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4.2 Medical Microbiology > Threat of Resistance and Their Mechanisms > Flashcards

Threat of Resistance and Their Mechanisms Flashcards

1
Q

Talk about the growing threat of antibiotic resistance

A

One of the top global public health and development threats
Estimated that bacterial AMR was directly responsible or 1.27 million global deaths and contributed to 4.95 million deaths in 2019
Thought to contribute to 50 million deaths by 2050
Rapidly increasing prevalence of MDR pathogens compicates treatment options

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2
Q

What is the main driver of resistance?

A

The misuse and overuse of antimicrobials in humans, animals and plants

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3
Q

What is mant by the dual threat of AMR?

A

Multi-drug resistance severly limits treatment options

Cross-infection facilitates spread and transmission

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4
Q

How does WHO combat AMR

A

In 2015 WHO launched the Global Action Plan on AMR in response to the growing AMR crisis

This lead to a need for a One Health approach

Who then launched the Global Antimicrobial Resistance and Use Surveillane System (GLASS)

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5
Q

What are the 5 objectives of the WHO global action plan

A

Improve awareness and understanding of antimicrobial resistance through effective communication, education and training

Strengthen the knowledge and evidence base through surveillance and research

Reduce the incidence of infection through effective sanitation, hygiene and infection prevenetion measures

Optimise the use of antimicrobial medicines in human and animal health

Develop the economic case for sustainable investment that takes account of the needs of al countries and to increase investment in new medicines, diagnostic tools, vaccines and other interventions

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6
Q

What does GLASS stand for?

A

Global Antimicrobial Resistance and Use Surveillance System

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7
Q

What has the last GLASS report in 2022 reported?

A

Highlights alarming resistance rates in 76 countries
42% third gen cephalosporin resistant E. Coli
35% methicillin resistant staph aureus
1 in 5 E. Coli UTIs show reduced susceptibility to ampicillin, co-trimoxazole, fluoroquinolones
K. pneumonia rising reliance on last resort antibiotics
Anticipated x2 surge in resistant to last resort antibiotis by 2035

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8
Q

Rate of resistant in E. Coli

A

42% third gen cephalosporin resistant E. Coli

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9
Q

Rate of resistance in S. aureus

A

35% methicillin resistant staph aureus

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10
Q

Rate of resistance in e. Coli UTIS

A

1 in 5 E. Coli UTIs show reduced susceptibility to ampicillin, co-trimoxazole, fluoroquinolones

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11
Q

How is the UN combatting resistance?

A

UN Genera Assembly held a high-level meeting on AMR in Septemeber 2024 to address the global threat of AMR

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12
Q

What is the WHO priority list and what is the point of is?

A

A list containing a catalogue of 15 families of bacteria that pose the greatest threat to human health

Intended to guide and promote research and development of new antibiotics

It classes bacteria as critical group, high group, medium group

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13
Q

What bacteria are part of the critical group according to WHO priority list
(4)

A

Enterobacterales -> Carbapenem resistant

Enterobacterales -> third gen cephalosporin resistant

Acinetobacter baumannii -> carbapenem resistant

M. tuberculosis -> rifampicin resistant

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14
Q

What bacteria are part of the high group according to WHO priority list

A

Salmonella typhi - fluoroquinolone resistant

Shigella species - fluoro resistant

E. faecium -> vancomycin resistant

P. aeruginosa -> carbapenem resistant

Non-typhoidal Salmonella -> fluoro resistant

N. gonorrhoeae -> third gen cephalosporin and/or fluoro resistant

S. aureus -> methicillin resistant

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15
Q

What bacteria are part of the medium group according to WHO priority list

A

Group A streptococci -> macrolide resistant
S. pneumoniae -> macrolide resistant
H. influenza -> ampicillin resistant
Group B streptococci -> penicillin resistant

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16
Q

What are the two classifications of resistance

A

Intrinsic resistance
Acquired resistance

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17
Q

What is intrinsic resistance?

A

The natural ability of the microorganism to resist specific antimicrobial agents, stemming from inherent biological characteristics rather than acquired mutations or gene transfer

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18
Q

What is acquired resistance?

A

This occurs when microorganisms gain the ability to resist agents through genetic mutations or the acquisition of resistance genes via horizontal gene transfer

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19
Q

How does intrinsic resistance affect the genotype of bacteria

A

There is a no change in genotype
Its a stable genetic property encoded in the chromosome, shared by all members of a genus

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20
Q

What are the two ways intrinsic resistance comes about?

A

Inaccessible Target

Target Not Susceptible to Antibiotic

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21
Q

Give an example of intrinsic resistance because of an inaccessible target

A

Anaerobic organisms that are inherently resistant to aminoglycosides because they lack an oxygen-dependent transport system to move the drgus across the cytoplasmic membrane

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22
Q

Give an example of intrinsic resistance because a targets not sussceptible to the antibiotic

A

Enterococci are inherently resistant to B-lactam antibiotics due to their low affinity of their PBP to them

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23
Q

How does acquired resistance affect the genome?

A

Arises by Alteration in genotype

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24
Q

What are the two methods of acquired resistance?

A

By Mutation through vertical gene transfer

Acquisition of exogenous genetic material through horizontal gene transfer

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25
Q

How is resistance acquired through mutation via vertical gene transfer?

A

This occurs within the endogenous makeup of a bacterial cell
This involves changes in the host chromosome, passed down to a daughter cell
If resistant mutats survive they usually show only reduced susceptibility i.e. low level resistance
Full resistance in a single step is rare

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26
Q

How is resistance acquired through acquisition of exogenous genetic material via horizontal gene transfer

A

Mechanisms include conjugation, transformation, or transduction
New resistance genes are incorporated into the bacterial chromosome
OR resistance genes are contained on a plasmid
MGEs such as transposons and integrons enhance the transfer of resistance genes through various mechanisms
MGEs provide bacteria numerous ways to spread and propagate resistance efficiently

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27
Q

What level of resistance is seen with vertical gene transfer, why is this?

A

Low level resistance
This is because its rare to see full resistance mutations evolveing in just a single step
-> way more likely to occur over multiple generations etc

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28
Q

What are the three mechanisms of horizontal gene transfer that can bring about resistance?

A

Conjugation
Transformation
Transduction

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29
Q

Where are resistance genes found in acquired resistance through horiontal gene transfer

A

Either incorporated into the bacterial chromosome or contained on a plasmid

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30
Q

What mobile genetic elements are responsible for acquired resistance through horizontal gene transfer?

A

Transposons and integrons

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31
Q

What is meant be selection of resistance?

A

Survival and proliferation of microorganisms with resistance traits under selective pressure, such as exposure to antimicrobial agents

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32
Q

How does selective resistance occur?

A

Antibiotics kill or inhibit susceptible bacteria allowing resistant strains to survive and multiply

Even low concentrations of antibiotics can create selective environments that favour resistant bacteria

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33
Q

What are three sources of selective pressure?

A

Inappropriate antibiotic use e.g. overprescription or misuse of antibiotics in healthcare settings

Agricultural Use e.g. antibiotics used in livestock for growth promotion or disease prevention

Environmental Contamination e.g. antibiotic residues in water, soil and wastewater

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34
Q

What are the four main mechanisms of resistance?

A

Enzymatic inactivation
Modification of target sites
Efflux pumps
Reduced permeability

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35
Q

What two mechanisms of resistance often go hand in hand?

A

Efflux pumps and reduced permeability

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36
Q

What is the mechanism behind enzymatic inactivation as a form of resistance

A

Bacterial production of specific enzymes that inactivate antibiotics

These enzymes hydrolyse, acetylate or otherwise modify antibiotics, preventing them from interacting effectively with bacterial targets

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37
Q

What are the three most common methods on enzymatic inactivation

A

Hydrolysis
Group transfer/acetylation
Redox process

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38
Q

Give two examples of hydrolysis as a methood of antibiotic inactivation

A

B-lactamase enzymes on B-lactams

Esterase on Macrolides

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39
Q

Give an example of group transfer as a methood of antibiotic inactivation

A

transferase-mediated resistance against aminoycosides

Most common in enterobacterales and enterococci

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40
Q

Give an example of a redox reaction as a method of enzymatic inactivation of antibiotics

A

Tetracycline modified into 11a-hydroxy-tetracycline
-> addition of O2

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41
Q

Talk about B-lactamase enzymes

A

These can degrade the B-lactam ring of penicillins, cephalosporins and carbapenems

This renders these drugs ineffective

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42
Q

In general where are B lactamase enzymes most commonly found

A

Enterobacteriaceae

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43
Q

Talk abut penicillinases

A

B-lactamases against penicillins

Mainly in gram positives

44
Q

Talk about cephalosporin b-lactamase enzymes

A

ESBLs

Mostly in GNBs

45
Q

Talk about carbapenemases

A

B-lactamases against carbapenems

Mostly in enterobacteriacae and pseudomonas

46
Q

Talk about the prevalence of B-lactamases

A

Prevalence of ESBLs and CPEs is concerning especially in hospital settings where these pathogens contribute to healthcare-associated infections

47
Q

Talk about acetylate/group transfer mediated resistance

A

Aminoglycoside resistance

Transferase mediated resistance

Commonly associated with enterobacterales and enterococci

48
Q

What are the three therapeutic implications of enzyme mediated resistance

A

Compelled to rely on B-lactamase inhibitors in combination with B-lactam antibiotics to counteract resistance

Evolution of carbapenemase-producing organisms has diminished the efficacy of even these combinations, this pushes clinicians towards alternatives like colistin or polymyxins which are toxic

The clinical burden of treatening infections with these last-resort antibiotics has heightened, demanding careful patient monitoring and increasing healthcare costs

49
Q

What are our two main B-lactamase inhibitors?

A

Clavulanic acid or tazobactam

NB: new resistance to these

50
Q

How does modification of target sites work as a mechanism of resistance

A

Bacteria can evade antibiotics by mutating or modifying the drug’s target site within the bacterial cell

This reduces the binding affinity of the antibiotic, this allowing the pathogen to survive

Altered target sites often arise from point mutations or horizontal gene transfer of resistance genes

51
Q

Through what two ways can altered target sites arise?

A

Point mutations or horizontal gene transfer

52
Q

What are the four ways that a bacteria can modify its target site?

A

Alteration of target enzyme e.g. peniciliin binding proteins
altered cell wall target
alteration of ribosomal target sites
production of auxotrophs bypass inhibited steps

53
Q

Give an example of alteration of target enzymes inducing resistance against penicillins

A

PBPs are enzymes located on the outer surface of the bacterial cytoplasm
These catalyse the cross-linking of peptidoglycan in the bacterial cell wall
These also serve as the target sites for B-lactam antibiotics
Thus mutations in these PBPs lead to PBPs losing afinity for B-lactam antibiotics
Reduced number of PBPs can also further limit the bindin of these B-lactam drugs (usually see both together)

54
Q

What are PBPs actually?

A

Enzymes such as transglycosylases and transpeptidases

55
Q

What is peptidoglycan also known as?

A

Murein

56
Q

Give five specific examples of alteration of a target enzyme

A

Methicillin resistance in S. aureus

Penicillin resistance in PNSP

Reduced cephalosporin susceptibility in N. gonorrhoeae

Quinolone resistance

Rifampicin resistance

57
Q

Talk about MRSA as an example of an altered target enzyme mechanism of resistance

A

Acquisition of the mecA gene which encodes a modified PBP2a which has reduced affinity for B-lactam antibiotics
This modification renders all B-lactam antibiotics ineffective against MRSA

58
Q

Talk about PNSP as an example of an altered target enzyme mechanism of resistance

A

Altered PBPs cause reduced susceptiblity to penicillin in certain S. pneumoniae strains

59
Q

Talk about N. gonorrhoeae as an example of an altered target enzyme mechanism of resistance

A

Altered PBP2 associated with reduced susceptibility to ceftriaxone

60
Q

Talk about quinolone resistance as an example of an altered target enzyme mechanism of resistance

A

Quinolones inhibit DNA synthesis, target bacterial DNA gyrase

Mutations in the gyrA gene (encoding NA gyrase) lead to broad-spectrum resistance against all fluoroquinolones

61
Q

Talk about Rifampicin resistance as an example of an altered target enzyme mechanism of resistance

A

Rifampiin inhibits RNA synthesis by binding to the B-subunit of RNA polymerase, thereby blocking mRNA synthesis

Mutations that alter the B-subuit of RNA polymerase reduce the drugs binding affinity, resulting in resistance to rifampicin

62
Q

How does alteration of cell wall precursor targets induce resisitance

A

Resistance arises through acquisition of genes encoding ligases which synthesis abnormal pentapeptide precursors with altered termini, reducing the binding affinity of antibiotics such as glycopeptides

63
Q

Give an example of where alteration of cell wall precursor targets induces resistance

A

Glycopeptide resistance in enterococci, such as VREs

64
Q

Explain glycopeptide resistance as an exaple of alteration of cell wall precursor targets as a mechanism of resistance

A

Vancomycin and teicoplanin bind to the D-ala-D-ala termin of pentapeptide chains in peptidoglycan subunits, inhibiting the cross-linking of the bacterial cell wall

65
Q

Give two examples of alteration of ribosomal target sites as a mecahnism of acquired resistance

A

Amionglycoside resistance e.g. streptomycin resistance in mycobacterium tuberculosis

Macrolide-Lincosamide-Streptogramin MLS Resistance

66
Q

Talk about aminoglycoside resistancfe as an example of alteration of ribomsal target sites

A

Aminoglycosides bind to multiple sites on the ribosom to block protein synthesis

Resistance occurs through the production of altered ribosomal binding proteins

e.g. streptomycin resistance in MTB

67
Q

Talk about macrolide-lincosamide-streptogramin resistance as an example of alteration of ribomsal target sites

A

Drugs like erythromycin and clindamycin bind to the 50S ribosomal sunit interfering with protein synthesis

Production of ribosomal enzymes with reduced macrolide binding affinity incur resistance

68
Q

What does MLS resistance stand for?

A

Macrolide-Lincosamide-Streptogramin resistance

69
Q

Give two examples of resistance whereby production of auxotrophs bypass inhibited steps

A

Sulphonamide and trimethoprim

-> both drugs work by competitively inhibiting the folic acid metabolic pathway which is essential for bacterial survival

70
Q

Talk about sulphonamide resistance as an example of auxotroph production

A

Acquired resistance arises from the production of an altered dihydropteroate synthase enzyme with reduced affinity for sulphonamides

71
Q

Talk about trimethoprim resistance as an example of auxotroph production

A

Resistance develops due to the production of a new dihydrofolate reductase enzyme that has reduced susceptibility to trimethoprim

72
Q

Talk about efflux pumps as a mechanism of resistance

A

Active efflux is a reconised common mechanism of resistance

Normal levels of efflux contribute to low level intrinsic resistance but bacteria can increase expression for high level

Resistance occurs due to active extrusion of drugs from the cell
This extrusion is mediated by multi-drug efflux pumps

Efflux pumps are categorised into five distinct protein superfamilies

73
Q

What is the function of efflux systems

A

They facilitate the removal of various secondary metabolites including antibiotics

They may be specific to a single substrate or broad spectrum expessling diverse compoints including antibiotics from multiple different classes (MDR)

74
Q

Talk about the expression of efflux pumps

A

Overexpression of efflux pumps or amino acid substitutions enhances pump efficiency, potentially leading to high-level multidrug resistance

Increased efflux pump activity may be an initial step in a bacterium’s progression to full resistance

Multi subunit efflux pumps are often encoded on the bacterial chromosome

75
Q

What is the effect of elevated efflux activity

A

Reduces intracellular antimicrobial levels enabling bacterial survival and facilitating the accumulation of additional resistance mutations

76
Q

Where are multi subunit efflux pumps encoded?

A

Encoded on the bacterial chromosome

77
Q

What are the five categories of efflux pumps?

A

Major Facilitator Superfamily (MFS)

Resistance-Nodulation-Division (RND)

Small Multidrug Resistance (SMR)

ATP-Binding Casette (ABC)

Multidrug and toxic compound extrusion (MATE)

78
Q

Talk about major facilitator superfamily of efflux pumps

A

MFSs found in E. Coli and S. aureus

Efflux antibiotics such as tetracyclines as well as dyes and sugars

79
Q

Talk about the resistance nodulation division of efflux pumps

A

RNDs found in P. aeruginosa and E. Coli

Efflux antibiotics such as beta lactams and fluoroquinolones as well as detergents

80
Q

Talk about the small multidrug resistance family of efflux pumps

A

SMRs found in E. Coli and M. tuberculosis

Efflux disinfectants and antiseptics

81
Q

Talk about the ATP-binding cassette family of efflux pumps

A

ABCs found in S. aureus and E. Coli

Efflux antibiotics such as macrolides and peptides

82
Q

Talk about the multidrug and toxic compound extrusion family of efflux pumps

A

MATEs found in Vibrio cholerae and P. aeruginosa

Efflux antibiotics such as fluoroquinolones and organic cations

83
Q

Talk about efflux pumps in GNBS

A

Efflux pumps in GNBs often span both the inner and outer membranes
This enables efficient extrusion of antibiotics directly into the external environment
RND pumps are major contributors to MDR in HAI caused by GNBS
Many of these pumps handle a variety of antibiotics, biocides and toxic compounds making infections very difficult to treat

84
Q

Why are we most concerned with RND family efflux pumps in GNBs

A

These pumps often work in conjunction with other resistance mechanisms such as enzyme degadation or permeability changes

85
Q

Talk about spread of resistance and efflux pumps in GNBs

A

Efflux pumps in pathogens like K. pneumoniae and A. baumannii are associated with global dissemination of MDR strains

86
Q

Talk about the role of efflux pumps in lastresort drug resistance

A

Pumps such as KpnEF in K. pneunoniae are linked to resistance against last-resort antibiotics like tigecycline

87
Q

Talk about efflux pumps in gram positives

A

Resistance mediated by efflux transporters located in the cytoplasmic membrane

The Major Facilitator Superfamily is the key efflux pump family in gram positives

Efflux pumps can bring about intrinsic or acquired resistance in gram positives

88
Q

Talk about resisistance mediated by efflux pumps in gram positives

A

Seen in S. aureus and S. pneumonia

intrinsic and transferable resistance

Resistance to a wide range of antimicrobials and biocides

89
Q

What are the two types of efflux pumps in gram positives, what is the importance of these

A

Plasmid encoded efflux pumps which facilitate horizontal spread of resistance

Chromosomally encoded pumps provide intrinsic resistance to key antibiotics

90
Q

Give two exampls of plasmid encoded efflux pumps in gram positives

A

QacA/B
MefA

91
Q

Give three examples of chromosomally encoded efflux pumps in gram positives

A

NorA
NorB
NorC

92
Q

How does multidrug resistance come about, in relation to porins?

A

Porin alterations o ften coexist with other resistance mechanisms such as eflux pumps or enzymatic degradation, making infections much more difficult to treat

93
Q

In what four ways can porins induce antibiotic resistance?

A

Reduced permeability leads to resistance

Mutations or loss of porins result in resistance

Altered porins slow drug penetration

Limited porin availability reduces efficacy

94
Q

Give an example of where reduced porin permeability leads to resistance

A

Normally beta lactams diffuse through general porins e.g. OmpF

But reduced permeabiblity leads to resistance

95
Q

Give an example of where mutations or loss of porins result in resistance

A

Carbapenems utilise specific porins such as OprD in P. aeruginosa but mmumtations in these or a loss of these porins results in resistance

96
Q

Give an example of where altered porins slow drug penetration

A

Fluroquinolones normally diffuse through porins into the cytoplasm

altering these porins slows down the penetration of the drug

97
Q

Give an example of where limited porin availability reduces efficacy

A

Aminoglycosides enter via porins and interact with ribosomes

Limiting porin availability prevents entry

98
Q

Talk about carbapenem resistance induced by porins

A

Loss or modification of specific porins like OmpK36 in K. pneumonia or OprD in P. aeruginosa is a hallmark of carbapenem resistance

99
Q

Talk about porin induced resistance and their relevance in HCAI

A

Pathogens like Acinetobacter baumannii and K. pneumoniae with altered porins are common causes of HCAI leading to treatment failures

100
Q

How do different mechanisms of resistance work together

A
  1. individual class of drugs inactivated by different mechanisms
  2. individual organism employs different mechanisms to generate resistance to single drug/different classes of drugs -> these mechanisms interact todetermine actual level of resistance
101
Q

What is synergistic resistance?

A

Whereby most clinically signigicant bacteria employ at least two or more resistant mechanisms for the same antibiotic class

A combination of mechanisms that leads to higher levels of resistance, often termed extensivelt drug-resistant or multidrug resistant

102
Q

What is cross-class resistance

A

Whereby one mechanisms has affects across more than one class of antibiotics

e.g. efflux pumps and permeability changes often provide cross-class resisistance impacting multile antibiotic classes simultaneously

103
Q

Talk about synergistic resistance in K. pneumoniae

A

Resistance to B-lactams by multiple mechanisms

Beta lactamase production e.g. ESBLs, KPC
Porin loss to reduce permeability -> porin Ompk35/OmpK36 are altered
Efflux pumps to actively remove beta-lactams from the cell

104
Q

Talk about synergistic resistance in P. aeruginosa

A

Resistance against fluoroquinolones through multiple mechanisms:
- efflux pumps encoded by MexAB-OprM system removes fluoros
- target modification encoded by mutations in DNA gyrase (gyrA) or topoisomeras IV (parC)
- outer membrane changes to limit drug penetration

105
Q

Talk about synergistic resistance in S. aureus

A

Resistance to macrolides through multiple mechanisms:
-target modification - ribosomal methylation via erm genes (ermA or ermC) reduces macrolide binding to 50S ribosomal subunit
-efflux pumps: MsrA pump actively expels macrolides

106
Q

Conclusions on resistance mechanisms

A

The molecular mechanismms underlying bacterial resistance highlight the formidable challenge facing modern medicine

Each resistance mechanism - enzymatic degradation, target modification, efflux pumping, or reduced permeability - constrains available treatment options and necessitates new approached in both clinical management and drug development

Multifaceted approach combining clinical vigilance, therapeutic innovation and policy support is essential to manage and mitigate the impact of resistance effectively

4.2 Medical Microbiology (20 decks)

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