Penicillin kills bacteria by interfering with the ability to synthesize cell wall. In this sequence, Escherichia coli were incubated in penicillin for 30 minutes. The bacteria lengthen, but cannot divide. Eventually the weak cell wall ruptures.

The inappropriate use of antibiotics (prophylactic treatment of herds in meat production and pointlessly treating viral infections with antibacterials) floods our environment with drugs that select for populations of antibiotic-resistant bacteria. Although penicillin was a wonder drug when discovered, some bacteria exposed to penicillin survived because they produced the enzyme β-lactamase that destroys penicillin’s structure. A solution was to devise other penicillin-like antibiotics (β-lactams) with structures that are not destroyed by β-lactamase. Methicillin is one of those drugs developed in the late 1950’s. Unfortunately, an increasing threat is now Methicillin-Resistant Staph aureus (MRSA) which avoids methicillin and other β-lactams by an alteration in MRSA's penicillin target-binding site. Bacteria are constantly evolving such new defenses, so treatment of bacterial infections requires a constant search for antibiotics with novel modes of action.