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JAMES MEADOW: When we're born we're
as close as we will ever get to being bacteria-free.
But as soon as we're in the world,
we're immediately covered with bacteria, bacteria
from everything we touch, everyone that touches us.
They're on our skin, fighting off infections.
They're in our guts or in our mouths, digesting our food.
Most of them are good for us, but they're constantly
evolving.
They can evolve and keep us healthy,
or they can evolve and make us sick.
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PAUL J. PLANET: Pinpoint colonies there.
SPEAKER: See this?
This big blue one here.
PAUL J. PLANET: Staphylococci are single-celled organisms.
They are bacteria.
We have Staph aureus, Staph epidermidis, Staph hominis,
Staph haemolyticus.
All of these are the species of bacteria that we
commonly culture from the skin.
And they've been with us for a very, very long time.
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But then we saw the emergence of MRSA.
MRSA can infect almost any part of the human body.
And infection is really when you start to do damage.
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A little cut, and MRSA gets into there
and can build a skin and soft tissue infection.
MRSA first showed up in hospitals
back in the '50s and '60s, but in the beginning of the 1990s,
now all of a sudden MRSA was showing up in the community
and became an epidemic.
So something happened that allowed
MRSA to take off like this.
This staph had somehow become optimized
for being transmitted between humans
and staying on humans once it gets there, potentially,
actually, optimized for being-- for life on skin.
The first thing we did was to look at DNA, because bacteria
can evolve by acquiring whole sets of genes that
have the potential to give them some completely new
characteristic instantaneously.
So one of the first things we wanted to know
was what differences were there between the genomes
of the epidemic strain and other closely related staph strains.
And you can see that here in this alignment of the two
genomes where these spaces indicate regions that
don't exist in the closest relative but do
exist in the epidemic strain, which
suggests that those areas of the genome
were actually acquired from some foreign source,
some other strain somewhere else.
So when we looked at some of the genes that
looked like they had been recently acquired
by the epidemic strain, one of the ones
that sort of jumped out at us was a gene called SPE-G.
SPE-G interacts with chemicals on human skin.
So we really wanted to know what the real benefit
of having the SPE-G gene was.
And the way we get at that is by knocking out the gene.
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So in essence, actually deleting the SPE-G gene from the genome
and then running side by side tests
with the naturally occurring MRSA and the knockout.
We introduced both strains onto human skin cells
grown in culture.
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And by comparing the two, we were
able to show that MRSA with the SPE-G gene
could actually survive on skin better.
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So for us, the central question was really
how had MRSA acquired the SPE-G gene?
It turns out that SPE-G was very similar to genes
that other people had seen in a close relative of MRSA
called Staph epidermidis.
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Staph epidermidis is an organism that lives on everybody's skin
and has been evolving to be optimally suited
to live on human skin.
Staph epidermidis is certainly there when MRSA comes in,
so we think that the Staph epidermidis, some of them
died, and there DNA was floating around in the medium.
And MRSA actively brings that DNA
through its membranes to incorporate that DNA then
into its genome.
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So the acquisition of the SPE-G gene gave, in an instant,
gave MRSA the ability to survive on the skin better.
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So these events some genes get transferred from one organism
to another can have profound effects on the epidemiology
and on human health.
So out there in the community, there
are many, many bacterial strains we need
to be investigating right now.
JAMES MEADOW: We live in a place,
whether we like it or not, that is full of bacteria.
Every time we reach up and hold the subway pole,
we're coming into contact with microbes
that someone else left there days
ago or just a few minutes ago.
And we don't understand how these things move around.
So we're doing an experiment right now to understand
where these bacteria are coming from and where they're going.
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The first step for in preparing this experimental chamber
is cleaning it the best that we can.
So we clean the walls on the box,
we clean the floor on the box, and we
filter the air that's going into the box,
because we're trying to find out just what a human is giving off
as they're sitting in a room.
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OK, so we're going to let the room settle down for 10 minutes
and then turn the filters on.
Good?
OK.
So we're collecting air at about shoulder height
and near the ground.
These cups have a sterile, clean filter right
at the base of them, so bacteria that
are being sucked in that air are going
to stop at that filter as air moves through.
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One thing that we know already just
by seeing the first bit of data that we've had
back is that when a human is in a room,
we're constantly giving off a lot of bacteria.
Every time I breathe, I'm giving out bacteria.
And just wiping my hands, I'm giving off a lot of bacteria.
But there's a lot of variability.
I have a dog.
None of the other two people have
a dog that are in this study, and so we
might be able to see dog-associated bacteria
on my samples.
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Or we might be able to see that I
went for a hike a few days ago and maybe it's
still on my clothes.
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And so now that we understand that there's
all these bacteria floating around
and that the vast majority of them are not bad for us,
the conversation is changing from doing battle with bacteria
to actually just managing our bacterial communities
in a sensible way.
When we knock back the bacteria on our hands
with antibiotic hand sanitizer or when we take antibiotics
when we don't need them, we are very likely making room
for something else to come in and either colonize
or actually to invade and affect our health.
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PAUL J. PLANET: We will always have bacteria on us.
We will always live with bacteria.
We can't, in some ways, live without them,
so understanding what makes a bacterium good
and what makes a bacterium bad, and what
makes a bacterium benign and what makes it cause disease--
those are the crucial questions.
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