Amoxicillin inhibits bacterial cell wall synthesis. It does this by binding to penicillin-binding proteins (PBPs), enzymes crucial for the formation of peptidoglycan, a major component of bacterial cell walls.
This binding prevents the cross-linking of peptidoglycan strands, weakening the cell wall and causing bacterial lysis (cell rupture) and ultimately, bacterial death. Amoxicillin is most effective against actively growing bacteria.
The specific PBPs targeted by amoxicillin vary depending on the bacterial species. Different bacterial species possess different PBPs with varying affinities for amoxicillin.
Importantly, resistance mechanisms in bacteria often involve alterations to these PBPs, reducing amoxicillin’s binding ability. This explains why amoxicillin isn’t always effective against Staphylococcus aureus infections.
Staphylococcus aureus, a common cause of skin infections, frequently displays resistance to amoxicillin, often producing beta-lactamases, enzymes that break down the amoxicillin molecule, rendering it ineffective.
