What if I told you there were trillions of tiny bacteria all around you?
It’s true.
Microorganisms called bacteria were some of the first life forms
to appear on Earth.
Though they consist of only a single cell,
their total biomass is greater than that of all plants and animals combined.
And they live virtually everywhere:
on the ground, in the water,
on your kitchen table, on your skin,
even inside you.
Don’t reach for the panic button just yet.
Although you have 10 times more bacterial cells inside you
than your body has human cells,
many of these bacteria are harmless or even beneficial,
helping digestion and immunity.
But there are a few bad apples that can cause harmful infections,
from minor inconveniences to deadly epidemics.
Fortunately, there are amazing medicines designed to fight bacterial infections.
Synthesized from chemicals or occurring naturally in things like mold,
these antibiotics kill or neutralize bacteria
by interrupting cell wall synthesis
or interfering with vital processes like protein synthesis,
all while leaving human cells unharmed.
The deployment of antibiotics over the course of the 20th century
has rendered many previously dangerous diseases easily treatable.
But today, more and more of our antibiotics
are becoming less effective.
Did something go wrong to make them stop working?
The problem is not with the antibiotics but the bacteria they were made to fight,
and the reason lies in Darwin’s theory of natural selection.
Just like any other organisms,
individual bacteria can undergo random mutations.
Many of these mutations are harmful or useless,
but every now and then, one comes along that gives its organism
an edge in survival.
And for a bacterium,
a mutation making it resistant to a certain antibiotic
gives quite the edge.
As the non-resistant bacteria are killed off,
which happens especially quickly in antibiotic-rich environments,
like hospitals,
there is more room and resources for the resistant ones to thrive,
passing along only the mutated genes that help them do so.
Reproduction isn’t the only way to do this.
Some can release their DNA upon death to be picked up by other bacteria,
while others use a method called conjugation,
connecting through pili to share their genes.
Over time, the resistant genes proliferate,
creating entire strains of resistant super bacteria.
So how much time do we have before these superbugs take over?
Well, in some bacteria, it’s already happened.
For instance, some strands of staphylococcus aureus,
which causes everything from skin infections to pneumonia and sepsis,
have developed into MRSA,
becoming resistant to beta-lactam antibiotics,
like penicillin, methicillin, and oxacillin.
Thanks to a gene that replaces the protein beta-lactams normally target and bind to,
MRSA can keep making its cell walls unimpeded.
Other super bacteria, like salmonella,
even sometimes produce enzymes like beta-lactams
that break down antibiotic attackers before they can do any damage,
and E. coli, a diverse group of bacteria
that contains strains that cause diarrhea and kidney failure,
can prevent the function of antibiotics,
like quinolones, by actively booting any invaders
that manage to enter the cell.
But there is good news.
Scientists are working to stay one step ahead of the bacteria,
and although development of new antibiotics
has slowed in recent years,
the World Health Organization has made it a priority to develop novel treatments.
Other scientists are investigating alternate solutions,
such as phage therapy or using vaccines to prevent infections.
Most importantly, curbing the excessive and unnecessary use of antibiotics,
such as for minor infections that can resolve on their own,
as well as changing medical practice to prevent hospital infections,
can have a major impact
by keeping more non-resistant bacteria alive
as competition for resistant strains.
In the war against super bacteria, deescalation may sometimes work better
than an evolutionary arms race.