2.  In 1928, Alexander Fleming was working with cultures of Staphylococcus aureus, a bacterium that causes boils and other types of infections.  He accidently left open one of the petri dishes (ooops!)  He later found mold growing, but no bacteria around the mold.  He concluded that the mold (Penicillium notatum) inhibited growth of bacteria, but he could not isolate and purify it.

3.  In 1941, Ernst Chain and Howard Florey were able to isolate the fungus and test it with mice which were injected with a deadly bacteria. The mice treated with penicillin survived.  After testing it on a policeman with an infection, the mass development of penicillin began in the U.S.  Thousands of troops during WWII survived infections caused by wounds due to the penicillin.

4.  Bacteria have cell walls which eukaryotic cells do not.  The cell walls are created by cross-linking of peptidoglycan.  Penicillin G interferes with the enzyme that creates these cross-links.  The cell wall weakens, causing the bacteria to burst (lyse) easily due to osmotic pressure.

5. Modifying the Side Chain  Penicillin G is deactivated by stomach acid, but can resistant to acid by modifying the side chain.

6.  Bacteria can also become resistant to penicillin by building enzymes which deactivate the penicillin (pencillinase) or having a modified enzyme for building the cell wall which does not allow the penicillin to bind to it.  Modifying the side chain can sometimes overcome these types of resistance.

7.  Antibacterials can wipe out helpful bacteria (especially in the gastrointestinal system).  Because of overprescription and use in animal feedstock, some bacteria have evolved to become extremely resistant to penicillin.  With drug-resistant bacteria, a “cocktail” of different antibacterials are used to overcome the infection.