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Clinical Pathology > Core Microbiology - Antibacterial Agents (1) > Flashcards

Core Microbiology - Antibacterial Agents (1) Flashcards

1
Q

Antibiotics

A

Chemical products of microbes that inhibit or kill other organisms

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2
Q

Antimicrobial agents

A
  • Antibiotics
  • Synthetic compounds with similar effect
  • Semi-Synthetic (modified from antibiotics)
    (Antibacterial, anti fungal, antiviral)
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3
Q

Bacteristatic

A

Inhibit bacterial growth (inhibit protein synthesis)

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4
Q

Bactericidal

A

Kill bacteria (cell wall-active agents)

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5
Q

Minimum Inhibitory Concentration (MIC)

A

Minimum concentration of antibiotic at which visible growth is inhibited

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6
Q

Synergism

A

Activity of two antimicrobials given together is greater than the sum of their activity if given separately

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7
Q

Antagonism

A

One agent diminishes activity of another

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8
Q

Indifference

A

Activity unaffected by addition of another agent

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9
Q

Which drugs is synergism confined to in treatment of streptococcal endocarditis?

A

B-lactam and aminoglycoside

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10
Q

Selective toxicity

A

Target not present/significantly different in human host

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11
Q

Antibiotic targets

A
  • Cell wall
  • Protein synthesis
  • DNA synthesis
  • RNA synthesis
  • Plasma membrane
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12
Q

Why is bacterial cell wall an ideal potential for selective toxicity?

A

No cell wall in animal cells

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13
Q

Peptidoglycan in bacterial cell wall is gram…

A

Can be both gram-positive and gram-negative

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14
Q

What are the glucose-derivatives that make up peptidoglycan’s polymer?

A

N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)

  • Tetrapeptides cross-linked by Gly5
  • Terminal D-Ala lost on cross-linking
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15
Q

Cell wall synthesis inhibitors

A
  • B-lactams
  • Glycopeptides
    (Cycloserine and Fosfomycin)
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16
Q

Structure of B-lactam antibiotics

A

All contain B-lactam ring, structural analogue of D-alanyl-D-alanine

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17
Q

How do B-lactam antibiotics work?

A

Interfere with function of ‘penicillin binding proteins’ - transpeptidase enzymes that are involved in peptidoglycan cross-linking

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18
Q

What was the first true antibiotic in clinical practice?

A

Benzylpenicillin (B-lactam antibiotic)

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19
Q

4 types of B-lactam antibiotics

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapenems
  4. Monobactams
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20
Q

Examples of penicillins

A
  • Benzypenicillin (PEN)
  • Amoxicillin (most commonly used)
  • Flucloxacillin
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21
Q

Penicillins are …. spectrum

A

Narrow

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22
Q

Examples of Cephalosporins

A
  • Cefuroxime (CXM) (most commonly used)

- Ceftazidime

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23
Q

Cephalosporins are … spectrum

A

Broad

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24
Q

Cephalosporins target gram

A

-ve, better than penicillins

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25
Q

Examples of Carbapenems

A
  • Meropenem (MER)

- Imipenem

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26
Q

Carbapenems are … spectrum

A

Extremely broad

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27
Q

Carbapenems target gram

A

negative, resistant

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28
Q

Examples of Monobactams

A

Aztreonam (AZT)

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29
Q

Monobactams target gram

A

negative only

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30
Q

Examples of Glycopeptides

A
  • Vancomycin (most commonly used)

- Teicoplanin

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31
Q

How do Glycopeptides work?

A
  • Large molecules, bind directly to terminal D-alanyl D-alanine on NAM pentapeptides - inhibits binding of transpeptidases - inhibits cross-linking
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32
Q

Glycopeptides target gram

A

positive activity (inability to penetrate gram negative outer membrane porins)

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33
Q

Protein synthesis in bacteria

A
  • Translation RNA > protein on ribosome

- ribonucleoprotein complexes (2/3 RNA 1/3 protein) catalyse peptide bond formation and synthesis polypeptides

34
Q

Stages of protein synthesis in bacteria

A
  1. Initiation
  2. Elongation
  3. Termination
  4. Ribosome recycling
35
Q

Subunits that make up ribosome

A

50S (large) and 30S (small) > 70S imitation complex

36
Q

In subunits S=?

A

Svedberg units, relative sedimentation rate

37
Q

Protein synthesis inhibitors

A
  • Aminoglycosides
  • Macrolides, Lincosamides, Streptogramins (MLS)
  • Tetracyclines
  • Oxazolidinones
  • Mupirocin
  • Fusidic acid (hardly used)
38
Q

Examples of aminoglycosides

A
  • Gentamicin (most commonly used)

- Amikacin

39
Q

Which protein synthesis inhibitors bind to 30S?

A
  • Aminogylcosides

- Tetracyclines

40
Q

Which protein synthesis inhibitors bind to 50S?

A
  • Macrolides, Lincosamides, Streptogramins (MLS)

- Oxazolidinones (maybe 70S)

41
Q

Adverse effects of Aminoglycosides

A
  • Reversible renal impairment on accumulation, can be irreversible (rare)
  • Need therapeutic drug monitoring
42
Q

MLS inhibit

A

Protein elongation, block exit tunnel by which newly synthesised peptic leaves ribosome

43
Q

Tetracyclines inhibit

A

RNA translation (interfere with rRNA and tRNA binding)

44
Q

MLS examples

A

Macrolides - Erythromycin, Clarithromycin (most commonly used)
Lincosamides - Clindomycin

45
Q

Tetracycline examples

A
  • Tetracycline

- Doxytetracycline (most commonly used)

46
Q

Oxazolidinones inhibit

A

Initiation of protein synthesis (inhibiting assembly of imitation complex)

47
Q

Adverse effect of Linezolid

A

Bone marrow depression

48
Q

Examples of Oxazolidinones

A

Linezolid

49
Q

DNA synthesis inhibitors

A
  • Trimethoprim (most commonly used) and sulfonamides

- Quinolones and Fluoroquinolones

50
Q

Tritemthoprim targets

A

Dihydrofolate reductase

51
Q

Sulfonamides target

A

Dihydropteroate synthetase

52
Q

Trimethoprim and sulfonamide inhibit

A

Folate synthesis (purine synthesis precursor)

53
Q

Co-trimoxazole

A

Trimethoprim-Sulfomethoxazole combined, bad side effects

54
Q

Quinolone and Fluoroquinolones examples

A
  • Nalidix acid
  • Ciprofoloxacin (most commonly used)
  • Levofloxacin
55
Q

Quinolone and Fluoroquinolones inhibit

A

DNA gyrate and/or topoisomerase IV (remodel DNA during DNA replication - supercoiling/strand separation)

56
Q

RNA synthesis inhibitors

A

Rifampicin - RNA polymerase inhibitor (prevents synthesis of mRNA)

57
Q

Plasma membrane agents

A
  • Daptomycin

- Colistin

58
Q

Daptomycin works by

A

It is a cyclic lipopeptide tail (frying pan shaped), inserts lipophilic tail into cell membrane > depolarisation and ion loss > destruction of cell membrane

59
Q

Daptomycin effects gram

A

positive only

60
Q

Colistin is a

A

Last resource for gram negative

61
Q

Adverse effects of all

A
  • Nausea
  • Vomiting
  • Headache
  • Rash
  • Allergies
  • Infusion reaction
  • Antibiotic resistance
  • Fungal infection - superficial/invasive candidasis
  • C.diff
62
Q

B-lactams intolerance

A

Nausea, diarrhoea and headache

63
Q

B-lactams minor allergy

A

Non-severe skin rash

64
Q

B-lactams minor allergy use … instead

A

Cephalosporins or carbapenems

65
Q

B-lactams severe allergy

A

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

66
Q

What drug can you use in a patient with any type of B-lactam allergy?

A

Aztreonam

67
Q

C.diff infection

A
  • Commonest cause of antibiotic-associated diarrhoea
  • Produces toxins A and B, caused by abolition of colonal resistance
  • Enterotoxin and spore production > clinical features and transmissibility
  • Hypervirulent strain 027 (more severe)
68
Q

Which antibiotics commonly precipitate C.diff?

A
  • Co-amoxiclav (amoxicillin-clavulanate)
  • Cephalosporins
  • Ciprofloxacin
  • Clindamycin
69
Q

Which antibiotics precipitate C.diff, but less commonly?

A
  • Benzylpenicillin
  • Aminoglycosides
  • Glycopepties
  • Piperacillin-tazobactam (broad spec)
  • Any
70
Q

What is Flucloxacillin used for?

A

Staphylococcus aureus (not MRSA)

71
Q

What is Benzypencillin used for?

A

Streptococcus pyogenes

72
Q

What is Cephalosporins used for?

A

Gram negative bacilli (avoid in elderly)

73
Q

What is Metronidazole used for?

A

Anaerobes

74
Q

What is Vancomycin used for?

A

Gram positive (MRSA)

75
Q

What is Meropenem used for?

A

Most clinically-relevant bacteria

76
Q

What has good availability in CSF?

A

B-lactams in inflammation

77
Q

What has poor availability in CSF?

A

Amino glycosides and vancomycin

78
Q

What has good availability in urine?

A

Trimethoprim and B-lactams

79
Q

What has poor availability in urine?

A

MLS antibiotics

80
Q

Reasons for combining antibiotics

A
  • Increase efficacy (synergy)
  • Broad spectrum (polymicrobial infection/empiric treatment of sepsis)
  • Decrease resistance (antituberculous chemo)

Clinical Pathology (60 decks)

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