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MIC3041 Medical Microbiology > Antibiotics > Flashcards

Antibiotics Flashcards

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
How did carbapenemases come about?
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.
26
Which bacterial species did carbapenemases come from?
Klebsiella pneumoniae
27
What mobile transposon does blaKPC originate from?
Tn4401
28
How can we combat beta-lactamase resistance?
We can use a beta-lactamase inhibitor in combination with a beta-lactam
29
What is the mode of action of a beta-lactamase inhibitor?
It interacts with the beta-lacatamase to save the antibiotic from degradation.
30
What do beta-lactamase inhibitors look like?
They look like beta-lactams but they have little/no antibiotic activity
31
What are 3 beta-lactamase inhibitors?
Clavulanic acid Sulbactam Tazobactam
32
What is amoxicillin forte/duo?
It is amoxicillin with clavulanic acid
33
What is the resistance mechanism for vancomycin?
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
34
What are the three groups of protein synthesis inhibitors?
Macrolides Tetracyclines Aminoglycoside
35
What are 3 macrolides?
Erythromycin Clarithromycin Azithromycin Suffix -thromycin
36
What are 4 tetracyclines?
``` Tetracycline Doxycycline Minocycline Tigecycline Suffix -cycline ```
37
What are 5 aminoglycosides?
``` Streptomycin Gentamicin Neomycin Tobramycin Suffix -mycin/micin ``` Amikacin
38
Are macrolides bactericidal or bacteriostatic?
They are bacteriostatic
39
Do macrolides bind reversibly or irreversibly?
Reversibly
40
Are tetracyclines bactericidal or bacteriostatic?
They are bacteriostatic
41
Do tetracyclines bind reversibly or irreversibly?
Reversibly
42
Are aminoglycosides bactericidal or bacteriostatic?
They are bactericidal
43
Do aminoglycosides bind reversibly or irreversibly?
Irreversibly
44
Which groups of protein synthesis inhibitors bind to the 30S subunit?
Tetracyclines | Aminoglycosides
45
Which groups of protein synthesis inhibitors bind to the 50S subunit?
Macrolides
46
What is the mode of action of macrolides?
They block the polypeptide exit tunnel of 50S and prevent peptide chain elongation
47
What is the mode of action of tetracyclines?
They bind to 30S and interfere with binding of tRNA to ribosomal complex
48
What is the mode of action of aminoglycosides?
They bind to 30S and cause mRNA codon to be misread; interfere with the initiation complex of 30S and 50S with mRNA
49
What is the mechanism of streptomycin (aminoglycoside) resistance?
ATP is used to phosphorylate streptomycin making it streptomycin phosphate.
50
What are the 8 mechanisms by which a bacterial cell can alter itself to become resistant to antibiotics?
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
What the antibiotics that target cell membranes?
Polymyxin | Daptomycin
52
What group of antibiotics do polymyxin and daptomycin belong to?
Cyclic lipopeptides
53
What charge is polymyxin?
Positivey charged
54
What charge is daptomycin?
Negatively charged
55
What is the trade name of daptomycin?
Cubicin
56
What is the mode of action of daptomycin?
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
What is the target of daptomycin?
Gram-positive bacteria | Cannot target Gram-negative bacteria as it cannot penetrate the outer membrane
58
What is the mode of action of polymyxin?
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
What is the target of polymyxin?
Gram-negative bacteria due to the negative charge of their LPS
60
What is a type of polymyxin?
Colistin
61
What is the target of colistin?
It is a last-line treatment for Acinetobacter baumannii
62
What does colistin look like?
- Short, cyclic antimicrobial peptide - Positively charged section - Hydrophobic tail
63
What is the mode of action Colistin?
It binds to Gram-negative outer and inner membrane and causes membrane destabilisation resulting in cell death
64
What are the 2 mechanisms of resistance to colistin?
1. Complete LPS loss | 2. Phosphoethanolamine (PEtn) addition to LPS
65
Explain the mechanism of complete LPS loss
Spontaneous mutations in lipid A biosynthesis genes IpxA, Ipxc, IpxD - > Loss of LPS alters membrane charge - > Reduced interaction with positively charged colistin
66
Does the complete loss of LPS confer high or low resistance?
High
67
Explain the mechanism of phosphoethanolamine (Petn) addition to LPS
Mutations in two-component regulatory system genes, pmrA or pmrB - > increased expression of Petn transferase pmrC - > reduces negative charge - > reduces colistin interaction
68
Does the addition of Petn to LPS confer high or low resistance?
High
69
What antibiotic/s inhibit mRNA synthesis?
Rifamycin
70
What is the mode of action of rifamycin?
It binds to DNA-dependent RNA polymerase and blocks the synthesis of mRNA
71
Is rifamycin bactericidal or bacteriostatic?
Bactericidal
72
What are the target/s of rifamycin?
It is broad-spectrum but not for enterobacteria such as Pseudomonas and Acinetobacter
73
Can rifamycin cross the blood-brain barrier?
Yes
74
What is rifamycin reserved for?
It is reserved for mycobacterial infections | It is used for prophylaxis of meningococcal and haemophilus close contacts
75
What are 4 types of rifamycin?
Rifampicin/Rifampin Rifabutin Rifapentine Prefix Rifa-
76
What is the mechanism of rifampin resistance?
Rifampin resistance can be due to mutations that alter the antibiotic target binding site in the RNA polymerase
77
How do many antibiotics enter bacterial cells?
They enter using membrane porins or specific channels
78
How do bacterial cells become resistant to antibiotics entering?
They used blocked penetration - > mutate: porin loss - > mutate: narrow porin - > mutate: decreased expression
79
How do bacterial cells become resistant to antibiotics that are already in them?
Increase efflux | -> mutations or transcriptional responses lead to increased efflux expression
80
What is the clinical definition of resistance?
Growth of a resistant organism will not be inhibited by an antibiotic at concentrations achievable in the body after approved dose
81
What does MDR mean?
Multi-drug resistant | non-susceptibility to at least one agent in three or more antimicrobial categories
82
What does XDR mean?
Extremely drug resistant | non-susceptibility to at least one agent in all but two or fewer antimicrobial categories
83
What does PDR mean?
Pan drug resistant | non-susceptibility to all agents in all microbial categories

MIC3041 Medical Microbiology (11 decks)

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