Microbiology-Antibiotics

Question 1

How does size make Gentamicin an effective antibiotic?

Answer 1

It cannot enter the eukaryotic membrane and thus only acts on extracellular microbes.

Question 2

Why do you see a sudden drop in turbidity when bacteria are exposed to penicillin?

Answer 2

Penicillin lyses the bacterial walls.

Question 3

You see a decline in bacterial growth when administering drugs A and B. When drug A is removed, bacterial growth remains stagnant. When drug B is removed bacterial growth resumes. What type of antibiotics are drugs A and B?

Answer 3

Drug B is a acteriostatic antibiotic and it inhibits cell growth. Drug A is a bactericidal and it kills the microbe.

Question 4

How does a lab use plate dilution to test the minimal inhibitory concentration (MIC)?

Answer 4

Add antibiotics until 99% of the bacteria are killed from the plate

Question 5

How does a lab use tube dilution to test the minimal lethal dose (MLD) of an antibiotic?

Answer 5

Bacteria is added to a tube of antibiotic of X concentration and watched to see if it grows.

Question 6

How do you use disc diffusion method to test which drug would be good for a particular bacteria?

Answer 6

Add the antibiotic disc and look to see if it inhibits growth.

Question 7

When considering combining antibiotics, you find that the combination is just as good as a single antibiotic. What is this called?

Answer 7

Indifference effect

Question 8

When considering combining antibiotics, you find that the combination is equal to the sum of both antibiotics’ effects. What is this called?

Answer 8

Additive effect

Question 9

When considering combining antibiotics, you find that the combination completely clears the infection better than any single one could’ve done. What is this called?

Answer 9

Synergistic effect

Question 10

When considering adding a bactericidal and bacteriostatic drug, you find that effect of the bactericidal is diminished because it targets cell wall synthesis and the bacteriostatic drug prohibits replication of the cell. What is this called?

Answer 10

Antagonist effect

Question 11

Why must you take special consideration when a patient wants an antibiotic for an abscess or necrotic tissue?

Answer 11

Blood flow is decreased to that area and oral antibiotic will have a hard time getting there.

Question 12

What ways are microbes resistant to antibiotics?

Answer 12

Intrinsically, acquired spontaneously and R plasmid transfer

Question 13

How did MRSA and MDTB become so rampant in the last decade?

Answer 13

Selective pressure from overprescribing of antibiotics

Question 14

You prescribe sulfa antibiotics to a patient with a bacterial infection. By prescribing this, what assumption are you making about the bacteria’s metabolism?

Answer 14

You assume that it needs and makes its own folic acid because sulfa drugs only work if they can target dihydropteroate synthetase in bacterial folic acid synthesis as competitive inhibitors for the enzyme.

Question 15

Why is Trimethoprim a good synergistic drug for sulfa drugs?

Answer 15

It inhibits folic acid production further down the pathway so that intermediates already in the cell cannot be used for synthesis.

Question 16

How do Rifampin and Rifabutin work as antibiotics?

Answer 16

They bind to the beta-subunit of RNA polymerase and inhibit transcriptional initiation. These work for Gram +, Neisseria and Mycobacteria. Eukaryotic structural differences make it selectively toxic.

Question 17

What type of antibiotics target DNA replication?

Answer 17

Quinolones. They target DNA topoisomerase II and thus replication.

Question 18

Metronidizole completely disrupts DNA structure, tearing it to pieces. Our DNA is similar to bacterial DNA, so how is it selectively toxic?

Answer 18

It is a pro-drug, meaning it must be metabolized before it becomes active. We do not have the enzymes to metabolize it and thus our cells remain unharmed.