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2.2 Microbiology > Antibiotic Activity > Flashcards

Antibiotic Activity Flashcards

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
How should broad and narrow antibiotics be used properly?
Use broad antibiotics initially when you haven't identified the organism but switch over to narrow spectrum antibiotics when you have the organism identidies
26
List the ideal properties of an antibiotic (4)
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
27
What is empiric therapy?
Use of broad spectrum antibiotics to treat an infection without knowing the causative organism
28
What four factors is choice of antibiotic influenced by? (4)
Antibiotic properties Pharmacological properties Host Pathogen
29
Why might the pharmacological properties of an antibiotic affect choice of antibiotic?
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
30
Why might the host affect choice of antibiotic?
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?
31
Why might the pathogen affect choice of antibiotic? (2)
The nature of the pathogen -> how doe sit evade the immune system etc Resistance profile - antimicrobial susceptibility test results from the lab
32
What does the duration of an antibiotic treatment depend on?
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
33
Why are antibiotics sometimes combined?
Some antibiotics work better together than alone (synergy)
34
How are antibiotics combined for treatment?
They are used together as a single antibiotic agent e.g. sulphonamide and trimethoprim
35
Give an example of where you would use more than one antibiotic as a single antibiotic agent (synergy antibiotics)
sulphonamide and trimethoprim
36
What is combination therapy?
Using 2 or more separate drugs in treatment Often used to prevent the emergence of resistance
37
Give an example of where combination therapy is used (2)
Triple treatment for tuberculosis Cephalosporin and gentamicin for ventilator associated pneumonia
38
When should combination therapy not be used?
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
List the modes of action of antibiotics (5)
Inhibit cell wall synthesis Inhibit protein synthesis Inhibit DNA/RNA synthesis Act on cytoplasmic cell/membrane Metabolic pathway inhibitors
40
What classes of antibiotics inhibit cell wall synthesis? (2)
B-lactams Glycopeptides
41
What classes of antibiotics inhibit protein synthesis? (3)
Aminoglycosides Tetracyclines Macrolides
42
What classes of antibiotics inhibit DNA/RNA synthesis?
Fluoroquinolones
43
What classes of antibiotics act on cytoplasmic/cell membranes? (2)
Polymyxin Polyenes
44
What classes of antibiotics act as metabolic pathway inhibitors?
Sulphonamides Trimethoprim
45
Write a note on cell wall inhibitors (3)
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
Write a note on peptidoglycan (2)
Component of bacterial cell walls Comprised of 2 sugar precursors - Uridine diphosphate-N-acetylglucosamine (UDP NAG) - UDP-N-acetyl muramyl-pentapeptide (UDP NAM)
47
How do B-lactams inhibit synthesis of peptidoglycan? (4)
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
What is the most common glycopeptide?
Vancomycin or teicoplanin
49
Write a note on glycopeptides (3)
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
What is the mode of action for glycopeptides (3)
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
What is the MurNac precursor?
UDP-N-acetyl muramyl-pentapeptide (UDP NAM)
52
Vancomycin is the first choice of drug for what? (3)
B-lactam resistant organisms particularly MRSA If allergic to B-lactams For C.difficile associated diarrhoae
53
Why aren't B-lactams used extensively
They are nephrotoxic i.e they damage the kidneys
54
Why are new classes and new generations within classes developed? (2)
To extend the spectrum of activity To reduce vulnerability to evolving resistance mechanisms
55
What are penicillins used for?
Gram positive bacteria and limited gram negative bacteria
56
What are cephalosporins used for?
Gram positive bacteria Extended enterobacterales Pseudomonas
57
What are carbapenems used for?
Reserved for resistant enerobacterales or pseudomonas
58
What are the two routes for B-lactams
Oral or IV
59
What is the principle behind protein synthesis inhibitors, aminoglycosides, tetracyclines and macrolides? (6)
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
How do aminoglycosides inhibit protein synthesis? (4)
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
What does binding of aminoglycosides to the 30S subunit do? (3)
This blocks initiation of protein synthesis, Blocks further translation and elicits premature termination Leads to incorporation of incorrect amino acid
62
What is gentamicin used for? (4)
Gram positive MRSA Enterococci Enterobacterales Extended Pseudomonas coverage
63
How is gentamicin often used? (2)
Used in combination with B-lactams such as ceftazidime in the treatment of serious invasive infection Frequently used in combination with B-lactams
64
Write a note on tetracyclines (4)
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
Write a note on macrolides (3)
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
How do the macrolides inhibit protein synthesis? (2)
They bind to the 50S ribosomal subunit This prevents elongation and inhibits protein synthesis
67
How are macrolides used? (3)
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
How does Linezolid work (2)
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
Write a note on fluoroquinolones (3)
An inhibitor of DNA synthesis -> by inhibiting DNA replication Ciprofloxacin is the main agent Levoflaxacin and moxifloxacin are more active quinolones
70
How do fluoroquinolones inhibit DNA synthesis? (3)
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
How are fluoroquinolones used? (4)
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
How do membrane active compounds work?
They work by disorganising the cell membrane
73
How do polymyxins work on the cell membrane (2)
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
How do polyenes act on the cell membrane? (2)
Polyenes such as amphotericin B (fungizone) work by binding to the cell membrane and creating pores This causes potassium leakage and eventually death
75
Daptomycin is a new type of antibiotic that acts on the cell membrane, how does it work?
It works selectively for bacterial cell membranes Doesn't have the toxicity associated with the polymyxins and polyenes
76
How are the polyenes used? (2)
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
What are competitive inhibitors and how do they work? (5)
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
What is a common side effect of using cephalosporins?
Vaginal candidiasis
79
What is a common side effect of using quinolones?
Photosensitivity
80
What classes of antibiotics cause renal toxicity?
Aminoglycosides -> gentamicin, tobramycin, amikacin Glycopeptides -> vancomycin, teicoplanin
81
What is an antibiotic assay and what is it for?
Used to monitor serum concentration of toxic antibiotics -> those that cause renal toxicity Trough serum or peak serum can be used
82
What is trough serum? (3)
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
What is peak serum? (3)
Post Taken 1 hour post dose Antimicrobial should have achieved active dose

2.2 Microbiology (60 decks)

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