Classes of Antibiotics and Mechanisms of Resistance Flashcards

2 SDLs in one

1
Q

How to cell wall targeting antibiotics work? Give examples

A

Inhibit the production of peptidoglycans that form cell walls.
e.g. prnicillins, cephalosporins and bacitracins

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2
Q

How do penicillins work

A

Penicillins  Acts on cell walls of growing bacteria inhibiting the enzyme responsible for the cross-linking between layers of peptidoglycans

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3
Q

How do cephalosporins work

A

Cephalosporins  similar activity to Penicillin

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4
Q

How do bacitracins work

A

Bacitracin  Interacts with bacterial cell membrane to prevent transfer of structural cell wall units

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5
Q

Describe how membrane targeting antibiotics work and give examples

A

Damage the membrane (mostly gram –ve) resulting in loss of osmotic control = loss of K ions and eventually cell death.
e.g. polymyxins

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6
Q

How do Antimetabolites or substrate analogue antibiotics work ? Give examples

A

Compete with metabolites forming non functional products. This prevents the further growth of such bacteria that require these substances
e.g. Sulphonamides
As many of these metabolites are only required for growth this kind of antibiotic can only inhibit growth and not kill bacteria.

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7
Q

How do sulphonamides work?

A

Compete with Para-aminobenzoic acid (PABA) in the formation of folic acid .

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8
Q

How do protein synthesis inhibitors work and give examples?

A

Interact with ribosomes either binding to the larger 50S chain (inhibiting protein synthesis) or the smaller 30S subunit (causing mis-coding of proteins and inhibition of protein elongation)
30S  Streptomycin, Neomycin, Gentomycin (all aminoglycosides and bacteriocidal)
50S  Chloramphenicol and Erythromycin

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9
Q

How do streptomycin, neomycin and gentomycin work?

A

Causing mis-coding of proteins and inhibition of protein elongation

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10
Q

Describe how antimicrobials that interfere with DNA work and give examples

A

Interference with DNA will result in effects on protein synthesis and therefore functioning and growth of the cell leading to cell death.e.g. quinolones

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11
Q

How do quinolones work

A

e.g. enroflaxin inhibit DNA Gyrase enzyme leading to loose coiling of DNA around RNA core. This leads to degradation of DNA into loose non-functional fragments by the action of endonucleases

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12
Q

Would resistance to one ribosome binding drugs lead to resistance to another?

A

Yes see above for details of the 50S and 30S binding antibiotics resistance to any in each of these categories could have the potential to develop resistance in any number of others in these groups.

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13
Q

How can point mutations lead to resistance to an antibiotic?

A

• Results in the changing of the amino acids that form a protein and therefore potentially the proteins structure, this could prevent binding of the antibiotic to its target site resulting in prevention of the activity of the antibiotic.

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14
Q

Why could efflux systems lead to resistance to multiple antibiotics while an enzyme to degrade an antibiotic may only lead to resistance to that single group?

A

Efflux systems are able to remove all toxic substrates (antibiotics) from the cell preventing them from binding and acting on the cell regardless of their route of action.
Enzymes have to be more specific (specific size and shape of active site to fit with the antibiotic).

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15
Q

What is clavulanic acid?

A

Clavulanic acid is a beta lactam that functions as a beta lactamase inhibitor, it works well with penicillin with is normally inactivated by Beta lactamase.

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16
Q

Is plasma mediated resistance more or less of a threat than resistance through selection of point mutations>

A

Plasmid Mediated Resistance
• The transfer of antibiotic resistance genes via plasmids between bacteria of the same or different species via conjugation
• More concerning as can occur over a shorter period of time and can spread to other species
Selective Point Mutation Resistance
• Where a point mutation in a bacteria cell results in its resistance to a particular antibiotic
• Limited by the growth and division rates of the bacteria

17
Q

Why might there be an increase in commensal e.coli with beta lactamase resistance after use of beta lactams in a dairy herd?

A

The use of beta-lactamas has targeted and reduced the number of E.coli in the population that are susceptible to this antibiotic type. This has created a selection pressure for those resistant to beta-lactams creating a population with this resistance.

18
Q

Is resistance in commensals an issue? And what factors make this a lower/higher risk?

A

It can be if they are spread to other areas of the body/ other animals that are more susceptible to the effects of these organisms
Factors include:
Particular commensal organ in question, contact between different species, other antibiotics that they are susceptible to.

19
Q

Define extended spectrum beta lactamase

A

Extended Spectrum Beta Lactamase  Beta lactamases that break down a wider spectrum of antibiotics than the norm