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2.2 Microbiology > Antibiotic Activity > Flashcards

Antibiotic Activity Flashcards

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1
Q

Define antimicrobials

A

Chemicals used to control microbial growth

Includes antibiotics and disinfectants

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2
Q

Define antibiotics

A

Chemical with inhibitory effect on microbial growth in human host

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3
Q

Write a note on the importance of antimicrobials
(4)

A

Over the past 80 years they have contributed to huge advances in medicine

The discovery of safe, systemic antibiotics have a major affect on the control of infectious diseases

Antibiotics have increased life expectancy from 47 in the the 1900s to 80 years today

Infant mortality has also greatly reduced from 100/1,000 in the 1900s to 6/1000 today

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4
Q

What was the first group of antibiotics found?

A

B lactams

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5
Q

When were B lactams discovered

A

1928

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6
Q

What is considered the golden age of antibiotic discovery?

A

1950s to 1960s

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7
Q

What was the innovation gap?

A

The years between 1962 and 2000 where no new major classes of antibiotics were found and there was limited development of new agents

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8
Q

List the six most commonly used antibiotic classes

A

B-lactams
Aminoglycosides
Glycopeptides
Macrolides
Quinolones
Tetracycline

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9
Q

What are the three most common types of B-lactams?

A

Penicillins
Cephalosporin
Carbapenems

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10
Q

List the four penicillins

A

Penicillin
Ampicillin
Amoxicillin
Augmentin

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11
Q

List the two most common cephalosporin

A

Cefotaxime
Ceftazidime

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12
Q

List the most common carbapenem

A

Meropenem

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13
Q

List the two aminoglycosides

A

Gentamicin
Amikacin

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14
Q

List the two glycopeptides

A

Vancomycin
Teicoplanin

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15
Q

List the two Macrolides

A

Clarithromycin
Azithromycin

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16
Q

List the three quinolones

A

Ciproflaxacin
Levoflaxacin
Moxifloxacin

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17
Q

What is the only group of tetracycline’s studied?

A

Tetracycline

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18
Q

What are our two newly developed agents?

A

Daptomycin
Linezolid

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19
Q

What are the four properties of antimicrobials

A

Selective toxicity
Inhibit or kill
Broad or Narrow Spectrum
Emergence of resistance

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20
Q

Write a note on the selective toxicity property of antibiotics
(3)

A

Selective toxicity is the ability to kill or inhibit growth of an organism without harming the cells of the host

The antimicrobial takes advantage of the biochemical differences between organism and host

In most cases selective toxicity is relative and nor absolute i.e. the antibiotic inhibits organisms at lower concentrations than what can cause toxic effects in host

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21
Q

Selective toxicity is said to be relative not absolute, what does this mean?

A

At low concentrations the antibiotic inhibits the organism but does not affect the host cells

However it can have toxic affects to the host at higher concentratinos

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22
Q

Write a note on the inhibit or kill property of antibiotics
(3)

A

Antibiotics may kill or inhibit microbial growth

Bacteriostatic - inhibit bacterial growth at concentrations attainable in the host body, this allows the host defence to cope with the static population

Bactericidal - have a rapid, lethal action at concentrations attainable in the host body, at least 99% of all pathogens are destroyed in the first 4-8 hours

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23
Q

What percentage of bacteria are killed by bactericidal antibiotics and in what time limit?

A

At least 99% are killed in the first 4-8 hours

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24
Q

Write a note on the broad or narrow spectrum principle of antimicrobials
(4 points on each)

A

Broad spectrum
- gram positive and gram negative
- useful if organism has not yet been identified
- disrupt the microbiome
- e.g. quinolones or carbapenems (B lactams)

Narrow spectrum
- act against a limited number of bacteria
- used preferably when organism has been identified
- causes less disruption to the microbiome
- e.g. glycopeptides such as vancomycin

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25
Q

How should broad and narrow antibiotics be used properly?

A

Use broad antibiotics initially when you haven’t identified the organism but switch over to narrow spectrum antibiotics when you have the organism identidies

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26
Q

List the ideal properties of an antibiotic
(4)

A

Selective toxicity
Cidal activity
Narrow spectrum of activity if appropriate or broad spectrum for empiric therapy or the treatment of polymicrobial infections
Slow emergence of resistance

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27
Q

What is empiric therapy?

A

Use of broad spectrum antibiotics to treat an infection without knowing the causative organism

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28
Q

What four factors is choice of antibiotic influenced by?
(4)

A

Antibiotic properties
Pharmacological properties
Host
Pathogen

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29
Q

Why might the pharmacological properties of an antibiotic affect choice of antibiotic?

A

Plasma life - how long it takes an antibiotic to degrade in plasma
Tissue distribution including CSF i.e. will it be able to get into CSF to treat an infection

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30
Q

Why might the host affect choice of antibiotic?

A

Where is the site of infection?
What dose is achievable in the site of infection?
What is the patient’s immune system like, what will the immune response be?

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31
Q

Why might the pathogen affect choice of antibiotic?
(2)

A

The nature of the pathogen -> how doe sit evade the immune system etc

Resistance profile - antimicrobial susceptibility test results from the lab

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32
Q

What does the duration of an antibiotic treatment depend on?

A

The nature and site of infection
The growth rate of the pathogen

e.g. UTI needs antibiotics for 5 days, BSI needs 2-3 weeks of treatment, endocarditis needs 6 weeks, tuberculosis needs 9 months of treatment

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33
Q

Why are antibiotics sometimes combined?

A

Some antibiotics work better together than alone (synergy)

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34
Q

How are antibiotics combined for treatment?

A

They are used together as a single antibiotic agent e.g. sulphonamide and trimethoprim

35
Q

Give an example of where you would use more than one antibiotic as a single antibiotic agent (synergy antibiotics)

A

sulphonamide and trimethoprim

36
Q

What is combination therapy?

A

Using 2 or more separate drugs in treatment
Often used to prevent the emergence of resistance

37
Q

Give an example of where combination therapy is used
(2)

A

Triple treatment for tuberculosis

Cephalosporin and gentamicin for ventilator associated pneumonia

38
Q

When should combination therapy not be used?

A

There is a tendency for young medics to over use antibiotics on patients when they’re not sure which one to use so they use both/multiple

39
Q

List the modes of action of antibiotics
(5)

A

Inhibit cell wall synthesis

Inhibit protein synthesis

Inhibit DNA/RNA synthesis

Act on cytoplasmic cell/membrane

Metabolic pathway inhibitors

40
Q

What classes of antibiotics inhibit cell wall synthesis?
(2)

A

B-lactams

Glycopeptides

41
Q

What classes of antibiotics inhibit protein synthesis?
(3)

A

Aminoglycosides

Tetracyclines

Macrolides

42
Q

What classes of antibiotics inhibit DNA/RNA synthesis?

A

Fluoroquinolones

43
Q

What classes of antibiotics act on cytoplasmic/cell membranes?
(2)

A

Polymyxin

Polyenes

44
Q

What classes of antibiotics act as metabolic pathway inhibitors?

A

Sulphonamides

Trimethoprim

45
Q

Write a note on cell wall inhibitors
(3)

A

B-lactams and glycopeptides

Bactericidal agents that block the synthesis of the rigid peptidoglycan component of the cell wall, so growing cells lyse and die

It targets peptidoglycan which is a vital component of bacterial cell walls and it is unique to bacteria

46
Q

Write a note on peptidoglycan
(2)

A

Component of bacterial cell walls

Comprised of 2 sugar precursors
- Uridine diphosphate-N-acetylglucosamine (UDP NAG)
- UDP-N-acetyl muramyl-pentapeptide (UDP NAM)

47
Q

How do B-lactams inhibit synthesis of peptidoglycan?
(4)

A

B-lactam antibiotics are analogues of D-alannyl-D-alanine -> the terminal amino acid residues on the precursor NAM/NAG peptide subunits.

The final step in the synthesis of peptidoglycan is facilitated by DD-transpeptidases also known as penicillin binding proteins (PBPs)

PBPs vary in their affinity for B-lactams and the number of PBPs varies between bacterial species

B-lactams bind to and inhibit transpeptidase enzymes (PBPS) and prevent the final stages of peptidoglycan cross-linking

48
Q

What is the most common glycopeptide?

A

Vancomycin or teicoplanin

49
Q

Write a note on glycopeptides
(3)

A

Large complex molecules

Too bulky to penetrate the outer membrane of gram-negative bacteria i.e. doesn’t work on gram negatives

Thus, glycopeptides only have gram positive bactericidal activity

50
Q

What is the mode of action for glycopeptides
(3)

A

They bind to the D-ala-D-ala termini of pentapeptide in MurNac PG precursor

This prevents transport of peptidoglycan subunits across the cytoplasmic membrane

This prevents incorporation of new PG subunits into the growing PG chain

51
Q

What is the MurNac precursor?

A

UDP-N-acetyl muramyl-pentapeptide (UDP NAM)

52
Q

Vancomycin is the first choice of drug for what?
(3)

A

B-lactam resistant organisms particularly MRSA

If allergic to B-lactams

For C.difficile associated diarrhoae

53
Q

Why aren’t B-lactams used extensively

A

They are nephrotoxic i.e they damage the kidneys

54
Q

Why are new classes and new generations within classes developed?
(2)

A

To extend the spectrum of activity

To reduce vulnerability to evolving resistance mechanisms

55
Q

What are penicillins used for?

A

Gram positive bacteria and limited gram negative bacteria

56
Q

What are cephalosporins used for?

A

Gram positive bacteria
Extended enterobacterales
Pseudomonas

57
Q

What are carbapenems used for?

A

Reserved for resistant enerobacterales or pseudomonas

58
Q

What are the two routes for B-lactams

A

Oral or IV

59
Q

What is the principle behind protein synthesis inhibitors, aminoglycosides, tetracyclines and macrolides?
(6)

A

They act by binding to the ribosome

They either prevent ribosome binding to mRNA or prevent elongation of the chains to form proteins

They disrupt many essential bacterial functions

The agents may be bactericidal or bacteriostatic

Linezolid is the new agent developed in this class

Antibiotics bind to the 30S and/or 50S ribosomal subunit and interfere with initiation, elongation or termination

60
Q

How do aminoglycosides inhibit protein synthesis?
(4)

A

Aminoglycosides are a family of related compounds e.g. gentamicin with bactericidal activity

The original structure has been modified by changing the side chains to produce more active agents such as tobramycin and amikacin

Aminoglycosides bind at multiple sites on 30S subunit

This blocks initiation of protein synthesis, blocks further translation and elicits premature termination and leads to incorporation of incorrect amino acid

61
Q

What does binding of aminoglycosides to the 30S subunit do?
(3)

A

This blocks initiation of protein synthesis,

Blocks further translation and elicits premature termination

Leads to incorporation of incorrect amino acid

62
Q

What is gentamicin used for?
(4)

A

Gram positive MRSA
Enterococci
Enterobacterales
Extended Pseudomonas coverage

63
Q

How is gentamicin often used?
(2)

A

Used in combination with B-lactams such as ceftazidime in the treatment of serious invasive infection

Frequently used in combination with B-lactams

64
Q

Write a note on tetracyclines
(4)

A

Bacteriostatic activity by bindinging to the 3oS ribosomal unit

Prevents elongation and inhibits protein synthesis

Limited use in treatment of STI (chlamydia) and acne

It chelates calcium so it shouldn’t be used in young children to prevent the blackening of teeth

65
Q

Write a note on macrolides
(3)

A

Class including erythromycin and newer agents such as clarithromycin and azithromycin which have improved activity

It has a bacteriostatic effect for most bacteria

It accumulates at the clinical site of infection which is a favourable pharmacokinetic property

66
Q

How do the macrolides inhibit protein synthesis?
(2)

A

They bind to the 50S ribosomal subunit

This prevents elongation and inhibits protein synthesis

67
Q

How are macrolides used?
(3)

A

They have good tissue distribution

They are the common treatment choice for gram positives, lower respiratory tract infections and STIs

They are active against some important gram negative pathogens such as Neisseria (STI) and Haemophilus (RTI)

68
Q

How does Linezolid work
(2)

A

Targets the 50S subunit and prevents formation of a functional 70S complex

It’s active against a range of Gram-positive cocci, including MRSA and VRE

69
Q

Write a note on fluoroquinolones
(3)

A

An inhibitor of DNA synthesis -> by inhibiting DNA replication

Ciprofloxacin is the main agent

Levoflaxacin and moxifloxacin are more active quinolones

70
Q

How do fluoroquinolones inhibit DNA synthesis?
(3)

A

They are bactericidal agents.

They act on enzymes DNA gyrase and topoisomerase IV that control DNA supercoiling and uncoiling during bacterial cell replication.

Trapping of enzymes leads to lethal double-strand DNA breaks

71
Q

How are fluoroquinolones used?
(4)

A

They are well tolerated broad spectrum agents

They have activity against staphylococci

They have good activity against gram-negative rods including P.aeuriginosa

Used in the treatment of UTI and chlamydia infections but also for systemic infections

72
Q

How do membrane active compounds work?

A

They work by disorganising the cell membrane

73
Q

How do polymyxins work on the cell membrane
(2)

A

Polymyxins such as colistin act by disorganising cell membranes

They’re uses are very limited due to toxicity but now increased as a last resort for MDROs

74
Q

How do polyenes act on the cell membrane?
(2)

A

Polyenes such as amphotericin B (fungizone) work by binding to the cell membrane and creating pores

This causes potassium leakage and eventually death

75
Q

Daptomycin is a new type of antibiotic that acts on the cell membrane, how does it work?

A

It works selectively for bacterial cell membranes
Doesn’t have the toxicity associated with the polymyxins and polyenes

76
Q

How are the polyenes used?
(2)

A

Polyenes such as amphotericin B are used in the treatment of systemic fungal infections

But use is associated with severe and potentially lethal side effects such as nephrotoxicity, hepatotoxicity and cardiac arrhythmias

77
Q

What are competitive inhibitors and how do they work?
(5)

A

Antimicrobials which inhibit bacterial metabolic pathways

Agents act as false substrates and compete for active sites on enzymes in metabolic pathways and therefore block production

Sulfonamide and tromethoprim (septrin) is the most common agent and it inhibits folic acid synthesis

These have synergistic action by blocking two steps in the same pathway resulting in bacteriostasis

They have limited use in the treatment of UTIs

78
Q

What is a common side effect of using cephalosporins?

A

Vaginal candidiasis

79
Q

What is a common side effect of using quinolones?

A

Photosensitivity

80
Q

What classes of antibiotics cause renal toxicity?

A

Aminoglycosides -> gentamicin, tobramycin, amikacin
Glycopeptides -> vancomycin, teicoplanin

81
Q

What is an antibiotic assay and what is it for?

A

Used to monitor serum concentration of toxic antibiotics -> those that cause renal toxicity

Trough serum or peak serum can be used

82
Q

What is trough serum?
(3)

A

Pre

Taken just before the next dose of an antibiotic

The antibiotic should be completely cleared from the body before taking the next dose

83
Q

What is peak serum?
(3)

A

Post

Taken 1 hour post dose

Antimicrobial should have achieved active dose

2.2 Microbiology (60 decks)

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