Question

1) Antimicrobial X targets a specific protein in the cytoplasm of the bacterial cell, causing the...

1) Antimicrobial X targets a specific protein in the cytoplasm of the bacterial cell, causing the bacteria to stop growing, but does not kill them. A few bacteria start to grow in the presence of antibiotic X. Analysis of the bacteria that can now grow shows that they have changed the shape of the target for antimicrobial X. What conclusion can be made?

a) The change in shape of the target for antimicrobial X had no effect on the effectiveness of antimicrobial X.
b) Antimicrobial X is less effective against the new shape of its target.
c) Antimicrobial X is more effective against the new shape of its target.

2) Penicillin’s target is transpeptidase, a protein involved in cell wall synthesis. For a Gram-positive bacterium, which of the following mechanisms would be most effective in resisting penicillin’s effects?

a) Drug inactivation via ?-lactamases
b) Drug inactivation via ?-lactamases and altered target binding site
c) Decreased permeability via alteration of porins and use of efflux pumps to move the drug out of the cell
d) Drug inactivation via ?-lactamases and use of efflux pumps to move the drug out of the cell
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Answer #1

1) Correct answer is:b) Antimicrobial X is less effective against the new shape of its target.

Reason:A change in the structure of the binding site in target molecule makes the interaction between the antimicrobial X and the target molecule less effective.

2)Correct answer is:b) Drug inactivation via ?-lactamases and altered target binding site

Reason: Inactivation of penicillin by beta lactamases and change in the binding site for penicillin would enable the bacteria to resist the penicillin's effect.

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Answer #2
Ans 1: (b)

it is given that few bacteria could escape the effects of antimicrobial X and could grow. This is possible when X cannot bind to altered shape of such bacteria.

Ans: Antimicrobial X is less effective against the new shape of its target.

Ans2: Drug inactivation via ?-lactamases and altered target binding site.
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