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Pharmacology & Toxicology > PHAR7: Antimicrobials > Flashcards

PHAR7: Antimicrobials Flashcards

1
Q

How do microorganisms cause toxicity?

A

In the wrong place, with the wrong activity, or in the wrong quantity they can cause toxicity and pathology through exhausting critical resources, invasion and killing of cells, or production of toxins.

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2
Q

List they types of microbes

A
  • Bacteria
  • Fungi
  • Viruses
  • Protoazoa
  • Helminths
  • Algae
  • Prions
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3
Q

List three characteristics of microbes

A
  • May be unicellular or multicellular
  • May exist individually as single cells or in colonies
  • Are present in all three domains of cellular life (Archaea, Bacteria and Eukarya)
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4
Q

How do bacteria divide?

A

Binary fission

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5
Q

Out of all the types of microbes, which have a cell wall?

A

Bacteria (peptidoglycan) and fungi (chitin), the rest do not.

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6
Q

What size of ribosomes do the different types of microbes have?

A

bacteria have 70S whereas all the others have 80S.

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7
Q

Viruses and prions can be considered as?

A

Non-cellular

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8
Q

What are the two types of DNA present in bacteria cells?

A

Plasmids and nucleoids

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9
Q

What does synergy mean?

A

The interaction of biological structures or substances that produce an overall effect greater than the sum of individual effects of any of them

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10
Q

What other factors can affect the pathology?

A
  • compromised host immunity

- translocation

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11
Q

What are the different types of bacterial shapes?

A
  • coccus
  • dilococci
  • tetrad
  • streptococci
  • coccobacillus
  • filamentous
  • staphylococci
  • bacillus
  • diplobacilli
  • palisades
  • strephtobacilli
  • club rod
  • vibrio
  • comma
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12
Q

Describe the cell wall structure of gram positive and gram negative bacteria.

A

+ve: thick peptidoglycan cell wall, one lipid bilayer

-ve: thin peptidoglycan layer in between two lipid bilayers (can have up to 40)

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13
Q

What was it found that arsenic-containing compounds helped cure? What was the compound called?

A

Syphilis infections

Organoarsenic compounds

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14
Q

What does magic bullet refer to?

A

Describes an ideal therapeutic agent, i.e. one that would only affect the target organism selectively. The more selectively toxic we can make a compound the greater the opportunity for application without side effects

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15
Q

How is DNA contained in the different types of microorganisms?

A
  • Bacteria: bacterial chromosomes and plasmids
  • Fungi: membrane bound nucleus containing chromosomes
  • Protoazoa: micronucleus and macronucleus containing chromosomes
  • Helminths: membrane bound nucleus containing chromosomes
  • Algae: membrane bound nucleus containing chromosomes
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16
Q

What are the therapeutic methods are there for targeting bacteria?

A
  • stopping genetic material replication
  • restricting genetic material component availability
  • compromising the structural integrity of the cell
  • preventing synthesis of membranes needed for growth
  • preventing synthesis of cellular proteins
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17
Q

Discuss the three main classes of biochemical reactions

A

Class I: target the production of metabolic precursors from substrates such as glucose, and therefore restrict any downstream processes.
Class II: target processes involved in the production of small molecules from metabolic precursors
Class III: target processes involved in the production of macromolecules from small molecule substrates

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18
Q

Antibacterial agents could also be classified how?

A
  • Cell wall inhibitors
  • bacterial cell membrane inhibitors
  • bacterial protein synthesis inhibitors
  • bacterial nucleic acid synthesis and action inhibitors
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19
Q

Name two nucleic acid synthesis inhibitors

A

PABA -> DHF inhibited by Sulfamethoxazole

DNF->THF inhibited by Trimethoprim

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20
Q

What does Ciprofloxacin do?

A

inhibition of DNA gyrase (gyrase: a bacterial enzyme that catalyzes the breaking and rejoining of bonds linking adjacent nucleotides in circular DNA to generate supercoiled DNA helices)

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21
Q

What does Rifampicin do?

A

it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis.

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22
Q

Name antibiotics that affect the ribosome (GETC)

A 
Tetracyclin
Gentamycin
Eythromycin
Chloramphenicol
Fusidic acid
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23
Q

What is the peptidoglycan polymer made up of? How is it bonded?

A

N-acetylglucosamine (NAG/NAGA) and N-acetylmuramic acid (NAM/NAMA), bonded in an alternating pattern by beta-(1,4)glycosidic linkages

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24
Q

Describe the structure of peptidoglycan cell walls

A

The peptidoglycan polymers are crossed linked by short peptide chains that give rise to a mesh-like structure composed of repeating parallel peptidoglycan

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25
Q

What is the benefit of the cross-linked structure of bacterial cell walls?

A

Provides structural rigidity, while remaining porous, and preventing the cell from lysis under the osmotic pressure of the local environment

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26
Q

What amino acid is in the middle of the cross chain linking the peptidoglycan chains?

A

D-alanine and 2 other amino acids

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27
Q

How do Beta-lactam drugs work?

A

Covalently binding to the DD-transpeptidase enzymes that are responsible for cross-linking the peptides between peptidoglycan chains.

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28
Q

What beta-lactam compounds are there? (Please Can Ceara Make Cake)

A
  • penicillin
  • Cephalosporins
  • Monobactams
  • Carbapenems
  • Clavulanic acid
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29
Q

What are the most common beta-lactam drugs

A

Penicillin

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30
Q

What does Vancomycin and related compound teichoplanin, do?

A

Prevent the synthesis of the bacterial cell wall by forming strong hydrogen bonds with the peptides that cross-link the peptidoglycan polymer chains, and thus prevent the formation of the normal lattice/mesh-like structure. Without cross-linking, the cell wall
integrity cannot be achieved, and therefore bacterial cell viability is compromised.

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31
Q

What does Vancomycin and related compound teichoplanin, do?

A

Prevent the synthesis of the bacterial cell wall by forming strong hydrogen bonds with the peptides that cross-link the peptidoglycan polymer chains, and thus prevent the formation of the normal lattice/mesh-like structure. Without cross-linking, the cell wall
integrity cannot be achieved, and therefore bacterial cell viability is compromised.

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32
Q

Name a bacterial cell membrane disruptor

A

daptomycin

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33
Q

How do bacterial cell membrane disruptors, such as daptomycin, work?

A

When multiple daptomycin molecules aggregate, their collective effect is to substantially distort the cell membrane shape, giving rise to holes. Loss of membrane integrity in this way causes depolarisation of the membrane, and consequently, chemical gradients necessary for many synthetic processes cannot be maintained. Ultimately, the bacterium dies though an inability to perform critical biochemical functions.

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34
Q

How do Polymixins work?

A

They compromise cell membrane integrity. They achieve their selectively for bacterial cells by binding to lipopolysaccharide (LPS) that is highly abundant in Gram-negative bacteria

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35
Q

Why aren’t Polymixins used very often?

A

Their treatment is often accompanied by a range of off-target effects that has limited their use, particularly since the development of agents with fewer associated toxicities.

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36
Q

What targets are used in bacterial cells to target protein synthesis?

A

70S ribosomes

37
Q

What are prokaryotic ribosomes made up of?

A

30S and 50S

38
Q

What are eukaryotic ribosomes made up of?

A

40S and 60S

39
Q

What does S for ribosomes mean?

A

Sedimentation coefficient: the ratio of the rate of sedimentation of a particle to the centrifugal acceleration applied to it). In general, the bigger the molecule/particle, the great the coefficient value

40
Q

What do the tetracyclines: Tetracycline, Doxycycline and Lymecycline work on? What is their common structural feature?

A

30S ribosome

Four connected and functionalised hydrocarbon rings

41
Q

What do the aminoglycosides: Gentamycin, Neomycin, Tobramycin work on? What is their common structural feature?

A

30S ribosomes

Amino-modified glycoside

42
Q

What do the macrolides: Erythromycin, Spiramycin, Telithromycin work on? What is their common structural feature?

A

50S ribosome

Macrocyclic lactone ring with one or more deoxy sugars

43
Q

What does Chloramphenicol work on? What is its common structural feature?

A

50S ribosome

small molecule

44
Q

What does Fusidic acid work on? What is its common structural feature?

A

50S ribosome

Small steroid

45
Q

Synthesis of DNA and RNA in bacteria is dependent on the availability of?

A

Folic Acid

46
Q

What precursor is folic acid synthesised from? What is this pathway called?

A

p-aminobenzoic acid (PABA): bacterial folate pathway

47
Q

What enzymes are involved in the catalyzing the necessary biotransformation of folic acid precursors?

A
  • dihydropteroate synthetase

- dihydrofolate reductase

48
Q

How is synthesis of nucleic acids inhibited?

A

Competitive inhibition of the enzymes that synthesis the precursor of folic acid which is needed for nucleic acid synthesis

49
Q

How is competitive inhibition of nucleic acids achieved?

A

Sulfonamides are structurally-similar to PABA (folic acid precursor), and trimethoprim is structurally similar to folic acid, and therefore introduction of these compounds will reduce the rate of bacterial DNA/RNA production and are bacteriostatic.

50
Q

List the key components in the bacterial folate acid pathway

A
  • Folate precursor p-aminobenzoic acid (PABA)
  • dihydropteroate synthetase inhibitor: sulfamethoxazole
  • Tetrahydrofolate (THF) precursor: dihydrofolic acid (DHF)
  • Dihydrofolate reductase Inhibitor: trimethoprim
51
Q

Bacterial DNA replication requires the action of what enzyme?

A

topoisomerase II

52
Q

What is topoisomerase II otherwise known as?

A

bacterial DNA gyrase

53
Q

Name some DNA gyrase inhibitors

A

quinolones such as ciprofloxacin, norfloxacin, and nalidixic acid

54
Q

How do DNA gyrase inhibitors work?

A

Inhibition of this process prevents bacterial gene translation or replication, and consequently bacterial cell division. Inhibition of: catalysis of the breaking and rejoining of bonds linking adjacent nucleotides in circular DNA to generate supercoiled DNA helices.

55
Q

Name a RNA synthesis inhibitor

A

rifampicin / rifampin

56
Q

How does rifampicin / rifampin (RNA synthesis inhibitor) work?

A

Inhibits bacterial DNA-dependent RNA polymerase

- prevent normal bacterial function and growth

57
Q

How can bacteria reduce the efficacy of antibacterial agents?

A

1) target modification
2) Immunity or bypass
3) Reducing the internal dose
4) Chemical inactivation

58
Q

Describe bacteria’s ability to increase resistance by target modification?

A

Largely responsible for resistance is the change in the target of the antibacterial agent; in general, this means that critical biochemical interactions are no longer effective, and the drug cannot act.

59
Q

Describe bacteria’s ability to increase resistance by immunity or bypass?

A

In some cases, the bacterial targets are not sufficiently well targeted or there is redundancy in the system (e.g. an enzyme may be inhibited, but the process is accomplished via another route).

60
Q

Describe bacteria’s ability to increase resistance by Reducing the internal dose?

A

Efflux pumps can be expressed on the cell membrane to pump out the active agent.

61
Q

Describe bacteria’s ability to increase resistance by Chemical inactivation?

A

Expression of enzymes or creation of an environment that inactivates a drug, or sequesters it.

62
Q

What are the three main ways that bacteria display resistance to a given antibacterial agent?

A
  • Inherent resistance of cells
  • Mutation and selection of resistant cells
  • Horizontal gene transfer to confer resistance mechanism on cells
63
Q

Describe inherent resistance of bacterial cells

A
  • existing degradation ability for the drug
  • the cell is impervious to the drug
  • the target is inaccessible and therefore cannot be acted upon
  • they do not utilise the specific target / mechanism of the drug
64
Q

Describe mutation and selection of resistant of bacterial cells

A

Variation in the population. Variation that leads to survival will be positively selected for if there is environmental pressure.

65
Q

What will lead to increased antimicrobial resistance?

A

A key driver for antimicrobial resistance results from inadequate control of bacterial populations by antibiotics or low-level chronic exposure such as through routine animal treatment or incomplete/unnecessary use of antibiotics in therapy

66
Q

What is the main/most common mechanism for antimicrobial resistance?

A

Horizontal gene transfer to confer resistance mechanism on cells

67
Q

Describe how horizontal gene transfer to confer resistance mechanism on cells can occur

A
  • Transformation through the uptake and incorporation of DNA containing a resistance gene
  • Phage (virus) mediated transfer of a resistance gene
  • Bacterial conjugation of a resistance gene
68
Q

Define antimicrobials

A

A naturally - or synthetically - derived agent that inhibits or kills (one or more types of) microorganism

69
Q

Define Antibiotic

A

Refers strictly to microorganism-produced substances that act against another microorganism

70
Q

Define Antibacterial

A

A naturally - or synthetically - derived agent that inhibits or kills (one or more types of) bacteria

71
Q

Define Bactericidal agent

A

An agent that kills bacteria

72
Q

Define Bacteriostatic agent

A

An agent that prevents/arrests bacterial growth and/or reproduction without necessarily killing them

73
Q

Define Commensal relationship

A

A symbiotic relationship between two organisms in which one benefits from the biological interactions while the other remains largely unaffected (no benefit or harm)

74
Q

Define Horizontal gene transfer

A

The transfer of genetic material from one bacterium to another by either i) transduction of DNA; ii) phage-mediated transfer; iii) bacterial conjugation

75
Q

Define Microbe

A

A microorganism

76
Q

Define Mutualistic relationship

A

A symbiotic relationship between two organisms in which both benefit from the biological interaction

77
Q

Define Vertical gene transfer

A

The transfer of genetic material from a parent to offspring

78
Q

You should know the mechanism of action for…

A 
Ciprofloxacin
Penicillin
Polymyxin
Rifampicin
Sulfamethoxazole
Trimethoprim
Vancomycin
79
Q

Antimicrobial agents of most types have a wide therapeutic window (index) why?

A

They are highly selective for bacterial processes either qualitatively or quantitatively

80
Q

What process does the antibacterial agent vancomycin inhibit?

A

Cell wall synthesis

81
Q

Why might a poorly absorbed, low bioavailability drug be used?

A

Because the bacteria target are located in the gastrointestinal tract

82
Q

What is Penicillin and how does it work?

A
  • Small molecule antibiotic
  • Covalently and irreversibly binds to DD-transpeptidase enzyme active site
  • Prevents cross-linking of peptidoglycan in cell wall
83
Q

What is Flucloxacillin and how does it work?

A

-Small molecule beta-lactam antimicrobial

  • Inhibits penicillin-binding proteins that are responsible for peptidoglycan synthesis
  • Prevents cell wall assembly
84
Q

How does Polymyxin work and what is it?

A
  • Peptide antimicrobial
  • Disrupts cell membrane integrity
  • Causes bacterial cell death
85
Q

What is Rifampicin and how does it work?

A
  • Medium-large heterocyclic compound
  • Inhibits DNA-dependent RNA polymerase
  • Prevents RNA synthesis, and therefore disrupts normal function and growth processes
86
Q

What is Sulfamethoxazole and how does it work?

A
  • PABA mimic
  • Inhibits dihydropteroate synthetase
  • Prevent synthesis of folate, a precursor in nucleic acid synthesis
87
Q

What is Trimethoprim and how does it work?

A
  • Folate mimic
  • Inhibits dihydrofolate reductase
  • Prevents synthesis of tetrahydrofolate, a precursor in nucleic acid synthesis
88
Q

What is Vancomycin and how does it work?

A
  • Glycopeptide
  • Inhibits cross-linking of peptides between peptidoglycan polymer chains
  • Prevents cell wall assembly

Pharmacology & Toxicology (8 decks)

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