Vancomycin works by interfering with what aspect of bacterial cell wall synthesis?

Vancomycin is an antibiotic that specifically targets bacterial cell wall synthesis, making it effective against certain types of bacteria, particularly Gram-positive organisms. The mechanism of action involves binding to the D-Ala-D-Ala terminus of the peptidoglycan precursors. This binding inhibits the transglycosylation step, which is essential for the polymerization of peptidoglycans, a crucial component of the bacterial cell wall.

By preventing the polymerization of these peptidoglycan strands, vancomycin effectively disrupts cell wall integrity, leading to cell lysis and ultimately the death of bacteria. This action is particularly critical in Gram-positive bacteria, which rely heavily on their robust peptidoglycan cell wall for structural support.

Additional mechanisms, like those posed by the other choices, do not describe how vancomycin works. For instance, inhibiting mRNA polymerase is related to antibiotic classes such as rifamycins, while blocking tRNA binding to mRNA pertains to some other antibiotics like tetracyclines. Furthermore, inhibiting protein synthesis at the ribosome is characteristic of antibiotics like aminoglycosides and chloramphenicol. However, vancomycin is distinct in its