D-alanyl-D-alanine

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22
Q

What do B-lactams interfere with?

A

The interfere with the function of “penicillin binding proteins” which are the enzymes involved in the construction of the peptidoglycan bacterial cell wall

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23
Q

What are “penicillin binding proteins”?

A

Transpeptidase enzymes involved in the peptidoglycan cross-linking which forms the bacterial cell wall

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24
Q

Which groups of antibiotics are B-lactam antibiotics?

A
  • penicillins
  • cephalosporins
  • carbapenems
  • monobactams
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25
Q

Give some examples of penicillins (B-lactams)

A
  • benzylpenicillin
  • amoxicillin
  • flucloxacillin
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26
Q

Give a feature of penicillins

A

Relatively narrow spectrum

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27
Q

Give some examples of cephalosporins (B-lactams)

A
  • cefuroxine

- ceftazidime

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28
Q

Give a feature of cephalosporins

A

Broad spectrum

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29
Q

Give some examples of carbapenems (B-lactams)

A
  • meropenem

- imipenem

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30
Q

Give a feature of carbapenems

A

Extremely broad spectrum

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31
Q

Give a monobactam (B-lactam)

A

Aztreonam

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32
Q

Give a feature of aztreonam (a monobactam, B-lactam)

A

Gram-negative activity only

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33
Q

Which B-lactam antibiotic works on gram-negative bacteria only?

A

Aztreonam

a monobactam

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34
Q

Glycopeptides are the other cell wall synthesis inhibitors, along with B-lactams. Give some examples

A
  • vancomycin

- teicoplanin

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35
Q

What do glycopeptide antibiotics do specifically?

A

Large molecules that bind directly to terminal D-alanyl-D-alanine on NAM pentapeptides, inhibiting binding of transpeptidases and thus peptidoglycan cross-linking

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36
Q

Glycopeptides work on which classification of bacteria?

A

Gram-positive

They are unable to penetrate gram-negative outer membrane porins

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37
Q

Vancomycin comes under which classification of antibiotics?

A

Glycopeptides

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38
Q

Summarise protein synthesis in bacteria

A
  • translation of RNA to protein takes place on the ribosome
  • ribonucleoprotein complex is 2/3 RNA and 1/3 protein
  • 50S (large) and 30S (small) subunits combine to form 70s initiation complex
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39
Q

Which groups of antibiotics are protein synthesis inhibitors?

A
  • aminoglycosides
  • macrolides, lincosamides, streptogramins (MLS)
  • tetracyclines
  • oxazolidinones
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40
Q

Give some examples of aminoglycosides

A
  • gentamycin

- amikacin

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41
Q

What do aminoglycosides do?

A

Bind to 30S ribosomal subunit

Mechanism of action not fully understood

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42
Q

Give some examples of MLS antibiotics

A
  • erythromycin, clarithromycin (macrolides)

- clindamycin (lincosamide)

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43
Q

What do MLS antibiotics do?

A

Bind to 50S ribosomal subunit
= blockage of exit tunnel

  • inhibition of protein elongation
44
Q

Give some examples of tetracyclines

A

Tetracycline, doxytetracycline

45
Q

What do tetracyclines do?

A

Bind to 30S ribosomal subunit

Inhibit RNA translation - interfere with binding of tRNA to rrNA

46
Q

Give an example of an oxazolidinone

A

Linezolid

47
Q

What does linezolid (an oxazolidinone) do?

A

Inhibits initiation of protein synthesis

Binds to 50S ribosomal subunit

Inhibits assembly of initiation complex

May also bind to 70S subunit

48
Q

Other than the aminoglycosides, MLS, tetracyclines and oxazolidinones, give some other protein synthesis inhibitors

A
  • mupirocin

- fusidic acid

49
Q

Which groups of antibiotics are DNA synthesis inhibitors?

A
  • trimethoprim and sulphonamides

- quinolones and fluoroquinolones

50
Q

What do trimethoprim and sulphonamides do?

A

Inhibit folate synthesis - folic acid is a purine synthesis precursor

51
Q

Specifically, what does trimethoprim inhibit?

A

Dihydrofolate reductase

52
Q

Specifically, what do sulphonamides inhibit?

A

Dihydropteroate synthetase

53
Q

What 2 antibiotics make co-trimoxazole when combined?

A

Trimethoprim and sulfamethoxazole

54
Q

What do quinolones and fluoroquinolones do?

A

Inhibit enzymes - DNA gyrase and topoisomerase IV

These are involved in remodelling of DNA during DNA replication

55
Q

Give some examples of quinolones and fluoroquinolones

A
  • nalidixic acid
  • ciprofloxacin
  • levofloxacin
56
Q

Which antibiotic is a RNA synthesis inhibitor?

A

Rifampicin

57
Q

What does rifampicin do?

A

It is an RNA polymerase inhibitor

Prevents synthesis of mRNA

58
Q

What is different about plasma membrane agents compared to other antibiotics?

A

They attack a structure (the plasma membrane) rather than disrupting a process

  • the plasma membrane must be intact for bacteria to survive
59
Q

Which plasma membrane agent works on gram-negative bacteria?

A

Colistin

60
Q

Which plasma membrane agent works on gram-positive bacteria?

A

Daptomycin

  • cyclic lipopeptides
  • destruction of cell membrane
61
Q

What are the general adverse effects of any drug?

A
  • nausea, vomiting, headache, skin rashes etc
  • infusion reactions
  • allergic reactions
62
Q

What type of infections can antibiotic treatment adversely cause?

A
  • fungal infection (superficial and invasive candidiasis)

- clostridium difficile infection

63
Q

Which group of antibiotics are most significant in allergy?

A

B-lactams

64
Q

What are the specific adverse effects of aminoglycosides?

A
  • reversible renal impairment on accumulation
  • irreversible ototoxicity

Therapeutic drug monitoring indicated

65
Q

What are the specific adverse effects of b-lactams?

A

Mainly allergic reactions

generalised rash = 1-10%
anaphylaxis = approx 0.01%

66
Q

What is the specific adverse effects of linezolid?

A

Bone marrow depression

67
Q

In which 3 ways can allergy to penicillins be classified?

A
  • intolerance
  • minor allergic reaction
  • severe allergic reaction
68
Q

What would an intolerance to penicillin cause?

A

Nausea, diarrhoea, headaches etc

69
Q

What would a minor allergic reaction to penicillin cause?

A

Non-severe skin rash

70
Q

What would a severe allergic reaction to penicillin cause?

A

Anaphylaxis, urticaria, angio-oedema, bronchospasm, severe skin reaction (Stevens-Johnson syndrome)

71
Q

Which B-lactams are safe to use in patents with non-severe penicillin allergy?

A
  • cephalosporins

- carbapenems

72
Q

Which B-lactams are safe to use in patients with any penicillin allergy?

A
  • aztreonam
73
Q

What is C. difficile infection caused by?

A

Abolition of colonisation resistance due to antibiotic consumption

74
Q

Which toxins does C. diff produce?

A

Toxins A and B

75
Q

What causes the clinical features and transmissibility of C. diff?

A

Combination of enterotoxin and spore production

76
Q

Which strain of C. diff causes more severe disease?

A

Hypervirulent strain 027

77
Q

What are the common precipitating antibiotics of C. diff?

A

4Cs

  • co-amoxiclav (amoxicillin-clavulanate)
  • cephalosporins
  • ciprofloxacin
  • clindamycin
78
Q

What are the less common precipitating antibiotics of C. diff?

A
  • benzylpenicillin, aminoglycosides, glycopeptides

- piperacillin-taxobactam (despite broad spectrum)

79
Q

May C. diff be precipitated by any antibiotics?

A

Yes!

80
Q

What are the 3 stages in the strategy of antibiotic use?

A
  1. empiric therapy (best guess)
  2. targeted therapy
  3. susceptibility-guided therapy
81
Q

Empiric therapy is the first stage in the strategy of antibiotic use. What is it based upon?

A
  • predicted susceptibility of likely pathogens
  • local antimicrobial policies

(after history, examination and clinical diagnosis)

82
Q

Targeted therapy is the second stage in the strategy of antibiotic use. What is it based upon?

A
  • predicted susceptibility of infecting organism(s)
  • local antimicrobial policies

(after laboratory investigations: microbiological diagnosis)

83
Q

Susceptibility-guided therapy is the third stage in the strategy of antibiotic use. What is it based upon?

A
  • susceptibility testing results

after the antimicrobial susceptibility test

84
Q

When can you use antimicrobials with the narrowest spectrum of agents?

A

When you have a higher level of knowledge of what the infecting organism is

85
Q

In the statement ‘Start Smart - then Focus’ relating to antibiotic use, what does the ‘start smart’ bit mean?

A
  • only use antibiotics if there is clinical evidence of bacteria infection
  • use local guidelines
  • document indication, duration or review date
  • obtain cultures first
  • use single dose antibiotics for surgical prophylaxis
86
Q

In the statement ‘Start Smart - then Focus’ relating to antibiotic use, what does the ‘focus’ part mean?

A

at 48 hours

  • stop antibiotics if there is no evidence on infection
  • switch antibiotics from intravenous to oral
  • change antibiotics, ideally to a narrower spectrum, or broader if required
  • continue and review again at 72 hours
  • outpatient parenteral antibiotic therapy (OPAT)
87
Q

What are some key antibiotic/bacteria combinations?

A
  • flucloxacillin/staph. aureus (not MRSA)
  • benzylpenicillin/strep. pyogenes
  • cephalosporins/gram-neg bacilli
  • metronidazole/anaerobes
  • vancomycin/gram-pos (MRSA)
  • meropenem/most clinically-relevant bacteria
  • cloisitin/last option for multi-resistant gram-negs
88
Q

What is a warning related to cephalosporins?

A

Avoid in the elderly

89
Q

The antibiotic colistin is used as a last option for which bacteria?

A

Multi-resistant gram-negatives

90
Q

Which antibiotic tends to be used for streptococcus pyogenes?

A

Benzylpenicillin

91
Q

Which antibiotic tends to be used for staphylococcus aureus?

A

Flucloxacillin

92
Q

Which antibiotic is used for MRSA (and other gram-positive bacteria)?

A

Vancomycin

93
Q

Anaerobic bacteria can be treated with which antibiotic?

A

Metronidazole

94
Q

Cephalosporins treat which type of bacteria?

A

Gram-negative bacilli

95
Q

What is an important determinant of in vivo efficacy?

A

Concentration at site of action

96
Q

What has good availability/ poor availability in the CSF?

A

B-lactams - good availability in presence of inflammation

Aminoglycosides and vancomycin = poor availability

97
Q

What has good availability/ poor availability in the urine?

A

Trimethoprim and B-lactams = good availability

MLS antibiotics = poor availability

98
Q

What is the main determinant of bacterial killing? (concentration dependent)

A

The factor by which concentration exceeds MIC

99
Q

How are high peaks of antibiotic concentration achieved? (concentration dependent)

A

By administering the antibiotic intermittently eg. aminoglycosides

100
Q

What is the main determinant of bacterial killing? (time dependent)

A

The amount of time of which antibiotic concentration exceeds MIC

101
Q

How is high concentration of antibiotic maintained? (time dependent)

A

Administered frequently e.g B-lactams

102
Q

What are the reasons for combining antibiotics? (combination therapy)

A
  • to increase efficacy
  • to provide adequately broad spectrum
  • to reduce resistance
103
Q

A reason for using combination therapy is to increase efficacy. How does this happen?

A

Synergistic combination may improve clinical outcome (B-lactam/aminoglycoside in streptococcal endocarditis)

104
Q

A reason for using combination therapy is to provide adequately broad spectrum. Explain this

A

Single agent may not cover all required organisms

  • polymicrobial infection
  • empiric treatment of sepsis
105
Q

How does using combination therapy reduce resistance?

A

The organism would need to develop resistance to multiple agents simultaneously

  • antituberculosis chemotherapy

1. CP - Core Microbiology (8 decks)

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