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Health Science > Antimicrobial Resistance & MDRO > Flashcards

Antimicrobial Resistance & MDRO Flashcards

Caoimhe

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Biology 101 flashcards
1
Q

Antibiotics may be bacteriostatic/bactericidal

What does a bacteriostatic antibiotic do?

A

The antibiotic prevents the growth of bacteria

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2
Q

Antibiotics may be bacteriostatic/bactericidal

What does a bactericidal antibiotic do?

A

The antibiotic kills bacteria

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3
Q

Various antimicrobial agents act by interfering with what? (4)

A
  1. Cell wall synthesis
  2. Plasma membrane integrity
  3. Nucleic acid synthesis
  4. Ribosomal function
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4
Q

Antibiotic Classes

What do B-Lactams do to kill bacteria? and an example?

A

Inhibit bacteria cell wall synthesis
Eg; Amoxicillin

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5
Q

AMR

When does AMR occur?

A

When microbes evolve mechanisms that protect them from the effects of antimicrobials

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6
Q

AMR

AMR consequences (4)

A
  1. Limited treatment for infections -> delayed treatment
  2. Increased risk of transmission
  3. Accumulation of antimicrobial resistance
  4. Panresistance -> microbe resistant to everything
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7
Q

AMR

(3) Stages of AMR evolution

A
  1. Genetic mutation as a result of selective pressures
  2. Horizontal gene transfer (HGT)
  3. Vertical gene transfer (clonal dissemination) and subsequent transmission of resistant strains from person -> person or from other sources (animals, environmental sources)
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8
Q

AMR

Main drivers of AMR (3)

A
  1. Overuse and misuse of antimicrobials
  2. Poor hygiene/ sanitation
  3. Substandard infection control measures in healthcare/agriculture
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9
Q

(3) Stages of horizontal gene transfer

A
  1. Transformation
  2. Translation
  3. Conjugation
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10
Q

What happens during the third stage of HGT?

A

Conjugation:
Cells need direct contact, with this a channel forms for DNA to pass

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11
Q

AMR

What are plasmids?

A

Small, extra-chromosomal DNA molecules that can replicate independently.

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12
Q

AMR

What were antibiotics used for in agriculture and what did this promote?

A

Antibiotics in low concentrations were used as growth promoters for animals in agriculture. This resulted in resistance among bacteria

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13
Q

AMR

MDRO definition

A

Microorganisms resistant to three or more classes of antimicrobial drugs

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14
Q

AMR

Beta lactam antibiotics examples? (2)

A
  1. Penicillins
  2. Carbapenems
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15
Q

AMR

Clinically significant resistance -> Gram positive organisms examples? (4)

A

Staphylococcus species:
1. Staphylococcus aureus
2. Coagulase negative Staphylococci (CNS)
Enterococcus species:
3. E. faecium
4. E. faecalis

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16
Q

AMR

CNS are examples of opportunistic bacteria. Define opportunistic bacteria?

A

Microorganisms that don’t usually cause disease, however can become pathogenic under certain conditions -> weakened immune system - immunocompromised

17
Q

Staph aureus infection associated with?

A
  1. Skin (abscesses, cellulitis)
  2. UTI
  3. BSI (blood stream infection)
  4. Osteomyelitis
  5. Foodpoisoning
18
Q

Staph aureus infection treatment (2)

A
  1. Cephalexin (beta lactam) for uncomlicated skin infection
  2. Vancomycin (glycopeptide antibiotic) for comlicated/invasive infections -> bacteraemia, pneumonia, etc.
19
Q

MRSA definiton

A

Any strain of S. aureus that has developed (through natural selection) or acquired (throughHGT) mutiple drug resistace to several beta-lactam antibiotics, most notably methicillin

20
Q

Explain how MRSA works !

A
  • Methicillin and beta-lactams bind to and inhibit penicillin binding protein (PBP)
  • PBP is an enzyme that assists with peptidoglycan assembly.
  • When PBP is inhibited the peptidoglycan matrix cannot properly be formed and the bacterial cell will burst
  • An alternative penicillin binding protein is coded for, preventing methicillin binding
  • Confers resistance to multiple beta-lactam antibiotics (penicillin based)
21
Q

Enterococcus Species

Infections caused by Enterococci species? (4)

A
  1. UTIs
  2. Bacteraemia
  3. Endocarditis (inflammation of the endocardium)
  4. Meningitis
22
Q

Enterococcus Species

Enterococcus species infection treatment? (2)

A
  1. Nitrofurantoin (nitrofuran class) for uncomplicated UTI
  2. Vancomycin (glycopeptide class) for invasive infections
23
Q

VRE

VRE description

A
  1. Nosocomial pathogens that are persistant in hospital environment
  2. Resistance to several antibiotics limits treatment options
  3. VRE infection liked with extended hospital stays
24
Q

How does vancomycin work?

A
  • Binds to the D-Ala-D-Ala terminus of peptidoglycan precursor, inhibiting transglycosylation and transpeptidation, and causing cell wall damage
25
Q

How is resistance to vancomycin conferred?

A

By the acquisition of the vanA or vanB gene that alter the D-Ala-D-Ala target of vancomysin

26
Q

Treatment for vancomycin resistant strains

A
  1. Linezolid and daptomycin
  2. Final resort antibiotics
27
Q

VRSA (Vancomycin Resistant S. Aureus)

What is VRSA mediated by?

A

A vanA gene cluster which is transferred from vancomycin resistant enterococci via transposon

28
Q

Clinically significant resistance-> gram negative microorganisms (2)

A

Primarily Enterobacterales
1. Extended spectrum beta-lactamase producers (ESBL)
2. Carbapenemase producing enterobacterales (CPE)

29
Q

How do ESBLs work?

A

They are associated with enzymes (beta-lactamases) that hydrolyse the beta-lactam ring of penicillins and cephalosporins

30
Q

Solution to ESBLs? (2)

A
  1. Supplement antibiotics with a beta-lactamase inhibitor eg: augmentin
  2. Use carbapenems
31
Q

CPEs

What are CPEs resistant to?

A

All antibiotics derived from penicillins

32
Q

What are Carbapenems?

A

Drugs of last resort, with broad spectrum of activity against gram negs and some gram pos.

33
Q

Antimicrobial control measures (4)

A
  1. Screening before entering intensive wards (for MRSA, VRE, CPE)
  2. Surveillance reporting
  3. Patient isolation
  4. Hygiene measures
34
Q

How is MRSA screened for

A

Swabs from nose, axilla, groin are plated on selective and differental media in hospital lab

35
Q

VRE screening

A

Culture from rectal swabs plated on selective and differential media in hospital lab

36
Q

CPE (and ESBL) screening

A

Culture from rectal swabs. Molecular approach available for urgent swabs.

37
Q

How could bacteriophages be used as an AMR solution?

A

Regulation of ecosystem: maintenance of population levels by predation

38
Q

Bacteriophage and viral infection of bacteria: how does it work?

A
  • Bacteriophage attaches itself to bacterium and infects host cell
  • It hijacks the bacteriums cellular machinary to produce viral components
  • New bacteriophages assmeble and burst out of bacterium -> called lysis

Health Science (10 decks)

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