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MCD Microbiology > 3 Hospital Acquired Infection and Antibiotic Resistance > Flashcards

3 Hospital Acquired Infection and Antibiotic Resistance Flashcards

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1
Q

Q: What is an antibiotic? Produced by? today?

A

A: -antimicrobial agent produced by a microorganism that kills or inhibits other microorganisms
-produced by soil-dwelling fungi/bacteria -> those used today have been altered eg semi-synthetic chemicals with antimicrobial activity

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2
Q

Q: What are antibiotics used for?

A

A: treating and preventing infection (eg in those that are immunosuppressed)

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3
Q

Q: What is an antimicrobial? Compared to antibiotics?

A

A: chemical that selectively kills or inhibits microbes (bacteria, fungi, viruses)
-broader target than antibiotics

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4
Q

Q: What is bactericidal behaviour? bacteriostatic? Relationship?

A

A: -kill bacteria
-stops bacterial growth

bactericidal activity is dose dependant (lower= bacteriostatic behaviour)

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5
Q

Q: What is an antiseptic?

A

A: chemical that kills or inhibits microbes that is usually used topically to prevent infection

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6
Q

Q: What does it mean for a bacteria to become resistant to antibiotics? (2) Spectrum?

A

A: that antibiotic can no longer be used against that bacteria // ability of an organism to replicate in the presence of an antibiotic at a particular concentration

there is a spectrum for different strains: the antibiotic concentration required to inhibit growth is different for different strains

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7
Q

Q: What is breakpoint? In relation to resistance?

A

A: an estimate of the reasonable concentration that might be achieved clinically

Any organism that can grow at a concentration of the breakpoint or greater than the breakpoint is resistant

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8
Q

Q: What is Minimal Inhibitory Concentration (MIC)?

A

A: the lowest concentration of the antibiotic required to inhibit growth

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9
Q

*Q: What occurs with greater use of antibiotics? Why? (2)

A

A: ->higher prevalence of resistance (less effective)

  • bacteria constitute as a moving target -> rapidly evolving and changing -> come up with new methods not to be killed
  • routine antibiotic use provides a selective pressure for the acquisition and maintenance (if a strain is already resistant) of resistant genes
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10
Q

*Q: Explain resistance in terms of natural selection. (3)

A

A: in any population-> get some variation

  • absence of selection pressures-> said diversity is maintained
  • presence of selection pressures-> allows specific phenotypes to thrive
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11
Q

*Q: What occurs soon after the arrival of a new antibiotic in hospitals? When is this not the case? Possible reason?

A

A: Resistance

Exceptions: Erythromycin and Vancomycin

Vancomycin - is toxic and not hugely effective so it wasn’t used much at the time of discovery so it took longer for resistance to develop

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12
Q

*Q: What does antibiotic resistance lead to? (3) Give 5 reasons for one. (5)

A

A: -increased mortality

  • increased morbidity
  • increased cost:
  • increased time to find a effective therapy therefore longer stay
  • use of less effective ‘second choice’ antibiotic therefore longer stay
  • use of more toxic drugs that need need additional supported therapy
  • use of more expensive therapy (newer drugs)
  • requirement of different approaches entirely eg surgery
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13
Q

*Q: What is a possible way around antibiotic resistance?

A

A: using vaccinations so that you prevent the infections from even occurring and therefore preventing the need of them

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14
Q

*Q: How are antibiotics often categorised? Name 7 classes. Which is the most commonly used class? Which is the only synthetic class of antibiotics?

A

A: according to their mechanism of action

  1. Beta-lactams **
  2. Tetracycline
  3. Chloramphenicol
  4. Quinolones (s)
  5. Sulphonamides
  6. Aminoglycosides
  7. Macrolides
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15
Q

*Q: What is the overall mechanism of action of beta-lactams? Explain. (3) 2 examples. Why is MRSA resistant to it?

A

A: Interfere with synthesis of the PEPTIDOGLYCAN component of the bacterial cell wall

  • beta-lactam ring is similar in structure to a precursor of peptidoglycan = AB mimics precursors for bacterial cell wall
  • once enzymes tries to use the AB (bind to Penicillin Binding Proteins (PBP)) they become deactivated
  • when bacteria are exposed to AB they lyse and die

Examples: Penicillin and methicillin

MRSA has a different PBP (PBP2a) which doesn’t bind with high affinity to beta-lactams

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16
Q

*Q: What is tetracycline? What is the overall mechanism of its action? Explain. (3)

A

A: -Bacteriostatic, broad spectrum
-Inhibits PROTEIN SYNTHESIS

  • Binds to the 16S component of the 30S ribosomal subunit thus
  • preventing charged aminoacyl tRNAs from binding to the mRNA/ribosome complex
  • prevents elongation of the polypeptide
17
Q

*Q: What is chloramphenicol? What is the overall mechanism of its action? Explain. (2) How is it often used? Current use?

A

A: -Bacteriostatic, broad spectrum
-Inhibits PROTEIN SYNTHESIS

  • Binds to 50S subunit and blocks peptidyl transfer step
  • prevents elongation of the polypeptide

Often used topically due to toxicity

as other drugs have become resistant-> it has been increasingly used as a systematic therapeutic

18
Q

*Q: What are quinolones? What do they represent? What is the overall mechanism of its action? Explain. (3)

A 
A: Bactericidal, broad spectrum 
-only synthetic class of AB

disrupt DNA replication
-targets DNA gyrase (in Gram NEGATIVE) and topoisomerase (in Gram POSITIVE)
(-DNA gyrase and topoisomerase is responsible for unravelling DNA)
-prevents DNA from sticking back together during unwinding process

19
Q

*Q: What are sulphonamides? (2) What is the overall mechanism of its action? Used to treat? (3) Give example and explain how it’s used. Use today?

A

A: Bacteriostatics that are not strictly antibiotics (synthesised)

Interferes with the folate pathway

-UTI, Reproductive Tract Infection (RTI) and bacteraemia

sulpha-methoxazole
-sometimes used with trimethoprim (co-trimoxazole) as they target separate components of the folate pathway

becoming more common despite some toxicity due to resistance to other antimicrobials

20
Q

*Q: What are aminoglycosides? What is the overall mechanism of its action? (3) Causes? 2 examples.

A

A: Bactericidal
-Target PROTEIN SYNTHESIS (30S ribosomal unit), RNA proofreading and cause damage to cell membrane

causes aberrant proteins and misfolding

EXAMPLES: Gentamycin, Streptomycin

21
Q

Q: What do macrolides treat? Method of action? (2) Example.

A

A: gram positive infections

  • Targets 50S ribosomal subunit preventing aminoacyl transfer
  • Causes truncation of polypeptides

EXAMPLE: Erythromycin

22
Q

*Q: What are the 4 distinct mechanisms of antibiotic resistance?

A

A: 1 Altered Target Site
2 Inactivation of Antibiotic
3 Altered Metabolism
4 Decreased Drug Accumulation

23
Q

Q: How can a bacteria ‘alter a target site’ in terms of antibiotic resistance? (2) Explain. 2 examples.

A

A: -arise from acquisition of an alternative gene or
-a gene that encodes a target-modifying enzyme (mutation)

You can acquire a gene which performs the same function but has a different structure and hence is not susceptible to the AB.

  1. MRSA acquired a gene which produces an alternative penicillin binding protein (PBP2a) - it performs the same function but has lower affinity to beta-lactams so methicillin is ineffective
  2. Streptococcus pneumoniae is resistant to erythromycin because it has acquired a gene which encodes an enzyme that methylates the AB target site in the 50S ribosomal subunit (ribosome still works) - this changes its structure so erythromycin can no longer act
24
Q

Q: How can a bacteria ‘inactivate an antibiotic’ in terms of antibiotic resistance? 4 examples. Alternative?

A

A: Acquire gene for an enzyme which breaks down the antibiotic (degradation or alteration)

  1. chloramphenicol acetyl-transferase (cat)
  2. beta-lactamase (bla)
    - ESBL and NDM-1 are examples of broad spectrum beta-lactamases

enzyme-independent: bacterium releases fragments of membrane that sequester antibiotic (act as decoy) and inactivate it

25
Q

Q: How can a bacteria ‘alter metabolism’ in terms of antibiotic resistance? Alternative? Example.

A

A: Re-engineer the metabolic pathways so you bypass the step that the antibiotic interferes with.

Increased production of enzyme substrate can be used to outcompete antibiotic inhibitor

EXAMPLE: increased production of PABA confers resistance to sulphonamides

26
Q

*Q: How can a bacteria ‘decrease drug accumulation’ in terms of antibiotic resistance? (2) Result?

A

A: -Reduced permeability of AB into bacterial cell
-Increase EFFLUX of AB out of cell

Drug does not reach sufficient concentration to be effective

27
Q

Q: What are the 3 sources of antibiotic resistance genes? 3 methods of conferring the DNA?

A

A: 1. Plasmids - extra chromosomal circular DNA, often multiple copy (more than one in cell) and often carry multiple AB res genes (selection for one maintains resistance to all)

  1. Transposons - allows DNA from plasmid to enter chromosomal DNA and vice versa
  2. Naked DNA - DNA from dead bacteria released into environment
  • transformation (uptake of extracellular DNA)
  • transduction (phage-mediated DNA transfer)
  • conjugation (pilus-mediated DNA transfer)
28
Q

Q: Name and explain 5 non-genetic mechanisms of resistance/treatment failure.

A

A: 1. biofilm= bacteria form slimy layer when attached to structures eg new hip/catheter -> hard for immune system to tackle

  1. intracellular location= hide in cells
  2. slow growth
  3. spores= are very resistant to heat and disinfectant and antibiotics
  4. persisters= adopt an inert dormant state which means blocking biosynthesis processes makes no difference
29
Q

*Q: Describe 5 reasons for treatment failure excluding antibiotic resistance.

A

A: 1. Inappropriate choice of organism (not all antibiotics kill bacteria- some are specific while others broad)

  1. Poor penetration of antibiotic into target site
  2. Inappropriate dose (half life)
  3. Inappropriate administration (oral vs IV)
  4. Presence of antibiotic resistance within commensal flora (another bacteria) e.g. secretion of beta-lactamase
30
Q

Q: How is resistance measured? 3 reasons for? Disadvantage? reason? Alternative approach?

A

A: -swabs are typically streaked out onto diagnostic agar to identify causative organism
-once identified, pathogen is streaked over a plate and then over-laid with antibiotic containing test strips/discs

  • quick
  • reproducable
  • cheap

measurements made in vitro will not fully reflect the situation in vivo (no immune or nutrition stress)

  1. microdilution and
  2. PCR detection of resistance genes
31
Q

*Q: What provides strong selective pressures for antibiotic resistance?

A

A: hospitals

32
Q

Q: Name 3 hospital acquired infections.

A

A: Methicillin-resistant S. aureus (MRSA)

Vancomycin-insensitive S. aureus (VISA)

Clostridium difficle

33
Q

*Q: Provide 7 risk factors for hospital acquired infections.

A

A: High number of ill people! (immunosuppression)

Crowded wards

Presence of pathogens from other people

Broken skin – surgical wound/IV catheter

Indwelling devices - intubation

AB therapy may suppress normal flora= usually outcompete pathogenic organisms (if removed (eg antibiotic) the pathogen has less competition so can proliferate and cause disease

Transmission by staff – contact with multiple patients

34
Q

*Q: How can we prevent the emergence of drug resistant bacteria? (6)

A

A: Tighter controls on prescription

Restriction of antibiotics for certain serious infections

Reduce use of broad spectrum antibiotics

Quicker identification of infections caused by resistant strains

Combination therapy

Knowledge of local strains/resistance patterns (experts in hospitals)

35
Q

*Q: How can we respond to the emergence of resistance? (2) Include examples.

A

A: 1. modification of existing medications eg prevent cleavage (beta-lactams) or enhance efficacy eg methicillin
2. combinations of antibiotic and inhibitor of eg beta-lactams eg augmentin

36
Q

*Q: Identify important bacterial pathogens that are multi-drug resistant? (2,3,1)

A

A: gram neg:

  • E coli (ESBL, NDM-1)
  • salmonella spp.

gram pos:

  • S aureus
  • S pneumoniae
  • C difficile

M tuberculosis

MCD Microbiology (12 decks)

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