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FD1 > Antimicrobial resistance > Flashcards

Antimicrobial resistance Flashcards

1
Q

What are antimicrobials?

A
  • chemicals that either kill or prevent the growth of microbes (bacteria, viruses, protozoa)
  • can be produced by microorganisms themselves/ lab
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2
Q

What are the impacts of antibiotic resistance?

A
  • health
  • welfare
  • economics
  • superbugs
  • reduced spectrum of drugs available to treat infections
  • no treatment available?
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3
Q

What are the drivers of AMR?

A
  • world travel (3 million flights/ get to any place in 48 hours)
  • mass treatment of livestock with antibiotics
  • bush meat imported (zoonotic bugs)
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4
Q

What % of emerging infectious diseases are of animal origin?

A

75%

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5
Q

Name examples of prophylactic and metaphylatic uses of antibiotics in animals

A
  • after surgery
  • dry cow therapy
  • before transport
  • potential outbreaks
  • stressful conditions
  • moving calves
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6
Q

What is metaphylatic?

A

-treat all animals when only a few are showing clinical signs

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7
Q

What are sub-therapeutic antibiotics?

A
  • resistance radiates from farms through water supplies etc.
  • travel through food chain
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8
Q

What is a withdrawal period?

A

-legal time to wait before using any products from the animal that had the antibiotics

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9
Q

What is antibiotic resistance?

A
  • bacteria can develop resistance through genetic mutation
  • the mutations enable the bacteria to alter the way it interacts with the antibiotic
  • may mean the antibiotic is ineffective
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10
Q

Name other resistance types

A
  • disinfections
  • heavy metals
  • antimicrobials incorporated into plastics
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11
Q

How do antibiotics work?

A
  • interfere with synthesis of the bacterial cell wall
  • prevent bacteria from making chemicals they need to survive
  • interfere with the genetic material in a bacterial cell and cause it to stop the bacterial cell dividing
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12
Q

Which antibiotics stop cell wall synthesis?

A
  • Penicillins
  • Cephalosporins
  • Carbapenems
  • Daptomycin
  • Glycopeptides
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13
Q

Which stop DNA synthesis?

A

-Fluoroquinolones

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14
Q

Which stop RNA synthesis?

A

-Rifampin

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15
Q

Which stops protein synthesis?

A
  • Macrolides
  • Chloramphenicol
  • Tetracycline
  • Aminoglycosides
  • Oxazolidonones
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16
Q

Which stops folic acid synthesis?

A
  • sulfonamides

- trimethoprim

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17
Q

Why has resistance emerged?

A
  • over use
  • ineffective antibiotics prescribed
  • use of antibiotic as growth promoters
  • illegal use
  • patients not completing courses
  • inappropriate use of disinfectants
  • evoluntionary pressures
  • antimicrobials in environment
18
Q

How can inadequate treatment of infections cause resistance?

A
  • wrong treatment
  • wrong initial diagnosis
  • treatment course too long/short
  • dilution of disinfectant wrong
  • exposure time to disinfectant wrong

(persistence of organisms/ DNA in environment)

19
Q

Bacterial fitness increased?

A
  • bacteria become fitter, due to other genes now being associated (can now colonise in the gut and survive more easily)
  • can now colonise more effectively and are more resistant
20
Q

How is antibiotic resistance acquired? (3)

A
  • transformation
  • conjugation
  • transduction
21
Q

what is transformation?

A

-uptake of free DNA in the environment (the free DNA usually comes from the breakdown of dead bacteria nearby)

22
Q

What is conjugation?

A

-the transfer of plasmids, or small circular pieces of bacterial DNA, containing resistance genes, from 1 bacterium to another

23
Q

What is transduction?

A
  • transfer of bacterial DNA via viruses, or bacteriophages, to other closely related bacteria
  • bacteriophages are viruses that only infect bacteria
24
Q

What are ESBL’s?

A
  • Extended-Spectrum Beta-Lactamases
  • enzymes that can be produced by bacteria making them resistant to cephalosporins e.g. cefuroxime
  • resistance is either plasmid or chromosomal encoded
  • dairy problem
25
Q

When was EBSL’s first described?

A

-1983

26
Q

Why are EBSL’s such a problem?

A
  • resistance can be carried on a plasmid
  • plasmids are highly promiscuous
  • many subtypes
  • plasmids may confer a fitness advantage

plasmid DNA could survive in the environment

-transfer to other organisms

27
Q

What are the different types of resistance?

A
  • Innate, natural or intrinsic
  • Mutational resistance
  • Extrachromosomal, chromosomal or acquired resistance (ESBL)
  • Phenotypic/ persister state
  • Physical mechanisms of resistance e.g. Biolfims, salmonella
28
Q

What are the mechanisms of resistance?

A
  • Efflux of the antibiotic
  • Membrane plug formation (protein produced to block uptake of drug)
  • Ribosomal blockade (protein to stop drug binging to ribosomes)
  • Enzymatic destruction
  • Alteration of the drug
  • Persister state/ phenotypic resistance
29
Q

What is the ‘Altered target site’ mechanism?

A
  • altered ribosomal protein
  • altered/ new binding proteins
  • ribosomal RNA methylation
  • altered DNA gyrase
  • insensitive dihydropteroate
  • ribosomal protection
  • insensitive dihydrofolate
  • altered cell wall stem peptide
30
Q

What are the antibiotic destroying mechanisms?

A
  • Aminoglycosides
  • Beta-lactamases
  • Chloramphenicol
31
Q

What is used by the bacterium to decrease the uptake of the drug?

A

-Beta-lactamase (alteration in bacterial permeability)

32
Q

What is cross resistance?

A
  • implies that a single mechanism covers resistance to multiple antimicrobial agents
  • multiple mechanisms involved
33
Q

What is MAR?

A
  • multiple antimicrobial resistance
  • group of genes = MAR
  • chromosomally encoded systems involved in low level resistance of bacteria to different classes of antibiotic (mainly B-lactams, disinfectants, organic solvents etc.)
34
Q

What is the MAR locus? (E.Coli/ Salmonella)

A
  • mediate AMR by up-regulating efflux of some antibiotics, disinfectants and organic solvents
  • via the AcrAB-TolC efflux pump
  • and down regulation influx through Outer Membrane Protein F
35
Q

What do efflux pumps do?

A
  • membrane proteins
  • act as an export for antimicrobials
  • exclude the antibiotic out of the cell as fast as it can enter

=low intracellular concs (insufficient to elicit an effect)

36
Q

What are the types of efflux pumps?

A
  • Primary active transporters- utilise the energy stored in ATP to catalase transport of drug across membrane by ATP hydrolysis
  • Secondary active transporters - driven by energy stored in ion gradients (generated by respiration)
  • Phosphotransferase system (PTS)
37
Q

What does phenotypic resistance allow?

A
  • allows bacteria to survive exposure to antimicrobials

- grow back when antibiotic pressure is removed

38
Q

What are the possible solutions to phenotypic resistance?

A

-Mutant prevention concentration (MPC)

39
Q

What is MPC?

A

-the lowest concentration of antibiotic to inhibit the emergence of mutants

40
Q

What is the persister state?

A
  • the bacteria have no resistant gene (but is resistant)
  • due to the metabolism of the bacteria (become dormant)
  • so 99 will die and 1 will survive - will keep happening
  • use 2/3 antibiotics at same time
41
Q

How are antibiotics administered?

A
  • injection
  • topical
  • oral
  • in feed
  • in water
  • pulse admin- reduce resistance
42
Q

Alternatives to antibiotics?

A
  • probiotics
  • prebiotics
  • synbiotics
  • phage therapy
  • natural plant extracts (oregano)
  • breed animals for resistance
  • vaccines
  • husbandry practises
  • education

FD1 (31 decks)

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