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MICB 308 > Antibiotic Resistance > Flashcards

Antibiotic Resistance Flashcards

1
Q

how does antibiotic resistance happen (4)

A
  1. lots of germs present, with few being drug resistant
  2. antibiotics kill bacteria causing illness and good bacteria protecting body from infection
  3. drug-resistant bacteria grow and take over without competition
  4. some bacteria give their drug resistance to other bacteria, causing more problems
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2
Q

what ultimately causes antibiotic resistance (2)

A
  • simply using antibiotics
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3
Q

why has antibiotic resistance (5)

A
  • mutation and selection
  • exchange of resistance genes between bacteria
  • exchange of bacteria between people
  • inappropriate use of antibiotics by physicians/patients
  • inappropriate use of antibiotics to enhance the growth of livestock
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4
Q

mechanisms of resistance (4)

A
  • intrinsic resistance
  • enzymatic inactivation of the antibiotic
  • efflux pumps
  • target modification
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5
Q

mechanisms of intrinsic resistance (2)

A
  • barrier function
  • detoxification
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6
Q

intrinsic resistance: barrier function (2)

A
  • outer membrane or cell wall
  • antibiotic is excluded from the cell
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7
Q

intrinsic resistance: detoxification (2)

A
  • scavenging-thiol mediated
  • compounds bind the antibiotic (the toxin) and neutralize it
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8
Q

what are the three general strategies to achieve drug resistance (3)

A
  • drug resistance due to altered targets
  • drug resistance due to decreased accumulation (low permeability or high efflux)
  • drug resistance due to enzymatic inactivation
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9
Q

efflux pumps: specificity (2)

A
  • hallmark of multi-drug resistance
  • some are very specific, whereas others can pump variety of antibiotics
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10
Q

efflux pumps: common features (3)

A
  • inner membrane pump
  • outer membrane pump
  • membrane fusion protein in periplasm that links IM to OM
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11
Q

enzymatic inactivation of the antibiotic: beta-lactam antibiotics

A
  • beta-lactamases inactivate penicillin and derivatives (beta-lactams)
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12
Q

enzymatic inactivation of the antibiotic: mechanism (2)

A
  • adds modifying groups to inactivate the antibiotic
  • mechanism of resistance to aminoglycosides
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13
Q

enzymatic inactivation of antibiotic: modifying groups (3)

A
  • methyl
  • acetyl
  • phosphate
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14
Q

how can beta-lactamases be overcome

A
  • augmentin
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15
Q

augmentin example and antibiotic it helps (2)

A
  • clavulanic acid
  • amoxicillin
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16
Q

how does clavulanic acid work (2)

A
  • covalently binds to serine residues in active site of the beta-lactamase
  • inactivates beta-lactamase and allows amoxicillin to work
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17
Q

bacteria outcome: beta-lactam

A
  • kills bacteria
18
Q

bacteria outcome: beta-lactam + beta-lactamase (2)

A
  • beta-lactam inactivated
  • no effect on bacteria
19
Q

bacteria outcome: beta-lactam + beta-lactamase + clavulanic acid (3)

A
  • inactivated beta-lactamase
  • beta-lactam unaffected
  • kills bacteria
20
Q

target modifications (2)

A
  • change the transpeptidase
  • change to PG precursors
21
Q

target modification of transpeptidase: which bacteria show this resistance

A
  • methicillin resistance S. aureus (MRSA)
22
Q

MRSA: transpeptidase (3)
- name
- gene
- similarity to other transpeptidases

A
  • Pbp2a
  • encoded by the mecA gene
  • 20% sequence identity to other Pbps
23
Q

how does the MRSA Pbp2a facilitate resistance (2)

A
  • has an altered or slightly distorted active site
  • prevents binding of methicillin while still allowing transpeptidases to occur
24
Q

how does resistance arise in MRSA (3)

A
  • mobile genetic element that houses the mecA gene
  • came from Staphylococcus strains (not S. aures)
  • rapidly spread between S. aures strains
25
Q

target modification of PG precursors: what antibiotic is affected

A
  • vancomycin
26
Q

what type of antibiotic is vancomycin

A
  • glycopeptide antibiotic
27
Q

vancomycin: mechanism of action (3)

A
  1. binds the D-ala D-ala part of the PG precursor
  2. prevents transglycosylation and transpeptidation
  3. PG biosynthesis is inhibited and eventually bacteria dies
28
Q

what is the vancomycin mechanism of resistance (3)

A
  1. vancomycin-PG precursors accumulate in cell membrane
  2. VanS senses this and phosphorylates itself and VanR
  3. VanR activates expression of vanX, vanH, and vanA genes
29
Q

VanR (2)

A
  • transcription factor
  • activated after it is phosphorylated
30
Q

vanX (2)

A
  • peptidase
  • eliminates D-ala D-ala PG precursor
31
Q

VanH and VanA

A
  • enable synthesis of D-ala D-lactate, which vancomycin does not bind
32
Q

what is the result of the vancomycin mechanism of resistance (3)

A
  • transglycosylation and transpeptidation can now occur
  • D-lac now hydrolyzed during peptidation instead of D-ala
  • results in “unaltered” PG synthesis
33
Q

how does vancomycin resistance arise (3)

A
  • all resistance genes carried on a transposon
  • transposon resides on a conjugative plasmid
  • resistance can spread quickly
34
Q

conjugative plasmid (2)

A
  • a mobile genetic element
  • encodes transfer apparatus
35
Q

multi-drug resistance (MDR) mechanism (2)

A
  • efflux
  • integrons
36
Q

why are integrons related to MDR (3)

A
  • found in many MDR strains
  • sequencing results showed that often resistance genes are found in tandem
  • strains resistant to a wide variety of anti-microbials
37
Q

integrons (2)
- what is it
- role

A
  • mobile genetic elements
  • capture and mobilize “gene cassettes” via site-specific recombination
38
Q

integrons: gene cassettes (2)

A
  • all have 59bp element
  • do not have their own promoters
39
Q

how do integrons and gene cassettes interact

A
  • 59bp element of gene cassette interacts with att site on the integron
40
Q

how are gene cassettes connected to a promoter (2)

A
  • rely on promoter in the integron
  • located within the integrase gene, int
41
Q

what are the origins of antibiotic resistance (2)

A
  • antibiotic-producing microbes
  • altered houeskeeping genes that recognize new substrates

MICB 308 (22 decks)

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