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Yr 2 - Clinical Pathology > Antibacterial & Antifungal Agents > Flashcards

Antibacterial & Antifungal Agents Flashcards

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1
Q

Antimicrobials inhibit critical process in bacterial/fungal cells.

These processes include:

A

Enzymes, molecules or physical structures

  • cell wall
  • protein synthesis
  • DNA synthesis
  • RNA synthesis
  • membrane function
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2
Q

Definition of antibiotics?

A

Chemical products of microbes that inhibit or kill other organisms

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3
Q

What are antimicrobial agents?

A

(antibacterial, antifungal, antiviral)

  • Antibiotics
  • Synthetic compounds with similar effect
  • Semi-synthetic i.e. modified from antibiotics

Different antimicrobial activity/spectrum, pharmacological properties or toxicity

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4
Q

What is selective toxicity?

A

Inhibit critical process in bacterial/fungal cells with minimal harm to the patient

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5
Q

Define bacteriostatic/fungistatic

A

Capable of inhibiting the GROWTH or reproduction of bacteria.

Mainly protein synthesis inhibitors

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6
Q

Define bacteriocidal/fungicidal

A

Causes cell death (kill organism outright)

Mainly cell wall-active agents

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7
Q

How do bacteriostatic/fungistatic antimicrobials typically work?

A

Mainly protein synthesis inhibitors

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8
Q

How does bacteriostatic differ from bacteriocidal?

A

Bacteriostatic: Capable of inhibiting the growth or reproduction of bacteria.

Different from bactericidal (capable of killing bacteria outright).

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9
Q

Define minimum inhibitory concentration (MIC)

A

The minimum concentration of an antimicrobial agent at which VISIBLE GROWTH is inhibited

i.e. lower MIC = organism more sensitive to antimicrobial

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10
Q

Define minimum bactericidal/fungicidal concentration (MBC/MFC)

A

The minimum concentration of antimicrobial agent at which most organisms ARE KILLED

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11
Q

Define synergy

A

When the effect of a COMBINATION of two antimicrobial agents is GREATER THAN the sum of the effects observed with the two drugs INDEPENDENTLY

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12
Q

Define antagonism

A

Activity of two antimicrobials given together is LESS THAN the activity of either if given separately

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13
Q

Define the antimicrobial spectrum

A

Range of bacterial/fungal species likely to be sensitive to a particular antibacterial/antifungal agent

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14
Q

What is a broad spectrum antibiotic?

A

Kills MOST TYPES of bacteria/fungi encountered

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15
Q

What is a narrow spectrum antibiotic?

A

Kills only a NARROW RANGE of organisms

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16
Q

Which spectrum of antibiotic should be used?

A

The narrowest spectrum antibiotic that is appropriate should be used at all times

(want to upset normal flora as little as possible)

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17
Q

How does the spectrum of organisms covered by an antimicrobial agent change during its clinical lifespan?

A

Tends to become narrower as resistance develops in the target microbial population

E.g. Penicillin was once a broad spectrum antibiotic, but now it is considered to be “narrow spectrum”.

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18
Q

One of the major groups of antimicrobial agents are CELL WALL SYNTHESIS INHIBITORS

What is the major structural component of bacterial cell wall?

A

Peptidoglycan

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19
Q

Why are cell wall synthesis inhibitors ideal?

A
  1. Cell wall required for survival of bacteria

2. no cell wall in animal cells –> ideal potential for selective toxicity

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20
Q

What is peptidoglycan?

A

Polymer of glucose-derivatives, N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)

Oligopeptide crosslinks formed by transpeptidases known as “penicillin binding proteins” (PBPs).

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21
Q

What are penicillin-binding proteins?

A

A group of proteins that are characterised by their affinity for and binding of penicillin. They are a normal constituent of many bacteria; the name just reflects the way by which the protein was discovered.

PBPs are members of a subgroup of enzymes called transpeptidases.

Involved in the synthesis and maintenance of peptidoglycan

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22
Q

What are the 2 main cell wall synthesis inhibitors among the antibacterial agents?

A
  1. β-lactams (beta-lactams, penicillins)

2. Glycopeptides

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23
Q

Describe structure and action of β-lactam antibiotics

A

All b-lactam antibiotics have a four-membered ring structure - the b-lactam ring

They act by inhibiting penicillin binding proteins: enzymes involved in the synthesis and maintenance of peptidoglycan.

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24
Q

What are the 4 major groups of β-lactam antibiotics?

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapenems
  4. Monobactams
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25
Give examples of penicillins What spectrum?
Benzylpenicillin, amoxicillin, flucloxacillin Relatively narrow spectrum§
26
Give examples of Cephalosporins What spectrum?
Cefuroxime, ceftazidime etc. Broad spectrum - Arranged into ‘generations’
27
Give examples of Carbapenems What spectrum?
Meropenem, imipenem Extremely broad spectrum
28
Give examples of Monobactams What spectrum?
Aztreonam Gram-negative activity only and has slightly different ring structure
29
Contraindications of β-lactam antibiotics?
the risk of cross-reactivity -contraindication of all β-lactam antibiotics in patients with a history of: severe allergic reactions (urticaria, anaphylaxis, interstitial nephritis) to any β-lactam antibiotic. N.B. patients with penicillin allergy can usually be given Aztreonam (different structure)
30
What are the 2 main examples of glycopeptides (cell wall synthesis inhibitor)?
Vancomycin, teicoplanin
31
Mechanism of glycopeptides?
Large molecules, bind to terminal amino acids on NAM pentapeptides Inhibit binding of transpeptidases and thus peptidoglycan cross-linking
32
What organisms are glycopeptides effective against?
Gram-positive --> unable to penetrate Gram-negative outer membrane
33
What are the 5 basic mechanisms of antibiotic action against bacterial cells?
1. Inhibition of Cell Wall Synthesis (most common mechanism) 2. Inhibition of Protein Synthesis (Translation) (second largest class) 3. Alteration of Cell Membranes. 4. Inhibition of Nucleic Acid Synthesis. 5. Antimetabolite Activity.
34
Where does protein synthesis take place in bacteria?
Protein synthesis takes place on the bacterial ribosome RNA moves through the ribosome and is translated into a polypeptide chain
35
What are bacterial ribosomes composed of? How does this differ to eukaryotic cells?
50S (large) and 30S (small) subunits combine to form 70S initiation complex 60S and 40S in eukaryotic cell
36
What does the S in 50S refer to?
S=Svedberg units; relative sedimentation rate
37
What are the 6 main types of bacterial protein synthesis inhibitors?
1. Aminoglycosides (e.g. gentamicin, amikacin) 2. Macrolides (e.g. erythromycin, clarithromycin) and lincosamides (clindamycin) 3. Tetracycline, doxycycline 4. Linezolid 5. Mupirocin 6. Fusidic acid (not used very much)
38
What are Tigecycline and eravacycline?
Synthetic derivatives of tetracyclines with a similar mechanism of action and a much broader spectrum
39
What does Linezolid target?
Gram-positive infections
40
What is Mupirocin used for?
Topical agent for staphylococcal/streptococcal infection
41
How do antibiotics that inhibit DNA synthesis work?
Inhibit folate synthesis --> Folic acid is a precursor of purine synthesis
42
What 2 drugs inhibit folate synthesis in order to inhibit DNA synthesis?
1. Trimethoprim - dihydrofolate reductase | 2. Sulfonamides
43
What is Trimethoprim commonly used to treat?
UTIs
44
DNA synthesis pathway in bacteria: 1. Bacterial para-amino benzoic acid (PABA) 2. Dihydropteroate 3. Dihydrofolate (dietary folate) 4. Tetrahydrofolate (folinic acid) 5. Thymidine/purine synthesis 6. DNA Which point of this pathway does: a) sulfonamides target? b) trimethoprim target?
a) The step from PABA --> dihydropteroate by inhibiting Dihydropteroate synthetase b) The step from Dihydrofolate (dietary folate) --> Tetrahydrofolate (folinic acid) by inhibiting Dihydrofolate reductase
45
What enzyme does sulfonamides inhibit?
Dihydropteroate synthetase
46
What enzyme does trimethoprim inhibit?
Dihydrofolate reductase
47
What is Co-trimoxazole a combination of? What is it used to treat?
trimethoprim-sulfamethoxazole 1. Has antibacterial effects 2. Has antifungal effects specific to Pneumocystis jiroweci 3. Has antiparasitic effects specific to Toxoplasma gondii
48
What are the antifungal effects of Co-trimoxazole specific to?
Pneumocystis jiroweci
49
What are the antiparasitic effects of Co-trimoxazole specific to?
Toxoplasma gondii (toxoplasmosis)
50
What is the action of fluoroquinolones? Mechanism?
DNA synthesis inhibitors: - Inhibit one or more of two related bacterial enzymes: DNA gyrase and topoisomerase IV - Involved in remodelling of DNA during DNA replication
51
What are 2 examples of fluoroquinolones?
Ciprofloxacin, levofloxacin
52
How do RNA synthesis inhibitors work?
- RNA polymerase inhibitor | - Prevents synthesis of mRNA
53
Whats an example of an antibiotic that acts as an RNA synthesis inhibitor?
Rifampicin
54
What is Rifampicin primarily used in the treatment of?
anti-tuberculous chemotherapy
55
Why is Rifampicin ALWAYS used in combination with other antimicrobial agents?
Easy for organisms to develop mutations in their RNA polymerase which render them resistant to Rifampicin
56
Some antibiotics target the cell membrane. What are some examples of these?
- Colistin/polymyxin E (Gram-negatives) | - Daptomycin (Gram-positives)
57
Mechanism of Daptomycin?
Is a cyclic lipopeptide that causes destruction of outer membrane or cytoplasmic membrane of Gram-positive agents
58
Summary of antibacterial mechanisms:
1. Cell wall synthesis - Glycopeptides - Beta-lactams - penicillins and cephalosporins 2. Protein synthesis: - Macrolides/lincosamides - Aminoglycosides - Tetracyclines - Linezolid Etc. 3. DNA synthesis - Trimethoprim/ sulfonamides - Quinolones - (Metronidazole) 4. RNA synthesis: - Rifampicin 5. Cytoplasmic membrane - Daptomycin 6. Outer membrane - Colistin (polymyxins)
59
What are pathogenic fungi divided into?
1. Filamentous fungi (moulds) | 2. Yeasts
60
What are dimorphic fungi?
Fungi that can exist in the form of both mould and yeast. This is usually brought about by change in temperature.
61
What parts of the fungal cell do antifungals target?
1. Cell wall 2. Cell membrane 3. DNA synthesis 4. Protein synthesis
62
What sterol is found in cell membranes of fungi and protozoa?
Ergosterol Serves many of the same functions that cholesterol serves in animal cells.
63
Why is selective toxicity for antifungals limited?
DNA and protein synthesis in animal cells is relatively similar to in fungal cells
64
What is the fungal cell wall composed of?
β-1,3-glucan (synthesized by β-1,3-glucan synthase)
65
Why is the fungal cell wall an excellent target for antifungal therapy?
As the components of the fungal cell wall are not present in humans i.e. animal cells have no cell wall
66
Main example of antifungal cell wall inhibitor?
Echinocandins (antifungal) - Anidulafungin - Caspofungin - Micafungin
67
Mechanism of Echinocandins?
- Enzyme inhibitors | - Inhibit β-1,3-glucan synthase
68
Why do Echinocandins have relatively few side effects?
Their target is specific to fungi
69
What are the 3 groups of antifungals that target the cell membrane (i.e. target Ergosterol)?
1. Azoles (clotrimazole, fluconazole, voriconazole) 2. Terbinafine 3. Amphotericin B (and nystatin)
70
Mechanism of Terbinafine?
Inhibit synthesis of ergosterol (a component of fungal cell membranes but not human or bacterial cells)
71
Mechanism of Amphotericin B (and nystatin)?
Bind to ergosterol causing physical damage to the membrane
72
What is the only antifungal agent to inhibit RNA/DNA synthesis?
5-fluorocytosine
73
Mechanism of 5-fluorocytosine?
Transported into fungal cells by a fungal enzyme (Cytosine permease) Metabolised into inhibitory molecules (mainly 5-fluorouracil)
74
What is 5-fluorocytosine used to treat?
Use largely historic but still used to treat cryptococcal meningitis
75
Summary of antifungal mechanisms
1. RNA/DNA synthesis - 5-fluorocytosine (5FC) 2. Cell membrane synthesis (ergosterol) - Azoles - Terbinafine 3. Cell membrane integrity - Amphotericin B 4. Cell wall synthesis - Echinocandins
76
Empiric vs targeted therapy?
Empiric Therapy. choosing antibiotic therapy with a clinical educated guess. Targeted Antibiotic Therapy. Choosing therapy based on a definitive organism As your level of knowledge of infecting organisms increases, the antimicrobial spectrum of agents used should decrease

Yr 2 - Clinical Pathology (80 decks)

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