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Antimicrobial and chemotherapy > General properties of antimicrobial agents > Flashcards

General properties of antimicrobial agents Flashcards

1
Q

What is meant by selective toxicity?

A

Drugs that disrupts microbial functions not found in the eukaryotic cells.

Leads to:

  • Greater selectivity
  • Greater therapeutic range
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2
Q

What are the classes of the antimicrobial agents?

A

1) cell wall synthesis inhibitors
2) Disruptors of cell wall/membrane
3) Protein synthesis inhibitors
4) Metabolic at antagonists
5) Nucleic acid synthesis/manipulation inhibitors

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3
Q

State agents of cell wall synthesis inhibition

A
  • Bacitracin
  • beta-lactam
  • Fosfomycin
  • Glycopeptides
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4
Q

which agents affect the Structure and function of the cell membrane

A
  • Colistin
  • Daptomycin
  • Polymyxin B
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5
Q

list agents that are Metabolic antagonists (Folic Acid synthesis)

A
  • Trimethoprim

- Sulfonamides

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6
Q

What agents are nucleic acid (DNA) inhibitors?

A
  • Quinolones
  • Nitrofurantoin
  • Nitroimidazole
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7
Q

Protein synthesis inhibition agents

A
  • Aminoglycosides
  • Lincosamide
  • Macrolides
  • Tetracyclines
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8
Q

G+ve cell wall structure and stain

A
  • Cytoplasmic membrane
  • Rigid, thick, cross-linked peptidoglycan
  • Purple stain
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9
Q

G-ve cell wall structure and stain

A
  • Cytoplasmic membrane
  • Thin, cross-linked peptidoglycan
  • Outer membrane
  • pink stain
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10
Q

What gives cell wall rigidity and what is it composed of?

A

-Peptidoglycan gives cell wall it rigidity
-Peptidoglycan is made of repeating sugars that are crossed linked:
+ N-acetyl glucosamine (NAG)
+ N-acetyl muramic acid (NAM)
- has peptide chain

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11
Q

What is the family of enzymes used to connect the sugar molecule peptide chain?

A

-Penicillin binding protein
or
-Transpeptidase
these are used interchangeably

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12
Q

How does PBPs work?

A
  • reactive serin residue in the PBP with the penultimate D-alanine on the peptide chain.
  • This remove the last reside (after the D-alanine).
  • The PBP grabs another pentaglycine chain for another peptidoglycan chain and join them together.
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13
Q

How does Beta-lactam work

A
  • It inhibits PBP.
  • B-Lactam ring resembles D-alanyl-D-alanine section of peptide side chain.
  • PBP bind irreversibly to lactam and not side chain
  • No cross-linking leads to bactericidal lysis.
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14
Q

Why is the lactam made of?

A

Made of Lactone and amide

- Lactone is a cyclic carboxylic ester

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15
Q

what makes Beta lactam ring so reactive?

A

Made of 4 rings and so is strained

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16
Q

What are the types of B-lactam resistance?

A
  • Intrinsic resistance

- Acquired resistance

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17
Q

what is intrinsic resistance?

A

Change in the structure or function of bacteria species.

eg no typical crosslinking

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18
Q

What is acquired resistance?

A

A previously sensitive bacterium acquires a mutation or new genetic material allowing it to resist activity of the agent

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19
Q

What is the mechanism of Beta-lactamase?

A

Lyses the 4 atom lactam ring. This reduces the strain and make it significantly less reactive.

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20
Q

What are the subgroups of penicillin?

A
  • Natural penicillin
  • Anti-staphylococcal penicillin
  • Aminopenicillin
  • Extended spectrum penicillin
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21
Q

Types of Natural penicillin

A

Penicillin V- oral

Penicillin G- injection (IM or IV)

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22
Q

Properties of natural penicillin

A

-Relatively hydrophobic side chain
-Majority of bacteria either intrinsically resistant or
have acquired resistance
-Susceptible to many β-lactamases

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23
Q

Examples of Anti-staphylococcal penicillin

A 
Flucloxacillin
Methicillin
Cloxacillin
dicloxacillin
oxacillin
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24
Q

Properties of Anti-staphylococcal penicillin

A

-Bulky side chains: reduced binding by staphylococcal lactamases
- MRSA / MRSE have different PBPs (mecA gene / PBP2)
- Bulky, relatively hydrophobic side chains prevent
penetration through porins (v poor G- action)

P.S MRSA=Methicillin-resistant Staphylococcus aureus

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25
Q

Examples of Aminopenicillins

A

Amoxicillin

Ampicillin

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26
Q

Properties of Aminopenicillin

A

-Additional amino group on side chains increases hydrophilicity
• Pass better through porins
• Extends spectrum of G– activity

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27
Q

Examples of extended-spectrum penicillin

A

piperacillin

ticarcillin

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28
Q

Properties of Extended-spectrum penicillin

A

– Side chains enhance porin penetration
– More resistant to G- lactamases
– Often less active against G+ organisms

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29
Q

What is penicillin augmentation

and give some examples

A

-Penicillin and beta-lactamase inhibitor is given in combination
-amoxicillin-clavulanate (augmentin)
piperacillin-tazobactam (tazocin)
additional lactams as “decoy” substrate

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30
Q

properties of B-lactamase inhibitors

A
  • Reactive molecule with high tendency to bind to βlactamases
  • Thus, active antibiotic doesn’t get cleaved
  • Increased activity against G+ / G- / anaerobes
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31
Q

Draw and describe the structure of cephalosporins.

A
  • It has the nucleus and 2 main side chain
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32
Q

What are the 2 side chain modifications on cephalosporins representative of.

A
  • R1: Antimicrobial activity including changed in water solubility and PBP affinity
  • R2: Pharmacokinetic properties
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33
Q

What is the name of the 1st, 2nd, 3rd , 4th and 5th gen cephalosporins.

A

1st: Cefalexin
2nd: Cefuroxime
3rd: Ceftazidime, ceftraixone
4th: Cefepime,
5th: Ceftaroline

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34
Q

Feature of first generation cephalosporins.

Features of the side chain.

A

Good for: activity against G+ cocci
R1: Protection from staphylococcal b-lactamases NOT G-VE
No R2

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35
Q

2nd gen cephalosporins features and R side chain features

A

-More activity G-ve than 1st gen.
-less activity against G+ve
-R1: increased polarity, better porin entry
R2: minimal but quite polar

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36
Q

3rd gen features and R side chain features

A
  • ceftriaxone, ceftazidime
    • R1 Polar: Increased porin penetration
    • Increased affinity for some PBPs
    • Increased stability vs. G- b-lactamases
  • ceftazidime active against Pseudomonas
    • R2 - ceftriaxone has a long t1/2
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37
Q

4th and 5th gen cephalosporin features

A

*cefepime (4th)
aminothiazolyl group on R1 and polar pyrolidine group on R2
Pseudomonas

*ceftaroline (5th)
good activity against G+, including MRSA (PBP2a)

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38
Q

What are the names of Carbapenems class drugs

A
  • Imipenem
  • meropenem
  • ertapenem
39
Q

What spectrum of antimicrobials does the carbapenems cover

A

It is a very broad spectrum antibiotic

- G-VE G+ve and anaerobic

40
Q

Name of a monobactam drug

A

-Aztreonam

41
Q

What range of bacterial classes do monobactams work against

A

Aerobic G-ve so it it a narrow spectrum

42
Q

feature of Monobactams

A
  • Lone b-lactam ring
  • Totally synthetic
  • Combines advantageous properties from 3G cephalosporins
  • Very low likelihood of reaction in penicillin-allergic patients (but R1 chain is very like ceftazidime)
43
Q

Name 2 of the glycopeptides

A

Vancomycin

Teicoplanin

44
Q

what are the origins of glycopeptides

A

From streptomyces organisms

45
Q

MOA of glycopeptides

A

Inhibit cell wall synthesis by forming complex with substrate that make D-ala-D-ala

“slowly/weakly” bactericidal

By binding to the D-Ala-D-Ala terminal of the growing peptide chain during cell wall synthesis, resulting in inhibition of the transpeptidase

46
Q

Glycopeptide spectrum

A

-Narrow spectrum

G+ve only as it is too large to enter into the porins of G-ve cells

47
Q

Origin of Fosfomycin

A

Streptomyces organisms

48
Q

What is the spectrum of Fofomycin

A

Broad-spectrum against G+ and G-

49
Q

What is the MOA of Fosfomycin

A
  • Inactivates MurA (inhibits peptidogylcan synthesis)
  • Fosfomycin resistance enzymes are in existence on chromosome and transferrable plasmids
  • FosA / FosB / FosX
  • weakly bactericidal
50
Q

Bacitracin origin

A

Bacillus subtilis organism

51
Q

MOA of Bacitracin

A

Interferes with peptidoglycan synthesis

52
Q

What is the spectrum of Bacitracin

A

Narrow-spectrum, usually for G+ organisms that cause skin infections

53
Q

Name the antibiotic that disrupt the cell wall envelope

A
  • Daptomycin

- Colistin

54
Q

MOA of Daptomycin

A

enters into G-ve cell membrane, aggregates and causes leakage of ions

Bactericidal

55
Q

MOA of Colistin

A

Attaches to lipopolysaccharide and phospholipid in G-ve cell membrane. Cause leaking of ions form within and major cell function

Bactericidal

56
Q

which part of the prokaryote do most anti microbials bind to?

A

Most bind to the ribosomes of the prokaryote. Includes both the 30S and 50S

57
Q

What are the different way a protein synthesis inhibitor can work?

A

They inhibit:

  • Aminoacyl-tRNA binding
  • Peptide bond formation
  • mRNA reading
  • Translocation
58
Q

Features of Aminoglycosides

A

-2+ amino sugars and an aminocyclitol (C6) ring

Broad spectrum: aerobic G- rod and -certain G+

59
Q

MOA of Aminoglycosides

A
  • Binds to 30s ribosomal subunit (interferes with translation proofreading)
  • Misreading of mRNA occurs
  • False proteins produced
  • Bactericidal
    • unusual for protein inhibitors
60
Q

What is the name of a common aminoglycosides

A

Streptomycin

gentamicin

61
Q

what are some features of Macrolides

A
  • contains 12 to 22 carbon lactone rings linked to one or more sugars
62
Q

List some drugs that are macrolides

A
  • Erythromycin
  • Azithromycin
  • Clarithromycin
63
Q

Features and MOA of erythromycin

A

Moderate spectrum
Bacterial statin

Binds to 23S rRNA of 50S ribosome subunit and inhibits protein chain elongation

64
Q

Features of azithromycin and clarithromycin

A

Broader spectrum and often time is more active that erythromycin

65
Q

Structure and spectrum of Tetracycline:

A

4 ring with a variety of side chains
Moderately broad spectrum (most are at G+ than G-)

Bacteriostatic

66
Q

MOA of tetracyclines

A
  • Combine with 30S ribosomal subunit.

- inhibits binding of aminoacyl-tRNA molecules to the A site of the ribosomes

67
Q

Tetracycline examples

A

Tetracycline
Doxycycline
Minocycline
Tigecycline

68
Q

what are tetracycline, minocycline, doxycycline used for?

A

Treat ATYPICAL organisms: pneumonia, chlamydia, Lyme disease, Acne

69
Q

Feature of tigecycline

A

It is a new variant

broad spectrum and given by IV

70
Q

Chloramphenicol structure and spectrum

A

Nitrobenzene structure
Broad spectrum
Bacteriostatic

71
Q

MOA of Chloramphenicol

A

Binds to 23S of 50S on ribosome.

Inhibits peptidyl transferase action

72
Q

What is chloramphenicol used to to treat.

A

Typhoid fever
brain abscesses,
rickettsial and
chlamydial infections

73
Q

Name some other protein synthesis inhibitors

A

Lincosamide

Oxazolidinone

74
Q

Lincosamides (clindamycin)

A

principally G+ and anaerobes,

often reserved for relatively “difficult”, possibly multiorganism infections.

Adverse reactions; notorious for C. diff (“unique”)

75
Q

oxazolidinone

A

synthetic antimicrobial that blocks the interaction of mRNA and ribosome

used to treat methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus (VRE)

76
Q

List antibiotic agents that are metabolic antagonists.

A
  • Trimethoprim

- Sulfamethoxazole

77
Q

MOA of metabolic antagonist

A

effects the synthetic of nucleotides especially tetrahydrofolate, which is used for many things.

78
Q

how does Sulfamethoxazole-trimethoprim combination work

A

Sulfamethoxazole has similar structure to para amino benzoic acid

Trimethoprim mimics dihydrofolate

synergistically inhibit synthesis of Tetrahydrofolate.

79
Q

What is trimethoprim-sulfamethoxazole used to treat?

A

Very serious infections such as pneumonia or Nocardia infection

This is due to it being toxic: skin reaction and bone marrow

80
Q

what ways can the resistance of sulfonamides occur in bacteria.

A
  • Alteration of target enzyme
  • Changes in permeability
  • Hyperproduction of PABA may overcome blockade
81
Q

Name some nucleic acid inhibitors

A
  • Quinolones

- Metronidazole

82
Q

Describe the structure of quinolones

A

It is a synthetic drug made with dual 4-quinolone rings

83
Q

Spectrum of quinolones

A

Broad spectrum

84
Q

MOA of quinolones

A

Act by inhibiting topoisomerases

  • DNA gyrase
  • Topoisomerase IV
85
Q

List some drugs under the class of quinolones

A
  • Nalidixic acid
  • Ciprofloxacin
  • Moxifloxacin
86
Q

How does the resistance of bacteria to quinolones occur?

A
  • Mutation in topoisomerase-encoding genes
  • Porins-poor outer membrane
  • Efflux pumps
87
Q

MOA of metronidazole

A

The nitro group on the core ring must be reduced so that the drugs is active.

Only achieved in anaerobes

Free radicals are generated with case DNA damage and cell death

88
Q

How does antimicrobial resistance occur

A

A random mutation that is selected

89
Q

Where does resistance usually originate from

A

From the recipients normal flora and when present can be bred due selection pressure.`

90
Q

Mechanism of Drug resistance

A
  • Prevent entrance of drug
    • drug can’t bind to or penetrate pathogen
    • bacterial decrease in permeability

-Pump drug out- efflux pumps

  • Inactivation of drug
    • chemical modification of drug by pathogen
  • Alteration of target enzyme or organelle
  • Use of alternative pathways or increased production of target metabolite
91
Q

what are the 6 potential b-lactam resistance

A

1) Peptidoglycan
Some organisms do not use peptidoglycan
2) Penetration into infected cells
b-lactams penetrate poorly into host cells
(ineffective against intracellular pathogens)
3) Porins in G-ve bacteria: reduce porins
Needed to gain access to PBPs. “Porin-poor” strains exist
4) Pumps
Efflux pumps transport antibiotics back out of the cell (most effective for G –ve as they can pump out of the outer membrane)
5) PBPs
Low affinity binding (may be acquired or intrinsic - vary between organisms anyway)(“acquired” includes MRSA, among others)
6) Penicillinases (b-lactamases)Enzymes that degrade b-lactam ring; descended from PBPs. Again many variations

92
Q

How is resistance transmitted

A

-Chromosomal genes
*Passed on during cell division to “all” progeny
-Mobile genetic elements (plasmids, transposons, integrons) Genes on these can move within and / or be freely exchanged between bacteria
-Gene cassettes
“sets” of related or unrelated resistance genes can exist as separate genetic elements or can be part of transposon, integron or chromosome

93
Q

How can the emergence of resistance be delayed.

A

1- Use drugs only when necessary
2- Achieve adequate concentration
3- use 2 or more drugs at the same time sometimes
4- develop new drugs, vaccination, use bacteriophages to treat bacterial disease.

94
Q

List the Classes of antibiotics available?

A 
Penicillin 
Cephalosporins
Macrolides
Carbapenems
Aminoglycoside
Glycoproteins
Sulfonamindes
Nitrofurans  
Licosamides
Tetracycline
Nitroimidazoles 
FLUOROQUINOLONES

Antimicrobial and chemotherapy (4 decks)

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