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My MCD- Microbiology > Lecture 3- Hospital Acquired Infections > Flashcards

Lecture 3- Hospital Acquired Infections Flashcards

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Biology 101 flashcards
1
Q

What is an antibiotic?

A

An antimicrobial agent produced by microorganisms which kill or inhibit other microorganisms

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2
Q

What is the difference between bactericidal and bacteriostatic?

A 
Bactericidal= kills bacteria
Bacteriostatic= inhibit bacterial growth
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3
Q

What is an antiseptic?

A

Chemical that kills or inhibits microbes that is used topically to prevent infection

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4
Q

What is the ‘minimal inhibitory concentration’ (MIC)?

A

The lowest concentration of AB required to inhibit growth

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5
Q

What is ‘resistance’?

A

The ability of an organism to replicate in the presence of an AB at a particular concentration

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6
Q

What is the ‘breakpoint’?

A

An estimate of the concentration that might be achieved clinically

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7
Q

What were the misconceptions at about antibiotics

A
  • resistance against more than one class of antibiotic at the same time would not occur
  • horizontal gene transfer would not occur
  • resistant organisms would be less’ fit’
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8
Q

When does resistance emerge?

A

Soon after the arrival of a new AB

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9
Q

How do antibiotics work?

A

SELECTIVE TOXICITY- inhibit specific pathways in certain types of bacteria

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10
Q

How do beta-lactams work as an antibiotic? Give examples of Beta lactams.

A
  • E.g. penicillin and methicillin
  • penicillin binds to Penicillin binding protein (PBP) and catalyses pathways
  • Beta lactam ring is similar in shape to peptidoglycan precursor and interferes with cell wall synthesis
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11
Q

Which bacteria is resistant to the action of beta- lactams and how?

A

MRSA

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

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12
Q

What sort of antibiotic is Tetracycline?

A

Bacteriostatic

Broad spectrum

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13
Q

How does Tetracycline work as an antibiotic?

A

Inhibits protein synthesis

  • Binds to the 16S component of the 30S ribosomal subunit
  • prevents interaction of charged aminoacyl tRNA with the mRNA ribosome complex
  • prevent elongation
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14
Q

What sort of antibiotic is Chlormaphenicol?

A

Bacteriostatic

Broad spectrum

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15
Q

What is the mechanism of action of Chloramphenicol?

A

Inhibits Protein Synthesis

- Binds to 50S ribosomal subunit and blocks peptidyl transferase step

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16
Q

Why is Chloramphenicol mainly used topically?

A

Because of its toxicity

17
Q

What sort of antibiotic are quinolone?

A

Synthetic
Broad spectrum
Bactericidal

18
Q

Which enzymes do quinolone target?

A

DNA gyrase-= Gram -ve

topoisomerase IV= Gram +ve

19
Q

What sort of ‘antibiotic’ are sulphonamides?

A

Bacteriostatic

Synthetic

20
Q

What are sulphonamides used to treat?

A

UTI’s, RTIs, bacteraemia

Interferes with folate pathway

21
Q

What sort of antibiotic are ahminoglycosides? give examples

A

Gentamicin, streptomycin

Bactericidal

22
Q

How do aminoglycosides work?

A

Target protein synthesis

- targets RNA proof reading–> msfolded proteins–> incorporated into cell membrane –> leakage –> rupture

23
Q

Give an example of a macrolide. Which sort of bacteria do they target and what is their mode of action?

A
  • Erythromycin
  • Gram positive infections
    _ Target 50S ribosomal subunit and prevent aminoacyl transfer
24
Q

What are the four main mechanisms of resistance?

A
  • altered target site
  • inactivation of antibiotic
  • altered metabolism
  • decreased drug accumulation (reduced uptake or increased efflux)
25
Q

Give an example of antibiotic inactivation

A

1) Beta- lactamase for beta-lactams

2) Chloramphenicol acetyl-transferase

26
Q

How might bacteria alter their metabolism to confer resistance to antibiotics?

A
  • increase enzyme substrate synthesis to out-compete the inhibitor
  • switch metabolic pathways
27
Q

How might AB resistant genes be acquired?

A
  • Transformation
  • Conjugation
  • Transduction
28
Q

What are the consequences of antibiotic resistance?

A
  • Increased morbidity
  • Increased mortality
  • increased length of hospital stay
  • increased cost
29
Q

What are the reasons of the high rate of hospital acquired infections?

A
  • High density of susceptible people
  • crowded wards
  • presence of pathogens
  • bone skin- surgical wounds/ IV catheter
  • Indeling devices (intubation)
  • AB therapy presses normal flora (commensals)
  • staff vectors
30
Q

How do you prevent the emergence of drug resistant bacteria?

A
  • prescribing strategies
  • reduced used of broad-spectrum antibiotics
  • quicker identification of infections caused by resistant strains
  • combination therapy
  • knowledge of resistance patterns

My MCD- Microbiology (9 decks)

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