Antibiotics Flashcards

1
Q

What is a bacteriostatic antibiotic?

A

One that causes cessation of growth, but the organism stays viable
- the body can then kill off by itself, because when the bacteria can’t multiply the balance is tipped towards the host

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2
Q

What is a bactericidal antibiotic?

A

One that kills the bacteria
- if the patient is immunocompromised need to use this because they don’t have any leucocytes to be able to do it themselves

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3
Q

What are the properties of penicillin G?

A

Has no toxic effects (unless allergic), but has to be injected and is painful (not orally active)
- useful on GPC, GPR, GNC
Mimics the D-ala-D-ala bond –> locks all the bacterial enzymes (DD-transpeptidase) up so the bacteria can’t make a cell wall

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4
Q

What are the properties of penicillin V?

A

Has an added side chain so it is more acid stable –> can be taken orally

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5
Q

What are the properties of methicillin?

A

Also needs to be injected, one of the more toxic penicillins but can be used to treat penicillin resistant staph
** now have MRSA though

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6
Q

What are the properties of ampicillin?

A

Has a broader spectrum - effective against GPC, GPR, GNC, GNR

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7
Q

What is the structure of peptidoglycan?

A

Repeating disaccharides in one layer and cross linking peptides in another which make a unique N-acetyl muramic acid

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8
Q

What is the biosynthesis of peptidoglycan?

A

Precursors are synthesised from intermediates in the cytoplasm which become immobilised on the inner aspect of the plasma membrane
- then using energy the blocks are transferred to the outside

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9
Q

What is the action of vancomycin?

A

It is a glycopeptide used to combat MRSA, binds directly to the D-ala-D-ala

  • doesn’t act on gram -ve bacteria at all because it is a very big molecule and highly charged
  • however can get VISA - intermediate staph aureus, which are furry on the outside and have made more cell wall material to mop up the vancomycin
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10
Q

What is a beta lactamase?

A

Enzymes produced by bacteria which recognise the same PBP as beta lactams and break open the ring structure, rendering them ineffective

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11
Q

What is clavulanic acid and how does it work?

A

A beta-lactamse inhibitor
- doesn’t have great antimicrobial action so cannot be used to treat infection on its own, but given with amoxicillin or ampicillin and they act synergistically

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12
Q

What is the mechanism of action of aminoglycosides?

A

Eg Gentamicin, acts on the recognition stage of protein synthesis

  • interfere with recognition by binding to the site where the amino acyl transferase will bind, distort the site so it doesn’t look the same
  • quite highly charged, so at first only get across the membrane in low concentrations, but as the membrane is weakened can get across in larger concentrations
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13
Q

What are the mechanisms of resistance to aminoglycosides?

A
  • enzymatic modification of the drug to make it inactive
  • modified outer membrane leading to reduced entry of the drug
  • efflux - ATP powered pump which pumps the drug out of the cell before it combines with the ribosomes
  • ribosomal mutation - which doesn’t let the drug bind to the ribosome
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14
Q

What is the mechanism of action of metronidazole?

A

A synthetic drug, needs to be reduced to become active

  • nitroreductase is needed, we don’t have it but bacteria that live in anaerobic environments do
  • drug is active against anaerobic bacteria and very effective against protozoa
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15
Q

What are the 3 mechanisms of transfer of genes between bacteria?

A

Transformation
Phage-mediated transduction
Plasmid-mediated conjugation

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16
Q

Describe the process of transformation?

A

ONLY OCCURS BETWEEN RELATED BACTERIA

- DNA is taken up by competent cells, homologous recombination occurs

17
Q

What is the lysogenic cycle? What is the lytic cycle?

A

Lysogenic cycle
- temperate phage, just sitting there, but can be encouraged to change into a virulent phage when the phage senses that there is something wrong with the bacteria
Lytic cycle
- phage replicating, becomes packaged, virus then kills the bacteria by lysis from within and hundreds of copies of the virus come out

18
Q

How is shiga-toxin related to phages?

A

Shiga-toxin is encoded by a phage, within E coli
- if take antibiotics for an infection the phage inside becomes aware that it is under threat, makes lots of copies of itself and its toxins and makes the infection much worse

19
Q

What is lysogenic conversion?

A

When a bacterium becomes infected with a phage and expresses a new phenotype as a result

20
Q

Describe the process of transduction

A

Donor bacteria is infected by a bacteriophage, normal and abnormal phages are formed (encapsulates part of the host DNA)
- abnormal phage then infects the recipient bacteria and get a transfer of DNA

21
Q

What is phage typing?

A

Phage can only infect certain bacteria, so you can determine which bacteria you have by the phage

22
Q

Describe plasmid-mediated conjugation

A

Can occur between entirely unrelated species

  • some plasmids can move between bacteria –> encode a cytoplasmic bridge and link
  • the plasmid makes a copy of itself while moving through the bridge so when it separates have 2 cells with the plasmid
    • requires direct contact between the donor and recipient
23
Q

What is a multiresistant plasmid?

A

A plasmid that has incorporated genes encoding resistance –> build up a whole lot of resistant genes
- can insert themselves right next to each other and can be driven by a single promoter and will get expression of all of the genes

24
Q

What is indifference in antibiotic combinations?

A
  • could just use drug A or drug B and get the same effect

- not much use using them together unless one is toxic

25
Q

What is synergy in antibiotic combinations?

A

When A + B = better than just A or just B

  • can be by blocking sequential steps of a metabolic pathway
  • by inhibiting enzymatic degradation
  • enhancing microbial uptake by bacterial cells
26
Q

What is antagonism in antibiotic combinations?

A

When A + B = worse than just A or just B

  • inhibition of bactericidal activity by a bacteriostatic agent
  • induction of enzymatic degradation
  • competition for binding to the same target
  • inhibition of target