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MIC3041 Medical Microbiology > Antibiotics > Flashcards

Antibiotics Flashcards

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1
Q

What can we do to change the present and future in terms of antibiotics and antibiotic resistance?

A
  • Prolong the lifespan of current antibiotics by best practice use
  • > infection control
  • > best practice prescribing
  • use current antibiotics in combinations that give improved activity and slow resistance development
  • develop new antibiotics
  • develop new strategies
  • > bacteriophage therapy
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2
Q

What does bactericidal mean?

A

Antibiotic that kills the bacteria

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3
Q

What does bacteriostatic mean?

A

Antibiotic that causes growth arrest of the bacteria

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4
Q

What is meant by the selectivity of antibiotics?

A

Antibiotics are molecules that have high toxicity for bacteria but low toxicity for humans.
They target molecules that are specific for (or very different in) microbes.

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5
Q

What are antibiotics that target cell wall synthesis?

A 
Penicillin
Beta-lactams
Vancomycin
Ampicillin
Cephalosporin
Carbapenem
Monobactam
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6
Q

How was penicillin discovered?

A

In was discovered in 1928 by Alexander Fleming when he left a plate of bacteria when he went on vacation. When he came back he found a fungi had grown on it and had a circle around it that showed no bacterial growth.

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7
Q

What does penicillin target?

A

Peptidoglycan

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8
Q

What is the role of peptidoglycan?

A

It gives the cell structural rigidity

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9
Q

Are antibiotics that target cell wall synthesis bactericidal or bacteriostatic?

A

They are bactericidal only against growing cells.

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10
Q

Describe the structure of peptidoglycan

A

Peptidoglycan consists of a backbone made up of N-acetylglucosamine (NAG) linked beta-1,4 to N-acetylmuramic acid (NAMA) (NAG-NAMA)
These polysaccharide chains are linked to other polysaccharide chains via crosslinking.
The crosslinking chains are L-Ala-D-Glu-DAP-D-Ala units. DAP = diaminopimelic acid
Prior to crosslinking each side chain ends in D-Ala-D-Ala. Crosslinking occurs via the enzyme transpeptidase.

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11
Q

What is the crosslinking enzyme for peptidoglycan called?

A

Transpeptidase

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12
Q

What do beta-lactams mimic?

A

They mimic D-Ala-D-Ala and contain a beta-lactam ring

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13
Q

Do all beta-lactams have a beta-lactam ring?

A

yes

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14
Q

What are 5 beta-lactams?

A 
Penicillin
Ampicillin
Cephalosporin
Carbapenem
Monobactam
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15
Q

What is the mode of action of beta-lactams?

A

The beta-lactam ring is recognised by glycopeptide transpeptidase. The Ser-OH recognises the beta-lactam ring and binds to it preventing it from binding to D-Ala-D-Ala

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16
Q

What class of antibiotics does vancomycin belong to?

A

Glycopeptide antibiotics

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17
Q

What is vancomycin active against?

A

It is only active against Gram positive bacteria

Vancomycin is too large to go through the outer membrane of Gram negative bacteria

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18
Q

What is vancomycin used for?

A

It is used for serious, life-threatening infections by Gram positive bacteria
In particular, it is used for MRSA as a last-line treatment

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19
Q

What is the mode of action of vancomycin?

A

It binds to D-Ala-D-Ala preventing transpeptidase from binding and crosslinking the polysaccharide chains. This eventually causing destabilisation of the peptidoglycan layer causing the cell to rupture and leak.

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20
Q

What is the mode of action of beta-lactam resistance?

A

Bacteria express many enzymes for degradation of antibiotics.
For beta-lactams they express beta-lactamases.

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21
Q

What is the resistance mechanism for penicillin?

A

Penicillinase, an enzyme that breaks the beta-lactam ring turning penicillin to penicilloic acid

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22
Q

What are carbapenams?

A

They are beta-lactams, that are broad-spectrum antibiotics.

They are derivatives of the natural product thienamycin.

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23
Q

Do beta-lactamases work on carbapenems?

A

No, carbapenems are resistant to most beta-lactamases.

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24
Q

What is the resistance mechanism for carbapenems?

A

Carbapenemase, an enzyme

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25
Q

How did carbapenemases come about?

A

It first began in India in 2006 with documented cases of carbapenem resistance.
In 2011, it was discovered that NDM1 beta-lactamase was being distributed among enterobacteria.
The carbapenem resistance mechanism came from the Klebsiella pneumoniae carbapenemase (KPC) resistance gene.
This gene made its way onto a mobile transposon on a plasmid, which can be transferred between bacteria via horizontal gene transfer.

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26
Q

Which bacterial species did carbapenemases come from?

A

Klebsiella pneumoniae

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27
Q

What mobile transposon does blaKPC originate from?

A

Tn4401

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28
Q

How can we combat beta-lactamase resistance?

A

We can use a beta-lactamase inhibitor in combination with a beta-lactam

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29
Q

What is the mode of action of a beta-lactamase inhibitor?

A

It interacts with the beta-lacatamase to save the antibiotic from degradation.

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30
Q

What do beta-lactamase inhibitors look like?

A

They look like beta-lactams but they have little/no antibiotic activity

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31
Q

What are 3 beta-lactamase inhibitors?

A

Clavulanic acid
Sulbactam
Tazobactam

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32
Q

What is amoxicillin forte/duo?

A

It is amoxicillin with clavulanic acid

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33
Q

What is the resistance mechanism for vancomycin?

A

Bacteria can have the vanA gene that alters peptidoglycan synthesis.
It changes the D-Ala-D-Ala to a D-Ala-D-Lac, which is resistant to vancomycin binding

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34
Q

What are the three groups of protein synthesis inhibitors?

A

Macrolides
Tetracyclines
Aminoglycoside

35
Q

What are 3 macrolides?

A

Erythromycin
Clarithromycin
Azithromycin
Suffix -thromycin

36
Q

What are 4 tetracyclines?

A 
Tetracycline
Doxycycline
Minocycline
Tigecycline
Suffix -cycline
37
Q

What are 5 aminoglycosides?

A 
Streptomycin
Gentamicin
Neomycin
Tobramycin
Suffix -mycin/micin

Amikacin

38
Q

Are macrolides bactericidal or bacteriostatic?

A

They are bacteriostatic

39
Q

Do macrolides bind reversibly or irreversibly?

A

Reversibly

40
Q

Are tetracyclines bactericidal or bacteriostatic?

A

They are bacteriostatic

41
Q

Do tetracyclines bind reversibly or irreversibly?

A

Reversibly

42
Q

Are aminoglycosides bactericidal or bacteriostatic?

A

They are bactericidal

43
Q

Do aminoglycosides bind reversibly or irreversibly?

A

Irreversibly

44
Q

Which groups of protein synthesis inhibitors bind to the 30S subunit?

A

Tetracyclines

Aminoglycosides

45
Q

Which groups of protein synthesis inhibitors bind to the 50S subunit?

A

Macrolides

46
Q

What is the mode of action of macrolides?

A

They block the polypeptide exit tunnel of 50S and prevent peptide chain elongation

47
Q

What is the mode of action of tetracyclines?

A

They bind to 30S and interfere with binding of tRNA to ribosomal complex

48
Q

What is the mode of action of aminoglycosides?

A

They bind to 30S and cause mRNA codon to be misread; interfere with the initiation complex of 30S and 50S with mRNA

49
Q

What is the mechanism of streptomycin (aminoglycoside) resistance?

A

ATP is used to phosphorylate streptomycin making it streptomycin phosphate.

50
Q

What are the 8 mechanisms by which a bacterial cell can alter itself to become resistant to antibiotics?

A
  1. Impaired influx
  2. Efflux
  3. Target mutation
  4. Target modification
  5. Overproduction of target mimic
  6. Factor-associated protection
  7. Drug modification
  8. Drug degradation
51
Q

What the antibiotics that target cell membranes?

A

Polymyxin

Daptomycin

52
Q

What group of antibiotics do polymyxin and daptomycin belong to?

A

Cyclic lipopeptides

53
Q

What charge is polymyxin?

A

Positivey charged

54
Q

What charge is daptomycin?

A

Negatively charged

55
Q

What is the trade name of daptomycin?

A

Cubicin

56
Q

What is the mode of action of daptomycin?

A

It directly interacts with membrane lipids, inserting itself and warping the shape of the cell membrane causing it to have open spaces through which cell division proteins can leak out.

57
Q

What is the target of daptomycin?

A

Gram-positive bacteria

Cannot target Gram-negative bacteria as it cannot penetrate the outer membrane

58
Q

What is the mode of action of polymyxin?

A

It inserts itself into the inner and out cell membrane leading to cell death.
The exact mechanism is unknown however it is believed to be possibly due to cell leakage of intracellular targets.

59
Q

What is the target of polymyxin?

A

Gram-negative bacteria due to the negative charge of their LPS

60
Q

What is a type of polymyxin?

A

Colistin

61
Q

What is the target of colistin?

A

It is a last-line treatment for Acinetobacter baumannii

62
Q

What does colistin look like?

A
  • Short, cyclic antimicrobial peptide
  • Positively charged section
  • Hydrophobic tail
63
Q

What is the mode of action Colistin?

A

It binds to Gram-negative outer and inner membrane and causes membrane destabilisation resulting in cell death

64
Q

What are the 2 mechanisms of resistance to colistin?

A
  1. Complete LPS loss

2. Phosphoethanolamine (PEtn) addition to LPS

65
Q

Explain the mechanism of complete LPS loss

A

Spontaneous mutations in lipid A biosynthesis genes IpxA, Ipxc, IpxD

  • > Loss of LPS alters membrane charge
  • > Reduced interaction with positively charged colistin
66
Q

Does the complete loss of LPS confer high or low resistance?

A

High

67
Q

Explain the mechanism of phosphoethanolamine (Petn) addition to LPS

A

Mutations in two-component regulatory system genes, pmrA or pmrB

  • > increased expression of Petn transferase pmrC
  • > reduces negative charge
  • > reduces colistin interaction
68
Q

Does the addition of Petn to LPS confer high or low resistance?

A

High

69
Q

What antibiotic/s inhibit mRNA synthesis?

A

Rifamycin

70
Q

What is the mode of action of rifamycin?

A

It binds to DNA-dependent RNA polymerase and blocks the synthesis of mRNA

71
Q

Is rifamycin bactericidal or bacteriostatic?

A

Bactericidal

72
Q

What are the target/s of rifamycin?

A

It is broad-spectrum but not for enterobacteria such as Pseudomonas and Acinetobacter

73
Q

Can rifamycin cross the blood-brain barrier?

A

Yes

74
Q

What is rifamycin reserved for?

A

It is reserved for mycobacterial infections

It is used for prophylaxis of meningococcal and haemophilus close contacts

75
Q

What are 4 types of rifamycin?

A

Rifampicin/Rifampin
Rifabutin
Rifapentine
Prefix Rifa-

76
Q

What is the mechanism of rifampin resistance?

A

Rifampin resistance can be due to mutations that alter the antibiotic target binding site in the RNA polymerase

77
Q

How do many antibiotics enter bacterial cells?

A

They enter using membrane porins or specific channels

78
Q

How do bacterial cells become resistant to antibiotics entering?

A

They used blocked penetration

  • > mutate: porin loss
  • > mutate: narrow porin
  • > mutate: decreased expression
79
Q

How do bacterial cells become resistant to antibiotics that are already in them?

A

Increase efflux

-> mutations or transcriptional responses lead to increased efflux expression

80
Q

What is the clinical definition of resistance?

A

Growth of a resistant organism will not be inhibited by an antibiotic at concentrations achievable in the body after approved dose

81
Q

What does MDR mean?

A

Multi-drug resistant

non-susceptibility to at least one agent in three or more antimicrobial categories

82
Q

What does XDR mean?

A

Extremely drug resistant

non-susceptibility to at least one agent in all but two or fewer antimicrobial categories

83
Q

What does PDR mean?

A

Pan drug resistant

non-susceptibility to all agents in all microbial categories

MIC3041 Medical Microbiology (11 decks)

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