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