Antibiotics Flashcards

1
Q

What are examples of organisms that produce antibiotics?

A

bacteria: streptomyces, bacillus
moulds: penicillium, cephalosporium

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2
Q

What are the two different types of antibiotics?

A

bacteriostatic - prevents it from growing further

bacteriocidal - kills it altogether

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3
Q

How do antibiotics work?

A

They target cellular targets - cell walls, cell membranes, nucleic acid, protein synthesis

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4
Q

What are examples of antibiotics?

A

penicillins, cephalosporins
tetracyclines, streptomycin
trimethoprim

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5
Q

Which antibiotics inhibit cell wall synthesis? How do these work?

A

penicillins, cephalosporins
bind to ‘penicillin binding proteins’ -> inhibit cross linking of cell wall -> accumulation of precursor cell wall units -> cell lysis

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6
Q

Which antibiotics inhibit protein synthesis? How do these work?

A

erythromycin - ribosome is prevented from translocating
tetracyclines - tRNA is blocked, no protein synthesised
streptomycin

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7
Q

Which antibiotics inhibit synthesis of essential metabolites?

A

trimethoprim

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8
Q

Which antibiotic causes injury to plasma membrane?

A

polymyxin B

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9
Q

Which antibiotics inhibit nucleic acid replication and transcription? How do these work?

A

quinolones - inhibit DNA gyrase -> prevents supercoiling of bacterial chromosome -> prevents ‘packing’ of DNA into bacterial cell

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10
Q

What are antibiotics?

A

naturally occurring antimicrobials - metabolic products of bacteria and fungi, reduce competition for nutrients and space
definition = a chemical substance produced by one organism that is destructive to another

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11
Q

How is antibiotic resistance developed? What are the causes of this?

A

Misuse of antibiotic selects for resistance mutants
Causes: using outdated/weakened antibiotics,
using antibiotics for common cold or other inappropriate conditions,
using antibiotics in animal feed
failing to complete the prescribed regimen
using someone else’s leftover prescription

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12
Q

What are some resistance mechanisms to antibiotics?

A

blocking entry
inactivating enzymes
alteration of target molecule
efflux of antibiotic

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