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2.2 Microbiology > Antimicrobial Resistance > Flashcards

Antimicrobial Resistance Flashcards

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1
Q

What are the two main problems surrounding drug resistance?

A

Multi-drug resistance which severely limits treatment options

Cross infection which facilitates spread and transmission

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2
Q

List the five most commonly implicated organisms in antibiotic resistance

A

Methicillin resistance staphylococcus aureus (MRSA)

Vancomycin resistant enterococcci (VRE)

Carbapenemase Producing Enterobacterales (CPE)

Carbapenemase Producing Organisms (CPO)

Extended Spectrum B-lactamase Producing GNBs (ESBLs)

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3
Q

What does the burden of antibiotic resistance referred to?
(4)

A

The increased mortality rates
The increased length of hospital stays
The increased healthcare costs

All of these are at least twice as great for patients infection with resistant bacteria versus susceptible bacteria

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4
Q

What has WHO said about MDRO/AMR?
(2)

A

There is a global epidemic of AMR

It a major threat to public health, leading to mounting healthcare costs, treatment failure and deaths

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5
Q

Comment on the different types of MDR (multi-drug resistance)

A

XDR - Extensively drug resistance
PDR - Pan drug resistance

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6
Q

How many people die a year due to antibiotic resistant strains in the EU?

A

37,000 die a year

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7
Q

How many people are expected to die from antibiotic resistance by 2050

A

10 million deaths by 2050
This is expected to cost 66 trillion

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8
Q

What are currently the four seen trends in AMR?
(4)

A
  1. Low grade PDR Healthcare associated pathogens
  2. More virulent XDR healthcare associated pathogens
  3. MDR pathogens prevalent in Healthcare and emerging in the community
  4. The boundary between hospital and community pathogens is also becoming increasingly blurred, with MDR pathogens causing both hospital and community- onset infections
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9
Q

How do you class PDR, XDR and MDR

A

PDR = resistant to all classes of antibiotics
XDR = susceptible to 2 or less than 2 antibiotic classes
MDR = Resistant to 3 or more classes

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10
Q

Give two examples of PDR organisms

A

e.g. VRE
e.g. CPO-Acinetobacter

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11
Q

Give three examples of XDR organisms

A

CPE
MRSA
ESBL-GNB

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12
Q

Give four examples of MDROs, two in community and two in healtchare

A

MRSA and CPEs in the community

S. pneumoniae and N. gonorrhoeae

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13
Q

Comment on the emergence of resistance
(4)

A

There is currently resistance to all antibiotics
The emergence of resistance is a function of time and use
The extend and speed of resistance development varies with each drug

Overcome by introduction of new classes of drug but there hasn’t been any developed

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14
Q

What are the two ways resistance can originate

A

Intrinsic
Acquired

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15
Q

Resistance is either intrinsic or acquired, what does this mean?

A

Exposure to antibiotics does not make bacteria resistance

The organism already has the resistance, the use of antibiotics just selects this out

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16
Q

What is intrinsic/inherent resistance

A

Stable genetic property encoded in the chromosome and shared by all members of genus

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17
Q

Which form of resistance is more common

A

Acquired resistance

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18
Q

What are the two ways acquired resistance can come about?

A

By alteration in genotype (mutation)

By acquisition of new/’foreign’ genetic material

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19
Q

Selection of resistance occurs naturally, what does this mean?
(3)

A

A phage has come in and given a bacteria resistance genes

But the potential for resistance hasn’t been unlocked yet

The antibiotic will kill all other organisms but the resistant strains -> this will then multiply

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20
Q

Comment on the misuse of antibiotics and resistance
(3)

A

This increases the rate at which natural selection of resistant strains occurs

Indiscriminate use of 1/3 of antibiotic prescriptions given on an outpatient basis are unnecessary

Widespread antibiotic use in animal husbandry e.g. pigs need a lot of antibiotics, cattle fed antibiotic feed in america

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21
Q

Comment on the evolution of antibiotic resistance
(4)

A

Evolution of resistant strains is a natural phenomenon

It occurs when microorganisms mutate or when resistant traits are exchanged

Again, the misuse of antibiotics accelerates this emergence

Poor infection control practices, encourage the further spread of antibiotic resistance

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22
Q

Antibiotic activity depends on what?
(4)

A

Stability - must not be inactivated
Access - muse be able to reach the target
Access - must not be extruded before binding to the target
Existence of a vital target that is susceptible to the agent

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23
Q

How can bacteria stop antibiotic activity

A

By production of drug-modifying enzymes which inactivate/modify the antibiotis

24
Q

How can bacteria stop antibiotic access?
(2)

A

Modification of cell envelope - to make it less permeable

Extrusion - expel drug from the cell

25
Q

How can bacteria stop the action of antibiotics by altering the target?

A

Modify the target - the antibiotic will bind less avidly

26
Q

Write about the production of drug-modifying enzymes
(4)

A

Enzymes destroy/modify the antibiotic

Bind to the antibiotic and destabilise it

e.g B-lactamase enzyme production

This is a widespread mechanism of resistance

27
Q

How do B-lactamases work?
(2)

A

By catalysing the hydrolysis of the B-lactam ring structure
This destroys the B-lactam activity

The B-lactamase ruptures the B-lactam ring and inactivates it

28
Q

Comment on B-lactamase mediated resistance

A

Widespread production in GN and GP bacteria

Extensively produced in Enterobacterales e.g. K. pneumonia and E. Coli

ESBL GNBs

CPEs

29
Q

What are ESBLs
(2)

A

Extended Spectrum B-lactamase Producing GNBs

These are resistant to 3rd and 4th generation cephalosporins

30
Q

What are CPEs

A

Carbapenemase Producing Enterobacterales

Resistant to Carbapenems and most other B-lactams

31
Q

Comment on resistant brought on by modification of the cell envelope
(4)

A

Antibiotics are designed to be hydrophilic so they can enter the bacterial cell through porins (water-filled channels) in their outer membrane

Gram negatives have a lot of these porins

Mutations reduce porin number or alter porins to impeded drug entry and mediate resistance

Mutation is only seen in gram negatives

32
Q

What organisms have porin mutations?
(2)

A

Pseudomonas
Enterobacterales

33
Q

Porin mutations mediate resistance against which classes of antibiotics

A

B-lactams
Fluoroquinolones

34
Q

What is extrusion of antibiotics also called

A

Antibiotic efflux

35
Q

How does antibiotic efflux mediate resistance
(4)

A

Found in gram positive and negative

Involves the active extrusion of drug from the cell due to action of export protein pumps (efflux pumps)

Efflux pumps normally facilitate removal of secondary metabolites from the cell

Efflux pumps are over expressed or altered to improve pump efficiency to induce MDR

36
Q

Where is efflux mediated resistance often seen

A

Gram positive and negative but especially in pseudomonas

37
Q

Efflux mutations mediate resistance against what classes of antibtiocs

A

Macrolides
Fluoroquinolones

38
Q

How is resistance mediated by target site modification
(4)

A

Seen in GP and GN but GP are better at this

Modify the antibiotic target so that is binds to antibiotic with less avidity

Very common mechanism with resistance seen against every class

Works by either altering the target that act as enzymes in the cell or alter targets that are of cell wall component

39
Q

Comment on target alteration of B-lactam antibiotics
(5)

A

This is seen in methicillin resistance

Penicillin Binding proteins are transpeptidase enzymes that facilitate the cross-linking of peptidoglycan

PBPs are the target sites for B-lactams (antibiotic looks like the D-ala, D-ala the PBPs need to bind)

Mutation in PBP enzymes causes a loss of affinity for B-lactam drugs

This is seen in MRSA = organism makes PBP2a which won’t bind any B-lactam

40
Q

Write about the target modification mediated resistance against Vancomycin
(5)

A

Vancomycin acts by binding to the D-ala, D-ala amino acid termini of the peptidoglycan subunits

This binding inhibits cell wall cross-linking

Acquisition of Van A or Van B genes encodes enzymes which synthesis abnormal PG subunits

These PG subunits have altered amino acid termini-reduced antibiotic affinity (D-ala, D-lac)

Seen in enterococcci VREs

41
Q

Comment on the resistance seen in E. faecium
(3)

A

Take in Van A or Van B genes

These make D-ala, D-lactace

This stops the vancomycin from working

42
Q

Antibiotic resistance is a complex process, comment on this
(4)

A

Individual class of drugs inactivated by more than one mechanism or resistance

Individual organisms may employ different mechanisms to generate resistance to single drug and to different classes of drugs- mechanisms interact to determine actual level of resistance

Genes that encode resistance determinants are often present on mobile genetic elements e.g. plasmids, phages

Spread of resistance between bacterial species, genera and even families

43
Q

Write a note on MRSA
(5)

A

First real significant type of resistance the world saw - biggest setback in history of antibiotic therapy

Usually if Methicillin resistant then resistant to other B-lactams as well, often to aminoglycosides and fluoroquinolones (HA MRSA)

Used to only be seen in HAI but now seen in community

Prevalence is dropping - we are now below EU average

40% of all BSI caused by staph were MRSA

44
Q

How do we investigate methicillin resistance
(4)

A

We use up cefoxitin disc diffusion

Incubate for 16-20 hours

Detect any colonies growing around disc or in zone of clearance

Cefoxitin can also be used in the MIC or in VITEK

45
Q

Write a note on Vancomycin Resistant Enterococci (VRE)
(7)

A

Altered cell wall targets

Emerged in 1990s

Resistance to fluoroquinolones and aminoglycosides in 30-60% of isolates also in VRE

Linezolid and daptomycin were developed to treat VRE but there is now resistance against these - XDR

XDR moving towards PDR

Healthcare associated infection

Ireland has really high amounts versus Europe

46
Q

How do we test for vancomycin resistance
(4)

A

Vancomycin disc diffusion for 24 hours (!!!)

Suspect resistance if zone edge is fuzzy or colonies grow within the inhibition zone

MIC or VITEK can be used

VITEK not good at detecting low levels or resistance

47
Q

Write a note on ESBL producing GNBs
(4)

A

Arose in 1980s

B-lactamase production - ability to hydrolyse extended spectrum B-lactams i.e. cephalosporins

Predominate in K. pneumonia and E.coli but increasingly seen in other Enterobacterales

Associated with HCAI resulting from cross-infection and lapse in infection control but also emerging in the community

48
Q

Comment on ESBL lab detection
(4)

A

Screen for ESBL production with routine cephalosporin AST

If reduced susceptibility to cefotaxime or ceftazidime observed confirm ESBL production with Combination Disc Test

CDT -> Disc diffusion with cephalosporin alone and cephalosporin plus Clavulanic acid (B-lactamase inhibitor).

If ESBL present the zone of inhibition will be 5mm smaller with the clavulanic acid as the B-lactamase enzymes are being inhibited

49
Q

Comment on CPEs
(6)

A

Production of B-lactamases

Carbapenemase enzymes - ‘Big 5’

OXA-48 and Klebsiellella pneumonia carbapenemase most common (only really seen in Galway)

Usually resistant to many other classes of antibiotics and are virulent

Vast majority of CPEs in Ireland are just colonisation in the gut -> not invasive but this high carriage rate could cause problems later when resistance spreads

70% of CPEs in Ireland were OXA-48

50
Q

How are CPEs detected in the lab?
(3)

A

Screen with routine Ertapenem AST

If ertapenem reduced susceptibility then confirm with Resist-5 lateral flow assay

Resist-Ab probes detection of OXA, KPC, NDM and VIM CPEs

51
Q

How do we combat antimicrobial resistance

A

Rational drug use
Ban on OTC antibiotics
AMR committee
National Policy
Increased collaboration
New AMR programmes
Std. treatment guidelines
Hand hygiene
Infection control and prevention
Antimicrobial surveillance
Immunisation coverage

Need new novel drugs

52
Q

What are the three main ways to combat antibiotic resistance

A

Develop new antibiotics
Antibiotic stewardship
Surveillance and infection prevention and control

53
Q

Comment on how new antibiotic would control antibiotic resistance
(4)

A

Novel classes urgently needed for the future

Linezolid and daptomycin are active against gram-positive bacteria such as MRSA but resistance emerging

Few classes in phase II or III clinical trials

Need new drugs for CPEs and CPOs (pseudomonas and acinetobacter)

54
Q

Comment on antibiotic stewardship
(3)

A

Judicious use of antibiotics must be promoted

Use of more appropriate drugs, shorter treatment courses and cyclic treatment regimens

Assuming comprehensive strategies are devised. continual audit must be undertaken

55
Q

How does the lab play a role in antibiotic resistance?

A
  • Labs can supress release of anti-microbial resistance results -> e.g. we put up 5 and 4 are susceptible but we only release the result on one so that the medics will only use one antibiotic – we can control the cycling of antibiotics
  • Pharmacist in charge of antimicrobials can also help do this by only issuing certain antimicrobials
56
Q

Comment on surveillance and infection prevention and control of antibiotic resistance
(3)

A

Most important options for control of resistance lie in implementation of effective surveillance and infection prevention control

Need for clinical laboratories to: provide accurate antibiotic susceptibility data, develop improved resistance detection methods, participate in local and national surveillance networks to collate resistance data

Need for Healthcare facilities to engage in IPC programmes -> patient isolation and facilities, hand hygiene and transmission-based precautions etc

57
Q

The iNAP2 framework alligns with 5 strategic objectives outlines in WHO AR Global Action plan, what are these 5 objectives

A

Improve awareness and knowledge (stewardship)

Enhance surveillance (IPC) of antibiotic resistance and antibiotic use (Stewardship)

Reduce the spread of infection and disease (IPC)

Optimise the use of antibiotics in human and animal health (stewardship)

Promote research and investment in new medicines, diagnostic tools, vaccines and other interventions (Research)

2.2 Microbiology (60 decks)

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