London, 1928: a group of mold spores
surf a breeze through a lab.
They drift onto a petri dish,
and when they land,
they germinate a medical revolution.
This lab belongs to Alexander Fleming,
a Scottish scientist
investigating the properties
of infectious bacteria.
At this time,
Fleming is away on vacation.
When he returns, he finds
a colony of mold growing on a petri dish
he’d forgotten to place in his incubator.
And around this colony of mold
is a zone
completely and unexpectedly
clear of bacteria.
In studying this mysterious phenomenon,
Fleming came to realize that the mold
was secreting some kind of compound
that was killing the bacteria.
The mold was a species
in the Penicillium genus,
so Fleming dubbed
the antibacterial compound “penicillin.”
What Fleming stumbled upon
was a microbial defense system.
The penicillium mold
constantly produces penicillin
in order to defend itself from threats,
such as nearby bacterial colonies
that might consume its resources.
Penicillin destroys
many types of bacteria
by disrupting synthesis
of their cell walls.
These walls get their strength
from a thick, protective mesh of sugars
and amino acids,
that are constantly being
broken down and rebuilt.
Penicillin binds to one of the compounds
that weaves this mesh together
and prevents the wall from being
reconstructed at a critical phase.
Meanwhile, penicillin stimulates
the release of highly reactive molecules
that cause additional damage.
Eventually, the cell’s structure
breaks down completely.
This two-pronged attack
is lethal to a wide range of bacteria,
whether in petri-dishes,
our bodies, or elsewhere.
It’s not, however,
harmful to our own cells,
because those don’t have cell walls.
For a decade or so
after Fleming’s discovery,
penicillin remained
a laboratory curiosity.
But during World War II,
researchers figured out how to isolate
the active compound
and grow the mold in larger quantities.
They then went on to win
the Nobel Prize for their work.
Teams at Oxford and several American
drug companies continued development,
and within a few years
it was commercially available.
Penicillin and similar compounds quickly
transformed the treatment of infections.
For the time being,
they remain some of the most important,
life-saving antibiotics used in medicine.
However, the more we use any antibiotic,
the more bacteria evolve resistance to it.
In the case of penicillin,
some bacteria produce compounds
that can break down the key structure
that interferes with cell wall synthesis.
As antibiotic use has increased,
more and more bacteria
have evolved this defense,
making these antibiotics ineffective
against a growing number
of bacterial infections.
This means it’s essential that doctors
not overprescribe the drug.
Meanwhile, 5 to 15% of patients
in developed countries
self-identify as allergic to penicillin,
making it the most commonly reported
drug allergy.
However, the vast majority— over 90%—
of people
who think they’re allergic
to penicillin actually are not.
Why the misperception?
Many patients acquire the allergy label
as children,
when a rash appears after they’re treated
for an infection with penicillin
or closely related drugs.
The rash is often blamed on penicillin,
while the more likely culprit
is the original infection,
or a reaction between the infection
and the antibiotic.
However, genuine penicillin allergies,
where our immune systems
mistake penicillin for an attacker,
do occur rarely
and can be very dangerous.
So if you think you’re allergic
but don’t know for sure,
your best bet is to visit an allergist.
They’ll complete an evaluation
that’ll confirm
whether or not you have the allergy.
Even if you do have a penicillin allergy,
your immune cells that react to the drug
may lose their ability to recognize it.
In fact, about 80% of people
who are allergic to penicillin
outgrow their allergy
within ten years.
This is great news for people
who currently identify
as allergic to penicillin;
the drug may one day save their lives,
as it has done for so many others.