3.1 Antimicrobial Resistance Flashcards

1
Q

What is intrinsic resistance?

A

the structure and/or biological characteristic of the microbe are not ameable to the effects of an antimicrobial

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2
Q

What is antimicrobial resistance?

A

the acquired ability of a microbe to resistance the effects of an antimicrobial that once could have successfully treated the microbe

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3
Q

What do we mean when we say AMR is binary?

A

it doesn’t creep up on you, it just happens out of nowhere

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4
Q

Name the 3 sites of antiobiotic action

A

Bacterial Wall and Cell membrane
nucleic acid synthesis
protein synthesis

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5
Q

What 6 antibiotics work on the bacterial cell wall and membrane?

A
penicillins
cephalosporins
carbapenems
monobactams
glycopeptides
polymyxins
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6
Q

Name 3 sorts of antibiotics working on nucleic acid synthesis

A
Folate antagonists
DNA Gyrase (quinolones)
RNA Polymerase (Rifampicin)
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7
Q

Why might we give HIV patients antibiotics which we know don’t work?

A

HIV will slow down its’ replication rate in order to survive

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8
Q

What is the most common form of AMR?

A

enzyme release

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9
Q

What is the principle of inducible resistance?

A

You have a bug which looks susceptible to the antibiotic…

however, it just switches a gene and sacrifices a bit of biological fitness to survive

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10
Q

What are the 3 most commonly seen antibiotic resistant bacteria?

A

Methicillin resistant staphylococcus aureus (MRSA)
Vanomycin resistant enterococci (VRE)
extended spectrum beta lactamase producing enterobacteriaceae (ESBL)

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11
Q

Why is ESBL so scary?

A

it produces enzymes which can break down our most broad spectrum antibiotics

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12
Q

What are the 2 types of resistance in TB?

What are their survival rates in the UK?

A

multidrug resistanct TB (MDR-TB) 80%

extensively drug resistant TB (XDR-TB) 30-50%

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13
Q

What is the definition of a multidrug resistant TB?

A

resistant to Rifampicin and Isoniazid

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14
Q

Why can HIV resistance come and go?

A

it copies itself like mad, making lots of mistakes in the process, this means that it could remain dormant for a bit, and then if you give someone antibiotics all of a sudden it goes crazy

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15
Q

name 2 M2 inhibitors, why are they important?

A

Amantadine, rimantadine

influenza A in humans is resistant to them

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16
Q

Name 6 factors accelerating AMR

A
drug prescribing
drug access
drug quality
Veterinary use
global travel
the environment
17
Q

What 2 techniques do we use to assess in vitro antibiotic effectiveness?

A

Minimum inhibitory concentration (MIC)

resistance mutations

18
Q

What is MIC?

A

minimum in vitro concentration which an antibiotic can inhibit growth

19
Q

What is the significance of the difference between in vitro efectiveness and in vivo effectiveness?

A

in vitro effectiveness doesn’t necessarily translate to in vivo effectiveness

20
Q

Name 8 mechanisms of antimicrobial resistance

A
Enzymes
Outer membrane permeability
Inner membrane permeability
Mutations in target sites
Antibiotic efflux pumps
Target site protection
Target site overproduction
Alternative metabolic 
pathways
21
Q

What antibiotics have influenza A in humans shown resistance to?

A

M2 inhibitors

22
Q

define an XDR-TB?

A

resistant to:

rifampicin
isoniazid
flouroquinolones
an injectable agent