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I&I WC1 > Antimicrobial resistance > Flashcards

Antimicrobial resistance Flashcards

1
Q

What are the modes of actions of antibiotics? (5)

A
  1. Interference with cell wall synthesis
  2. Interference with DNA synthesis
  3. Interference with RNA synthesis
  4. Interference with protein synthesis
  5. Interference with folic acid metabolism
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2
Q

Which groups of antibiotics are members of the β-lactams? (4)

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapenems
  4. Monobactam
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3
Q

Which process in bacteria is targeted by β-lactam antibiotics? Which part of the bacterium does this concern?

A

Cell wall synthesis, specifically the peptidoglycan layer

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4
Q

When is monobactam (β-lactam antibiotic) used?

A

In case of allergy to other β-lactam antibiotics (penicillins, cephalosporins, carbapenems)

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5
Q

What is the general structural makeup of the peptidoglycan layer of bacteria?

A

Alternating NAM-NAG sugar chains, connected by peptide bridges

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6
Q

What are the three stages of bacterial cell wall synthesis?

A
  1. Cytoplasmic stage
  2. Cell surface stage
  3. Lysis/maintenance of peptidoglycan layer
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7
Q

What happens during the cytoplasmic stage of bacterial cell wall synthesis? Which enzyme is involved?

A

Assembly of smaller units of peptidoglycan by pyruvyl transferase

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8
Q

What happens during the cell surface stage of bacterial cell wall synthesis?

A

Assembly of smaller subunits on the cell surface by penicillin-binding proteins (PBPs)

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9
Q

Which stage of the cell wall synthesis do β-lactam antibiotics target?

A

Cell surface stage -> prevents assembly of peptidoglycan subunits into a cell wall, leading to cell wall lysis

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10
Q

What happens during the lysis/maintenance stage of the bacterial cell wall? Which enzymes are involved? (3)

A

Constant refreshment of the peptidoglycan layer

  1. Glycosidases
  2. N-acetyl-muramyl-L-alanine amidases
  3. Endopeptidases
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11
Q

Which enzymes fall within the PBPs? (3)

A
  1. Transglycosidases
  2. Transpeptidases
  3. Carboxypeptidases
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12
Q

What is an important condition for β-lactam antibiotics to have effect?

A

Bacteria have to be metabolically active -> otherwise there is no cell wall synthesis to interfere with

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13
Q

On which factors do differences in activity among β-lactam antibiotics (in Gram- bacteria) depend? (3)

A
  1. Penetration into Gram- cell
  2. Lability to periplasmic β-lactamases
  3. Affinity to PBPs
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14
Q

Which mechanisms of β-lactam resistance are there? (3) Which is most common in Gram- bacteria? Which is more common in Gram+ bacteria?

A
  1. Impaired permeability of outer membrane
  2. Mutated PBPs with changed affinity = most common in Gram+ bacteria
  3. Enzymatic hydrolysis of the β-lactam ring = most common in Gram- bacteria
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15
Q

How do β-lactams enter Gram- bacteria?

A

Via proins in the outer membrane

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16
Q

Which physicochemical factors influence uptake of β-lactams through porins? (3)

A
  1. Size
  2. Hydrophobicity
  3. Charge
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17
Q

How can Gram- bacteria block β-lactam antibiotics from entering through their outer membrane?

A

Changes in porins that hamper the influx of antibiotics

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18
Q

In which two locations can β-lactamase genes be present?

A
  1. Chromosomal
  2. Plasmids
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19
Q

True or false: if β-lactamases are present in the bacterial chromosome, bacteria constantly produce β-lactamases, thus becoming resistant to β-lactam antibiotics

A

False; some bacteria constitutively express β-lactamases, whilst others have inducible β-lactamases (induced by the presence of antibiotics)

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20
Q

What are four important penicillins?

A
  1. Penicillin
  2. Ampicillin
  3. Piperacillin
  4. Ticarcillin
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21
Q

The higher the generation of cephalosprin, the [lower/higher] its activity against Gram-

A

The higher the generation, the higher the activity against Gram-

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22
Q

What is the only available monobactam?

A

Aztreonam

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23
Q

What is an ESBL? To which class of antibiotics are bacteria expressing ESBL usually still sensitive?

A

Extended-spectrum β-lactamase -> against multiple classes of β-lactam antibiotics. Usually still carbapenem-sensitive

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24
Q

What are β-lactamases that produce resistance against carbapenems called?

A

Carbapenemases

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25
Q

How can antibiotics have specific toxicity to bacterial protein synthesis?

A

Bacterial ribosomes differ from eukaryotic ribosomes, allowing for specific toxicity

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26
Q

What is an important class of antibiotics that interferes with bacterial protein synthesis?

A

Aminoglycosides

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27
Q

What is an important physiochemical characteristic of aminoglycosides? How does this help them enter the bacterial cell?

A

Highly positively charged, causing them to electrostatically bind to the outer membrane of bacteria

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28
Q

What are the three stages in the mechanism of action of aminoglycosides?

A
  1. Energy-independent phase
  2. Energy-dependent phase
  3. Binding to 30S ribosomal subunit
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29
Q

What is the energy-independent phase of aminoglycoside action?

A

Electrostatic binding to the bacterial outer membrane

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30
Q

What is the energy-dependent phase of aminoglycoside action? When is entry enhanced?

A

Transport into cytoplasm by proton motive force. The greater the membrane potential, the more efficient this process is.

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31
Q

In which cases is the transmembrane potential of bacteria lowered? (3) Why is this detrimental to the action of aminoglycosides?

A
  1. Low oxygen environment
  2. Low pH
  3. Hyperosmolarity

Aminoglycosides need a high transmembrane potential to enter bacteria effectively -> they will not enter effectively under these conditions

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32
Q

To which bacterial ribosomal subunit do aminoglycosides bind? What are the effects of this? (2)

A

30S subunit

  1. Inhibition of protein synthesis
  2. Misreading of codons
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33
Q

Which mechanisms of resistance to aminoglycosides are there? (3) Which is most important?

A
  1. Aminoglycoside-modifying enzymes = most important
  2. Alteration in uptake
  3. Change in ribosomal binding sites
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34
Q

What are the classes of aminoglycoside-modifying enzymes? (3) What are their abbreviations?

A
  1. Acetyltransferases (AAC)
  2. Adenyltransferases (ANT)
  3. Phosphotransferases (APH)
35
Q

What is the action performed by acetyltransferases (aminoglycoside-modifying enzymes)

A

Acetyl-CoA-depedent acetylation of an amino group

36
Q

What is the action performed by adenyltransferases (aminoglycoside-modifying enzymes)

A

ATP-dependent adenylation of a hydroxyl group

37
Q

What is the action performed by phosphotranferases (aminoglycoside-modifying enzymes)

A

ATP-dependent phosphorylation of a hydroxyl group

38
Q

What is an important class of antibiotics that interferes with bacterial DNA synthesis?

A

Quinolones

39
Q

What are important quinolones? (3)

A
  1. Ciprofloxacin
  2. Levofloxacin
  3. Moxifloxacin
40
Q

How do quinolones enter a cell? What enables them to enter via this way?

A

Passive diffusion -> small and hydrophobic molecules that easily pass the plasma membrane

41
Q

Which mechanism of entry can quinolones employ when there is some degree of hydrophobicity of the quinolones?

A

Enter via LPS

42
Q

What determines the amount of quinolones in a bacterial cell?

A

Balance between the efficacy of efflux pumps and the influx through the membrane

43
Q

What is the mechanism of action of quinolones?

A

Interference of topoisomerases II and IV

44
Q

What is the function of topoisomerases? (2) How can quinolones target these without causing toxicity in humans?

A
  1. Regulate super-coiling of DNA
  2. Cut dsDNA to initiate replication

Not present in humans

45
Q

How do quinolones block topoisomerase function?

A

By forming a complex with them, blocking their enzymatic function

46
Q

Into which groups (2) and subgroups (3, 3) can resistance to quinolones be divided?

A
  1. Chromsomally encoded
    1.1 - Decreased target affinity
    1.2 - Decreased accumulation
    1.3 - Combination of 1.1 & 1.2
  2. Plasmid-mediated
    2.1 - qnrA
    2.2 - Aminoglycoside acetyltransferase
    2.3 - Quinolone efflux pumps
47
Q

How can bacteria decrease the target affinity of quinolones? (2) What kind of resistance does this lead to?

A
  1. Mutations in topoisomerases
  2. Mutations in quinolone-resistance determining region

Individual mutations lead to low-level resistance, but as mutations accumulate, resistance grows

48
Q

How can bacteria decrease accumulation of quinolones? (2)

A
  1. Decreased porine expression
  2. Hyper-expression of natural efflux
49
Q

True or false: decreased porine expression can lead to high-level quinolone resistance

A

False; this leads to low-level resistance

50
Q

What is qnrA? Where is it encoded?

A

A quinolone resistance mechanism -> a protein that binds to topoisomerases and prevents quinolones from binding

Plasmid-encoded

51
Q

What is the effect of aminoglycoside acetyltransferase on quinolones?

A

Acetylates quinolones, blocking their effect

52
Q

Which two quinolone efflux pumps are known?

A
  1. qepA
  2. oxqAB
53
Q

What is an MDRO?

A

Multi-drug resistant organism

54
Q

What are the two main pillars of prevention of MDRO spread in healthcare?

A
  1. Infection prevention & control measures
  2. Search & isolation of colonized/infected patients
55
Q

Which group has the highest risk to be carrying a MDRO?

A

Patients who were hospitalized abroad

56
Q

In which geographical areas is the prevalence of MDROs highest? (2)

A
  1. Southern Asia
  2. Africa
57
Q

True or false: only hospitalized travellers can carry MDROs into hospitals

A

False; healthy travellers can also spread MDROs without being ill

58
Q

In which geographical area is the prevalence of ESBL highest?

A

Soutern Asia

59
Q

What are risk factor for acquisation of ESBL? (6) Which are specific for geographical areas?

A
  1. Antibiotics during travel
  2. Traveller’s diarrhoea
  3. Meal at street food halls
  4. Raw vegetable consumption
    (Southeast Asia)
  5. Visiting local markets daily (Eastern Africa)
  6. Staying in rural areas (Eastern Africa)
60
Q

What are protective factors for acquisation of ESBL? (2)

A
  1. Washing hands before meals
  2. Beach holiday
61
Q

What is the medium time till loss of resistant bacteria?

A

30 days after travel

62
Q

How many % of travellers who had acquired a MDRO still carry them after 1 year?

A

11%

63
Q

What can unkown MDRO carriage lead to?

A
  1. Difficult to treat infections
  2. Hospitalization without appropriate infection prevention/control measures
  3. Spread of MDROs to other patients, healthcare personnel or the hospital environement
64
Q

What are preventitive measures taken to prevent the spread of MDROs in the hospital? (4)

A
  1. Single occupancy isolation rooms
  2. Personal protective equipment
  3. Search and isolation of colonized/infected patients
  4. Source- and contact tracing if appropriate measures were not taken
65
Q

How are patients screened for MDROs before hospitalization? Which step is taken if an increased risk is detected?

A

Universal risk assesment combined with risk-based screening of all incoming patients

In case of increased risk: culture of throat and rectum for MDRO identification

66
Q

How many yearly deaths will be attributable to antimicrobial resistance in 2050?

A

~9 million

66
Q

Which problems with antimicrobial resistance surveillance has the WHO detected (2014)? (2)

A
  1. Gaps are largest where health systems are weak
  2. No agreement on surveillance standards
67
Q

What is an important characteristic of the 2015 WHO Global Action Plan on Antimicrobial Disease?

A

One Health approach, focussing on human disease, animal disease & the environment

68
Q

What are important pillars of the 2015 WHO Global Action Plan on Antimicrobial Resistance? (4)

A
  1. Improving awareness through communcation, education & training
  2. Strengthen knowledge through surveillance & research
  3. Reduce incidence of infection through sanitation, hygiene & infection prevention measures
  4. Optimize use of antimicrobial medicines in human and animal health
69
Q

What are contributing factors to antimicrobial resistance in low- and middle income countries? (3)

A
  1. High infectious burden
  2. Cost constraints prevent application of newer, more extensive antibiotics
  3. Systemic surveillance systems absent or rudimentary
70
Q

True or false: eukaryotic viruses outnumber bacteriophages

A

False; bacteriophages are the most numerous biological entity on earth

71
Q

What is an important function of bacteriophages for human health (under natural circumstances)?

A

Important regulators of bacterial populations -> contribute to homeostasis of bacterial flora in humans

72
Q

Which types of genome can bacteriophages have? (3)

A
  1. dsDNA
  2. ssDNA
  3. RNA
73
Q

How do bacteriophages enter bacteria?

A

Through entry receptors (like any virus)

74
Q

Which stages does a phage infection have? (2)

A
  1. Lysogenic stage -> phage being incorporated in the bacterium
  2. Lytic stage -> production & release of new phages
75
Q

What is the danger in using temperate bacteriophages in antibacterial therapy?

A

These can transfer genes between bacteria -> could spread AMR or virulence genes

76
Q

True or false: only a minority of phages are so-called temperate phages, capable of transferring genetic elements

A

False; the majority of phages is capable of transferring genetic elements

77
Q

How can bacteria protect themselves from coming into contact with phages? (3)

A
  1. Hiding under mucosal layers
  2. Withdrawing to areas where they are difficult to reach
  3. Formation of biofilms
78
Q

How do bacteria defend themselves from infection by phages? (5)

A
  1. Change surface structures
  2. Blockage of invader DNA entry
  3. Restriction modification system
  4. Abortive infection -> infected bacteria lyse to prevent further spreading
  5. CRISPR-Cas
79
Q

What is the most common solution to picking the right phage for therapy in humans?

A

Picking a cocktail of phages instead of a single variety

80
Q

What kind of host immune responses are there against phages? (3)

A
  1. Innate immunity can remove circulating phages
  2. Sera of non-immunized individuals contain IgM against phages -> natural antibodies
  3. Phages stimulate bacterial phagocytosis -> bacterial cells taken up
81
Q

Which parts of the innate immune system are especially adapt at removing circulating phages?

A

Components of the reticuloendothelial system

82
Q

What are properties of phages that can be used in antibacterial therapy? (7)

A
  1. Don’t disturb homeostasis of commensal flora
  2. Don’t encode toxins
  3. Are unable to facilitate transfer of genetic material
  4. Are able to circumvent bacterial defence systems
  5. Are not neutralized by host humoral immune responses
  6. Collaborate with the host immune system to clear the bacteria
  7. Don’t directly or indirectly cause anaphylactic shock
83
Q

What is a mechanism by which phages can help the (innate) immune system clear bacteria?

A

They can opsonize bacteria, making them easier to phagocytose

I&I WC1 (20 decks)

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