Phamacodynamic
Penicilin G inhibits the third and final stage of bacterial cell wall synthesis by binding to specific penicillin-binding proteins located inside the bacterial cell wall.
After binding with specific PBPs, Penicillin inhibits transpeptidase, an enzyme that is responsible for developing cross-bridges within the cell wall.
These cross-bridges give the cell wall its strength.
Additionally, penicillin affects auto-lytic enzymes (autolysins) that promote active cell wall destruction.
The relationship between PBPs and autolysins is unclear; possibly, penicillin interferes with an autolysin inhibitor.
As the cell wall weakens, the internal osmotic pressure of the bacteria changes, allowing the cell to swell, the burst.
The body's immune system completes the process of fighting the infection and cleans up debris from ruptured bacteria.
Penicillin has selective toxicity to bacteria because human cells do not use the biochemical process that the bacteria use to form a cell wall and thus protected from destruction.