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Microbiology > Antimicrobials (1) > Flashcards

Antimicrobials (1) Flashcards

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1
Q

Name 3 selective targets of 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

Name 2 Inhibitors of Cell Wall Synthesis

A

beta-lactam antibiotics and glycopeptides

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3
Q

Name examples of beta-lactam antibiotics and what targets they have

A

penicillin, cephalosporins, carbapenems o Broad spectrum

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4
Q

Name examples of glycopeptides antibiotics and what targets they have

A

– vancomycin, teicoplanin o Gram-positive

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5
Q

What is the difference between gram positive and negative cell walls?

A

• Gram-positive cell wall – thick peptidoglycan cell wall (made of NAG - N-acetylglucosamine and NAM - N-acetylmuramic acid components) • Gram-negative cell wall – thinner peptidoglycan cell wall, outer membrane conferring resistance to some antibiotics o Can be more resistant and harder to treat due to outer membrane

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6
Q

What do Beta-lactams do?

A

• Inactivate enzymes involved in terminal stages of cell wall synthesis = transpeptidases / penicillin binding proteins o Beta lactam is a structural analogue of the enzyme substrate

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7
Q

Beta-lactams are bactericidal what does this mean and what are the consequences?

A

• Bactericidal (active against rapidly dividing bacteria) – if cell wall has already been formed, they have no effect o Ineffective against bacteria lacking peptidoglycan cell walls (mycoplasma, chlamydia) o Cause cell lysis

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8
Q

Name the penicillins

A

o Penicillin o Amoxicillin o Flucloxacillin o Piperacillin

o Clavulanic acid (Co-amoxiclav) and tazobacterm (Tazocin/Piptazobactam)

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9
Q

What bacteria does penicillin work on?

A

Gram positive organisms, Streptococci, Clostridia

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10
Q

What is penicillin broken down by?

A

Beta lactamases produced by S.aureus

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11
Q

What bacteria does amoxicillin act on?

A

Broad spectrum penicillin, extends coverage to Enterococci and Gram negative organisms

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12
Q

What is amoxicillin broken by?

A

broken down by β-lactamase produced by S.aureus and many Gram negative organisms

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13
Q

Which penicillin is stable to ß-lactamase by S.Aureus (gram -ve and e.coli)?

A

Flucloxacillin (and co-amoxiclav)

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14
Q

What bacteria does piperacillin act on?

A

Broad-spectrum (pseudomonas, non-enteric gram -ve)

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15
Q

What breaks down piperacillin?

A

broken down by β-lactamase produced by S. aureus and many Gram negative organisms

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16
Q

Name the cephalosporins.

A

First Generation: Cephalexin Second Generation: Cefuroxime Third Generation: Cefotaxime, Ceftriaxone and Ceftazidime

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17
Q

Which cephalosporin is resistant to beta lactamases produced by gram -ve bacteria?

A

Cefuroxime - Stable to many β-lactamases produced by Gram negatives. Similar cover to co-amoxiclav but less active against anaerobes

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18
Q

What is Ceftriaxone associated with? What does it treat?

A

C. difficile

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19
Q

What is Ceftazidime used for?

A

Activity against pseudomonas (HAIs often)

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20
Q

What are Extended Spectrum β-lactamase producing organisms always resistant to?

A

all cephalosporins regardless of in vitro results

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21
Q

Name the carbapenems

A

Meropenem, Imipenem, Ertapenem

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22
Q

What are carbapenem used for?

A

Stable to ESBL enzymes – used against the ESBL organisms

However, carbapenemase enzymes becoming more widespread  MDR organisms

Danger from MDR – Acinetobacter and klebsiella species

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23
Q

How toxic is beta lactams?

A

Relatively not

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24
Q

How is beta lactams excreted

A

Renally so decrease dose if renal impairment

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25
Q

What is the short life of beta lactams?

A

Short

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26
Q

How cross-allergenic are beta lactams?

A

penicillin has 10% cross reactivity with cephalosporins and carbapenems

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27
Q

What type of bacteria are glycopeptides effective against?

A

gram +ve (inhibit cell wall synthesis) o Large molecules so unable to penetrate gram -ve

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28
Q

What are glycopeptides uses?

A

o MRSA infections (IV) o C. difficile infection (oral – Vancomycin, teicoplanin)

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29
Q

How toxic are glycopeptides?

A

Nephrotoxic – must monitor for accumulation

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30
Q

How bactericidal are glycopeptides?

A

Slowly

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31
Q

Name the inhibitors of protein synthesis

A
  • Aminoglycosides -Tetracyclines - Macrolides -Cloramphenicol - Oxazolidinones
32
Q

Name the aminoglycosides

A

gentamicin, amikacin, tobramycin

33
Q

Describe the MOA of aminoglycosides

A
  • Bind to amino-acyl site of 30s ribosome subunit
  • Rapid, concentration-dependent bactericidal
  • Require specific transport mechanisms to enter
    • Accounts for some intrinsic resistance
34
Q

Why must be monitor levels of aminoglycosides?

A

• Ototoxic & nephrotoxic, therefore must monitor levels

35
Q

What aminoglycosides are effective against pseudomonas aeruginosa? What are aminglycosides ineffective against?

A

Gentamicin and tobramycin but not against anaerobes

No activity vs anaerobes

36
Q

What do aminoglycosides work synergistically with?

A

Beta lactams

37
Q

What bacteria do tetracyclines act on?

A

• Broad-spectrum agents with activity against intracellular pathogens (e.g. chlamydiae, rickettsiae & mycoplasmas) as well as most conventional bacteria

38
Q

Describe the MOA of tetracyclines

A
  • Bacteriostatic
  • Reversibly bind to the ribosomal 30s subunit
  • Prevent binding of aminoacyl-tRNA to the ribosomal acceptor site, so inhibiting protein synthesis
    *
39
Q

Tetracyclines are bacteriostatic, what does this mean?

A

A bacteriostatic agent or bacteriostat, abbreviated Bstatic, is a biological or chemical agent that stops bacteria from reproducing, while not necessarily killing them otherwise.

40
Q

What are the problems with tetracyclines?

A

Widespread resistance limits usefulness to certain defined situations • Do not give to children or pregnant women • Light-sensitive rash

41
Q

What bacteria are macrolides effective/not effective against?

A

• Minimal activity against Gram –ve bacteria • Useful agent for treating mild Staphylococcal or Streptococcal infections in penicillin-allergic patients • Also active against Campylobacter sp and Legionella. Pneumophila • Newer agents include clarithromycin & azithromycin with improved pharmacological properties

42
Q

What is the MOA of macrolides?

A
  • Bacteriostatic
  • Binds to the 50s subunit of the ribosome
43
Q

What is the MOA of chloramphenicol?

A
  1. Binds to the peptidyl transferase of the 50S ribosomal subunit
  2. Inihibits the formation of peptide bonds during translation
  3. Bacteriostatic
44
Q

When would you use cholramphenicol?

A

Broad antibacterial activity

Rarely used apart from eye preparations

Risk of aplastic anaemia

Risk of grey-baby syndrome in neonates because of inability to metabolise the drug

45
Q

What are oxazolidinones used against?

A

Highly active against Gram positive organisms, including MRSA and VRE. Not active against most Gram negatives.

46
Q

What is the MOA of Oxazolidinones?

A

Binds to the 23S component of the 50S subunit to prevent the formation of a functional 70S initiation complex (required for the translation process to occur).

47
Q

What is the issue with Oxazolidinones?

A

Expensive, may cause thrombocytopenia & optic neuritis; should only be used with micro/ID approval

48
Q

Name the inhibitors of DNA synthesis

A

• Quinolones • Nitroimidazoles

49
Q

Name the quinolones

A

ciprofloxacin (old), levofloxacin (new), moxifloxacin (new)

50
Q

What bacteria do quinolones act on? Whats the MOA?

A

.Act on alpha unit of DNA gyrase, bactericidal

51
Q

What illnesses are quinolones used for?

A
  • Broad antibacterial activity, especially vs Gram –ve organisms, including Pseudomonas aeruginosa
  • Newer agents (e.g. levofloxacin, moxifloxacin) → activity vs G +ves and intracellular bacteria, e.g. Chlamydia spp
52
Q

Name the Nitroimidazoles

A

metronidazole, tinidazole

53
Q

What is the MOA of nitroimidazoles?

A

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

• Rapidly bactericidal

54
Q

What microorganisms are nitroimidazoles effectuve against?

A

Active against anaerobic bacteria and protozoa (e.g. Giardia)

Nitrofurans are related compounds: nitrofurantoin is useful for treating simple UTIs

55
Q

Name an inhibitor of RNA synthesis

A

• Rifamycins

56
Q

Name the Rifamycins

A

rifampicin and rifabutin

57
Q

What is the MOA of rifampicin?

A

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

Bactericidal

58
Q

What bacteria is rifampicin active against?

A

•Active against certain bacteria, including Mycobacteria & Chlamydiae

59
Q

What must be taken into account when giving rifampicin?

A
  • Monitor LFTs
  • Beware of interactions with other drugs that are metabolised in the liver (e.g oral contraceptives)
  • May turn urine (& contact lenses) orange
60
Q

Describe resistance to rifampicin.

A
  • Except for short-term prophylaxis (vs. meningococcal infection) you should NEVER use as single agent because resistance develops rapidly
  • Resistance is due to chromosomal mutation.
  • This causes a single amino acid change in the ß subunit of RNA polymerase which then fails to bind Rifampicin.
61
Q

Name the cell membrane toxins

A

• Daptomycin • Colistin

62
Q

Which bacteria does daptomycin act on?

A

– a cyclic lipopeptide with activity limited to G+ve pathogens. It is a recently-licenced antibiotic likely to be used for treating MRSA and VRE infections as an alternative to linezolid and Synercid

63
Q

What bacteria is colistin effective against?

A

a polymyxin antibiotic that is active against Gram negative organisms, including Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella. pneumoniae

64
Q

What is the problem with colistin?

A

It is not absorbed by mouth. It is nephrotoxic and should be reserved for use against multi-resistant organism

65
Q

Name the 4 mechanisms of resistance and the bacteria that use them or the antibiotic that they evade

A
  1. B Bypass antibiotic-sensitive step 2. E Enzyme chemical modification / inactivation of antibiotic –> ESBLs 3. A Accumulation reduced of antibiotic i. Impaired uptake–> Doxycycline ii. Enhanced efflux –> Flucytosine 4. T Target modification or replacement–> MRSA, S. pneumoniae, flucloxacillin, macrolides
66
Q

Name the inhibitors of Folate Metabolism

A

• Sulphonamides • Diaminopyrimidines

67
Q

How do inhibitors of Folate Metabolism work

A

• These act indirectly on DNA through interference with folic acid metabolism

68
Q

Describe the inactivation mechanism of Beta lactams

A

• Beta lactamases are a major mechanism of resistance to beta lactam ABx in SA and gram -ve bacilli (coliforms) This is NOT the mechanism of resistance in penicillin resistant Penumococci and MRSA • Penicillin resistance not reported in group A (strep pyogenes), B, C, or G beta haemolytic streptococci

69
Q

Name a Diaminopyrimidines

A

Trimethoprim - used to treat UTIs

70
Q

Describe the altered target mechanism from Beta lactams

A
  • Used by streptococcus pneumoniae - penicillin resistance is the result of the acquisition of a series of stepwise mutations in PBP genes
71
Q

What type of antibiotics do ESBL act against? Which organisms is it becoming more common in?

A

• ESBLs can enzymatically break down cephalosporins (cefotaxime, ceftazidime, cefuroxime) as well as penicillins o But, not carbapenems Becoming more common in E.coli and Klebsiella species.

72
Q

Describe the altered target mechanism in macrolides?

A
  • Adenine-N6 methyltransferase modifies 23S rRNA
  • Modification reduces the binding of (MLS) Macrolide, lincosamide and streptogramin antibiotics and results in resistance
  • Encoded by erm (erythromycin ribosome methylation) gene
73
Q

What are sulphonamides used to treat? Whats the problem with them?

A
  • Act indirectly on DNA through interference with folic acid metabolism
  • Synergistic action between the two drug classes because they act on sequential stages in the same pathway
  • Sulphonamide resistance is common, but the combination of sulphamethoxazole+trimethoprim (Co-trimoxazole) is a valuable antimicrobial in certain situations (e.g. Treating Pneumocystis jiroveci pneumonia)
  • Trimethoprim is used for Rx community-acquired UTIs
74
Q

What are ESBLs? Where can they be found?

A

Extended Spectrum ß Lactamases (ESBL)

  • Able to break down cephalosporins (cefotaxime, ceftazidime, cefuroxime)
  • Becoming more common in E. coli and Klebsiella species.
  • Treatment failures reported with ß Lactam/ ß Lactamase inhibitor combinations (eg. Augmentin/Tazocin)
75
Q
A

3

76
Q
A

2

Microbiology (19 decks)

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