The Truth About... s01e19 Episode Script

Antibiotics

There's a wonder drug we all rely on.
It fights infections.
It's extraordinary! And makes it possible for us to have life-saving operations.
It's vital in modern medicine.
We're going to give you an antibiotic.
Antibiotics are our front-line medical weapon.
Since the very first antibiotic, penicillin, was developed in these laboratories in Oxford, they've gone on to save some 100 million lives.
But we've taken them for granted.
We've been overusing antibiotics and the bacteria that cause infections are becoming resistant to them.
The headlines are saying we're on the verge of an apocalypse.
If nothing is done, then antibiotic resistance could become a greater cause of death than cancer.
And that would mean that annually, worldwide, ten million people will die.
I'm Angela Rippon and I'm setting out on a very personal journey, to discover the truth behind the headlines.
I want to find out what we can all do to fight back.
How we can cut down on the antibiotics we use.
No need for antibiotics? No need for antibiotics.
And target when we should be using them.
Right now, scientists are racing to find new antibiotics and I'll be joining them.
Are new antibiotics still to be discovered if we look in the right places? You've got to keep out of the way of that jaw.
Or, will scientists have to come up with an entirely new kind of treatment? That's cool.
That's a first.
Yes.
Whether you've taken antibiotics before or not, this affects all of us, unless we act now.
That is amazing.
This is The Truth, About Antibiotics.
My journey begins, in my childhood.
So, I have travelled to Plymouth, the city where I was born.
This was my very first school.
It's a little nursery school, which is just on the edge of Plymouth Hoe and it is one of the few buildings, that is exactly as it was when I was a little girl.
It was while I was growing up in this city that I contracted tuberculosis.
In 1949, TB was a killer.
I had to be quarantined, in the hope that my natural defences would come to my rescue.
I wasn't allowed to see my parents for weeks on end.
It was common practice at the time.
Yet, a quarter of all those who contracted TB, still died.
But I was very lucky.
Because a couple of years before, a new drug had been released.
It was called, streptomycin.
It was an antibiotic.
And it saved my life.
But if the headlines are to be believed, these very same families of antibiotics that cured me, are now failing.
So, I want to know what a post-antibiotic apocalypse actually means for us.
Infections are caused by viruses, bacteria, fungi and parasites.
Now, viral infections include colds and the flu.
A bacterial infection can range from meningitis and tuberculosis, right through to the dangers of E.
coli and MRSA.
Because viruses and bacteria are entirely different organisms, they need entirely different treatment.
Antibiotics only work against bacteria.
So, just what is the problem we're facing? Imagine these pins are bacteria, and these bowling balls are antibiotics.
When we get a bacterial infection, we take antibiotics and they wipe them out.
At least, that's what's meant to happen.
When we started using antibiotics, they were extremely effective.
But, we've overused them, so the bacteria they attack have adapted and become resistant to them.
So, if nothing is done, our miracle cure could stop working altogether, leaving us with no protection from bacterial infections.
For us to play our part in the fight back, we all need to understand what we're up against.
But, how many of us really know what antibiotic resistance, actually is? I guess I've heard of it, I don't really know much about it.
It's when you take a lot of antibiotics and your body becomes resistant to it.
Hmm, I have to think about that one.
No, I'm not clued-up on it, to be honest with you, no.
Probably because we're taking them too much, so our body is becoming immune.
I haven't a clue.
I go by what the doctor says.
I guess like an alien chemical drug coming into your body and then your body rejecting it, I guess.
But it's not.
It's the bacteria themselves that are developing that resistance and that's because they've been around for billions of years, and in that time, they've learned how to defend themselves against whatever the natural world throws at them.
So, here we are, human beings in the 21st century, with what we think is a miracle drug, antibiotics.
But, as far as bacteria are concerned, they're just another challenge, something else to be defeated, and so far, the bacteria are winning.
If you need scientific proof, here it is.
At Harvard University, they grew bacteria in a large dish, to show E.
coli developing resistance to antibiotics.
On the outside strip there's no antibiotic.
Then there's a single dose that normally kills E.
coli.
The strength increases to ten times, 100 times and finally, in the middle, the antibiotic is 1,000 times stronger than normal.
At each end of the dish, they introduced E.
coli.
And they filmed what happened.
I think this is staggering.
The normal E.
coli spread where there's no antibiotic, but they can't survive where they encounter the first dose.
Then, a resistant strain breaks through.
It spreads, able to defeat the single-strength dose.
At the next boundary, the resistant bacteria have to pause and develop new resistance to survive in ten times as much antibiotic as normal.
Then, the mutated strains repeat this at 100 times normal strength and finally, after acquiring ever greater resistance, the bacteria can survive antibiotics that are 1,000 times stronger.
If you needed proof, there it is.
The bacteria are clever little so-and-sos and they have learned how to become resistant to antibiotics.
That process took just ten days.
When bacteria develop resistance to not just one but many different kinds of antibiotics, they're known as superbugs.
Our bodies are full of bacteria, and most are harmless, even the dangerous ones strike only when we're vulnerable, when we're older or our immune system is compromised.
The infections they cause can usually be stopped by antibiotics, but some bacteria, like the E.
coli in the Harvard experiment are becoming more and more difficult to stop.
I've tracked down a young woman who has survived repeated attacks from a bacterial superbug.
I've been living with the superbug for around seven, eight years now.
I first found out when I was about 17.
The superbug Emily Morris carries causes repeated attacks of the urinary tract infection, cystitis.
Now, for most women, antibiotics will cure cystitis, but Emily's is caused by a strain of E.
coli that is resistant to those antibiotics, making it harder for her to fight the infection.
Obviously, like a teenager, I thought I was quite fit and healthy, so it was quite hard to get my head round that.
I did feel very ill.
Like, it didn't feel like a normal cystitis.
I did feel very unwell.
That was the first one and I think that was probably one of the worst ones.
Emily was hospitalised, but recovered from that infection.
Since then, she's continued to have repeated attacks.
The E.
coli she carries is resistant to all but the strongest antibiotics.
Her fear is that one day, the drugs won't work at all, putting her life at risk.
The superbug has already forced her to make some tough decisions.
I think it must have been about my third or fourth attack, and it was in my early pregnancy.
The doctor that was seeing me at A&E said, "This antibiotic "we're going to give you hasn't been tested "on a pregnant person before.
"We don't know how it will affect your baby," and obviously the fear of being a first-time mum anyway, it was the worst fear you could ever have.
The antibiotic was called a carbapenem.
It's a drug of last resort, but without it, both Emily and her baby could have died.
So, I had to choose to take the antibiotic, but, unfortunately, if I didn't, me or the baby aren't going to be here.
Emily's son, Emerson, was born healthy, and is now four years old.
But he has recently developed a rare form of epilepsy.
Doctors can't tell if it's a side-effect of the very antibiotic she was forced to take to save both their lives.
Is there a doubt in the back of your mind that it might be as a result of having taken the antibiotics? Sorry.
Take a moment.
Yeah.
But you had no choice.
I know.
But I don't think anybody would even be able to answer me that question.
I just sort of hope that it wasn't for that, but I do.
I do.
There is something at the back of my head, just something I've done, of course.
As antibiotic resistance grows, more and more of us will be affected like Emily.
If you think about it, I don't know a lot of people that have survived a superbug this many times.
If all our antibiotics fail, the effect on modern medicine will be catastrophic.
This group of people are going to show us what will happen when the medical procedures that we all now take for granted become, life-threatening.
These 60 volunteers represent the population of Britain.
Nearly half could die, if we no longer had antibiotics.
Some would go because births by Caesarean section would be a thing of the past.
They rely on antibiotics to fight infection.
Chemotherapy needs them just as much, so cancer patients would die.
Without antibiotics, hip and knee replacements become an invitation to infection, and routine operations put lives at risk.
And premature babies would not have vital assistance in those early days, to help them make it through.
Before antibiotics, 40% of us would die from infection.
Without antibiotics, we are going to return to the Dark Ages of medicine, when even a simple scratch could be a death sentence.
And these aren't just statistics.
These are human lives.
Good Hope Hospital in Sutton Coldfield provides a stark example of just how vital antibiotics are in our war against infection.
The latest arrival at A&E is delirious.
The medics believe Elizabeth Blunt is suffering from a condition called sepsis, and sepsis is a killer.
It's caused when an infection triggers our body's immune system to attack our vital organs.
Good Hope Hospital has pioneered best practice for its treatment.
Doctors here are alert to the symptoms of the condition and know to treat it with an immediate course of antibiotics.
So, how important are antibiotics to you in the work that you do? Well, they're critically important, they are the single most effective life-saving intervention in patients with sepsis.
Blood tests will help to establish the infection that has triggered Elizabeth's sepsis, but she needs treatment, fast.
Sepsis already kills 40,000 people in Britain every year.
Resistance is already a huge problem.
As many as 40% of cases of sepsis are known to be caused by E.
coli.
More than 40% of E.
coli in some laboratories are now resistant to first-line antibiotics.
And the effectiveness of all our antibiotics is becoming more and more uncertain.
But it's not too late to take action.
There are things we can all do to defeat the superbugs.
The most well-known superbug is MRSA.
Just a decade ago, it was killing thousands every year.
Nothing matters until it becomes personal.
Derek Butler is one of the people who helped us to fight back.
His stepfather, John, was in hospital when he contracted MRSA and he died in the midst of the outbreak in 2003.
John wasn't just my stepfather, he was my best friend.
And on the day that he died, we had a telephone call from the hospital to say that he was deteriorating quite rapidly.
Just minutes before he died, he opened his eyes and looked at me and I just said, "Just go, son.
" "Just let go.
" "Don't fight it any more, just go.
" And with that, he took his last breath, and I held his head in my arms, and it was heartbreaking.
I can't say anything else than that.
When John was dying, I said to him, "You will not be forgotten" and that, "Your death will not be in vain" - and we have to learn the lessons of the past.
We have to learn that this cannot carry on, because there are others, besides John, that have been lost to health-care infections that are untreatable.
Derek's wife, Maria, lost her mother to MRSA, too.
My dad misses her terribly.
You never know when you're going to need an antibiotic and you don't want to be in the position, that our family was in.
Derek now helps run the charity MRSA Action UK.
They campaigned for improved hygiene and screening in hospitals.
Alongside initiatives by both the NHS and government, the impact was quick and dramatic.
Deaths in the UK from MRSA have dropped by 80% from their peak in 2006.
The story of MRSA shows that if we change the way we do things, we can find success, in our battle against bacterial resistance.
This is a war we cannot win.
But it's one we cannot afford to lose, either.
And for me, that's the key in this.
We have to keep striving to keep ahead of the bacteria.
They're not politicians.
They're not scientists.
They're just ordinary people, who have had tragedy in their lives, and as individuals, every one of us can actually play a role, in what Derek says is a battle we just can't afford to lose.
So, what can we all do to help? I'm at Oxford University, at the labs where the early work was done on turning Fleming's penicillin into a prescription drug.
At the Sir William Dunn School of Pathology, Susan Lea says the answer's quite simple.
Good hygiene.
Washing your hands for 20 seconds, but hardly any of us spend anything like that! Susan, I think we're all aware that we really should wash our hands when we've been to the bathroom, but in general, what are we doing actually when we're washing our hands? What's the purpose of it? The primary purpose is to actually just wash the bacteria away physically, and the reason we want to do this is that we touch our hands to our face, we touch our hands to things other people touch, and we can communicate things if we don't wash them away.
And why is it so important that we do it when we've been to the bathroom? When we've been to the bathroom, we have the potential bacteria which normally live inside of us that have been transferred to the outside and if we don't wash them off our hands, we spread them further around, both on ourselves and on the environment, for others to pick them up and this is potentially unhealthy.
Many of us wash our hands and clean surfaces with antibacterial soaps, wipes and sprays.
They may kill 99.
9% of bacteria, but as the Harvard experiment showed us, it's the few that survive that are the problem.
These products aren't antibiotics, but anything that attacks bacteria risks increasing resistance.
In fact, there's no need to kill the bacteria on us at all, you just need to wash them off, and for that, soap is effective and safe.
Does the water have to be hot? No, the hot is for our own comfort.
The bacteria don't like water, it's a hostile environment for them, being in water, but hot is just so that it's more comfortable for us.
We don't like plunging our hands in icy water.
So, water generally just drowns them? Yes.
They pop in water.
Now, is this a question of time or technique? What is the technique? I think it's a combination of both.
We need water and we need detergent, because these two things are unfriendly to the bacteria, and then we need to wash the entirety of our hands, and we need to make sure that we wash all the surfaces, including the backs, including between the fingers, and then the nails, don't forget about the nails.
They're a wonderful little haven for them to lurk in.
And if we do that - and then wash it off.
So, what difference does all of this actually make to our health? It's one of the few things that we can do as individuals to stop the spread of bacteria in our environment.
It's self-help for ourselves, self-help for our families, and it's help for our community and colleagues around us as well, and it's simple.
One of the biggest causes of resistance is overuse.
The more we use antibiotics, the less effective they become.
Between 2000 and 2015, global antibiotic use went up by a staggering 65%.
Yet in Britain, it's estimated that almost a quarter of prescriptions are totally wasted.
Patients often demand antibiotics when GPS have no way of checking if we really need them.
So, how can we test if an infection is caused by bacteria, which means we need antibiotics, or a virus, which means we don't? In a village in the Lancashire countryside, one GP surgery has been carrying out a brand-new trial of a machine that can do just that.
And soon, we could see it in use in every surgery across the country.
The machine carries out a simple blood test to measure something known as CRP, a protein that shows the body's response to infection.
High levels indicate a bacterial infection, a low level and you're more likely to be suffering from a virus.
We take a drop of blood, similar to when our diabetics take their blood sugars, and we load it into a cartridge and it tells us the level.
We'll just prick your finger.
- Tiny bit of blood.
- Tiny bit of blood.
And we just have to hold this there.
Until it's full.
In the machine.
And how long is that going to take? It'll take about three minutes.
So, during this time, what we're usually doing is having a conversation with the patient - what we do, depending on the result.
So, we use a level of 20.
If that level is less than 20, we know categorically that there's no inflammation going on anywhere in the body.
Between 20 and 100, there could be, and over 100, there almost certainly is.
So, those patients, we usually would recommend a prescription of antibiotics.
But how do you deal with a patient who sits where I am now and says, "I want an antibiotic.
" I suppose they may get frustrated, because historically, they've known that every year, they've had a course of antibiotics and they've perceived themselves to have got better.
The classic phrase that you get is, "This cold has gone to my chest, Doctor.
" If the infection is viral, antibiotics are useless.
Demanding them, just increases the risk of resistance.
Our number-one rule in medicine is to do no harm, and at the moment, by issuing antibiotics inappropriately, we could potentially be doing harm for our future generations.
BEEPS Does that tell us it's done? It is, it's done.
So, your CRP level is seven, which is normal.
- Perfectly normal.
- Perfectly normal.
What difference has this machine made to the amount of antibiotics that you're now prescribing from this surgery? What we've noticed is that over the winter months particularly, when we tend to see more respiratory infections, our antibiotic levels have fallen drastically.
So, when you say you've had a reduction, what sort of numbers? Over one particular month, we saw as many as 1,000 less respiratory antibiotics from 2017 to 2018.
That's one heck of a drop, isn't it? It is, it is.
I'm told that the cost of the test at the moment is a lot more expensive than a course of antibiotics, but that really is a very short-term view.
Surely, it's the high-cost of antibiotic resistance that's going to be so much greater in the long run? But if you're determined to get antibiotics, then you can still obtain them online, without ever seeing a doctor.
This kind of misuse can only add to the risk of resistance.
How can we possibly tell if we have an infection? And even if we do, do we know whether or not it can be treated by an antibiotic? That kind of self-prescribing really is, a complete, waste of time! You could just be throwing your money away on something that's going to do you no good at all.
But the problem of overuse isn't just the number of antibiotics prescribed.
It's also the type of antibiotic.
It's very hard to isolate the specific bacteria causing an infection without detailed and time-consuming blood tests.
But one bad apple does not spoil the whole bunch.
We commonly use what's known as broad-spectrum antibiotics.
They attack a wide range of bacteria, to make sure of targeting and killing the cause of the infection, but that means getting rid of everything in its path.
Narrow-spectrum antibiotics attack specific bacteria, allowing more targeted use.
Better targeting means less unnecessary exposure, and that means less resistance.
So, what if doctors knew exactly which narrow-spectrum antibiotic to prescribe? I've gone back to my home county of Devon, where new technology is being developed to pinpoint bacterial resistance, so that we can do just that.
Doctor Tina Joshi has found a way of using the DNA in bacteria to work out, in just minutes, which antibiotics are likely to be most effective.
She uses microwaves to break down the bacteria and isolate its DNA, but as the DNA in bacteria is too small to be seen by the naked eye, she's showing us how the process works using something which is packed with DNA that we can see.
Strawberries.
Strawberries have eight times the amount of DNA inside of them compared to a normal cell.
Now, when we look at bacteria, they're on a nanoscale, we can't see the DNA inside of them.
Which is why we're in the middle of this wonderful strawberry patch here in the Devon countryside with a microwave! Yes, that's exactly right.
Because that's an important part of what you're going to do? Yes, it is.
It's actually going to break open some of the cells within the strawberries, that's what we are going to be doing.
We're going to see the DNA? We're actually going to see the DNA.
- How are you going to do it, then? - So Just take some strawberries.
Mash them up.
Yeah.
And put them in the microwave.
The microwaves are actually breaking open the cells, releasing that DNA, and we'll be able to see that by just adding a bit of alcohol in a minute.
So, what you can see here is just a bit of strawberry gloop.
Gloop, that's a technical term? It is, a scientific technical term! So, I'm going to add some alcohol here.
- Yeah.
And what you're going to be able to see, very shortly, is this.
- Is that DNA? - This is DNA .
.
that's come out of the strawberry.
- Fascinating.
- Wow! - That's the DNA! - That's the DNA coming out.
It's quite crude.
It's not purified.
And it's the white stuff that you can just see.
Tina is using the same technique on bacteria, and she's got the rest of her equipment back at the lab.
At Plymouth University, she's developing a diagnostic device that will allow doctors to pinpoint bacterial resistance in minutes.
And that's the beauty of this, it's going to be small and hand-held, something like a mobile phone.
Tina's invention will take an infected blood sample and a built-in miniature microwave will isolate the DNA.
This will then be analysed using Tina's breakthrough, a sophisticated sensor chip.
Any doctor will be able to get a diagnosis within minutes, with the results shown in an easy to understand display.
And it will be like a traffic light system.
In the timeframe of a five-minute doctor's appointment, the GP can say, "Ah, I'm going to prescribe you this narrow-spectrum antibiotic, that's actually going to treat you.
" And it should really assist the clinician in appropriate prescribing.
It'll take two more years to develop a prototype, but Tina is already generating significant interest from investors in new technology.
And when her machine does arrive, it will be a key weapon in our struggle against bacterial infection.
The first antibiotic, penicillin, was discovered really by accident back in 1928 and it then took more than a decade for them to work out, how they could mass-produce it.
Since then, of course, a lot more antibiotics have been discovered, but they can almost all be grouped into just seven antibiotic families, and they were all discovered in the 20th century.
And that's part of the problem.
Because we're now in the 21st century.
Think of it as a race.
Us against bacteria.
At first, pharmaceutical companies developed one new medicine after another.
Each new drug was a weapon against new forms of infection.
Penicillin was the first-ever antibiotic, in 1928.
New families of antibiotics followed, each capable of fighting different forms of infection.
But the stark truth is that the drugs companies have not kept pace with bacterial resistance.
The '50s, the '60s and '70s saw great strides made, each new drug strengthening our hand.
But in the '80s, we dropped the baton spectacularly.
The drugs companies have not discovered any new families of antibiotics, since the mid '80s, a gap of more than 30 years, during which time, bacteria have been free to develop resistance to the antibiotics we already have.
I need to find out why the pharmaceutical companies stopped.
Since the 1980s, they've found new ways of fighting cancer, HIV and heart disease, to name just three other killers.
Did they really believe, that they'd won the war against bacteria? At the headquarters of the Association of the British Pharmaceutical Industry, I'm meeting head of research, Sheuli Porkess.
She tells me the steps that are needed to make a new drug.
You start with a number of different medicines and then because for each medicine, each antibiotic, you need to show that it works and that it's safe, and that it can be made to the right quality.
A number of antibiotics that you try to develop won't meet those standards and that's why the process takes 8-12 years.
8-12 years? No quick-fix, then.
Roughly how much would an antibiotic cost to bring to market? From the science through to a medicine you can actually give to a patient, is of the order of hundreds of millions of pounds, yes.
And that's where the problems start.
How can we get more investment into research and development in antibiotics, understanding that actually, you might be developing a medicine that you hope will only be used in very limited circumstances? If bacteria aren't exposed to a new drug too often, there's less chance of them developing resistance, keeping the drug effective.
So, presumably, it's not going to be financially viable, sometimes, for you to come up with that antibiotic? In the case of antibiotics, where you're developing a medicine which you hope will only be used in very rare cases, we need a different way of looking at the investment.
The pharmaceutical industry seem to be saying that if they can't actually make any money out of a new antibiotic, then it's not exactly high on their list of priorities.
But as clearly we do desperately need new antibiotics, then that raises a fundamental issue that needs sorting.
Who's going to pay for them? The woman who may have the answer made headlines warning that we face an antibiotic apocalypse.
She's Chief Medical Officer, Dame Sally Davies.
What we need to do is separate paying for the research from the money that companies get for manufacturing and selling the drugs.
We need to fund it in a way that they will make them, and we hold them and use them where they will have most effect, and they are not abused.
But we're not talking about a one-off, quick-fix payment.
Even if we gee up the system to produce new drugs, we will need to do that for ever, not just now, and crack it, and feel complacent, as we have done for the last 30 years, but every decade, we will need more.
So, how long have we got before the apocalypse - a time when bacterial-resistant infections run rife, and millions of people die? Well, Asia is on the brink, so they've got, perhaps ten years.
Maybe that gives us another five, ten, at maximum.
That's not very long.
Is that long enough for the pharmaceutical companies to come up with this new family of antibiotics that will confound the bacteria? It is if they get down to it.
But we have yet to make the move.
What's it going to take, then, to make pharmaceutical companies come up with a new family of antibiotics? Money.
They want money.
Then they'll put their people to it, and I have no doubt, when they really go for it, they can find things.
If Dame Sally is right, then we need government and the pharmaceutical companies to get together and work out exactly how we can fund the development of new antibiotics as soon as possible.
And in the meantime, well, I would just like to see who has actually already picked up the baton.
Who is looking for those new antibiotics right now? Many antibiotics come from the natural world around us, because Mother Nature has already done the job for us.
Alexander Fleming's discovery in 1928 was a complete accident.
He found a mould growing on a Petri dish.
The mould was killing bacteria.
He'd discovered penicillin.
Penicillin is a fungus, but many antibiotics are made by bacteria themselves.
It's their own form of self-defence against other bacteria.
So, scientists can look anywhere for new antibiotics where bacteria thrive, including on us.
Now, to find out how many bacteria are living on me at the moment, I'm going to make a print of my hand in this Petri dish.
At the Liverpool School of Tropical Medicine, Doctor Adam Roberts is showing me the bacteria present on my own skin.
What did you discover? We found quite a wide array of different bacteria from your hand.
I mean, that is my hand.
I'm crawling with those bacteria, am I? Not just me, everybody else.
Everybody.
It's normal.
They live with us all of the time.
We've evolved together.
Adam is running a project to harness the power of bacteria, asking people to send him samples from wherever bacteria might be growing.
He's hoping to repeat the happy accident that gave us the first-ever antibiotic, penicillin.
What I wanted to do was to engage the public, but what I also wanted to do was to recreate that randomness that Alexander Fleming encountered when he was working on penicillin, and I thought, "What better way of combining those two, than asking the public to decide where we look for bacteria which may produce antibiotics themselves?" He calls his project Swab and Send, and we have enlisted the help of these wild swimmers to take part.
Our volunteers lost a friend to a bacterial infection.
It's the kind of thing that can affect anybody, healthy, unhealthy person, it doesn't really matter.
They're taking swabs where bacteria breed.
If people send random samples from places filled with bacteria, we might find the next penicillin.
My boyfriend's mum, she has a lot of problems with repeat infections and she's always on antibiotics, and they're just not working, and it's a horrible, horrible situation, so We've asked these swimmers to choose out-of-the-ordinary places to collect samples.
It's something we need to wake up to.
If we don't do something, it's going to be the next cancer.
One of our Swab and Send samples just might be the source of a new antibiotic.
I am delivering them to Adam for analysis, but not before taking some samples of my own.
Should be nice and filthy up here, I think.
Yeah.
That's pretty good.
Well, I've brought the swabs from the wild swimmers, Adam, and these are the couple that I've done today.
- What are we going to do with them? - Excellent.
So, the first thing we'll do is put these onto agar plates, - to see what grows on there.
- OK.
What Adam hopes to see are clear circles like these on earlier samples.
It's a sign of one bacteria being attacked by the antibiotic activity of another.
When we talk about activity, we're talking about this, these zones of inhibition.
So, that tells us that that strain is talented.
Talented? Oh, I love that! So, we call it talented if it's producing something of interest.
There's no bacterial activity there in that bit because the bacteria have been killed off.
Where did this come from? That one was from a school cupboard.
This is one of the largest zones of inhibition - off the dirt on a magnifying glass.
The bacteria in the middle was isolated from a broken tooth.
Adam's right.
It could easily be a random sample that strikes gold.
So, who knows? It could be something from the samples I've taken, or the wild swimmers, that actually comes up with the basis for a new antibiotic? Quite possibly.
It'll take two weeks for our samples to grow, so I'll be back when Adam has the results.
Industry also has its part to play in the fight against antibiotic resistance.
Around the world, more antibiotics are used in farming than anywhere else.
A staggering 80% of all the antibiotics are given to livestock, and that means that farming practices have a huge impact on antibiotic resistance.
Here in Britain, we have some of the toughest regulations over their use.
But that's not true of every country.
Antibiotics prevent livestock catching and passing on infections.
In some countries, farm animals are given them as a matter of course, and there's an unexpected side-effect.
Some antibiotics make animals grow larger, quicker, and that's good for profits.
So, rather than using fewer antibiotics, some countries are using even more.
Now, that's causing a problem.
Resistance is passing from those bacteria that infect animals to the bacteria that can do harm to people.
And that increases the risk to every one of us.
The regulations in Britain and Europe are helping set the standard, and others are already following.
For example, China has now banned the use of antibiotics as a growth-promoter for pigs.
Scientists at Cambridge University have been looking at other ways of reducing the use of antibiotics in agriculture.
Not in its libraries or even its laboratories, but, here, at the University of Cambridge farm.
Farmers usually milk dairy cows for six months at a time.
They then give them a three-month rest or dry period.
It's during this time that it's common for them to get udder infections, like mastitis.
Usually, antibiotics are used to prevent this.
But this cow, which is used to this veterinary procedure, is part of a trial aimed at keeping cows healthy without resorting to antibiotics.
Traditionally, all cows are given an antibiotic into the udder.
Just to prevent any mastitis occurring in that period.
- That's what you use to do.
- That's what we used to do.
But now, all we need to do is stop any bacteria getting in By effectively plugging the teat? Exactly, so we're putting a sealant in, just to act as a barrier to stop any new infections getting in.
- No need for antibiotics? - No need for antibiotics.
Perfect.
And that'll last for how long? That'll last for the whole dry period, so she'll be dry until July now, so, two months' time and then when she starts milking, that sealant will just strip out with the first milking.
Never been a farmer but I've been around a lot of farm animals in my time.
It's great to see that you can actually do something as simple as that, to keep this cow healthy without antibiotics, and keep the rest of the herd healthy, too.
Back in Liverpool, Adam Roberts has the results of our Swab and Send experiment.
What has he managed to grow from the samples that I delivered? He's been looking for what he calls isolates.
Isolated samples, capable of fighting other bacteria.
And he's got something surprising to show me from the bacteria he grew from my handprint in a Petri dish.
What have you found? We have found isolates that are able to kill MRSA - from your hands.
- Me? - Yeah, these are your bacteria isolates.
You can see the zones of inhibition around them? Yeah.
So, it's killing the MRSA.
It's extraordinary.
If it's novel, then there's no reason why that can't be developed into a medicine.
I'm reeling from the fact that I've got some kind of thing on my hands that might work against MRSA.
I find that quite extraordinary, I must say.
I did not expect my hand to harbour something that could help in the fight against bacteria, but what about the swabs? Did you find anything exciting on the stuff that you got from the swimmers? So, one of the isolates from the swimmers, I think it was here, inhibits Micrococcus luteus, which is another bacteria.
And this was from a life buoy in the lake.
How exciting is that for you to find that? It's really, really cool, actually.
It just shows that you can find antibiotics pretty much anywhere that you look for them, so, there's a huge untapped resource that we need to investigate.
These Petri dishes are just the first step in the complicated process of drug development.
How many lines of investigation has Adam found in the three years that he's been running this project? We've got thousands of different swabs from all over the world.
We're interested now in about 50 isolates which can kill MRSA, including yours.
We've got about 40 isolates which can kill E.
coli.
And that'll take how long before something like that is safe enough to be given to someone? So, that process is a lengthy one, and we're probably looking at about 20 years.
What happens in the meantime? In the meantime, we have to rely on the antibiotics that we've got, and hope somebody else comes up with some elsewhere in the world.
If drug development takes so long, I want to find out if there's anything that can help speed up the process.
I've heard of a project at Bristol University, using new technology that might help.
So, that's my next destination.
Dr Paul Race is growing bacterial samples from some of the most remote places on Earth, deep-sea sponges from the bottom of our oceans.
One of the interesting things about the work that we do in deep-sea sediments is our capacity to sample environments which have never even been looked at before.
So, areas of the ocean that people have never accessed, and our theory is that the bacteria that live in those environments have never been discovered before.
They're new and interesting and they make new and interesting, novel and natural products, which have antibiotic activity.
What Paul is studying is intriguing enough.
But it's the equipment he's using that might help in our race against time.
Paul doesn't use a Petri dish, instead he's 3-D printing its state-of-the-art replacement, the Isolation Chip or iChip.
The iChip harnesses the power of nature.
Once it's loaded with bacterial samples, it's buried in the same substance in which they were found.
So, an iChip full of bacteria from a deep-sea sponge is buried in sediment from the sea floor.
By maintaining contact with their natural surroundings, many more of the bacteria will grow in any one sample.
Up to 50 times more than in a Petri dish.
The beauty of this system is, it speeds up the discovery process, but also, our success rate in terms of recovering the number of new and interesting hits is much, much higher.
Thanks to the iChip, Paul is getting five times more leads to pursue.
You're getting them quicker? Yes.
Does that mean that also, then, we're likely to be discovering new antibiotics a lot quicker? That's the hope.
And certainly, the evidence that's available so far suggests this could be an incredibly powerful way to expedite that process of antibiotic discovery.
Paul has already found five new compounds that could lead to new antibiotics.
And he's not the only individual trying to harness the forces of nature to find antibiotics.
I've heard of an intriguing project taking place on the other side of the Atlantic.
So, my investigation now takes me overseas.
These are the swamplands on the Texas/Louisiana border.
I'm meeting someone who's hoping to find potential new antibiotics with a little help from .
.
alligators.
Mark Merchant is a professor of biochemistry at McNeese State University.
But he first noticed something special about alligators when he was just a little boy.
I'll tell you the story, I can remember when I was, I guess I was eight years old, maybe? I was fishing with my grandfather in a small canoe, and we were paddling along the bayou and I can remember going by quite a large alligator.
It scared me cos the alligator was probably three metres, three-and-a-half metres, this was a big one.
And it was completely missing its leg.
I can remember thinking, "That's a tough animal.
"In this environment, how does he feed, how does he get along "and compete with other alligators?" Of course, it wasn't until I'd been through graduate school, until I started thinking about why didn't that animal come down with some sort of infection? Because I spend a lot of time in the marsh and if I get a little scratch on my arm in that water, it gets red and puffy and highly infected.
There must be something amazing about the immune systems of these animals.
I've joined Mark on a research trip into the bayou.
He thinks alligators are protected by something special in their blood.
So, for the past 20 years, he's been taking alligator blood samples, thinking, if he can find out what works for them, it just might work for us.
Alligators are nocturnal, so we'll have to wait for it to get dark.
But it gives me a chance to ask a question that's been bothering me.
Isn't it risky for you doing this? Ah, it's not as bad as one might think.
We do this a lot, so, you know, I've still got them all! And what about the alligators? Oh, no, with the alligators, we take a blood sample quick.
Get some weights and measurements maybe, and put them right back, and we try to get them right back in the water to minimise the stress on the animal.
Well, the sun is going down, so we'd better get out there - and find some 'gators.
- Let's do it.
When it gets too dark for filming on our normal cameras, we switch to infrared.
There are hundreds of square miles of swamp for the alligators to hide in.
But then, there are thousands of alligators.
The hardest part for Mark is catching them, when all he's equipped with is a noose on a stick.
Then, we spot our first alligator.
There? There.
Although Mark is a past master at this, I've never before shared a small boat like this with a deadly predator.
All the power in an alligator bite is in the snap of its jaw.
So, a little tape is all Mark needs to keep it shut.
- OK.
- Right.
Mark has a special licence to do this and he takes such a small amount of blood, it doesn't harm the alligator.
The first alligator has done its bit.
What Mark has been pursuing is brand-new research, so he needs hundreds of samples to pinpoint exactly what it might be in the alligator blood that protects them from infection.
Then, he'll have to find out if it's effective on humans, and how to reproduce it.
After plenty of dead ends, Mark says he has now discovered two small proteins in the alligator blood that could become antibiotics.
And a pharmaceutical company has picked up his work, but how close they are to producing a commercially viable medicine is top secret, with millions of dollars at stake.
1,800 miles away, at Yale University in Connecticut, Dr Ben Chan is studying an alternative to antibiotics that's also found in the natural world - microscopic particles called phages.
These alien-looking, spiderlike viruses reproduce by killing bacteria.
The science of phages was developed in Eastern Europe in the 1950s, in countries that didn't have access to Western medicine or antibiotics.
As Ben has discovered, there are countless different phages to catalogue.
In a single millilitre of sea water, there's maybe a billion phages in it, so they are everywhere.
It looks a bit like a spider with these little legs, what are these for? These little feet here are what it uses to identify the host bacteria that it's going to infect.
So, it clings onto them? So, it clings on and then it shifts the whole thing down and it jams the DNA from here and it just goes .
.
and it injects it into the bacteria.
And when it injects that DNA into its host, it sets to work destroying the bacteria.
- So, you found a killer? - Yes, yeah.
So, if it bumps into the right bacteria, it can infect it, kill it, and produce 100 or so more that go on and find other hosts, other bacteria.
Though phages were discovered in the early 20th century and their use pioneered in Eastern Europe, in the West, scientists ignored them and instead pressed ahead with the development of antibiotics.
They were found before chemical antibiotics, but then when penicillin came along, a chemical that was pretty easy to administer, so we went in that direction.
Penicillin can affect a pretty broad spectrum of pathogens.
Whereas not one phage can affect all bacteria.
So, are you saying then that a phage is particular to a bacteria, in other words, there may be hundreds of hundreds of millions and billions of phages around, but there are similarly millions and millions of bacteria? You have to marry up the phage, you have to do that kind of, like a dating agency, you've got to find the phage that will kill a specific bacteria? Yeah.
So, Ben is constantly on the hunt, looking wherever bacteria thrive, and where phages are most active.
One of his preferred sources is the local sewage plant.
It'll take weeks to isolate the new phages, but back in the lab, Ben has something else remarkable to show me.
A Petri dish that had been covered with E.
coli, then treated with a phage.
Just look at it now! Ben, I don't think I've ever seen a Petri dish where whatever you've introduced has wiped out the bacteria completely.
That is a remarkable example of just how effective the phages can be.
Yeah, and they're able to do that because they replicate, right? So, they'll grow and grow and grow, and reproduce and produce many more particles until there's no more bacteria, and they can just wipe out an entire population.
- And there's no antibiotic involved in this at all? - Correct.
Wow! That is amazing.
So, why aren't we using phages in the UK? Well, as yet, they haven't undergone the necessary trials, but I've discovered a British woman who took it upon herself to get treatment.
I could understand it if it was just a prototype treatment somewhere.
But for something that's been used for so many years in other countries with great success, I just can't understand why it's not even looked at in the UK.
Susan Simpkiss has to look after her health.
Over 20 years ago, she developed a condition called bronchiectasis.
When a recurring chest infection stopped responding to antibiotics and threatened to overwhelm her, she turned elsewhere for help.
Doctors in Eastern Europe assessed her condition before the phages she needed were shipped to her from a clinic in Georgia.
And this is what came through the post? This is what came through the post and this is actually a bacterial phage and this is what you inhale via this nebuliser over a period of ten days.
I was able to go five months without another infection, which, to me, is a big bonus.
How long since you've been able to do that? Years.
How frustrating is it, then, for you to know that this is not something you can actually get here in this country? It's frustrating because it's not something that's been developed overnight.
They've been using it in the old Iron Curtain countries with great success.
There must be thousands affected by antibiotic resistance.
I just can't understand why there isn't an appetite to investigate it more.
Clearly, there's no way that I would advocate the use of unlicensed drugs here in Britain, but I think I'm beginning to share Sue's frustration that when it comes to phages, let's face it, they've been used for decades now in Iron Curtain countries, where they've been tried and tested and they work, and clearly, they worked for her.
And yet here in Britain, we don't seem to be prepared to give them at least a chance to help people like Sue, whose condition has become antibiotic resistant, and frankly, there is nowhere else to go.
Antibiotic resistance is one of the biggest threats facing us all today.
Yet, I've seen just how vital antibiotics are to our continued good health.
Thanks to antibiotics, sepsis patient Elizabeth Blunt survived her attack.
I've discovered it's not too late to act, as I've met some of the people showing us the way.
Individuals, looking for whole new families of antibiotics, with potential answers all around us in the natural world.
Living on my own hands, we've discovered a bug that could fight MRSA.
And I've learned we can all help by simply using the correct technique for washing our hands, and never demanding an antibiotic from our doctors.
But when the Chief Medical Officer is warning that we have perhaps 15 years before thousands more people start dying from antibiotic-resistant infections, we can only hope that we stop sleepwalking into an apocalypse.
But also, government and pharmaceutical companies really have to make a concerted effort to find those new families of antibiotics.
And frankly, they'd better get a move on, because we are running out of time.