Michael Mosley vs. the Superbugs (2017) Movie Script
1
For more than 70 years,
we've waged war
against bacterial infections
using antibiotics.
But it's a war we're now losing.
Drug-resistant superbugs...
..are spreading.
To find out what
we're up against,
I'm donating my body to
an extraordinary experiment.
We are going to unleash
bacterial hell on a clone of my body.
Woohoo!
We're hoping this experiment -
which is novel and rather spooky -
will give us a whole new
insight into the way that bacteria
fight back against antibiotics.
- That is absolutely revolting.
- It's fabulous!
I'll search high and low
for radical solutions...
Die, bacteria, die!
..to stop the spread
of the superbugs.
When I remove the bandage,
we should see quite a difference.
Oh, yeah!
Is it too late to prevent
antibiotic Armageddon?
Me and my body
are about to find out.
Hello.
- Good to see you upright.
- Well, it's nice to be upright.
- Come and have a seat.
- Thank you.
Hi there.
A month ago, 57-year-old
John Shelton was fighting
for his life against a
sudden bacterial infection.
- Good.
- When I arrived here, they opened me up, there was a big mass.
It was very, very infected,
and the bacteria were already
working their merry havoc,
trashing my body,
shutting down my lungs,
shutting down my kidneys, shutting
down everything, pretty much.
- You don't remember anything?
- Not a thing.
His lung had almost
completely filled up with bacteria,
or infection, and he wasn't
able to oxygenate his blood.
Bacteria called staph
aureus caused the infection.
They were eventually stopped
by a concoction of antibiotics,
but for a while it
was touch and go.
- HE INHALES AND
EXHALES - Brilliant.
- EMOTIONAL: - When they thought
he'd had a brain haemorrhage -
sorry -
that was not a great moment.
You know, just one day at a time,
really, and you do place your faith
in the fact there's going to be
another antibiotic to come up.
It's interesting that, you know,
there is a lot of technology here,
there is obviously a fantastic staff
but, in the end, it's kind of
antibiotics versus bacteria.
That's it. Simple as that.
There is no doubt in my
mind that, without antibiotics,
I would not be here.
Before the 1940s, up to a
third of deaths were caused
by bacterial infection.
A simple cut could kill you.
Then came antibiotics -
drugs able to kill bacteria.
The first was penicillin,
discovered by Alexander
Fleming in 1928.
More followed.
But then, the pipeline dried up.
No totally new antibiotics
have been found for
more than 30 years.
And more and more bacteria
are becoming resistant
to our dwindling stock...
..including superbugs,
which threaten to send modern
medicine back to the Dark Ages.
Around 700,000 people die every
year because of drug-resistant
strains of
infections like E. coli
and TB, but that figure could
soar to around 10 million a year
by the middle of this century
if urgent action isn't taken.
Increasing numbers of people are finding
that antibiotics are no longer working.
People like Slawa.
Slawa's foot is so
infected with E. coli.
It could lead to her whole
leg being amputated.
Be warned, this glimpse
into a post-antibiotic world
is gruesome.
So, if you are squeamish,
look away now.
'If we do nothing,
'modern medicine in all its finery
will become much more hazardous.'
Cancer therapy, immunotherapy...
I mean, just simple
infections like meningitis.
All of these things
become more hazardous.
So anti-microbial resistance
is the biggest single issue
which is affecting modern
medicine at the moment.
In 2015, 34
million prescriptions
were issued for
antibiotics in the UK alone.
Have we created superbugs by
popping too many of these pills?
I want to find out exactly
what antibiotics do and why
bacteria are resisting them.
Time for an unusual experiment.
So I have done a lot of
strange things in my time,
and a lot of self experiments,
but nothing quite like this.
Now, I'm in pretty good
health and I only take antibiotics
when I absolutely have to,
but I am going to explore what
a powerful antibiotic
does to my body
by making my bacteria visible.
If you'd like to know, I have
not washed for two days.
- Great.
- All right! Yeah, that's...
When I start doing these
things, I always think,
"Oh, it sounds
like a good idea,"
and when I actually get there,
I start to wonder if it really is.
Artist Mellissa Fisher
specialises in creating
living biological sculptures.
- Oooh!
- Right in between your toes.
With Professor Mark
Clements of Lincoln University,
she is leading a team to make
a living bacterial
sculpture out of me.
So, that's the...the right here.
Step one - collect material
from all over my body
using cotton-wool swabs.
On the skin, you've got over
1,000 different types of bacteria.
And each person is unique.
All different parts of the
body will have slightly different
micro flora, depending on
whether it's a moist area,
whether it's a dry
area, oily area...
By moist, I'm thinking
armpits, probably.
Yeah, the very moist areas...
The armpit and the
groin are particularly good.
- OK. I might do my own groin.
- Yes. Yeah, yeah, yeah.
Next, I'm wrapped in plaster
to create a mould of me...
Woo!
..and given a full body
wax in the process.
Do you want your hair back?
Our home for this experiment
is Imperial College in London.
It's right on that edge, there.
Here, our team of scientists
and sculptors turn my body mould
into possibly the world's
largest Petri dish by filling it
with a nutrient-rich
jelly called agar.
Good morning,
gang. Good morning.
After 12 hours, the
agar jelly has set.
It is like Tutankhamen's
tomb, isn't it?
All right, so nice and
gently, up and out.
There's two parts
to this experiment,
which is why my rather
spooky clone is split in half.
- The foot's out.
- Woohoo!
That is wonderfully weird.
On one side, we want to grow
bacteria from all over my skin
to see what's living on me.
It kind of looks like
me, I must admit that.
A slightly bald
version of me, but...
THEY CHUCKLE Wow.
On the other side, we've added
a broad-spectrum antibiotic used
in hospitals against a
wide range of infections.
But before we even get the
chance to add my bacteria,
something else has snuck in.
What's the green stuff?
- Does this suggest the presence of bacteria already, then?
- It does.
On this side, where we
don't have any antibiotics,
- then there has been some growth of bacteria.
- Right.
So even given the
tiniest opportunity,
the bacteria have got stuck in.
They do, they do. Yes, yep,
yep. They're everywhere.
We don't know where these
green bacteria have come from.
But you can see that the antibiotic
embedded on the left-hand side
have so far stopped
the invader from growing.
Time to add bacteria
collected from my body.
These are all the swabs
we've taken of your body.
We're going to start with the
bottom of the feet, so number 20.
We want to make visible
the invisible microbes -
mainly bacteria - that
live on a healthy human.
So we're adding each of my
samples to the corresponding
part of my clone.
Let's see what they
make of their new home.
OK, we can do this.
Our giant Petri dish is
sealed into an airtight case.
It really does feel like they're
taking my body and embalming it.
Whoa!
- Oop, the foot's gone.
- Oh, no!
Despite a couple of
rather nasty foot injuries...
..Microbial Michael is now
ready for our experiment to start.
Which microbes
will thrive and where?
I would expect, within
the next few days,
we'll start seeing them
emerge on that side.
The question is, will they be
able to overcome the antibiotics
and start growing on this side?
The truth is, we have absolutely
no idea what is going to happen
next, because this sort of thing
has never been done on
this sort of scale before.
We simply have
to wait to find out.
Time for a road trip.
I want to dig deeper
into the roots of the crisis.
So why are more and more
bacteria becoming resistant?
Is it simply that we're
overdoing the antibiotics,
or is it more
complicated than that?
I recently read about a
fascinating discovery made here,
in New Mexico, which changed the
way I think about antibiotic resistance.
Now, this is the spot.
Gorgeous, isn't it?
Unfortunately, what I am looking
for is not here, on the surface.
It is deep underground.
And I say unfortunately because
I am pretty claustrophobic.
My guide is Dr Hazel Barton.
- Hey-ho. Hello. - Hi, Michael, how are you doing?
- Glad to see you.
Hazel's a microbiologist
who searches for new species
of bacteria living deep
under Carlsbad National Park,
in a vast network of caves.
- Thank you. What's the longest you've been down here for?
- Eight days.
- Eight days? Cool. Journey to the centre of the earth.
- Yeah.
So we're getting off
the tourist trail here.
Blimey. It gets
narrower, doesn't it?
- It's quite big in here.
- Yeah. It's cool.
It was in 2012 in a cave much
deeper than I'm able to go that
Hazel's team made their
breakthrough discovery.
So the kind of areas that we
sample look quite a bit like this.
Hazel took a bunch of bacterial
samples from the cave and
sent them off to
a lab for analysis.
The results shocked everyone.
So I sent him just 100, right?
He started testing
them, and he's like,
"You're not going
to believe this,
"but they are
resistant to everything."
- Blimey.
- Everything that's used...
So these were bacteria
you found on a wall in a cave.
Much more remote than this,
- much further away.
- That had not seen humans for...
We know humans had never
been in there because we know...
we had the exploration records,
so there was no impact on it.
And they were resistant to
practically every antibiotic
- that's used in the clinic.
- Wow.
That is both incredibly
exciting and incredibly scary.
Nobody had ever thought that
you would find resistant bacteria
down in the bottom
of a bloody cave.
They'd had no
interaction with humans,
but the bacteria Hazel found
in the cave were resistant to
a huge array of antibiotics
we use in modern medicine.
This resistance had clearly
evolved over millions of years
without us having
anything to do with it.
Why?
Well, it makes sense
when you think of antibiotics
not as man-made but the
by-product of war between microbes.
They make chemical weapons
to destroy their enemies and
steal their resources...
..weapons we have learnt
to exploit as antibiotics.
The bacteria living deep in the
cave have had millions of years to
evolve weapons that can target
and destroy even their toughest rivals.
The battle for scarce resources
like nutrients and energy is
particularly brutal
down here, in the caves.
It's really starved down
here. There's no resources.
It's probably one of the most
starved environments on Earth
because, if you think about it, any
energy needs to come in through
the rock, and so there's a
big competition for nutrients.
The fewer the resources, the
more intensely the microbes battle,
and that creates resistance
because the bacteria under
attack don't just
lie back and die.
When billions of bacterial
cells are bombarded,
all it takes is for one
cell to mutate its DNA...
..in such a way that the
antibiotic can no longer kill it.
This ability to resist
then spreads...fast.
So developing resistance
to antibiotics is an entirely
natural process,
which the bacteria
of Carlsbad have
taken to the extreme.
- So, a fierce competition going around us all the time.
- Uh-huh.
Microbes producing antibiotics,
but this is all happening millions
of years before Fleming and
his friends at Oxford
actually developed penicillin.
Right. And that's what we
discovered down here that kind of blew
everybody's mind, is the thought
that resistance and that antibiotic
battle is because we've
been using antibiotics,
but it can't be down here cos
these guys have never seen
the antibiotics that Fleming,
everyone has made since.
But if resistance to
antibiotics arises naturally,
what does that mean for us?
Let's see if Microbial
Michael has any answers.
Bloody hell. That is grotesque.
We've left him
alone for a few days,
and the bacteria swabbed
from my body have run riot.
I'm hoping immunologist
Dr Sheena Cruickshank
from Manchester University
can help me make
sense of what's happening.
Michael, meet Michael.
That is so weird.
- I just think it's so exciting to be able to see...
- It is both exciting
and really, really
disgusting, I have to say.
There's something, as well, about
seeing me down there, effectively
covered with this stuff.
I think you should be looking
at this as showing you the
amazing life that
is living on you.
We're starting on
the right-hand side,
where there's no
added antibiotic.
That means these different-coloured
bacteria should be part of my
normal skin flora.
Look at this
amazing white, blue...
OK, I thought white, blue meant there was
nothing growing there, but there is something?
No, that's actually
growing over the blue,
and that's really exciting
- because it suggests that perhaps it is battling with the blue.
- OK.
It's competing with it.
And I think that's
Staphylococcus epidermidis,
and that's a really
common skin bacteria.
And we actually know that some
bacteria make anti-bacterials,
so they compete with each
other and they kill other bacteria.
So, perhaps that's
what's happening here.
So we're kind of seeing warfare
in action between the bacteria.
Absolutely.
What this side of this experiment
is showing us very colourfully is
how bacteria in a healthy body
keep each other in check as they
battle for space and nutrients.
Because most bacteria living
on us are harmless or beneficial,
in a balanced ecosystem,
they leave limited room
for the bad bugs
- the pathogens.
Behind the scenes, our team is
identifying exactly what's grown
using DNA analysis.
And they found something
potentially nasty up my nose.
This is really interesting.
If you look around your nose
there, around your nostril,
there is Staphylococcus
aureus growing there.
That is the sort of orangey...
- They call it the golden staph, don't they?
- Yeah.
A lot of people -
about a third of people -
have Staphylococcus
aureus in their nostrils.
It's quite, quite normal.
But a lot of people associate
it with being a pathogen.
In the right
circumstances, it's fine.
In the wrong, it can be deadly.
If our immune system takes a hit,
some species amongst our bacteria
can get out of control
and do serious harm.
That's what then relatives of the
golden staph aureus in my nose did
to patient John Shelton,
overrunning his body's defences
and very nearly killing him.
On this side of the experiment,
my bacteria are keeping each
other in check, just as I'd expect.
But on the other side,
it's a different story.
So we are coming across to the
side which was actually enriched
- with antibiotics, wasn't it?
- Mm-hm.
Peer past the fog of
condensation caused by
so much microbial activity,
and our time-lapse cameras
reveal that even on the side which
is heavily impregnated with
broad-spectrum antibiotics,
there are still
bacteria growing.
Though, admittedly,
there are a lot less of them.
Here, just here, at the top
of the head, you can see,
there's actually quite
a few clear zones.
So that suggests that certainly
the antibiotic is doing its job
in areas, and it's certainly
been controlling in this area
the blue, which was kind
of taking over everything.
One of the things that
is very striking to me
- is that on the other side, there's competition going on...
- Mm-hm.
..which suggests that
wiping out all your bacteria is
a bad idea because actually
you do want sort of good bacteria,
if you like, to kind of compete
with the pathogens and stop them
- encroaching.
- Absolutely.
What this demonstrates very
clearly is you shouldn't take
a broad-spectrum antibiotic
unless you really need to.
As the caves of New
Mexico showed us,
the more bacteria are
attacked, the more they will resist.
But there is also an unfortunate
fact - that broad-spectrum
antibiotics carpet bomb
friend and foe indiscriminately.
There is a lot of collateral
damage amongst the benign
and beneficial species.
This accelerates resistance
because surviving pathogens now have
less competition for resources,
and they can colonise
the whole battlefield.
If one of these survivors
is resistant to multiple drugs
and potentially
harmful, it's a superbug.
The bad news for me is the team
have found two growing on my clone.
One that is particularly
interesting is an organism called
Enterococcus faecium.
And this is an entirely
normal part of our gut flora.
But if it gets into the
wrong parts of the body,
or if the person has a
compromised immune system,
it can cause really
serious invasive infections.
And because it's inherently
resistant to antibiotics,
it's very, very hard to treat.
The team has also found Pseudomonas
growing through the antibiotic.
It's not part of my skin flora,
but a travelling pathogen
that can cause
infection and pneumonia
if it gets inside our bodies...
..say, through an open wound.
Microbial Michael has shown
me superbugs on my skin.
But what about inside me, where
some really important stuff happens?
I've sent off a very personal
sample to be analysed.
So, we've received our
poo sample from Michael.
And we want to have a look
to determine if he's got any
resistant bacteria.
When you think
about antibiotics,
most of these us will take
these orally, and also we'll take it
with a drink of water,
so therefore, the
antibiotics will hit the gut first.
Our guts and intestines are
home to at least 1,000 different
species of bacteria.
But now there's new research
about what can happen to them when
we take antibiotics.
The striking thing about
a healthy person
who takes an antibiotic
is that, in all likelihood,
they will get resistant bacteria
in their tummies - in
their colon, actually -
after about seven days.
And with some antibiotics,
these resistant bugs last in
their tummies for up to a year.
That sounds like another compelling
reason not to take antibiotics
unless you really have to.
I'm hoping my gut doesn't
contain resistant bacteria.
Right, so you had my poo
samples. What did you find?
- So...
- 'Lindsay has tried growing my gut bacteria
'on plates containing four
clinically important antibiotics.'
- Presumably, these plates should be clear of bacteria.
- Yeah.
If you had susceptible bacteria,
then they should be clear,
but as you can see, there's
multiple colonies on each of
the plates, which would suggest
they are resistant to that antibiotic.
That does surprise me.
I haven't had that many
antibiotics in my life.
Well, I was going to ask,
when was the last time you
had a course of antibiotics?
Probably about four years ago.
Yeah, OK, so that's quite a long time ago,
but maybe does correlate with
some of the data that we've shown.
That's a nasty surprise. I've
got bacteria growing inside me
which are resistant
to all four antibiotics -
one of which I've
never even taken.
I know the name, but I
think I would know if I'd had it.
Yeah, you would probably
know if you had vancomycin.
It's a last-resort antibiotic,
- so this is what you get if you're really ill.
- OK.
That is really quite
worrying, I must admit.
And what is really quite
striking is the fact that the main
culprit in terms of having
antibiotic resistant genes
is E. coli.
Blimey. I have E. coli in my gut
which is resistant to everything.
- Yes.
- Blimey. That's bad news!
OK. That's not what
I was hoping to hear.
There are lots of different strains
of E. coli. A few are very nasty.
We don't know
what strain I've got,
but we do know
it is very resistant.
Now, that was an
unpleasant surprise.
It's one thing to talk
about antibiotic resistance,
but to discover that
I've got these E. coli,
and they are resistant to
all sorts of antibiotics is,
I must admit, worrying.
I'm not really worried
by the fact it's E. coli.
It's the resistance bit.
Why?
Well, once resistance emerges
in one species of bacteria,
it can spread to other species.
It's all to do with the way
they exchange genes,
as Sheena can explain.
We get all our DNA from our parents,
- so you get half from your mum,
half from your dad. That's
your lot. You don't get any more.
You might see that chap down
the corridor who never catches
a cold and think, "Oh, I'd love
to be able to steal that ability."
But we can't.
But imagine you could.
Imagine you could steal DNA and
swap DNA just as easily as you swap your
e-mail or your telephone number.
And basically, bacteria can do that.
It's called horizontal
gene transfer,
and this is the way antibiotic
resistance can spread.
Using this trick,
different species of bacteria
share genetic information...
..including the ability to
resist a specific antibiotic.
The bacteria don't even have to
be touching because they can also
pick up bits of genetic information
left in the environment around them.
That means the E. coli
inside me could, theoretically,
share its genes
with other species...
..and turn my gut into a
factory of resistant bacteria.
And we have plenty of
evidence that really does happen.
Resistance is spreading
from microbe to microbe.
Wherever antibiotics are used
intensively, such as hospitals,
more resistant bacteria emerge.
They share their
genes. They multiply.
This explains how superbugs
like MRSA and E. coli can resist
so many different drugs.
And they don't stay
confined inside our hospitals...
..because, like us,
bacteria can travel.
And people aren't the only
source of resistant bacteria.
Globally, half of all
antibiotics are given to animals.
In countries like
America and China,
they are even widely
used as growth promoters.
Animals and humans alike pump
out more and more resistant bacteria.
But how far is the wave
of resistance spreading?
In Cornwall,
a pioneering new study has found
evidence that resistant bacteria are
travelling through our waterways,
out to sea, and then back again,
into humans.
Hi. I'm going to talk to you
about the Beach Bums survey.
We recruited 300
people to our survey -
surfers and people
who don't surf, as well -
and asked them to collect
swabs of their faecal material.
You take the swab, send
it back to us in the post,
and then we test it for the
presence of resistant bacteria.
What we found is that a
greater proportion of surfers have
resistant bacteria in their guts
compared to people who don't surf.
We think that, if you
swallow a lot of seawater,
that some of the bacteria
that are present in the seawater
survive and go on to live
inside...inside your gut.
If resistant bacteria can make it
out to sea and then into surfers,
I could have picked up the
resistant E. coli in my gut from, well,
just about anywhere.
The good news is that in the
UK and some other countries,
antibiotic use in farming
has started to come down.
But there's no putting the
genie back in the bottle.
Resistant bugs are in our
bodies and all around us.
There isn't any doubt that
we have been complacent
and we have walked
into this huge problem.
But humans have been between
a rock and a hard place here.
They want to use antibiotics,
but as soon as they use them,
resistance arises.
Because they are life-saving, if
you stop using antibiotics, people die.
At the end of the day,
we need new antibiotics.
Trouble is, modern
medicine hasn't found
a totally new type of
antibiotic in more than 30 years.
Each new drug involves a long
and complex process of chemical
engineering and testing.
They are certainly difficult
to make from scratch.
Instead, scientists have
relied on finding new microbes,
growing them and then
trying to identify and extract any
chemicals with potential
antibiotic properties.
One problem is that many
microbes simply won't grow using
traditional lab techniques.
And without being
able to grow them,
we will struggle to
develop new antibiotics.
Time to search out
some novel solutions.
Here in Boston, I've come to
meet a maverick microbiologist who,
I'm told, has developed a whole
new way of growing bacteria
and, in the process, discovered
possibly the first new class
of antibiotics in decades.
Dr Slava Epstein has
promised to show me his secret.
Do you see a suitable spot
somewhere around here?
We can find a suitable spot just
about anywhere on the planet.
So, the first thing that
happens, we collect soil.
We collect soil.
We don't have to
have too much of it
because every gram of soil is
easily a billion
or 10 billion cells.
But what we're going to do
with the cells in the lab is going to
be very different.
Two thirds of our most important
antibiotics were originally found
in microbes living in soil, a well
which looked like it had run dry.
But now, Slava has thrown out
the 130-year-old Petri dish and
replaced it with a device that, to
my eyes, looks equally low-tech -
a plastic tray into which
his assistant adds a diluted
solution of the soil sample.
In this vial, there
is about 100 cells.
- 100 cells down from a few billion?
- Yes. - And these are all bacteria?
These are all bacteria.
It is starting from this point that
things are going to be different
because we are not going
to put them into a Petri dish.
Instead, we are
preparing this device.
- It is just a collection of wells with a porous bottom.
- OK.
So, I have to say, this
doesn't look that radical.
Not being a microbiologist,
I probably don't understand
why it is so different.
It is radical because
- have I ever mentioned any word nutrient?
- No.
- Because there is none.
- OK. - We don't need them.
Unlike the Petri
dish, we do not.
We do not want to
create artificial conditions.
- Now that will go into the soil...
- OK.
- ..from which these cells came from.
- Ah!
- That is clever.
- So inside... Thank you.
- Inside... - I get it at last.
- ..chemically... - OK, yeah.
..it will not be different
from the outside.
So if the cells can
grow in nature...
- You are returning them to their normal environment...
- Yes.
..rather than
sticking them in agar.
- They should be able to grow inside.
- Ah!
By putting the bacteria back
into the soil they came from,
Slava is encouraging them to
grow just like they would in the wild.
Compared to using agar jelly,
the results are astounding.
The difference in colony
count between the two methods
- is 30,000%.
- Wow.
You can grow 30,000% more
cells if you do it this way than if
you do it the conventional way.
That's correct.
This technique means they can
grow bacteria that would normally
be missed, and they have
created versions of the device to
look for novel bacteria in
all sorts of environments,
including the human mouth.
- Very neat.
- It's also very simple.
You can really build this
device in your garage.
What excites me about
Slava's discovery is it means
there's clearly a whole
world of microbes out there,
just waiting to be found.
Imagine you are an ancient
Greek looking up at the sky.
You'd only see a tiny handful
of the stars and planets that are
actually out there.
In some ways, we are a bit like
that ancient Greek when it comes to
the microbial world.
There is a vast
galaxy of tiny creatures,
and we are currently only aware
of a very small proportion of them.
We need to start looking for
new antibiotics much further
afield than the
soil under our feet.
Some scientists think seabeds
could be rich in antibacterial potential.
Easier pickings are washing
up on our shores with evidence
clips of seaweed contain microbial
agents effective against MRSA.
And deep in the caves under
New Mexico, Hazel Barton's team
has discovered that millions
of years of intense bacterial
warfare has produced
chemicals we may be able to use.
One of the organisms
that we found
made 38 novel
antimicrobial compounds,
- of which three were new antibiotics.
- Hm.
So the potential is that people
turn their attention to these
extreme environments - like
caves, like the deep ocean, like,
you know, the Arctic - we
are going to have this explosion
in new compounds over
the next ten, 15 years.
The hunt for antibiotics is not
just in extreme environments
but anywhere that's
home to novel microbes.
Professor Matt Hutchings
has found what could be
a novel antibiotic in...
an ant farm.
It's an amazing system.
They've been using antibiotics
for 50 to 60 million years.
The secret Matt's team has
unlocked is in the relationship
between these leaf-cutter
ants and their food source.
The fungus is the only food
for this whole ant colony.
And if they smell any foreign fungi
that might cause disease in there,
they cut it out, they
carry it over to this part,
which is the waste dump,
which is usually outside the nest.
They rub their bodies against
it and then they dig it back into
the ground.
The really interesting thing for us
is the reason they rub their bodies
against it is because
their bodies are covered in
antibiotic-producing bacteria
that the ants can use to defend
their fungus against disease.
Matt's lab has extracted a couple
of experimental new antibiotics
from the bacteria on the ants.
They haven't yet been
tested on humans.
So, time for part two of our
experiment, using my body -
well, bits of my body - to test
out some of these novel drugs.
We are creating a biohazard
and infecting different parts of
me with three of the most common
multi-drug-resistant superbugs -
MRSA, salmonella
and Pseudomonas.
Where should I put it, then?
- On the fingers.
- On the fingers, in there? OK.
Then, we'll try to cure them.
First, I want to see if
ant antibiotic can tackle
an infection of MRSA...
..on my face.
MRSA can cause skin infections.
If it gets inside us
and attacks our lungs,
it can be particularly
dangerous.
We've given my face a few
days for the bacteria to take hold.
So, this is the ant antibiotic,
and it is genuinely new and
really rather exciting because,
as you can see, it is really working,
because that white disc
on my forehead there,
there's a zone of death
around it which suggests
that it really is killing
all those bacteria.
So the good news is,
it's new and it's working.
The bad news is it's probably
ten, 15, 20 years away.
Why so long?
Well, finding an antibiotic in
nature is just the first stage in
an expensive and very
complicated process.
To discover a new
antibiotic, I mean,
you have to go from the
early stage of discovery -
so isolate bacteria from a
place like a leaf-cutter ant nest -
get those bacteria
growing on a plate,
solve the chemical structure of
that antibiotic - which is not trivial -
and then, of course, you have
to get a drug company interested
because they're the only
people with enough money
to get things through clinical trials.
The reality is, less than 1%
are actually suitable candidates
and make it through to actually
get them to the stage where they're
approved as safe to use in humans.
So it can take 15, 20
years and cost, well,
between half and 1 billion.
A time lag of 15 to 20 years is
massive given that around 700,000
people already die annually
because of antibiotic-resistant bacteria.
So what are we going to
do until new drugs emerge?
For starters, surely we could use
our existing stock more carefully.
Half of all hospital prescriptions
are for broad-spectrum antibiotics.
And given everything I've
learnt, that can't be a good idea.
Why do doctors continue to
use broad-spectrum antibiotics?
It strikes me as like carpet bombing
everything and you'd be better off
if you were a bit more targeted.
Well, as a doctor, you're
confronted with a dilemma.
When you see a new patient,
you don't necessarily have
the diagnosis in front of you.
- So you want to save the patient...
- Mm-hm.
..and you want to cover
all the eventualities.
And hence, you use a
broad-spectrum antibiotic.
- Right, because you don't know what it is you're trying to hit.
- Exactly.
To use targeted narrow-spectrum
antibiotics, doctors need to
be able to quickly diagnose
the specific infection in a patient.
For some bugs, like the
ones that cause tuberculosis,
that means taking samples,
growing the bacteria
and sequencing its DNA -
a process that can
take up to ten weeks.
But Tim's part of
a team working on
a prototype gadget that could
massively speed up DNA sequencing.
So, you see the patient
and they spit into your pot.
Yep. And the DNA from
your phlegm goes on there.
- OK.
- You close it.
- And then it... This sequences it?
- That sequences it. - Bloody hell.
- Now...
- That is really, really impressive, I have to say.
That is impressive.
So, how quickly would you
then be able to make a diagnosis?
- The sequencing of the genome will take less than an hour.
- Yeah.
The analysis takes
about two minutes.
OK, right.
- OK. Two minutes as opposed to ten weeks?
- Yes.
Right, that is really
crunching it, isn't it?
And this, presumably,
isn't just for TB.
No. It's of great use for TB, but
it can be used for any bacterium.
If you're able to get a diagnosis
within minutes of seeing your
patient, it enables you to give
the correct narrow-spectrum
antibiotic that targets just those
bacteria that are causing the
illness and nothing else,
so it's precision bombing
rather than carpet bombing.
If trials in clinics over the next
couple of years are successful,
this device could extend the
life of antibiotics by slowing
the pace of resistance.
But what if we could also stop
some bugs from resisting altogether?
Some commonly prescribed
antibiotics work by getting into
bacterial cells, and when
they hit a lethal dose,
this causes the
bacteria to rupture -
something they have
evolved ways to resist.
Dr Jess Blair is part of a team
from Birmingham University
with a plan to stop the
bacteria fighting back.
She is going to try and explain
the principle behind her approach
using a bucket
as a bacterial cell.
OK, so you've got a watering
can here full of antibiotic.
If you start pouring that into
our bacterial cell, what we hope,
then, is that this will
kill off the bacterial cell.
So, for argument's sake,
let's say our level at which the
antibiotic becomes
toxic is here.
So you need to keep pouring.
However, bacteria
have a nifty trick.
In their membranes, they
have pumps called efflux pumps.
So I'm pouring in antibiotics,
and the bacteria are
just pumping them out.
Pumping them
straight back out again.
So now it's not
looking quite so good.
- Sorry, I'm getting your feet wet.
- Yep.
It's going to become a bit
more difficult for you to get
the antibiotic towards our line at
which it's going to become toxic.
Right.
And what happens when they
become really antibiotic resistant
is they make more and
more of these pumps.
OK, that's a very neat trick.
So, what can you do about it?
Well, in my pocket,
I've got a cable tie to
sort of demonstrate this.
So, we have inhibited
the efflux pump.
- So you're able to keep pouring the antibiotic in...
- There we go!
..and we're about
to reach the level
which is going to
kill our bacterial cell.
Die, bacteria, die!
There we go. OK.
So that's the theory.
I mean, how close
are we to it in practice?
When I say we, I
mean you, of course.
Well, people have been able
to find molecules that do this.
The problem is there's no molecules
at the moment which are able
to both inhibit efflux pumps but
also are OK to be given to a person.
Most of the ones that we
currently have are toxic to people.
Because she can't test her inhibitor
chemical on a living human being,
Jess is going to test it instead on
a salmonella infection in my hand.
While she does that,
Dr Andy Edwards and I are trying
out another experimental chemical
on my other hand, which
we have infected with MRSA.
Andy wants to show me what
he calls an antibiotic amplifier.
It's designed to stop this
superbug from resisting
an existing antibiotic
called ciprofloxacin.
So, what ciprofloxacin does
is to break up bacterial DNA.
It smashes it into
lots of small pieces.
And MRSA is really good at
then sticking that back together
and surviving.
So what we want to do
with our antibiotic amplifier is
prevent the bacterium from
sticking the DNA back together again.
MRSA has a very bad
reputation, doesn't it?
It has a bad reputation
for a good reason.
So, MRSA causes lots of lots
of surgical-site infections and
other skin infections,
particularly in hospitals.
And once it gets into the
blood, it is very, very serious.
It can attach to your
heart, bones and joints.
So you're going to try and
make this non-resistant again,
reverse it if you like.
That's right, that's right. We're
trying to outsmart the bug.
Andy's antibiotic amplifier
and Jess's pump inhibitor are
amongst a number of so-called
resistance breakers currently
in development.
The results from our test
certainly suggest they could have
a promising future.
Though, the first one
is easier to make out on
a Petri dish than
on my agar hand.
This is the pump inhibitor,
the one that stops the bacteria
pumping out the antibiotics.
And this one is
working rather well.
You've got the
salmonella infection here,
and it is resistant
to the antibiotic
which is in the
rest of the plate.
But here, in the middle,
that bit there is working
because the area around it is clear.
So that's promising.
That's good.
Next, the hand that
was infected with MRSA.
What's encouraging is
the area that I painted
on the back of the hand, here,
which was a mixture
of the amplifier
and the antibiotic,
that is clean.
So that would suggest the
amplifier is doing what it should do,
which is preventing bacteria
from reforming their DNA,
and therefore, the
bacteria are being killed.
That one I give high
marks to. That one worked.
That's encouraging results
from one experimental antibiotic
and two resistance-breakers.
But none of these cures will
be ready to use on you or me
any time soon.
The final thing I want to look
at is something which will kill
bacteria but which isn't
actually an antibiotic.
This is where I normally come.
At Oxford University,
microbiologist
Dr Alex Betts is investigating
viruses which
naturally attack bacteria.
Mind your feet, cos we are
looking for...something, actually,
a lot like that. Perfect.
Alex is one of a handful of
scientists in the UK working
with bacterial phages.
All right, here we go. Oh, look
at that. Isn't that disgusting?
This is a fresh goose
poo, and from these,
I can isolate the bacteria
and the viruses that are inside
the digestive tract of geese.
And that I can take back to the
lab, and it should be a treasure
trove of things that could
potentially treat disease in humans.
Lovely.
I want to see if Alex's
viruses can cure me.
- Here we go. - Oh, wow.
- I have a gift for you, my lovely face.
For the scientist
who has everything.
- It's quite weird, isn't it?
- Look at that nose!
LAUGHING: Thank you(!)
What we're going to do
now is test a type of virus Alex
has acquired from a sewage farm
against a superbug - Pseudomonas.
This bug causes
septicaemia and pneumonia.
In short, it's very nasty.
It's a powerhouse of antibiotic
resistance. It's a real problem.
And it's been
isolated from food,
soil, drinking water,
even really extreme
environments like aviation fuel.
This thing can grow on
pretty much anything. So it's...
- It's a good test, basically.
- Very much so.
If we can beat this, then
we are in a good position.
- So these are billions of viruses, is that right?
- Yes, indeed.
These are viruses that
infect and kill bacteria,
just as part of their
natural life cycles.
It's not something we've
engineered in the lab.
These images were taken with
a hugely powerful microscope.
You can see the tiny viruses
known as phages clamped on to
a single bacterial cell.
Phages are
parasites for bacteria.
They inject their genetic
material into a cell,
forcing it to produce a
huge number of new phages.
These then burst out
of the cell, destroying it.
Research into phages is
just getting started in the UK.
But in Eastern Europe,
they've been experimenting with
viruses therapeutically
for almost a century.
And in the Polish
city of Wroclaw,
there's a specialist clinic that's
achieving really impressive results
in treating people with
antibiotic-resistant infections.
Remember the gruesome
wound in Slawa's foot?
Her E. coli infection is
so bad and so untreatable,
there's a serious risk she
will have to have it amputated.
Now she's hoping
phages can save it.
Through our experimental
phage therapy,
we want to protect
her against amputation.
I'm going to apply
phage preparation
into the wound.
And I show you how I do it.
This is a phage
preparation against E. coli.
The doctors hope to get
Slawa's infection under control
and then perform an
operation to save the foot.
Look away for a minute
if you're squeamish.
The patient will have
surgery, which aim is to cut
this dead tissue,
but we apply phages before
to decrease a lot of bacteria.
After surgery, Slawa will
receive combination therapy using
phages and targeted antibiotics.
It will be months before Slawa
knows if the therapy is working.
Fingers crossed.
In the meantime, let's see how
my virus treatment is getting on.
- Here we go.
- OK.
Now, it doesn't look
obviously different.
So, under white lights, the
bacteria aren't particularly visible,
cos they have kind of a
similar colour to the agar,
but there is this neat trick. They produce
a molecule that fluoresces very intensely
under UV light.
- Look at that.
- Yeah!
- And hopefully, when I remove the bandage...
- Yeah.
- ..we should see quite a difference.
- Oh, yeah!
That is very, very
striking, isn't it?
- And that is because the bacteria were unable to grow in there.
- Right.
- It's really done the business, hasn't it?
- It has done, yeah.
The viruses are
natural parasites.
They haven't evolved to
completely obliterate their hosts,
but what you will
get is, hopefully,
in the context of therapy
where you're treating
a patient with an immune system,
that you'll push the
bacteria far enough
the patient's immune system
can take care of whatever's left.
There have been no
clinical trials in the UK yet.
But I'm hoping that one
day phages will make
a significant contribution
to frontline medicine.
They're not going
to replace antibiotics,
but there are certain roles
that they can fulfil that would
ease the pressure on
our existing therapeutics,
buy us some time to
develop new antimicrobials,
and it can certainly be
used alongside antibiotics.
Phages are going to have
to step up and take a role.
So what have I learnt
about antibiotic resistance?
Well, the biggest lesson is
that bacteria will never stop
evolving ways to fight back...
..which means we need
a multi-pronged response,
including, of course, new,
better-targeted antibiotics.
It's going to take serious resources
to turn things around and prevent
the projected death toll.
If ten million people a year
are going to die by 2050,
that's not that far away
if you consider that it
takes 20 or 25 years
to get a new drug to market.
And you don't just
need one new antibiotic -
you need a whole
generation of new antibiotics,
so it's going to cost tens of
billions of dollars, basically.
And the reality is that,
if you spend 1 billion getting
an antibiotic to the clinic,
you probably won't
make your money back.
So it's not great business.
That money has got to come
from somewhere and, presumably,
it's going to be at
a government level.
Last year, the United
Nations passed a resolution,
unanimously signed
by 193 countries,
saying that all countries
should get together
and take action,
so I do detect
movement forwards,
but these things are slow.
If we fail to act, we risk plunging
medicine back into the Dark Ages.
But I'm encouraged by the
fact there's a vast world of
microbes out there, packed
with potential allies as well as
enemies - a world which we
are only just beginning to explore.
I'm actually feeling more confident
than I was at the beginning of
this film that we will find
ways to combat the threat of
antibiotic resistance.
I can only hope that when we
develop new weapons, we will treat them
with greater care and respect
than we have in the past.
For more than 70 years,
we've waged war
against bacterial infections
using antibiotics.
But it's a war we're now losing.
Drug-resistant superbugs...
..are spreading.
To find out what
we're up against,
I'm donating my body to
an extraordinary experiment.
We are going to unleash
bacterial hell on a clone of my body.
Woohoo!
We're hoping this experiment -
which is novel and rather spooky -
will give us a whole new
insight into the way that bacteria
fight back against antibiotics.
- That is absolutely revolting.
- It's fabulous!
I'll search high and low
for radical solutions...
Die, bacteria, die!
..to stop the spread
of the superbugs.
When I remove the bandage,
we should see quite a difference.
Oh, yeah!
Is it too late to prevent
antibiotic Armageddon?
Me and my body
are about to find out.
Hello.
- Good to see you upright.
- Well, it's nice to be upright.
- Come and have a seat.
- Thank you.
Hi there.
A month ago, 57-year-old
John Shelton was fighting
for his life against a
sudden bacterial infection.
- Good.
- When I arrived here, they opened me up, there was a big mass.
It was very, very infected,
and the bacteria were already
working their merry havoc,
trashing my body,
shutting down my lungs,
shutting down my kidneys, shutting
down everything, pretty much.
- You don't remember anything?
- Not a thing.
His lung had almost
completely filled up with bacteria,
or infection, and he wasn't
able to oxygenate his blood.
Bacteria called staph
aureus caused the infection.
They were eventually stopped
by a concoction of antibiotics,
but for a while it
was touch and go.
- HE INHALES AND
EXHALES - Brilliant.
- EMOTIONAL: - When they thought
he'd had a brain haemorrhage -
sorry -
that was not a great moment.
You know, just one day at a time,
really, and you do place your faith
in the fact there's going to be
another antibiotic to come up.
It's interesting that, you know,
there is a lot of technology here,
there is obviously a fantastic staff
but, in the end, it's kind of
antibiotics versus bacteria.
That's it. Simple as that.
There is no doubt in my
mind that, without antibiotics,
I would not be here.
Before the 1940s, up to a
third of deaths were caused
by bacterial infection.
A simple cut could kill you.
Then came antibiotics -
drugs able to kill bacteria.
The first was penicillin,
discovered by Alexander
Fleming in 1928.
More followed.
But then, the pipeline dried up.
No totally new antibiotics
have been found for
more than 30 years.
And more and more bacteria
are becoming resistant
to our dwindling stock...
..including superbugs,
which threaten to send modern
medicine back to the Dark Ages.
Around 700,000 people die every
year because of drug-resistant
strains of
infections like E. coli
and TB, but that figure could
soar to around 10 million a year
by the middle of this century
if urgent action isn't taken.
Increasing numbers of people are finding
that antibiotics are no longer working.
People like Slawa.
Slawa's foot is so
infected with E. coli.
It could lead to her whole
leg being amputated.
Be warned, this glimpse
into a post-antibiotic world
is gruesome.
So, if you are squeamish,
look away now.
'If we do nothing,
'modern medicine in all its finery
will become much more hazardous.'
Cancer therapy, immunotherapy...
I mean, just simple
infections like meningitis.
All of these things
become more hazardous.
So anti-microbial resistance
is the biggest single issue
which is affecting modern
medicine at the moment.
In 2015, 34
million prescriptions
were issued for
antibiotics in the UK alone.
Have we created superbugs by
popping too many of these pills?
I want to find out exactly
what antibiotics do and why
bacteria are resisting them.
Time for an unusual experiment.
So I have done a lot of
strange things in my time,
and a lot of self experiments,
but nothing quite like this.
Now, I'm in pretty good
health and I only take antibiotics
when I absolutely have to,
but I am going to explore what
a powerful antibiotic
does to my body
by making my bacteria visible.
If you'd like to know, I have
not washed for two days.
- Great.
- All right! Yeah, that's...
When I start doing these
things, I always think,
"Oh, it sounds
like a good idea,"
and when I actually get there,
I start to wonder if it really is.
Artist Mellissa Fisher
specialises in creating
living biological sculptures.
- Oooh!
- Right in between your toes.
With Professor Mark
Clements of Lincoln University,
she is leading a team to make
a living bacterial
sculpture out of me.
So, that's the...the right here.
Step one - collect material
from all over my body
using cotton-wool swabs.
On the skin, you've got over
1,000 different types of bacteria.
And each person is unique.
All different parts of the
body will have slightly different
micro flora, depending on
whether it's a moist area,
whether it's a dry
area, oily area...
By moist, I'm thinking
armpits, probably.
Yeah, the very moist areas...
The armpit and the
groin are particularly good.
- OK. I might do my own groin.
- Yes. Yeah, yeah, yeah.
Next, I'm wrapped in plaster
to create a mould of me...
Woo!
..and given a full body
wax in the process.
Do you want your hair back?
Our home for this experiment
is Imperial College in London.
It's right on that edge, there.
Here, our team of scientists
and sculptors turn my body mould
into possibly the world's
largest Petri dish by filling it
with a nutrient-rich
jelly called agar.
Good morning,
gang. Good morning.
After 12 hours, the
agar jelly has set.
It is like Tutankhamen's
tomb, isn't it?
All right, so nice and
gently, up and out.
There's two parts
to this experiment,
which is why my rather
spooky clone is split in half.
- The foot's out.
- Woohoo!
That is wonderfully weird.
On one side, we want to grow
bacteria from all over my skin
to see what's living on me.
It kind of looks like
me, I must admit that.
A slightly bald
version of me, but...
THEY CHUCKLE Wow.
On the other side, we've added
a broad-spectrum antibiotic used
in hospitals against a
wide range of infections.
But before we even get the
chance to add my bacteria,
something else has snuck in.
What's the green stuff?
- Does this suggest the presence of bacteria already, then?
- It does.
On this side, where we
don't have any antibiotics,
- then there has been some growth of bacteria.
- Right.
So even given the
tiniest opportunity,
the bacteria have got stuck in.
They do, they do. Yes, yep,
yep. They're everywhere.
We don't know where these
green bacteria have come from.
But you can see that the antibiotic
embedded on the left-hand side
have so far stopped
the invader from growing.
Time to add bacteria
collected from my body.
These are all the swabs
we've taken of your body.
We're going to start with the
bottom of the feet, so number 20.
We want to make visible
the invisible microbes -
mainly bacteria - that
live on a healthy human.
So we're adding each of my
samples to the corresponding
part of my clone.
Let's see what they
make of their new home.
OK, we can do this.
Our giant Petri dish is
sealed into an airtight case.
It really does feel like they're
taking my body and embalming it.
Whoa!
- Oop, the foot's gone.
- Oh, no!
Despite a couple of
rather nasty foot injuries...
..Microbial Michael is now
ready for our experiment to start.
Which microbes
will thrive and where?
I would expect, within
the next few days,
we'll start seeing them
emerge on that side.
The question is, will they be
able to overcome the antibiotics
and start growing on this side?
The truth is, we have absolutely
no idea what is going to happen
next, because this sort of thing
has never been done on
this sort of scale before.
We simply have
to wait to find out.
Time for a road trip.
I want to dig deeper
into the roots of the crisis.
So why are more and more
bacteria becoming resistant?
Is it simply that we're
overdoing the antibiotics,
or is it more
complicated than that?
I recently read about a
fascinating discovery made here,
in New Mexico, which changed the
way I think about antibiotic resistance.
Now, this is the spot.
Gorgeous, isn't it?
Unfortunately, what I am looking
for is not here, on the surface.
It is deep underground.
And I say unfortunately because
I am pretty claustrophobic.
My guide is Dr Hazel Barton.
- Hey-ho. Hello. - Hi, Michael, how are you doing?
- Glad to see you.
Hazel's a microbiologist
who searches for new species
of bacteria living deep
under Carlsbad National Park,
in a vast network of caves.
- Thank you. What's the longest you've been down here for?
- Eight days.
- Eight days? Cool. Journey to the centre of the earth.
- Yeah.
So we're getting off
the tourist trail here.
Blimey. It gets
narrower, doesn't it?
- It's quite big in here.
- Yeah. It's cool.
It was in 2012 in a cave much
deeper than I'm able to go that
Hazel's team made their
breakthrough discovery.
So the kind of areas that we
sample look quite a bit like this.
Hazel took a bunch of bacterial
samples from the cave and
sent them off to
a lab for analysis.
The results shocked everyone.
So I sent him just 100, right?
He started testing
them, and he's like,
"You're not going
to believe this,
"but they are
resistant to everything."
- Blimey.
- Everything that's used...
So these were bacteria
you found on a wall in a cave.
Much more remote than this,
- much further away.
- That had not seen humans for...
We know humans had never
been in there because we know...
we had the exploration records,
so there was no impact on it.
And they were resistant to
practically every antibiotic
- that's used in the clinic.
- Wow.
That is both incredibly
exciting and incredibly scary.
Nobody had ever thought that
you would find resistant bacteria
down in the bottom
of a bloody cave.
They'd had no
interaction with humans,
but the bacteria Hazel found
in the cave were resistant to
a huge array of antibiotics
we use in modern medicine.
This resistance had clearly
evolved over millions of years
without us having
anything to do with it.
Why?
Well, it makes sense
when you think of antibiotics
not as man-made but the
by-product of war between microbes.
They make chemical weapons
to destroy their enemies and
steal their resources...
..weapons we have learnt
to exploit as antibiotics.
The bacteria living deep in the
cave have had millions of years to
evolve weapons that can target
and destroy even their toughest rivals.
The battle for scarce resources
like nutrients and energy is
particularly brutal
down here, in the caves.
It's really starved down
here. There's no resources.
It's probably one of the most
starved environments on Earth
because, if you think about it, any
energy needs to come in through
the rock, and so there's a
big competition for nutrients.
The fewer the resources, the
more intensely the microbes battle,
and that creates resistance
because the bacteria under
attack don't just
lie back and die.
When billions of bacterial
cells are bombarded,
all it takes is for one
cell to mutate its DNA...
..in such a way that the
antibiotic can no longer kill it.
This ability to resist
then spreads...fast.
So developing resistance
to antibiotics is an entirely
natural process,
which the bacteria
of Carlsbad have
taken to the extreme.
- So, a fierce competition going around us all the time.
- Uh-huh.
Microbes producing antibiotics,
but this is all happening millions
of years before Fleming and
his friends at Oxford
actually developed penicillin.
Right. And that's what we
discovered down here that kind of blew
everybody's mind, is the thought
that resistance and that antibiotic
battle is because we've
been using antibiotics,
but it can't be down here cos
these guys have never seen
the antibiotics that Fleming,
everyone has made since.
But if resistance to
antibiotics arises naturally,
what does that mean for us?
Let's see if Microbial
Michael has any answers.
Bloody hell. That is grotesque.
We've left him
alone for a few days,
and the bacteria swabbed
from my body have run riot.
I'm hoping immunologist
Dr Sheena Cruickshank
from Manchester University
can help me make
sense of what's happening.
Michael, meet Michael.
That is so weird.
- I just think it's so exciting to be able to see...
- It is both exciting
and really, really
disgusting, I have to say.
There's something, as well, about
seeing me down there, effectively
covered with this stuff.
I think you should be looking
at this as showing you the
amazing life that
is living on you.
We're starting on
the right-hand side,
where there's no
added antibiotic.
That means these different-coloured
bacteria should be part of my
normal skin flora.
Look at this
amazing white, blue...
OK, I thought white, blue meant there was
nothing growing there, but there is something?
No, that's actually
growing over the blue,
and that's really exciting
- because it suggests that perhaps it is battling with the blue.
- OK.
It's competing with it.
And I think that's
Staphylococcus epidermidis,
and that's a really
common skin bacteria.
And we actually know that some
bacteria make anti-bacterials,
so they compete with each
other and they kill other bacteria.
So, perhaps that's
what's happening here.
So we're kind of seeing warfare
in action between the bacteria.
Absolutely.
What this side of this experiment
is showing us very colourfully is
how bacteria in a healthy body
keep each other in check as they
battle for space and nutrients.
Because most bacteria living
on us are harmless or beneficial,
in a balanced ecosystem,
they leave limited room
for the bad bugs
- the pathogens.
Behind the scenes, our team is
identifying exactly what's grown
using DNA analysis.
And they found something
potentially nasty up my nose.
This is really interesting.
If you look around your nose
there, around your nostril,
there is Staphylococcus
aureus growing there.
That is the sort of orangey...
- They call it the golden staph, don't they?
- Yeah.
A lot of people -
about a third of people -
have Staphylococcus
aureus in their nostrils.
It's quite, quite normal.
But a lot of people associate
it with being a pathogen.
In the right
circumstances, it's fine.
In the wrong, it can be deadly.
If our immune system takes a hit,
some species amongst our bacteria
can get out of control
and do serious harm.
That's what then relatives of the
golden staph aureus in my nose did
to patient John Shelton,
overrunning his body's defences
and very nearly killing him.
On this side of the experiment,
my bacteria are keeping each
other in check, just as I'd expect.
But on the other side,
it's a different story.
So we are coming across to the
side which was actually enriched
- with antibiotics, wasn't it?
- Mm-hm.
Peer past the fog of
condensation caused by
so much microbial activity,
and our time-lapse cameras
reveal that even on the side which
is heavily impregnated with
broad-spectrum antibiotics,
there are still
bacteria growing.
Though, admittedly,
there are a lot less of them.
Here, just here, at the top
of the head, you can see,
there's actually quite
a few clear zones.
So that suggests that certainly
the antibiotic is doing its job
in areas, and it's certainly
been controlling in this area
the blue, which was kind
of taking over everything.
One of the things that
is very striking to me
- is that on the other side, there's competition going on...
- Mm-hm.
..which suggests that
wiping out all your bacteria is
a bad idea because actually
you do want sort of good bacteria,
if you like, to kind of compete
with the pathogens and stop them
- encroaching.
- Absolutely.
What this demonstrates very
clearly is you shouldn't take
a broad-spectrum antibiotic
unless you really need to.
As the caves of New
Mexico showed us,
the more bacteria are
attacked, the more they will resist.
But there is also an unfortunate
fact - that broad-spectrum
antibiotics carpet bomb
friend and foe indiscriminately.
There is a lot of collateral
damage amongst the benign
and beneficial species.
This accelerates resistance
because surviving pathogens now have
less competition for resources,
and they can colonise
the whole battlefield.
If one of these survivors
is resistant to multiple drugs
and potentially
harmful, it's a superbug.
The bad news for me is the team
have found two growing on my clone.
One that is particularly
interesting is an organism called
Enterococcus faecium.
And this is an entirely
normal part of our gut flora.
But if it gets into the
wrong parts of the body,
or if the person has a
compromised immune system,
it can cause really
serious invasive infections.
And because it's inherently
resistant to antibiotics,
it's very, very hard to treat.
The team has also found Pseudomonas
growing through the antibiotic.
It's not part of my skin flora,
but a travelling pathogen
that can cause
infection and pneumonia
if it gets inside our bodies...
..say, through an open wound.
Microbial Michael has shown
me superbugs on my skin.
But what about inside me, where
some really important stuff happens?
I've sent off a very personal
sample to be analysed.
So, we've received our
poo sample from Michael.
And we want to have a look
to determine if he's got any
resistant bacteria.
When you think
about antibiotics,
most of these us will take
these orally, and also we'll take it
with a drink of water,
so therefore, the
antibiotics will hit the gut first.
Our guts and intestines are
home to at least 1,000 different
species of bacteria.
But now there's new research
about what can happen to them when
we take antibiotics.
The striking thing about
a healthy person
who takes an antibiotic
is that, in all likelihood,
they will get resistant bacteria
in their tummies - in
their colon, actually -
after about seven days.
And with some antibiotics,
these resistant bugs last in
their tummies for up to a year.
That sounds like another compelling
reason not to take antibiotics
unless you really have to.
I'm hoping my gut doesn't
contain resistant bacteria.
Right, so you had my poo
samples. What did you find?
- So...
- 'Lindsay has tried growing my gut bacteria
'on plates containing four
clinically important antibiotics.'
- Presumably, these plates should be clear of bacteria.
- Yeah.
If you had susceptible bacteria,
then they should be clear,
but as you can see, there's
multiple colonies on each of
the plates, which would suggest
they are resistant to that antibiotic.
That does surprise me.
I haven't had that many
antibiotics in my life.
Well, I was going to ask,
when was the last time you
had a course of antibiotics?
Probably about four years ago.
Yeah, OK, so that's quite a long time ago,
but maybe does correlate with
some of the data that we've shown.
That's a nasty surprise. I've
got bacteria growing inside me
which are resistant
to all four antibiotics -
one of which I've
never even taken.
I know the name, but I
think I would know if I'd had it.
Yeah, you would probably
know if you had vancomycin.
It's a last-resort antibiotic,
- so this is what you get if you're really ill.
- OK.
That is really quite
worrying, I must admit.
And what is really quite
striking is the fact that the main
culprit in terms of having
antibiotic resistant genes
is E. coli.
Blimey. I have E. coli in my gut
which is resistant to everything.
- Yes.
- Blimey. That's bad news!
OK. That's not what
I was hoping to hear.
There are lots of different strains
of E. coli. A few are very nasty.
We don't know
what strain I've got,
but we do know
it is very resistant.
Now, that was an
unpleasant surprise.
It's one thing to talk
about antibiotic resistance,
but to discover that
I've got these E. coli,
and they are resistant to
all sorts of antibiotics is,
I must admit, worrying.
I'm not really worried
by the fact it's E. coli.
It's the resistance bit.
Why?
Well, once resistance emerges
in one species of bacteria,
it can spread to other species.
It's all to do with the way
they exchange genes,
as Sheena can explain.
We get all our DNA from our parents,
- so you get half from your mum,
half from your dad. That's
your lot. You don't get any more.
You might see that chap down
the corridor who never catches
a cold and think, "Oh, I'd love
to be able to steal that ability."
But we can't.
But imagine you could.
Imagine you could steal DNA and
swap DNA just as easily as you swap your
e-mail or your telephone number.
And basically, bacteria can do that.
It's called horizontal
gene transfer,
and this is the way antibiotic
resistance can spread.
Using this trick,
different species of bacteria
share genetic information...
..including the ability to
resist a specific antibiotic.
The bacteria don't even have to
be touching because they can also
pick up bits of genetic information
left in the environment around them.
That means the E. coli
inside me could, theoretically,
share its genes
with other species...
..and turn my gut into a
factory of resistant bacteria.
And we have plenty of
evidence that really does happen.
Resistance is spreading
from microbe to microbe.
Wherever antibiotics are used
intensively, such as hospitals,
more resistant bacteria emerge.
They share their
genes. They multiply.
This explains how superbugs
like MRSA and E. coli can resist
so many different drugs.
And they don't stay
confined inside our hospitals...
..because, like us,
bacteria can travel.
And people aren't the only
source of resistant bacteria.
Globally, half of all
antibiotics are given to animals.
In countries like
America and China,
they are even widely
used as growth promoters.
Animals and humans alike pump
out more and more resistant bacteria.
But how far is the wave
of resistance spreading?
In Cornwall,
a pioneering new study has found
evidence that resistant bacteria are
travelling through our waterways,
out to sea, and then back again,
into humans.
Hi. I'm going to talk to you
about the Beach Bums survey.
We recruited 300
people to our survey -
surfers and people
who don't surf, as well -
and asked them to collect
swabs of their faecal material.
You take the swab, send
it back to us in the post,
and then we test it for the
presence of resistant bacteria.
What we found is that a
greater proportion of surfers have
resistant bacteria in their guts
compared to people who don't surf.
We think that, if you
swallow a lot of seawater,
that some of the bacteria
that are present in the seawater
survive and go on to live
inside...inside your gut.
If resistant bacteria can make it
out to sea and then into surfers,
I could have picked up the
resistant E. coli in my gut from, well,
just about anywhere.
The good news is that in the
UK and some other countries,
antibiotic use in farming
has started to come down.
But there's no putting the
genie back in the bottle.
Resistant bugs are in our
bodies and all around us.
There isn't any doubt that
we have been complacent
and we have walked
into this huge problem.
But humans have been between
a rock and a hard place here.
They want to use antibiotics,
but as soon as they use them,
resistance arises.
Because they are life-saving, if
you stop using antibiotics, people die.
At the end of the day,
we need new antibiotics.
Trouble is, modern
medicine hasn't found
a totally new type of
antibiotic in more than 30 years.
Each new drug involves a long
and complex process of chemical
engineering and testing.
They are certainly difficult
to make from scratch.
Instead, scientists have
relied on finding new microbes,
growing them and then
trying to identify and extract any
chemicals with potential
antibiotic properties.
One problem is that many
microbes simply won't grow using
traditional lab techniques.
And without being
able to grow them,
we will struggle to
develop new antibiotics.
Time to search out
some novel solutions.
Here in Boston, I've come to
meet a maverick microbiologist who,
I'm told, has developed a whole
new way of growing bacteria
and, in the process, discovered
possibly the first new class
of antibiotics in decades.
Dr Slava Epstein has
promised to show me his secret.
Do you see a suitable spot
somewhere around here?
We can find a suitable spot just
about anywhere on the planet.
So, the first thing that
happens, we collect soil.
We collect soil.
We don't have to
have too much of it
because every gram of soil is
easily a billion
or 10 billion cells.
But what we're going to do
with the cells in the lab is going to
be very different.
Two thirds of our most important
antibiotics were originally found
in microbes living in soil, a well
which looked like it had run dry.
But now, Slava has thrown out
the 130-year-old Petri dish and
replaced it with a device that, to
my eyes, looks equally low-tech -
a plastic tray into which
his assistant adds a diluted
solution of the soil sample.
In this vial, there
is about 100 cells.
- 100 cells down from a few billion?
- Yes. - And these are all bacteria?
These are all bacteria.
It is starting from this point that
things are going to be different
because we are not going
to put them into a Petri dish.
Instead, we are
preparing this device.
- It is just a collection of wells with a porous bottom.
- OK.
So, I have to say, this
doesn't look that radical.
Not being a microbiologist,
I probably don't understand
why it is so different.
It is radical because
- have I ever mentioned any word nutrient?
- No.
- Because there is none.
- OK. - We don't need them.
Unlike the Petri
dish, we do not.
We do not want to
create artificial conditions.
- Now that will go into the soil...
- OK.
- ..from which these cells came from.
- Ah!
- That is clever.
- So inside... Thank you.
- Inside... - I get it at last.
- ..chemically... - OK, yeah.
..it will not be different
from the outside.
So if the cells can
grow in nature...
- You are returning them to their normal environment...
- Yes.
..rather than
sticking them in agar.
- They should be able to grow inside.
- Ah!
By putting the bacteria back
into the soil they came from,
Slava is encouraging them to
grow just like they would in the wild.
Compared to using agar jelly,
the results are astounding.
The difference in colony
count between the two methods
- is 30,000%.
- Wow.
You can grow 30,000% more
cells if you do it this way than if
you do it the conventional way.
That's correct.
This technique means they can
grow bacteria that would normally
be missed, and they have
created versions of the device to
look for novel bacteria in
all sorts of environments,
including the human mouth.
- Very neat.
- It's also very simple.
You can really build this
device in your garage.
What excites me about
Slava's discovery is it means
there's clearly a whole
world of microbes out there,
just waiting to be found.
Imagine you are an ancient
Greek looking up at the sky.
You'd only see a tiny handful
of the stars and planets that are
actually out there.
In some ways, we are a bit like
that ancient Greek when it comes to
the microbial world.
There is a vast
galaxy of tiny creatures,
and we are currently only aware
of a very small proportion of them.
We need to start looking for
new antibiotics much further
afield than the
soil under our feet.
Some scientists think seabeds
could be rich in antibacterial potential.
Easier pickings are washing
up on our shores with evidence
clips of seaweed contain microbial
agents effective against MRSA.
And deep in the caves under
New Mexico, Hazel Barton's team
has discovered that millions
of years of intense bacterial
warfare has produced
chemicals we may be able to use.
One of the organisms
that we found
made 38 novel
antimicrobial compounds,
- of which three were new antibiotics.
- Hm.
So the potential is that people
turn their attention to these
extreme environments - like
caves, like the deep ocean, like,
you know, the Arctic - we
are going to have this explosion
in new compounds over
the next ten, 15 years.
The hunt for antibiotics is not
just in extreme environments
but anywhere that's
home to novel microbes.
Professor Matt Hutchings
has found what could be
a novel antibiotic in...
an ant farm.
It's an amazing system.
They've been using antibiotics
for 50 to 60 million years.
The secret Matt's team has
unlocked is in the relationship
between these leaf-cutter
ants and their food source.
The fungus is the only food
for this whole ant colony.
And if they smell any foreign fungi
that might cause disease in there,
they cut it out, they
carry it over to this part,
which is the waste dump,
which is usually outside the nest.
They rub their bodies against
it and then they dig it back into
the ground.
The really interesting thing for us
is the reason they rub their bodies
against it is because
their bodies are covered in
antibiotic-producing bacteria
that the ants can use to defend
their fungus against disease.
Matt's lab has extracted a couple
of experimental new antibiotics
from the bacteria on the ants.
They haven't yet been
tested on humans.
So, time for part two of our
experiment, using my body -
well, bits of my body - to test
out some of these novel drugs.
We are creating a biohazard
and infecting different parts of
me with three of the most common
multi-drug-resistant superbugs -
MRSA, salmonella
and Pseudomonas.
Where should I put it, then?
- On the fingers.
- On the fingers, in there? OK.
Then, we'll try to cure them.
First, I want to see if
ant antibiotic can tackle
an infection of MRSA...
..on my face.
MRSA can cause skin infections.
If it gets inside us
and attacks our lungs,
it can be particularly
dangerous.
We've given my face a few
days for the bacteria to take hold.
So, this is the ant antibiotic,
and it is genuinely new and
really rather exciting because,
as you can see, it is really working,
because that white disc
on my forehead there,
there's a zone of death
around it which suggests
that it really is killing
all those bacteria.
So the good news is,
it's new and it's working.
The bad news is it's probably
ten, 15, 20 years away.
Why so long?
Well, finding an antibiotic in
nature is just the first stage in
an expensive and very
complicated process.
To discover a new
antibiotic, I mean,
you have to go from the
early stage of discovery -
so isolate bacteria from a
place like a leaf-cutter ant nest -
get those bacteria
growing on a plate,
solve the chemical structure of
that antibiotic - which is not trivial -
and then, of course, you have
to get a drug company interested
because they're the only
people with enough money
to get things through clinical trials.
The reality is, less than 1%
are actually suitable candidates
and make it through to actually
get them to the stage where they're
approved as safe to use in humans.
So it can take 15, 20
years and cost, well,
between half and 1 billion.
A time lag of 15 to 20 years is
massive given that around 700,000
people already die annually
because of antibiotic-resistant bacteria.
So what are we going to
do until new drugs emerge?
For starters, surely we could use
our existing stock more carefully.
Half of all hospital prescriptions
are for broad-spectrum antibiotics.
And given everything I've
learnt, that can't be a good idea.
Why do doctors continue to
use broad-spectrum antibiotics?
It strikes me as like carpet bombing
everything and you'd be better off
if you were a bit more targeted.
Well, as a doctor, you're
confronted with a dilemma.
When you see a new patient,
you don't necessarily have
the diagnosis in front of you.
- So you want to save the patient...
- Mm-hm.
..and you want to cover
all the eventualities.
And hence, you use a
broad-spectrum antibiotic.
- Right, because you don't know what it is you're trying to hit.
- Exactly.
To use targeted narrow-spectrum
antibiotics, doctors need to
be able to quickly diagnose
the specific infection in a patient.
For some bugs, like the
ones that cause tuberculosis,
that means taking samples,
growing the bacteria
and sequencing its DNA -
a process that can
take up to ten weeks.
But Tim's part of
a team working on
a prototype gadget that could
massively speed up DNA sequencing.
So, you see the patient
and they spit into your pot.
Yep. And the DNA from
your phlegm goes on there.
- OK.
- You close it.
- And then it... This sequences it?
- That sequences it. - Bloody hell.
- Now...
- That is really, really impressive, I have to say.
That is impressive.
So, how quickly would you
then be able to make a diagnosis?
- The sequencing of the genome will take less than an hour.
- Yeah.
The analysis takes
about two minutes.
OK, right.
- OK. Two minutes as opposed to ten weeks?
- Yes.
Right, that is really
crunching it, isn't it?
And this, presumably,
isn't just for TB.
No. It's of great use for TB, but
it can be used for any bacterium.
If you're able to get a diagnosis
within minutes of seeing your
patient, it enables you to give
the correct narrow-spectrum
antibiotic that targets just those
bacteria that are causing the
illness and nothing else,
so it's precision bombing
rather than carpet bombing.
If trials in clinics over the next
couple of years are successful,
this device could extend the
life of antibiotics by slowing
the pace of resistance.
But what if we could also stop
some bugs from resisting altogether?
Some commonly prescribed
antibiotics work by getting into
bacterial cells, and when
they hit a lethal dose,
this causes the
bacteria to rupture -
something they have
evolved ways to resist.
Dr Jess Blair is part of a team
from Birmingham University
with a plan to stop the
bacteria fighting back.
She is going to try and explain
the principle behind her approach
using a bucket
as a bacterial cell.
OK, so you've got a watering
can here full of antibiotic.
If you start pouring that into
our bacterial cell, what we hope,
then, is that this will
kill off the bacterial cell.
So, for argument's sake,
let's say our level at which the
antibiotic becomes
toxic is here.
So you need to keep pouring.
However, bacteria
have a nifty trick.
In their membranes, they
have pumps called efflux pumps.
So I'm pouring in antibiotics,
and the bacteria are
just pumping them out.
Pumping them
straight back out again.
So now it's not
looking quite so good.
- Sorry, I'm getting your feet wet.
- Yep.
It's going to become a bit
more difficult for you to get
the antibiotic towards our line at
which it's going to become toxic.
Right.
And what happens when they
become really antibiotic resistant
is they make more and
more of these pumps.
OK, that's a very neat trick.
So, what can you do about it?
Well, in my pocket,
I've got a cable tie to
sort of demonstrate this.
So, we have inhibited
the efflux pump.
- So you're able to keep pouring the antibiotic in...
- There we go!
..and we're about
to reach the level
which is going to
kill our bacterial cell.
Die, bacteria, die!
There we go. OK.
So that's the theory.
I mean, how close
are we to it in practice?
When I say we, I
mean you, of course.
Well, people have been able
to find molecules that do this.
The problem is there's no molecules
at the moment which are able
to both inhibit efflux pumps but
also are OK to be given to a person.
Most of the ones that we
currently have are toxic to people.
Because she can't test her inhibitor
chemical on a living human being,
Jess is going to test it instead on
a salmonella infection in my hand.
While she does that,
Dr Andy Edwards and I are trying
out another experimental chemical
on my other hand, which
we have infected with MRSA.
Andy wants to show me what
he calls an antibiotic amplifier.
It's designed to stop this
superbug from resisting
an existing antibiotic
called ciprofloxacin.
So, what ciprofloxacin does
is to break up bacterial DNA.
It smashes it into
lots of small pieces.
And MRSA is really good at
then sticking that back together
and surviving.
So what we want to do
with our antibiotic amplifier is
prevent the bacterium from
sticking the DNA back together again.
MRSA has a very bad
reputation, doesn't it?
It has a bad reputation
for a good reason.
So, MRSA causes lots of lots
of surgical-site infections and
other skin infections,
particularly in hospitals.
And once it gets into the
blood, it is very, very serious.
It can attach to your
heart, bones and joints.
So you're going to try and
make this non-resistant again,
reverse it if you like.
That's right, that's right. We're
trying to outsmart the bug.
Andy's antibiotic amplifier
and Jess's pump inhibitor are
amongst a number of so-called
resistance breakers currently
in development.
The results from our test
certainly suggest they could have
a promising future.
Though, the first one
is easier to make out on
a Petri dish than
on my agar hand.
This is the pump inhibitor,
the one that stops the bacteria
pumping out the antibiotics.
And this one is
working rather well.
You've got the
salmonella infection here,
and it is resistant
to the antibiotic
which is in the
rest of the plate.
But here, in the middle,
that bit there is working
because the area around it is clear.
So that's promising.
That's good.
Next, the hand that
was infected with MRSA.
What's encouraging is
the area that I painted
on the back of the hand, here,
which was a mixture
of the amplifier
and the antibiotic,
that is clean.
So that would suggest the
amplifier is doing what it should do,
which is preventing bacteria
from reforming their DNA,
and therefore, the
bacteria are being killed.
That one I give high
marks to. That one worked.
That's encouraging results
from one experimental antibiotic
and two resistance-breakers.
But none of these cures will
be ready to use on you or me
any time soon.
The final thing I want to look
at is something which will kill
bacteria but which isn't
actually an antibiotic.
This is where I normally come.
At Oxford University,
microbiologist
Dr Alex Betts is investigating
viruses which
naturally attack bacteria.
Mind your feet, cos we are
looking for...something, actually,
a lot like that. Perfect.
Alex is one of a handful of
scientists in the UK working
with bacterial phages.
All right, here we go. Oh, look
at that. Isn't that disgusting?
This is a fresh goose
poo, and from these,
I can isolate the bacteria
and the viruses that are inside
the digestive tract of geese.
And that I can take back to the
lab, and it should be a treasure
trove of things that could
potentially treat disease in humans.
Lovely.
I want to see if Alex's
viruses can cure me.
- Here we go. - Oh, wow.
- I have a gift for you, my lovely face.
For the scientist
who has everything.
- It's quite weird, isn't it?
- Look at that nose!
LAUGHING: Thank you(!)
What we're going to do
now is test a type of virus Alex
has acquired from a sewage farm
against a superbug - Pseudomonas.
This bug causes
septicaemia and pneumonia.
In short, it's very nasty.
It's a powerhouse of antibiotic
resistance. It's a real problem.
And it's been
isolated from food,
soil, drinking water,
even really extreme
environments like aviation fuel.
This thing can grow on
pretty much anything. So it's...
- It's a good test, basically.
- Very much so.
If we can beat this, then
we are in a good position.
- So these are billions of viruses, is that right?
- Yes, indeed.
These are viruses that
infect and kill bacteria,
just as part of their
natural life cycles.
It's not something we've
engineered in the lab.
These images were taken with
a hugely powerful microscope.
You can see the tiny viruses
known as phages clamped on to
a single bacterial cell.
Phages are
parasites for bacteria.
They inject their genetic
material into a cell,
forcing it to produce a
huge number of new phages.
These then burst out
of the cell, destroying it.
Research into phages is
just getting started in the UK.
But in Eastern Europe,
they've been experimenting with
viruses therapeutically
for almost a century.
And in the Polish
city of Wroclaw,
there's a specialist clinic that's
achieving really impressive results
in treating people with
antibiotic-resistant infections.
Remember the gruesome
wound in Slawa's foot?
Her E. coli infection is
so bad and so untreatable,
there's a serious risk she
will have to have it amputated.
Now she's hoping
phages can save it.
Through our experimental
phage therapy,
we want to protect
her against amputation.
I'm going to apply
phage preparation
into the wound.
And I show you how I do it.
This is a phage
preparation against E. coli.
The doctors hope to get
Slawa's infection under control
and then perform an
operation to save the foot.
Look away for a minute
if you're squeamish.
The patient will have
surgery, which aim is to cut
this dead tissue,
but we apply phages before
to decrease a lot of bacteria.
After surgery, Slawa will
receive combination therapy using
phages and targeted antibiotics.
It will be months before Slawa
knows if the therapy is working.
Fingers crossed.
In the meantime, let's see how
my virus treatment is getting on.
- Here we go.
- OK.
Now, it doesn't look
obviously different.
So, under white lights, the
bacteria aren't particularly visible,
cos they have kind of a
similar colour to the agar,
but there is this neat trick. They produce
a molecule that fluoresces very intensely
under UV light.
- Look at that.
- Yeah!
- And hopefully, when I remove the bandage...
- Yeah.
- ..we should see quite a difference.
- Oh, yeah!
That is very, very
striking, isn't it?
- And that is because the bacteria were unable to grow in there.
- Right.
- It's really done the business, hasn't it?
- It has done, yeah.
The viruses are
natural parasites.
They haven't evolved to
completely obliterate their hosts,
but what you will
get is, hopefully,
in the context of therapy
where you're treating
a patient with an immune system,
that you'll push the
bacteria far enough
the patient's immune system
can take care of whatever's left.
There have been no
clinical trials in the UK yet.
But I'm hoping that one
day phages will make
a significant contribution
to frontline medicine.
They're not going
to replace antibiotics,
but there are certain roles
that they can fulfil that would
ease the pressure on
our existing therapeutics,
buy us some time to
develop new antimicrobials,
and it can certainly be
used alongside antibiotics.
Phages are going to have
to step up and take a role.
So what have I learnt
about antibiotic resistance?
Well, the biggest lesson is
that bacteria will never stop
evolving ways to fight back...
..which means we need
a multi-pronged response,
including, of course, new,
better-targeted antibiotics.
It's going to take serious resources
to turn things around and prevent
the projected death toll.
If ten million people a year
are going to die by 2050,
that's not that far away
if you consider that it
takes 20 or 25 years
to get a new drug to market.
And you don't just
need one new antibiotic -
you need a whole
generation of new antibiotics,
so it's going to cost tens of
billions of dollars, basically.
And the reality is that,
if you spend 1 billion getting
an antibiotic to the clinic,
you probably won't
make your money back.
So it's not great business.
That money has got to come
from somewhere and, presumably,
it's going to be at
a government level.
Last year, the United
Nations passed a resolution,
unanimously signed
by 193 countries,
saying that all countries
should get together
and take action,
so I do detect
movement forwards,
but these things are slow.
If we fail to act, we risk plunging
medicine back into the Dark Ages.
But I'm encouraged by the
fact there's a vast world of
microbes out there, packed
with potential allies as well as
enemies - a world which we
are only just beginning to explore.
I'm actually feeling more confident
than I was at the beginning of
this film that we will find
ways to combat the threat of
antibiotic resistance.
I can only hope that when we
develop new weapons, we will treat them
with greater care and respect
than we have in the past.