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MicroPath > Antibiotics 1 > Flashcards

Antibiotics 1 Flashcards

1
Q
  1. What are three targets for antibiotics?
A

Peptidoglycan layer of cell wall
Inhibition of bacterial protein synthesis
DNA gyrase and other prokaryote-specific enzymes

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2
Q
  1. Name two groups of antibiotics that inhibit cell wall synthesis.
A

Beta-lactams

Glycopeptides

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3
Q
  1. What are the three groups of beta-lactam antibiotics?
A

Penicillins
Cephalosporins
Carbapenems

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4
Q
  1. Give two examples of glycopeptides.
A

Vancomycin

Tiecoplanin

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5
Q
  1. What is the difference between Gram-positive and Gram-negative bacteria?
A

Gram-positives has a thick peptidoglycan cell wall

Gram-negatives have an outer membrane with a thin peptidoglycan cell wall

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6
Q
  1. Outline the mechanism of action of beta-lactam antibiotics.
A 
Inactivate enzymes that are involved in the terminal stages of cell wall synthesis 
Inhibits transpeptidases (aka penicillin-binding protein) 
This means that there are no peptide crosslinks between peptidoglycan chains so the cell wall is weak 
Beta-lactam is a structural analogue of the enzyme substrate
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7
Q
  1. During which phase of the cell cycle will beta-lactams be ineffective?
A

Stationary phase

The cells need to be rapidly dividing

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8
Q
  1. Which type of bacteria are beta-lactams ineffective against?
A

Bacteria with no cell wall (e.g. Mycoplasma and Chlamydia)

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9
Q
  1. List four types of penicillin.
A

Penicillin
Amoxicillin
Flucloxacillin
Piperacillin

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10
Q
  1. For each of the following antibiotics, describe their coverage and mechanisms of resistance:

Penicillin
Amoxicillin
Flucloxacillin
Piperacillin

A

a. Penicillin
Active against Gram-positives (e.g. Streptococci, Clostridia)
Broken down by beta-lactamases (mainly produced by S. aureus)
NOTE: penicillin is the MOST ACTIVE beta-lactam antibiotic
b. Amoxicillin
Broad-spectrum penicillin
Extends coverage to Enterococci and Gram-negative organisms
Broken down by beta-lactamase produced by S. aureus and many Gram-negatives
c. Flucloxacillin
Similar to penicillin but less active
Does NOT get broken down by beta-lactamase produced by S. aureus
d. Piperacillin
Similar to amoxicillin
Extends coverage to Pseudomonas and other non-enteric Gram-negative organisms
Broken down by beta-lactamase produced by S. aureus and many Gram-negatives

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11
Q
  1. Name two beta-lactamase inhibitors. What is the benefit of giving beta-lactamase inhibitors with beta-lactams?
A

Clavulanic acid
Tazobactam
Protect penicillins from breakdown by beta-lactamases thereby increasing the coverage to include S. aureus, Gram-negatives and anaerobes

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12
Q
  1. List examples of 1st, 2nd and 3rd generation cephalosporins.
A

1st = cephalexin
2nd = cefuroxime
3rd = ceftriaxone, ceftazidime, cefotaxime
NOTE: as you go up the generations you get increasing activity against Gram-negatives and less activity against Gram-positives

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13
Q
  1. What is the benefit of cephalosporins over penicillins?
A

They are not broken down by beta-lactamases

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14
Q
  1. What is a disadvantageous association of ceftriaxone?
A

Associated with C. difficile infection

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15
Q
  1. What is a benefit of ceftazidime?
A

Good anti-Pseudomonas cover

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16
Q
  1. List three examples of carbapenems.
A

Meropenem
Imipenem
Ertapenem

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17
Q
  1. List examples of bacteria that have shown carbapenem resistance.
A

Acinetobacter

Klebsiella

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18
Q
  1. Which type of bacteria are glycopeptides effective against and why?
A

Gram-positives

They are large molecules so they cannot cross the outer membrane of Gram-negative cell walls

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19
Q
  1. What is a major side-effect of glycopeptides?
A

Nephrotoxic

Monitor blood levels to prevent accumulation

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20
Q
  1. Outline the mechanism of action of glycopeptides.
A

Glycopeptides bind to amino acid chains at the end of peptidoglycan precursors and prevent glycosidic bonds being formed (via transglycosidase) and prevent peptide crosslinks being formed (via transpeptidase)
NOTE: they are similar to beta-lactams but instead of binding to the enzymes, they bind to substrates (cell wall component precursors)

21
Q
  1. List some classes of antibiotics that work by inhibiting protein synthesis.
A 
Aminoglycosides
Tetracyclines
Macrolides 
Lincosamides (e.g. clindamycin)
Streptogramins (e.g. Synercid)
Chloramphenicol
Oxazolidinones (e.g. linezolid)
22
Q
  1. Outline the mechanism of action of aminoglycosides.
A

Binds to amino-acyl site of the 30S ribosomal subunit and prevents elongation of the polypeptide chain
It also causes misreading of the codons along the mRNA

23
Q
  1. What are some major side-effects of aminoglycosides?
A

Ototoxic and nephrotoxic

24
Q
  1. Which aminoglycosides are particularly active against Pseudomonas aeruginosa?
A

Gentamicin

Tobramycin

25
Q
  1. What is a major issue with tetracyclines?
A

Widespread resistance (most Gram-negatives)

26
Q
  1. Which groups of patients should not receive tetracyclines?
A

Children and pregnant women

Because it can deposit in bone and cause discoloration of growing teeth

27
Q
  1. Outline the mechanism of action of tetracyclines.
A

Binds to the ribosomal 30S subunit and prevents the binding of aminoacyl-tRNA to the ribosomal acceptor site, thereby inhibiting protein synthesis

28
Q
  1. Outline the mechanism of action of macrolides.
A

Binds to the 50S ribosomal subunit and interferes with translation
Also stimulates the dissociation of peptidyl-tRNA

29
Q
  1. What are two major risks of taking chloramphenicol?
A

Aplastic anaemia

Grey baby syndrome – neonates have reduced ability to metabolise the drug

30
Q
  1. Outline the mechanism of action of chloramphenicol.
A

Binds to the peptidyl transferase of the 50S ribosomal subunit and inhibits the formation of peptide bonds during translation

31
Q
  1. Outline the mechanism of action of oxazolidinones.
A

Binds to the 23S components of the 50S subunit to prevent the formation of a functional 70S initiation complex (needed for translation)

32
Q
  1. Which organisms are oxazolidinones active against?
A

Gram-positives (including MRSA and VRE)

Not active against Gram-negatives

33
Q
  1. List two groups of antibiotics that inhibit DNA synthesis.
A

Quinolones

Nitroimidazoles

34
Q
  1. List 3 examples of quinolones.
A

Ciprofloxacin
Moxifloxacin
Levofloxacin

35
Q
  1. List 2 examples of nitroimidazoles.
A

Metronidazole

Tinidazole

36
Q
  1. Outline the mechanism of action of quinolones.
A

Acts on the alpha-subunit of DNA gyrase predominantly with other actions

broad spectrum especially against gram -ve and intracellular organisms

37
Q
  1. Outline the mechanism of action of nitroimidazoles.
A

Under anaerobic conditions, an active intermediate is formed, which causes DNA strand breakage

38
Q
  1. Outline the mechanism of action of rifampicin.
A

Inhibits protein synthesis by binding to DNA-dependent RNA polymerase thereby inhibiting initiation

39
Q
  1. Name two cell membrane toxins.
A

Daptomycin

Colistin

40
Q
  1. Describe the activity of daptomycin.
A

Gram-positives

Likely to be used in treating MRSA and VRE

41
Q
  1. Describe the activity of colistin.
A

Active against Gram-negatives including Pseudomonas aeruginosa, Acinetobacter baumanii and Klebsiella pneumoniae
NOTE: it is a polymyxin

42
Q
  1. Name two families of antibiotics that work by inhibiting folate metabolism.
A

Sulphonamides

Diaminopyrimidines

43
Q
  1. What is co-trimoxazole?
A

Sulphamethoxazole + trimethoprim

44
Q
  1. List some mechanisms of antibiotic resistance.
A

Chemical modification or inactivation of the drug
Modification or replacement of the target
Reduced antibiotic accumulation (impaired uptake or enhanced efflux)
Bypass antibiotic-sensitive step in cell division

45
Q
  1. Which bacteria produce beta-lactamases?
A

S. aureus and Gram-negative bacilli (coliforms)

NOTE: this is not the mechanism of resistance in pneumococcus and MRSA

46
Q
  1. In which groups of bacteria is penicillin resistance not reported in?
A

Group A, B, C and G beta-haemolytic streptococci

47
Q
  1. Describe how MRSA uses ‘altered targets’ as a mechanism of resistance.
A

MRSA has a mecA gene which encodes novel PBP2a

This has a low affinity for binding beta-lactams therefore is not inactivated by beta-lactams

48
Q
  1. Describe the mechanism of resistance in Streptococcus pyogenes.
A

Results from acquisition of a series of stepwise mutations in PBP genes
Lower level resistance can be overcome by increasing the dose

49
Q
  1. Describe the mechanism of resistance to macrolides.
A

Adenine-N6 methyltransferase modifies the 23S RNA
This reduces the binding of macrolides thereby resulting in resistance
Encoded by erm (erythromycin ribosome methylation) genes
NOTE: caution when using clindamycin in Staphylococcus and Streptococcus which is resistant to macrolides because lincosamides can induce this mechanism of resistance

MicroPath (10 decks)

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