Question

8. Vancomycin may still be used to treat MRSA infections for all of the following reasons EXCEPT:

a. Vancomycin inhibits cross-linking in the peptidoglycan.

b. Vancomycin inhibits the transpeptidase enzyme.

c. Vancomycin binds to penicillin-binding protein 2a (PBP2a).

d. Vancomycin binds directly to the peptidoglycan.

e. Vancomycin is effective against MRSA for all of the above reasons.

9. For some time, people have used tetracycline to treat malaria infections, although they did not know why it worked because the malarial organism is ____.

a. eukaryotic

b. prokaryotic

c. acellular (neither eukaryotic nor prokaryotic)

10. The malarial organism possesses the remnants of a chloroplast, called an apicoplast. How does tetracycline inhibit growth of the malarial organism? Be sure to make it clear why it is more toxic to cells of the pathogen than human cells in your answer. "Because it has an apicoplast" is not a sufficient answer!

Answer 1

8. Vancomycin binds to the terminal D-alanine-D-alanine complex. This prevents release of the 5th D-alanine that hinders the formation of cross-linking between the L-lysine and the 4th D-alanine.

Hence, the correct option is (a). Vancomycin inhibits cross-linking in the peptidoglycan.

9. For some time, people have used tetracycline to treat malaria infections, although they did not know why it worked because the malarial organism is a. eukaryotic.

10. Apicoplasts have separate protein synthesis mechanism just like chloroplasts and mitochondria. The tetracycline inhibits the translation in binding to 30s ribosomes in apicoplasts. So, the tetracycline is more toxic to bacteria than the human as human cells don't carry the 30S ribosome subunit.