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1. CP - Core Microbiology > (1) Intro to antibacterial agents > Flashcards

(1) Intro to antibacterial agents Flashcards

1
Q

What is the ‘spectrum’ of an antibiotic?

A

The organisms against which they are active

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2
Q

What is an antimicrobial agent?

A

Umbrella term - can be antibacterial, anti fungal, antiviral agents etc.

Includes antibiotics, synthetic compounds and semi-synthetic compounds

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3
Q

Define antibiotic

A

Chemical products of microbes that inhibit or kill other organisms

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4
Q

What is a semi-synthetic antimicrobial agent?

A

Modified from antibiotics

May have a different antimicrobial activity/spectrum or different pharmacological properties or toxicity

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5
Q

The term ‘antibiotic’ is often used interchangeably with which other term?

A

Antibacterial agent

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6
Q

In which 2 general ways do antibacterial agents act to stop bacteria?

A
  • inhibit bacterial growth (= bacteristatic)

- kill bacteria (=bactericidal)

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7
Q

What is the minimum inhibitory concentration (MIC)?

A

The minimum concentration of antibiotic at which visible growth is inhibited

The smaller the MIC, the more active the antibiotic

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8
Q

Can antibiotics be both bacteristatic and bactericidal?

A

Some antibiotics are bacteristatic at low concentrations and bactericidal at high concentrations

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9
Q

What are the 3 types of antimicrobial interactions?

A
  • synergism
  • antagonism
  • indifference
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10
Q

Synergism is a type of antimicrobial interaction. What does it mean?

A

The activity of 2 antimicrobials given together is greater than the sum of their activity if given separately

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11
Q

Antagonism is a type of antimicrobial interaction. What does it mean?

A

One agent diminishes the activity of another

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12
Q

Indifference is a type of antimicrobial interaction. What does it mean?

A

Activity unaffected by the addition of another agent

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13
Q

Give a clinical example of synergism

A

B-lactam/aminoglycoside therapy of streptococcal endocarditis

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14
Q

What is selective toxicity?

A

The target of the antibacterial is not present in human host or is significantly different in the human host

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15
Q

Give some examples of targets of antibiotics

A
  • cell wall
  • protein synthesis
  • DNA synthesis
  • RNA synthesis
  • plasma membrane
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16
Q

What does the bacterial cell wall consist of?

A

Peptidoglycan

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17
Q

Peptidoglycan is the major component of cell walls in which type of bacteria?

A

Both Gram-positive and Gram-negative bacteria

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18
Q

What is peptidoglycan a polymer of?

A

It is a polymer of glucose-derivatives, N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)

(NAMs joined together by NAGs, forms a network)

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19
Q

Why is targeting the bacterial cell wall good in terms of selective toxicity?

A

There is no cell wall in animal cells

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20
Q

Which classes of antibiotics are cell wall synthesis inhibitors?

A
  • B-lactams

- glycopeptides

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21
Q

What do B-lactams (a cell wall synthesis inhibitor) all contain?

A

The b-lactam ring

Four-membrered ring structure (C-C-C-N)

Structural analogue of D-alanyl-D-alanine

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22
Q

What do B-lactams interfere with?

A

The interfere with the function of “penicillin binding proteins” which are the enzymes involved in the construction of the peptidoglycan bacterial cell wall

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23
Q

What are “penicillin binding proteins”?

A

Transpeptidase enzymes involved in the peptidoglycan cross-linking which forms the bacterial cell wall

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24
Q

Which groups of antibiotics are B-lactam antibiotics?

A
  • penicillins
  • cephalosporins
  • carbapenems
  • monobactams
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25
Give some examples of penicillins (B-lactams)
- benzylpenicillin - amoxicillin - flucloxacillin
26
Give a feature of penicillins
Relatively narrow spectrum
27
Give some examples of cephalosporins (B-lactams)
- cefuroxine | - ceftazidime
28
Give a feature of cephalosporins
Broad spectrum
29
Give some examples of carbapenems (B-lactams)
- meropenem | - imipenem
30
Give a feature of carbapenems
Extremely broad spectrum
31
Give a monobactam (B-lactam)
Aztreonam
32
Give a feature of aztreonam (a monobactam, B-lactam)
Gram-negative activity only
33
Which B-lactam antibiotic works on gram-negative bacteria only?
Aztreonam | a monobactam
34
Glycopeptides are the other cell wall synthesis inhibitors, along with B-lactams. Give some examples
- vancomycin | - teicoplanin
35
What do glycopeptide antibiotics do specifically?
Large molecules that bind directly to terminal D-alanyl-D-alanine on NAM pentapeptides, inhibiting binding of transpeptidases and thus peptidoglycan cross-linking
36
Glycopeptides work on which classification of bacteria?
Gram-positive They are unable to penetrate gram-negative outer membrane porins
37
Vancomycin comes under which classification of antibiotics?
Glycopeptides
38
Summarise protein synthesis in bacteria
- translation of RNA to protein takes place on the ribosome - ribonucleoprotein complex is 2/3 RNA and 1/3 protein - 50S (large) and 30S (small) subunits combine to form 70s initiation complex
39
Which groups of antibiotics are protein synthesis inhibitors?
- aminoglycosides - macrolides, lincosamides, streptogramins (MLS) - tetracyclines - oxazolidinones
40
Give some examples of aminoglycosides
- gentamycin | - amikacin
41
What do aminoglycosides do?
Bind to 30S ribosomal subunit Mechanism of action not fully understood
42
Give some examples of MLS antibiotics
- erythromycin, clarithromycin (macrolides) | - clindamycin (lincosamide)
43
What do MLS antibiotics do?
Bind to 50S ribosomal subunit = blockage of exit tunnel - inhibition of protein elongation
44
Give some examples of tetracyclines
Tetracycline, doxytetracycline
45
What do tetracyclines do?
Bind to 30S ribosomal subunit Inhibit RNA translation - interfere with binding of tRNA to rrNA
46
Give an example of an oxazolidinone
Linezolid
47
What does linezolid (an oxazolidinone) do?
Inhibits initiation of protein synthesis Binds to 50S ribosomal subunit Inhibits assembly of initiation complex May also bind to 70S subunit
48
Other than the aminoglycosides, MLS, tetracyclines and oxazolidinones, give some other protein synthesis inhibitors
- mupirocin | - fusidic acid
49
Which groups of antibiotics are DNA synthesis inhibitors?
- trimethoprim and sulphonamides | - quinolones and fluoroquinolones
50
What do trimethoprim and sulphonamides do?
Inhibit folate synthesis - folic acid is a purine synthesis precursor
51
Specifically, what does trimethoprim inhibit?
Dihydrofolate reductase
52
Specifically, what do sulphonamides inhibit?
Dihydropteroate synthetase
53
What 2 antibiotics make co-trimoxazole when combined?
Trimethoprim and sulfamethoxazole
54
What do quinolones and fluoroquinolones do?
Inhibit enzymes - DNA gyrase and topoisomerase IV These are involved in remodelling of DNA during DNA replication
55
Give some examples of quinolones and fluoroquinolones
- nalidixic acid - ciprofloxacin - levofloxacin
56
Which antibiotic is a RNA synthesis inhibitor?
Rifampicin
57
What does rifampicin do?
It is an RNA polymerase inhibitor Prevents synthesis of mRNA
58
What is different about plasma membrane agents compared to other antibiotics?
They attack a structure (the plasma membrane) rather than disrupting a process - the plasma membrane must be intact for bacteria to survive
59
Which plasma membrane agent works on gram-negative bacteria?
Colistin
60
Which plasma membrane agent works on gram-positive bacteria?
Daptomycin - cyclic lipopeptides - destruction of cell membrane
61
What are the general adverse effects of any drug?
- nausea, vomiting, headache, skin rashes etc - infusion reactions - allergic reactions
62
What type of infections can antibiotic treatment adversely cause?
- fungal infection (superficial and invasive candidiasis) | - clostridium difficile infection
63
Which group of antibiotics are most significant in allergy?
B-lactams
64
What are the specific adverse effects of aminoglycosides?
- reversible renal impairment on accumulation - irreversible ototoxicity Therapeutic drug monitoring indicated
65
What are the specific adverse effects of b-lactams?
Mainly allergic reactions generalised rash = 1-10% anaphylaxis = approx 0.01%
66
What is the specific adverse effects of linezolid?
Bone marrow depression
67
In which 3 ways can allergy to penicillins be classified?
- intolerance - minor allergic reaction - severe allergic reaction
68
What would an intolerance to penicillin cause?
Nausea, diarrhoea, headaches etc
69
What would a minor allergic reaction to penicillin cause?
Non-severe skin rash
70
What would a severe allergic reaction to penicillin cause?
Anaphylaxis, urticaria, angio-oedema, bronchospasm, severe skin reaction (Stevens-Johnson syndrome)
71
Which B-lactams are safe to use in patents with non-severe penicillin allergy?
- cephalosporins | - carbapenems
72
Which B-lactams are safe to use in patients with any penicillin allergy?
- aztreonam
73
What is C. difficile infection caused by?
Abolition of colonisation resistance due to antibiotic consumption
74
Which toxins does C. diff produce?
Toxins A and B
75
What causes the clinical features and transmissibility of C. diff?
Combination of enterotoxin and spore production
76
Which strain of C. diff causes more severe disease?
Hypervirulent strain 027
77
What are the common precipitating antibiotics of C. diff?
4Cs - co-amoxiclav (amoxicillin-clavulanate) - cephalosporins - ciprofloxacin - clindamycin
78
What are the less common precipitating antibiotics of C. diff?
- benzylpenicillin, aminoglycosides, glycopeptides | - piperacillin-taxobactam (despite broad spectrum)
79
May C. diff be precipitated by any antibiotics?
Yes!
80
What are the 3 stages in the strategy of antibiotic use?
1. empiric therapy (best guess) 2. targeted therapy 3. susceptibility-guided therapy
81
Empiric therapy is the first stage in the strategy of antibiotic use. What is it based upon?
- predicted susceptibility of likely pathogens - local antimicrobial policies (after history, examination and clinical diagnosis)
82
Targeted therapy is the second stage in the strategy of antibiotic use. What is it based upon?
- predicted susceptibility of infecting organism(s) - local antimicrobial policies (after laboratory investigations: microbiological diagnosis)
83
Susceptibility-guided therapy is the third stage in the strategy of antibiotic use. What is it based upon?
- susceptibility testing results | after the antimicrobial susceptibility test
84
When can you use antimicrobials with the narrowest spectrum of agents?
When you have a higher level of knowledge of what the infecting organism is
85
In the statement 'Start Smart - then Focus' relating to antibiotic use, what does the 'start smart' bit mean?
- only use antibiotics if there is clinical evidence of bacteria infection - use local guidelines - document indication, duration or review date - obtain cultures first - use single dose antibiotics for surgical prophylaxis
86
In the statement 'Start Smart - then Focus' relating to antibiotic use, what does the 'focus' part mean?
at 48 hours - stop antibiotics if there is no evidence on infection - switch antibiotics from intravenous to oral - change antibiotics, ideally to a narrower spectrum, or broader if required - continue and review again at 72 hours - outpatient parenteral antibiotic therapy (OPAT)
87
What are some key antibiotic/bacteria combinations?
- flucloxacillin/staph. aureus (not MRSA) - benzylpenicillin/strep. pyogenes - cephalosporins/gram-neg bacilli - metronidazole/anaerobes - vancomycin/gram-pos (MRSA) - meropenem/most clinically-relevant bacteria - cloisitin/last option for multi-resistant gram-negs
88
What is a warning related to cephalosporins?
Avoid in the elderly
89
The antibiotic colistin is used as a last option for which bacteria?
Multi-resistant gram-negatives
90
Which antibiotic tends to be used for streptococcus pyogenes?
Benzylpenicillin
91
Which antibiotic tends to be used for staphylococcus aureus?
Flucloxacillin
92
Which antibiotic is used for MRSA (and other gram-positive bacteria)?
Vancomycin
93
Anaerobic bacteria can be treated with which antibiotic?
Metronidazole
94
Cephalosporins treat which type of bacteria?
Gram-negative bacilli
95
What is an important determinant of in vivo efficacy?
Concentration at site of action
96
What has good availability/ poor availability in the CSF?
B-lactams - good availability in presence of inflammation Aminoglycosides and vancomycin = poor availability
97
What has good availability/ poor availability in the urine?
Trimethoprim and B-lactams = good availability MLS antibiotics = poor availability
98
What is the main determinant of bacterial killing? (concentration dependent)
The factor by which concentration exceeds MIC
99
How are high peaks of antibiotic concentration achieved? (concentration dependent)
By administering the antibiotic intermittently eg. aminoglycosides
100
What is the main determinant of bacterial killing? (time dependent)
The amount of time of which antibiotic concentration exceeds MIC
101
How is high concentration of antibiotic maintained? (time dependent)
Administered frequently e.g B-lactams
102
What are the reasons for combining antibiotics? (combination therapy)
- to increase efficacy - to provide adequately broad spectrum - to reduce resistance
103
A reason for using combination therapy is to increase efficacy. How does this happen?
Synergistic combination may improve clinical outcome (B-lactam/aminoglycoside in streptococcal endocarditis)
104
A reason for using combination therapy is to provide adequately broad spectrum. Explain this
Single agent may not cover all required organisms - polymicrobial infection - empiric treatment of sepsis
105
How does using combination therapy reduce resistance?
The organism would need to develop resistance to multiple agents simultaneously - antituberculosis chemotherapy

1. CP - Core Microbiology (8 decks)

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