Evolution (2002) s01e04 Episode Script
The Evolutionary Arms Race
NARRATOR: The cold war is history.
But Russia is in the grips of another arms race.
No warheads are involved.
The enemy is a microbe and the battleground is the human body.
The race between predator and prey is a driving force in evolution.
But this, too, is a predator.
And we are its prey.
Russia's crowded prisons have spawned the evolution of a deadly new microbe, resistant to our best medicine.
(men coughing in background) As it escapes prison walls it attacks new prey without preference, without warning.
(woman speaking Russian) TRANSLATOR: Like any medical student I knew about the disease.
I knew its symptoms.
But I had no idea it could be like this.
NARRATOR: Now the killer is spreading beyond Russia and everyone is fair game.
The arms race between humans and microbes cannot be won by drugs alone.
But if we learn to harness evolution we may reach a truce with our mortal enemies.
NARRATOR: On a misty morning, western Oregon seems a mild place fit for gentle creatures, like beaver and duck.
Yet this is home to one of the deadliest animals on Earth.
Local legend long hinted at its lethal power.
Eventually, a tale of untimely death attracted the scrutiny of science.
MAN: When I was an undergraduate student 37 years ago my professor told me a story about three hunters out here in the Coast Range being found dead and there was a newt boiled in their coffeepot.
That's a good one.
MAN: So his question to me was "Go find out if these newts are poisonous.
" NARRATOR: Edmund Brodie Jr.
has studied the rough-skinned newt ever since the last decade or so with his son, Edmund Brodie III.
It turns out the newt is extremely poisonous.
Its skin glands secrete one of the most potent toxins found in nature.
When ingested the toxin can paralyze a victim within minutes and shut down vital functions within hours.
An amount equivalent to a pinhead can kill an adult human.
BRODIE JR.
: This is probably the most poisonous animal in the world with enough skin toxin to kill tens of thousands of mice or perhaps a hundred people.
Of course, they don't bite so this isn't really dangerous holding it unless I were to eat it, which I won't.
The question was, why should a small animal like this be so many times more toxic than necessary to kill all predators? Why should a salamander evolve that much toxin? Yeah, I can smell the secretion.
Don't lick your hands.
(chuckling) I'll try not to.
NARRATOR: No environmental factor can explain the evolution of the newt's extreme toxicity.
The Brodies discovered another animal is responsible.
I'm going to head over to these brambles.
Okay.
NARRATOR: The common garter snake thrives in these parts.
Harmless to humans, it feeds on earthworms, frogs and toads.
But there's one prey in the snake's diet few other predators ever touch.
She's got a food item.
Oh, yeah.
Look at that.
It's a pretty big object.
I don't know if it's big enough to be a newt but it could be.
Come on, honey.
Here it comes.
Yeah, here it is.
Aha! How about that? It had eaten a full-sized male newt.
Yeah.
BRODIE III: This species of garter snake is the predator that we think is driving the evolution of the high toxin levels in the newts.
This is the only thing that can survive an encounter with a newt.
It's the only thing that can therefore represent a selective pressure for increasing toxicity.
As the snakes get better at resisting the effects of the toxin the prey has to evolve higher levels of toxin.
You can think of this as this sort of escalating- counterescalating arms race between the predator and the newt, the prey.
NARRATOR: But the toxin does take a toll.
Some snakes are slowed down.
Others are immobilized for a few hours after eating a newt.
(device beeps) NARRATOR: In the lab, the Brodies can measure the garter snake's resistance to the toxin.
They coax a baby snake down a track wired with motion sensors and record its time.
Time.
MAN: 3.
4.
NARRATOR: Then they inject the snake with a small amount of purified toxin to simulate the effects of eating a newt.
(device beeps) NARRATOR: Now the snake is raced again.
BRODIE JR.
: It's aggressive.
Sometimes when they can't crawl, they do that.
NARRATOR: A snake with low resistance can be stalled to a standstill.
MAN: 6.
3.
BRODIE III: Oh! (device beeps) NARRATOR: A resistant snake is much less affected by the toxin but it, too, pays a price.
The more resistant a snake the more slowly it moves without any toxin.
BRODIE JR.
: The snake experiences a cost from evolving the resistance.
That snake would be more susceptible to its own predators.
4.
1.
BRODIE JR.
: So there's a trade-off between speed in a snake and the level of resistance.
BRODIE III: All through Oregon, you've got this BRODIE JR.
: We were very surprised to see that the arms race is a predator evolving to a prey and a prey evolving to the predator.
And this has allowed us to get a better understanding of evolution.
It's now abundantly clear that evolution is driven not just by physical forces such as storms and fire and climatic change but much more by biological forces.
That is, particularly the way species interact with one another: cooperating with one another, parasitizing one another preying on one another.
NARRATOR: What made the lion fierce and the zebra fast? What sparked the development of tooth and claw? The deadly dance of predator and prey drives evolution.
Surely there was a time on an ancient savanna when hungry beasts hunted our ancestors.
Perhaps the hot breath of carnivores once drove our own evolution and made us faster, stronger or smarter.
But today, we have only one kind of predator left to fear.
Microorganisms that cause disease consume us from the inside out.
The human body is the food that fuels their rapid-fire reproduction.
Some bacteria can reproduce a million times more quickly than we do.
These microscopic predators have cast a long, dark shadow on our history.
The bacteria that cause tuberculosis riddled the bodies of Egyptian nobles over 4,000 years ago.
Another microbe spawned the dreaded Black Death.
In the 14th century bubonic plague killed one in three Europeans.
The influenza virus claimed some 20 million lives on the heels of World War I.
We were virtually defenseless against infectious disease until recently.
ANNOUNCER: This is a battlefield: a battlefield in man's total war against disease.
Here, man has locked his heaviest artillery against premature death: antibiotics, the miracle drugs of our time.
NARRATOR: In the 20th century scientists began to focus on the chemicals that microbes produce to attack each other.
Perhaps some of these compounds would kill disease organisms without harming the human body.
The first so-called antibiotic, penicillin saved countless lives in World War II.
Now doctors had a weapon to fight the infections that commonly killed soldiers wounded on the battlefield.
By the 1950s, hundreds of antibiotics were on the market.
Defeating deadly germs seemed like child's play.
In 1969, the U.
S.
Surgeon General declared it was "time to close the book on infectious disease.
" He spoke too soon.
(men coughing and speaking softly) NARRATOR: The Russian prison system is ground zero of a new epidemic.
An old killer is back with a vengeance.
Since the collapse of the Soviet Union Russia's incarceration rate has soared to the highest in the world.
More than one million inmates are confined to a penal system designed for a fraction of that number.
But overcrowding, poor nutrition and scant sanitation are not the worst of a prisoner's nightmares.
Now tuberculosis stalks these men.
The bacteria that cause TB can lie dormant for decades in a healthy person.
But if the immune system is weakened the microbes begin to multiply and consume the lungs.
MAN: Prisoners are malnourished.
Many of them are alcoholics.
Many of them are smokers.
And just the stress of being in prison all these factors together make you very, very susceptible to probably not only being infected with TB but also coming down with active disease.
NARRATOR: When a person with active TB coughs or even speaks he expels contagious droplets that linger in the air for hours.
The next victim needs only to inhale to be infected.
At least 100,000 inmates have active TB but antibiotics are in short supply.
Many men will die before their terms are up.
Sasha Belevich is serving time for his second burglary conviction in Tomsk a city in western Siberia.
His four-year term now seems like a death sentence.
(Belevich speaking Russian) TRANSLATOR: I never thought I'd be infected.
I never gave it much thought.
At first, I didn't believe what the doctor told me.
I thought that maybe it was any other illness but not tuberculosis.
NARRATOR: Diagnosed during his first prison term Sasha was given antibiotics.
He improved but after his release, he stopped getting treatment.
Now his TB is back, but the same drugs cannot cure him.
The microbes in his body have evolved.
When Sasha first took antibiotics the drugs killed off most of the TB bacteria.
But when his treatment stopped, it left some microbes alive, the ones that were most resistant to the drugs.
As these survivors multiplied all their offspring acquired that same resistance.
An entirely new strain of bacteria evolved untreatable with standard drugs.
(man speaking Russian) NARRATOR: Sasha is now beyond help by prison doctors.
He's not alone.
At least 30,000 Russian inmates have multi-drug-resistant TB and their numbers are growing.
This epidemic has brought Alex Goldfarb from New York back to his homeland.
Working with Russian authorities he's developing a pilot program in the Tomsk prison to change the way TB is treated.
GOLDFARB: This prison system is the ideal incubator for those drug-resistant strains.
Russians have been using inadequate treatment regimens.
Particularly in prisons, for the past decade they use a low quality drug they never finish the treatment course, and as the result these resistant strains are spreading on their own through coughing, and that's a major problem.
NARRATOR: For drug-resistant cases Goldfarb has a small supply of so-called "second-line drugs.
" Far more expensive than standard TB treatments second-line drugs can cause dangerous side effects.
But Goldfarb's supply won't even begin to cover 300 inmates quarantined in the drug resistance ward much less all the cases just outside prison walls.
When a prisoner's term is up he's released into the heart of Tomsk; population: half a million.
Healthy or sick, he's now free to walk these streets and ride these buses with unsuspecting citizens.
(young woman speaking Russian) TRANSLATOR: Like any medical student, I knew about the disease.
I knew its symptoms.
But I had no idea it could be like this.
NARRATOR: Anna Kolosova doesn't know how she became infected with a strain of TB resistant to five drugs.
(speaking Russian) TRANSLATOR: I found out completely by accident.
I went to take my driving test and I had to have a medical exam.
They took an X ray and they told me I had tuberculosis.
NARRATOR: Six months later, she began coughing up blood.
On leave from medical school she has been hospitalized ever since.
(speaking Russian) TRANSLATOR: If we had second-line drugs Anna's prognosis might be positive.
Without them, her prognosis is not positive in the least.
Anna's case is not unique.
In my care, I have another college student and other young patients with drug-resistant TB.
NARRATOR: Their symptoms can be eased.
Their active disease may subside for a time.
But the drugs that could save their lives are not yet within reach.
(speaking Russian) NARRATOR: For now, just 30 inmates will receive second-line drugs.
All have at least two more years to serve, a guarantee they'll complete their treatment and prevent the evolution of new drug-resistant bacteria.
Still, there's grumbling.
GOLDFARB: People are asking why you are spending $5,000 to $8,000 to cure or treat a convicted killer.
So we have to explain and explain and explain that we chose prisons for epidemiological reasons.
This is the hub where this problem can be addressed.
(speaking Russian) NARRATOR: A gesture of good faith, Goldfarb has removed his mask to address 30 men who are getting a second chance at life.
He tells them "The treatment we're offering you is no experiment.
"It has never been used in Russia "because it's too expensive.
"It's a complicated and painful process.
"For some of you, it will last a year and a half.
"But all of you must take this as seriously as possible and complete the entire course of your treatment.
" Belevich! NARRATOR: Sasha was a victim of evolution but now the odds are good he'll live out his sentence.
(Belevich speaking Russian) TRANSLATOR: I've got 2½ years left to serve.
I'm not afraid of the side effects.
I just want to get better, that's all.
NARRATOR: But in a facility for TB patients on the edge of town others remain prisoners of the disease.
(Kolosova speaking Russian) TRANSLATOR: The new drugs are the only hope we have.
There's nothing else to wait for.
It's the only thing I'm waiting for.
My family is very supportive.
They visit every other day, my mother and father, my grandparents.
I'm only 19.
I have to be optimistic.
NARRATOR: Siberia once seemed the most remote spot on Earth.
Not anymore.
Planes, trains and highways now crisscross Russia.
Strains of drug-resistant TB have spread to thousands of citizens and some are leaving the country.
KREISWIRTH: What's dramatically affected the spread of TB is our ability to travel.
All the strains that are in the Russian prisons among prisoners will eventually come to our doorstep.
NARRATOR: The global spread of TB is monitored in New York City at the Public Health Research Institute.
On the rise nearly everywhere, TB now rivals AIDS: it claims two to three million lives a year.
TB bacteria collected worldwide help researchers chart the evolution of new strains.
DNA extracted from the bacteria can be displayed in a bar code pattern, a genetic fingerprint of the enemy, for Barry Kreiswirth.
KREISWIRTH: We've been able to look literally at the DNA from the bacteria and we use this as a detective story.
We can go from bacteria to bacteria which infect different people and ask, are these bacteria the same? Are we getting one person who is spreading his or her strain to many others? Based on our fingerprint database we've actually seen the most prominent strain that is running rampant throughout the Tomsk prison already in the U.
S.
Hi, Barry, what's up? Look at this.
NARRATOR: Kreiswirth shares this grim discovery with Alex Goldfarb.
So this is a fingerprint of that 148 strain that we see all over the Tomsk prisons, that multi-drug- resistant strain.
Look at this one: same exact pattern.
But this isn't from the prison; this is from a New York patient we received from the Department of Health in New York City.
It's identical.
Is he a Russian? Well, this is a Russian who has MDR-TB.
So I think it's a nice find but it's a scary one, too.
NARRATOR: How long before another traveler carries drug-resistant TB to New York or any other city? How long before others are infected? If an epidemic erupted most cities would be caught unprepared: not enough personnel trained to diagnose and treat TB; no stockpiles of second-line drugs; and TB is just the tip of the iceberg.
The microbes that cause malaria, pneumonia, gonorrhea and scores of other infectious diseases are also evolving drug resistance.
Misuse of antibiotics is one cause.
Overuse is another.
In the United States, nearly half of all prescriptions are unnecessary or inappropriate.
KREISWIRTH: We've created this problem.
Multi-drug resistance is a manmade problem.
And we do that by putting antibiotics in animal feeds we have antibiotics running rampantly through hospitals we have antibiotics in the environment.
By developing as many antibiotics that we have over the last 50 years we've essentially accelerated an evolutionary process.
The outcome is that we're going to have more drug-resistant microbes to the point where some of the most dangerous bacteria will not be treatable.
We're racing against the microbe every day and unfortunately we're losing.
NARRATOR: It's an arms race without end.
The more drugs we launch at microbes the more resistance they evolve.
Maybe it's time to change our strategy.
If we can drive microbes to evolve drug resistance then we can also make them evolve in ways that benefit us.
This is the radical proposition of Amherst biologist Paul Ewald.
EWALD: When people are looking at the antibiotic resistance problem they see evolution as sort of the the bad guy.
It's the evolutionary process that's led to antibiotic resistance and that's true.
But, just as easily, we can have evolution being the solution.
In other words, we can have evolutionary processes leading to organisms becoming more mild.
NARRATOR: Disease organisms evolve to be more or less harmful depending on how they are spread.
Microbes that depend on close contact between people tend to be mild.
EWALD: The rhinovirus that causes a common cold is transmitted by people walking around sneezing or coughing on other people.
Since it really does depend on fairly healthy people to be transmitted not surprisingly, it's one of the mildest viruses that we know about.
NARRATOR: But microbes that are transmitted by insects or by tainted food or water tend to make people very sick.
EWALD: The worst of all of the diarrheal bacteria that we know of have been waterborne.
The bacteria that cause cholera and typhoid fever are often waterborne.
So even if the organism is so harmful that the sick person can't move from bed the organism can still be transmitted to large numbers of people.
Once we understand the factors that favor increased harmfulness and decreased harmfulness then we can look at all of the things we do in society and we can ask the question: Are we doing certain things or can we do certain things that would favor organisms evolving towards mildness? We can look at the cholera outbreak in South America as a kind of natural experiment that allows us to evaluate these ideas.
NARRATOR: In 1991, cholera invaded Peru and spread quickly.
Over the next five years, more than one million people were stricken with diarrhea and vomiting, some severely.
Over 10,000 people died.
The disease was transmitted through water contaminated with human waste or through food that was washed or handled by infected people.
Ewald collected strains of cholera bacteria from South America and measured the amount of toxin they produced, an indication of their virulence.
Over time, he would document evolution in action.
EWALD: If you have contaminated water, allowing transmission we expect the cholera organism to evolve to a particularly high level of harmfulness and that's exactly what we see.
We find that the bacteria that had invaded countries with poor water supplies evolved increased harmfulness over time; they've actually become more toxigenic, they produce more toxin than they did at the outset.
If, instead, we clean up the water supplies then we force the bacteria to be transmitted only by routes that require healthy people.
And what we find is that when cholera invaded countries with clean water supplies the organism dropped in its harmfulness.
Those bacteria evolved lower levels of toxin production; they actually became more mild through time.
People would still be getting infected but the infections would be so mild that most people won't even be sick.
So, the cholera outbreak in Latin America suggests that we may need only a few years to change the cholera organism from one that would often kill people to one that hardly ever causes the disease.
What we're suggesting here is that we can domesticate these disease organisms, very much in the same way that we have domesticated other organisms that are potentially harmful.
For example, wolves have been harmful to us throughout our evolutionary history but through domestication some wolves have evolved into dogs that instead of harming us, actually help us.
And I think we can do the same thing with these disease organisms.
NARRATOR: Working with evolution instead of against it we might eventually subdue even the deadliest microbes.
Evolution has already forged such surprising truces.
WOMAN: Okay.
NARRATOR: Most wild cats have evolved a way to live with a virus closely related to one that is decimating humans.
The story was unraveled by Stephen O'Brien, here at the National Zoo to examine a tranquilized cheetah.
Well, we originally became interested in the cats because I was interested in the interplay between infectious diseases and the genes of the species that suffer them.
We began working with cheetahs and subsequently started to study each of the 37 different species in the cat family.
What we're learning from them is that they are mirrors of evolutionary processes in humans.
NARRATOR: It all began in the 1980s when O'Brien became concerned that small populations of endangered cats were especially vulnerable to the ravages of infectious disease.
Then he heard that domestic cats were falling prey to a newly discovered and lethal virus: The Feline Immunodeficiency Virus, or F.
I.
V.
F.
I.
V.
is associated with very skinny and malnourished and wasting disease in house cats.
And that disease was the result of the collapse of the immune system.
So, the parallels with Human Immunodeficiency Virus were very strong.
I was curious as to whether or not the virus had also been able to infect nondomestic cats.
NARRATOR: O'Brien had collected biological specimens from thousands of wild cats around the world.
He began to screen them for the presence of the virus.
O'BRIEN: Well, when we did that in cheetahs from East Africa and the pumas in the Rockies and the ocelots down in the Andes and the lions in the Serengeti, it turned out that virtually every species of cats on the planet had been exposed to and infected with a version of Feline Immunodeficiency Virus.
Well, I was terrified because I thought that we were just a heartbeat away from a epidemic that was going to decimate some of these cats and, since 36 of 37 of these cat species are already considered endangered or threatened then this could be the final wallop.
NARRATOR: For years, O'Brien feared the worst.
He urged zoo keepers and game wardens around the world to test their animals for the virus and to watch for AIDS-like symptoms.
O'BRIEN: What we discovered, though, over time is that these cats were really not getting ill.
It was as if they had somehow come up with a resistance to a fatal virus.
NARRATOR: O'Brien's research suggests F.
I.
V.
first infected the cats' ancestors around one million years ago.
It decimated the animals but a few cats carried mutations that made them resistant to the virus.
These survivors passed on their protective genes to their offspring and to most wild cats alive today.
Over time, the virus may also have evolved into less lethal strains.
Today, wild cats and F.
I.
V.
have reached the end of a long evolutionary process and have adapted to each other.
Humans and H.
I.
V.
only recently embarked on the path that might eventually lead to a truce.
But the example of the wild cats convinced O'Brien there must be people endowed with mutations that protect them from H.
I.
V.
He set out to find them.
O'BRIEN: Over a ten-year period of time I quietly collected blood samples from 10,000 individuals that are high risk.
My colleagues and I extracted the DNA and we were stunned to discover a whopping mutation which protected against H.
I.
V.
infection.
And it was the first gene that we could definitively say was influencing the outcome of exposure to this deadly virus.
NARRATOR: Most people have receptors on their immune cells that allow H.
I.
V.
to dock and gain entry.
But people with the mutation discovered by O'Brien lack some or all of these receptors.
Infection by H.
I.
V.
becomes impossible.
The mutation is present in about ten percent of European Caucasians but completely absent in native African and East Asian peoples.
Something in the evolutionary history of Caucasians must have favored the survival of people with this mutation.
O'BRIEN: We've actually used precise dating techniques to date the last time such a selective pressure took place.
And that came out 700 years ago.
Well, if you look in the history books that was the time of a rather dramatic infectious disease a pandemic, which was the Black Death or the bubonic plague.
And at that time, a third of Europeans were wiped out.
NARRATOR: A mutation that saved people from the plague seven centuries ago may now protect their descendants from infection by H.
I.
V.
O'BRIEN: Today, when we scroll through the genes of cats or humans we discover that they're littered with these footprints of historic epidemics that have defined the survival of today's living species.
NARRATOR: We all bear the marks of our ancestors' struggle for survival but evolution is driven not just by conflict and competition.
Cooperation and teamwork have also ensured the "survival of the fittest.
" Toward the end of the 20th century biologists began to realize that there's another force equally important and responsible for the buildup of a great deal of the magnificent superstructure of the Earth's biodiversity.
And that is cooperation, what we call symbiosis, and, particularly, mutualistic symbiosis; that is, intimate living together of different kinds of organisms in which there's a partnership which benefits both of the partners.
NARRATOR: Nature abounds in symbiosis.
Many species depend on a partner for their very survival.
A grouper enjoys a cleaning as tiny shrimp eat the parasites on its skin.
Anemones give safe harbor to clownfish who bring food and chase off predators.
With nectar and pollen, flowers entice birds and bees to help fertilize them.
Most plants rely on fungi living on their roots to extract nutrients from the soil.
And grazing animals could not digest their diet without the bacteria that live in their gut and break down plant matter.
We, too, are symbiotic creatures.
Beneficial bacteria cover every inch of our skin and the length of our intestines.
They help digest food, produce vitamins and keep dangerous microbes out.
(forest buzzing with insect and animal calls) Symbiosis has deep roots in the history of life.
Some 50 to 60 million years ago just after the age of the dinosaurs two species formed a lasting bond here in the dense thicket that would become the Amazonian rain forest.
MAN: A big mature Atta nest.
NARRATOR: These huge mounds of earth are the product of that partnership, one that brought Ted Schultz and Ulrich Mueller to a remote corner of Brazil.
The unlikely excavators of all this dirt are leaf-cutter ants.
MAN: Look, they're bringing stuff in.
There're some foragers here starting.
Yeah NARRATOR: Leaf-cutter ants make their nests in underground chambers.
They emerge regularly to forage, blazing trails that extend hundreds of feet into the forest.
Most tropical plants are permeated with toxic chemicals, a deterrent against browsers.
The ants cut fresh vegetation, but they don't eat it.
They feed it to another organism.
Foragers carry their cargo down into the nest and turn it over to smaller worker ants.
They clean the leaf fragments and chew them into a pulpy mulch.
Leaf-cutters cultivate a fungus that breaks down the toxins in the leaves and swells with proteins and sugars.
This is the ants' food.
MUELLER: Both the ants and the cultivated fungus are dependent on each other for living.
The ants need the fungus as a food, they're dependent on it; you take away the fungus, they will die.
In reverse, the fungus cannot do without the ants.
So, it's a mutual co-dependency.
SCHULTZ: A mature colony of leaf-cutter ants can consist of as many as eight million individuals and they're the dominant herbivores of the New World tropics.
They take an estimated 15% to 20% of all the fresh vegetation.
A mature colony of Atta leaf-cutter ants are the equivalent of an adult cow sitting in the middle of the rain forest foraging on the vegetation in their immediate area.
NARRATOR: The entire rain forest is affected by the symbiosis of ant and fungus.
To understand how it evolved Schultz and Mueller collect ant nests throughout Latin America.
Here's one.
Where? Oh, yeah.
NARRATOR: An experienced eye can spot the subtle signs of a young nest founded perhaps six months ago when a new queen left home with a bit of fungus in her mouth and burrowed into the ground.
BOTH: There it is.
SCHULTZ: Beautiful.
MUELLER: Opening a nest is a very exciting moment.
Suddenly, the cavity opens and you see the fungus garden and then you may see the queen.
SCHULTZ: There's the queen.
MUELLER: Yes, there she is.
The size of a peanut.
MUELLER: What we've learned from studying the ants is that you can have a long-term existence, over 50 million years as an agriculturist.
There's clear parallels between the ant agriculture and the human agriculture.
Both types of societies are dependent on cultivation of some other organism and have very sophisticated procedures how to promote the growth of these organisms.
NARRATOR: But human farmers are plagued by pests in their crops while the ants' gardens seemed pest-free.
A century of research had concluded that the ants are probably so adept at weeding that no infestation can take hold.
A graduate student in 1998 Cameron Currie just didn't buy it.
I actually had some people tell me that looking at diseases in the ant gardens was kind of a silly project, that the ants maintained their gardens free of diseases and so why would you be going there to look for diseases? So I went out and collected ant colonies and then I isolated pieces of the garden to see what was there other than the fungus the ants cultivated.
NARRATOR: He cultured 1,500 fungus samples and the same aggressive mold kept showing up.
When he removed the ants from a nest he saw the mold devastate the fungus in a matter of days.
So the antsdidhave a pest in their gardens.
But how did they keep it so completely under control? Cameron began to wonder about a white, waxy coating on the body parts of some ants.
What really intrigued him were the ants working deep in the gardens that were covered with the stuff.
He asked the experts about it.
SCHULTZ: In the past people had just considered this to be some sort of nondescript secretion that was produced by the ants for unknown, probably uninteresting reasons.
And Cameron was the first to put this waxy secretion under the microscope and notice it was not inert and lifeless but it was actually alive.
NARRATOR: The "wax" turned out to be tangled mats of bacteria.
But what shocked Cameron was these were the same types of bacteria that produce half the antibiotics used in human medicine.
CURRIE: I remember my graduate advisor and I were laughing thinking that wouldn't this be exciting if these ants had been effectively using these bacteria for production of antibiotics for millions of years when humans only discovered this 60 years ago.
And we thought at the time that this was maybe a bit farfetched.
NARRATOR: Farfetched but true.
It seems the ants have been using antibiotics to control the pest in their gardens for some 50 million years.
So why hasn't the mold evolved antibiotic resistance? SCHULTZ: I think that the answer probably lies in the fact that the ants are using cultures of millions of cells of bacteria to produce these antibiotics.
And so these bacteria are evolving.
Likewise the pathogen that is the target of these antibiotics is also evolving, and it's an evolutionary arms race that has continued for 50 million years.
NARRATOR: And so the symbiosis of ant and fungus also includes the aggressive mold in the fungus garden and the bacteria living on the ants.
Nature is often more complex than it first appears.
WILSON: Scientists have just begun to understand how two species can interact, or three or four.
But they're a long way from understanding how thousands, or tens of thousands of species can interact to create the monumental ecosystems of the world, like rain forests and coral reefs.
And the most remarkable gap in our knowledge is in bacteria and other microorganisms because these make up the base of the living world.
We need them; they don't need us.
NARRATOR: And yet we do everything in our power to avoid microbes.
A barrage of new products states the message loud and clear: The only good germ is a dead one.
Are we making our world too clean? Consider the research of pediatrician Erika von Mutius.
Du musst feste einatmen, bitte.
Stelltest richtig fest Gut, noch mal.
NARRATOR: She treats allergies and asthma, conditions in which the immune system overreacts to harmless substances.
Rates of both disorders are on the rise in affluent, industrialized regions.
Perhaps children are growing up in surroundings too germ-free for their own good.
VON MUTIUS: Microbes do a lot of harmful things to us but they may also be important for our immune system to learn how to deal with the environment and how to tolerate and fight viruses, bacteria and infections.
NARRATOR: To understand the causes of allergies and asthma Von Mutius is conducting research in a place where these conditions are rare The Bavarian countryside.
She wants to sort out exactly which environmental factors may be protecting children who grow up here.
VON MUTIUS: The study we're doing is a comparison within little villages.
So we compare children who live on the farm to children in the same village who do not live on the farm.
NARRATOR: She has enlisted over 800 families with children between the ages of six and 12 to participate in a detailed survey of health and lifestyle.
Dann, wieviel Zeit VON MUTIUS: In each questionnaire, we asked for allergic conditions and then most importantly we asked for the contact to farm animals and farming activities.
(interview proceeding in German) NARRATOR: Her goal is to create a profile of environmental exposures for each child.
Her team analyzes dust samples from carpets and bedding throughout the house for the presence of animal hair, dust mites and microorganisms.
If the family keeps livestock samples from the stables are screened for microbes released in the shedding and droppings of animals.
The study is in progress but preliminary results suggest one very strong correlation.
VON MUTIUS: One of the factors that seems to be important is the contact to the livestock.
These children, the more they are in the stables, um and the earlier they are in the stables that this gives a protection against the development of allergies.
NARRATOR: High levels of microorganisms in the stables may help prime a child's immune system for life.
VON MUTIUS: Microbes have been around us always and probably we need to find a balance between eradicating the harmful effect of bacteria and maybe also taking the beneficial components of this.
But this is really into the future.
(cows mooing) NARRATOR: Our species evolved in a world awash with microbes crowded with other creatures.
We've only begun to understand the value of this heritage.
WILSON: Scientists and medical researchers who have focused on the subject are more and more in agreement that it's a big mistake for humanity to separate itself from the rest of the living world too much.
The vast majority of species out there are our friends; they're not our enemies.
And we not only benefit from them but as a whole, they are essential to our existence.
We're the fortunate heirs of more than three billion years of evolution that created this stupendous diversity.
We need to learn a lot more about the living world and the way that humanity itself is affecting evolution.
NARRATOR: Like all living things, humans are a product of evolution.
But we're the only species that knows it.
We alone can see into the distant past and marvel at the history of life.
We alone are beginning to understand that we can use evolution to shape the future for all of life.
More than anything else this unique vision may be what makes us human.
Continue the journey into where we're from and where we're going at the Evolution web site.
The seven-part Evolution boxed set and the companion book are available from WGBH Boston Video.
To place an order, please call:
But Russia is in the grips of another arms race.
No warheads are involved.
The enemy is a microbe and the battleground is the human body.
The race between predator and prey is a driving force in evolution.
But this, too, is a predator.
And we are its prey.
Russia's crowded prisons have spawned the evolution of a deadly new microbe, resistant to our best medicine.
(men coughing in background) As it escapes prison walls it attacks new prey without preference, without warning.
(woman speaking Russian) TRANSLATOR: Like any medical student I knew about the disease.
I knew its symptoms.
But I had no idea it could be like this.
NARRATOR: Now the killer is spreading beyond Russia and everyone is fair game.
The arms race between humans and microbes cannot be won by drugs alone.
But if we learn to harness evolution we may reach a truce with our mortal enemies.
NARRATOR: On a misty morning, western Oregon seems a mild place fit for gentle creatures, like beaver and duck.
Yet this is home to one of the deadliest animals on Earth.
Local legend long hinted at its lethal power.
Eventually, a tale of untimely death attracted the scrutiny of science.
MAN: When I was an undergraduate student 37 years ago my professor told me a story about three hunters out here in the Coast Range being found dead and there was a newt boiled in their coffeepot.
That's a good one.
MAN: So his question to me was "Go find out if these newts are poisonous.
" NARRATOR: Edmund Brodie Jr.
has studied the rough-skinned newt ever since the last decade or so with his son, Edmund Brodie III.
It turns out the newt is extremely poisonous.
Its skin glands secrete one of the most potent toxins found in nature.
When ingested the toxin can paralyze a victim within minutes and shut down vital functions within hours.
An amount equivalent to a pinhead can kill an adult human.
BRODIE JR.
: This is probably the most poisonous animal in the world with enough skin toxin to kill tens of thousands of mice or perhaps a hundred people.
Of course, they don't bite so this isn't really dangerous holding it unless I were to eat it, which I won't.
The question was, why should a small animal like this be so many times more toxic than necessary to kill all predators? Why should a salamander evolve that much toxin? Yeah, I can smell the secretion.
Don't lick your hands.
(chuckling) I'll try not to.
NARRATOR: No environmental factor can explain the evolution of the newt's extreme toxicity.
The Brodies discovered another animal is responsible.
I'm going to head over to these brambles.
Okay.
NARRATOR: The common garter snake thrives in these parts.
Harmless to humans, it feeds on earthworms, frogs and toads.
But there's one prey in the snake's diet few other predators ever touch.
She's got a food item.
Oh, yeah.
Look at that.
It's a pretty big object.
I don't know if it's big enough to be a newt but it could be.
Come on, honey.
Here it comes.
Yeah, here it is.
Aha! How about that? It had eaten a full-sized male newt.
Yeah.
BRODIE III: This species of garter snake is the predator that we think is driving the evolution of the high toxin levels in the newts.
This is the only thing that can survive an encounter with a newt.
It's the only thing that can therefore represent a selective pressure for increasing toxicity.
As the snakes get better at resisting the effects of the toxin the prey has to evolve higher levels of toxin.
You can think of this as this sort of escalating- counterescalating arms race between the predator and the newt, the prey.
NARRATOR: But the toxin does take a toll.
Some snakes are slowed down.
Others are immobilized for a few hours after eating a newt.
(device beeps) NARRATOR: In the lab, the Brodies can measure the garter snake's resistance to the toxin.
They coax a baby snake down a track wired with motion sensors and record its time.
Time.
MAN: 3.
4.
NARRATOR: Then they inject the snake with a small amount of purified toxin to simulate the effects of eating a newt.
(device beeps) NARRATOR: Now the snake is raced again.
BRODIE JR.
: It's aggressive.
Sometimes when they can't crawl, they do that.
NARRATOR: A snake with low resistance can be stalled to a standstill.
MAN: 6.
3.
BRODIE III: Oh! (device beeps) NARRATOR: A resistant snake is much less affected by the toxin but it, too, pays a price.
The more resistant a snake the more slowly it moves without any toxin.
BRODIE JR.
: The snake experiences a cost from evolving the resistance.
That snake would be more susceptible to its own predators.
4.
1.
BRODIE JR.
: So there's a trade-off between speed in a snake and the level of resistance.
BRODIE III: All through Oregon, you've got this BRODIE JR.
: We were very surprised to see that the arms race is a predator evolving to a prey and a prey evolving to the predator.
And this has allowed us to get a better understanding of evolution.
It's now abundantly clear that evolution is driven not just by physical forces such as storms and fire and climatic change but much more by biological forces.
That is, particularly the way species interact with one another: cooperating with one another, parasitizing one another preying on one another.
NARRATOR: What made the lion fierce and the zebra fast? What sparked the development of tooth and claw? The deadly dance of predator and prey drives evolution.
Surely there was a time on an ancient savanna when hungry beasts hunted our ancestors.
Perhaps the hot breath of carnivores once drove our own evolution and made us faster, stronger or smarter.
But today, we have only one kind of predator left to fear.
Microorganisms that cause disease consume us from the inside out.
The human body is the food that fuels their rapid-fire reproduction.
Some bacteria can reproduce a million times more quickly than we do.
These microscopic predators have cast a long, dark shadow on our history.
The bacteria that cause tuberculosis riddled the bodies of Egyptian nobles over 4,000 years ago.
Another microbe spawned the dreaded Black Death.
In the 14th century bubonic plague killed one in three Europeans.
The influenza virus claimed some 20 million lives on the heels of World War I.
We were virtually defenseless against infectious disease until recently.
ANNOUNCER: This is a battlefield: a battlefield in man's total war against disease.
Here, man has locked his heaviest artillery against premature death: antibiotics, the miracle drugs of our time.
NARRATOR: In the 20th century scientists began to focus on the chemicals that microbes produce to attack each other.
Perhaps some of these compounds would kill disease organisms without harming the human body.
The first so-called antibiotic, penicillin saved countless lives in World War II.
Now doctors had a weapon to fight the infections that commonly killed soldiers wounded on the battlefield.
By the 1950s, hundreds of antibiotics were on the market.
Defeating deadly germs seemed like child's play.
In 1969, the U.
S.
Surgeon General declared it was "time to close the book on infectious disease.
" He spoke too soon.
(men coughing and speaking softly) NARRATOR: The Russian prison system is ground zero of a new epidemic.
An old killer is back with a vengeance.
Since the collapse of the Soviet Union Russia's incarceration rate has soared to the highest in the world.
More than one million inmates are confined to a penal system designed for a fraction of that number.
But overcrowding, poor nutrition and scant sanitation are not the worst of a prisoner's nightmares.
Now tuberculosis stalks these men.
The bacteria that cause TB can lie dormant for decades in a healthy person.
But if the immune system is weakened the microbes begin to multiply and consume the lungs.
MAN: Prisoners are malnourished.
Many of them are alcoholics.
Many of them are smokers.
And just the stress of being in prison all these factors together make you very, very susceptible to probably not only being infected with TB but also coming down with active disease.
NARRATOR: When a person with active TB coughs or even speaks he expels contagious droplets that linger in the air for hours.
The next victim needs only to inhale to be infected.
At least 100,000 inmates have active TB but antibiotics are in short supply.
Many men will die before their terms are up.
Sasha Belevich is serving time for his second burglary conviction in Tomsk a city in western Siberia.
His four-year term now seems like a death sentence.
(Belevich speaking Russian) TRANSLATOR: I never thought I'd be infected.
I never gave it much thought.
At first, I didn't believe what the doctor told me.
I thought that maybe it was any other illness but not tuberculosis.
NARRATOR: Diagnosed during his first prison term Sasha was given antibiotics.
He improved but after his release, he stopped getting treatment.
Now his TB is back, but the same drugs cannot cure him.
The microbes in his body have evolved.
When Sasha first took antibiotics the drugs killed off most of the TB bacteria.
But when his treatment stopped, it left some microbes alive, the ones that were most resistant to the drugs.
As these survivors multiplied all their offspring acquired that same resistance.
An entirely new strain of bacteria evolved untreatable with standard drugs.
(man speaking Russian) NARRATOR: Sasha is now beyond help by prison doctors.
He's not alone.
At least 30,000 Russian inmates have multi-drug-resistant TB and their numbers are growing.
This epidemic has brought Alex Goldfarb from New York back to his homeland.
Working with Russian authorities he's developing a pilot program in the Tomsk prison to change the way TB is treated.
GOLDFARB: This prison system is the ideal incubator for those drug-resistant strains.
Russians have been using inadequate treatment regimens.
Particularly in prisons, for the past decade they use a low quality drug they never finish the treatment course, and as the result these resistant strains are spreading on their own through coughing, and that's a major problem.
NARRATOR: For drug-resistant cases Goldfarb has a small supply of so-called "second-line drugs.
" Far more expensive than standard TB treatments second-line drugs can cause dangerous side effects.
But Goldfarb's supply won't even begin to cover 300 inmates quarantined in the drug resistance ward much less all the cases just outside prison walls.
When a prisoner's term is up he's released into the heart of Tomsk; population: half a million.
Healthy or sick, he's now free to walk these streets and ride these buses with unsuspecting citizens.
(young woman speaking Russian) TRANSLATOR: Like any medical student, I knew about the disease.
I knew its symptoms.
But I had no idea it could be like this.
NARRATOR: Anna Kolosova doesn't know how she became infected with a strain of TB resistant to five drugs.
(speaking Russian) TRANSLATOR: I found out completely by accident.
I went to take my driving test and I had to have a medical exam.
They took an X ray and they told me I had tuberculosis.
NARRATOR: Six months later, she began coughing up blood.
On leave from medical school she has been hospitalized ever since.
(speaking Russian) TRANSLATOR: If we had second-line drugs Anna's prognosis might be positive.
Without them, her prognosis is not positive in the least.
Anna's case is not unique.
In my care, I have another college student and other young patients with drug-resistant TB.
NARRATOR: Their symptoms can be eased.
Their active disease may subside for a time.
But the drugs that could save their lives are not yet within reach.
(speaking Russian) NARRATOR: For now, just 30 inmates will receive second-line drugs.
All have at least two more years to serve, a guarantee they'll complete their treatment and prevent the evolution of new drug-resistant bacteria.
Still, there's grumbling.
GOLDFARB: People are asking why you are spending $5,000 to $8,000 to cure or treat a convicted killer.
So we have to explain and explain and explain that we chose prisons for epidemiological reasons.
This is the hub where this problem can be addressed.
(speaking Russian) NARRATOR: A gesture of good faith, Goldfarb has removed his mask to address 30 men who are getting a second chance at life.
He tells them "The treatment we're offering you is no experiment.
"It has never been used in Russia "because it's too expensive.
"It's a complicated and painful process.
"For some of you, it will last a year and a half.
"But all of you must take this as seriously as possible and complete the entire course of your treatment.
" Belevich! NARRATOR: Sasha was a victim of evolution but now the odds are good he'll live out his sentence.
(Belevich speaking Russian) TRANSLATOR: I've got 2½ years left to serve.
I'm not afraid of the side effects.
I just want to get better, that's all.
NARRATOR: But in a facility for TB patients on the edge of town others remain prisoners of the disease.
(Kolosova speaking Russian) TRANSLATOR: The new drugs are the only hope we have.
There's nothing else to wait for.
It's the only thing I'm waiting for.
My family is very supportive.
They visit every other day, my mother and father, my grandparents.
I'm only 19.
I have to be optimistic.
NARRATOR: Siberia once seemed the most remote spot on Earth.
Not anymore.
Planes, trains and highways now crisscross Russia.
Strains of drug-resistant TB have spread to thousands of citizens and some are leaving the country.
KREISWIRTH: What's dramatically affected the spread of TB is our ability to travel.
All the strains that are in the Russian prisons among prisoners will eventually come to our doorstep.
NARRATOR: The global spread of TB is monitored in New York City at the Public Health Research Institute.
On the rise nearly everywhere, TB now rivals AIDS: it claims two to three million lives a year.
TB bacteria collected worldwide help researchers chart the evolution of new strains.
DNA extracted from the bacteria can be displayed in a bar code pattern, a genetic fingerprint of the enemy, for Barry Kreiswirth.
KREISWIRTH: We've been able to look literally at the DNA from the bacteria and we use this as a detective story.
We can go from bacteria to bacteria which infect different people and ask, are these bacteria the same? Are we getting one person who is spreading his or her strain to many others? Based on our fingerprint database we've actually seen the most prominent strain that is running rampant throughout the Tomsk prison already in the U.
S.
Hi, Barry, what's up? Look at this.
NARRATOR: Kreiswirth shares this grim discovery with Alex Goldfarb.
So this is a fingerprint of that 148 strain that we see all over the Tomsk prisons, that multi-drug- resistant strain.
Look at this one: same exact pattern.
But this isn't from the prison; this is from a New York patient we received from the Department of Health in New York City.
It's identical.
Is he a Russian? Well, this is a Russian who has MDR-TB.
So I think it's a nice find but it's a scary one, too.
NARRATOR: How long before another traveler carries drug-resistant TB to New York or any other city? How long before others are infected? If an epidemic erupted most cities would be caught unprepared: not enough personnel trained to diagnose and treat TB; no stockpiles of second-line drugs; and TB is just the tip of the iceberg.
The microbes that cause malaria, pneumonia, gonorrhea and scores of other infectious diseases are also evolving drug resistance.
Misuse of antibiotics is one cause.
Overuse is another.
In the United States, nearly half of all prescriptions are unnecessary or inappropriate.
KREISWIRTH: We've created this problem.
Multi-drug resistance is a manmade problem.
And we do that by putting antibiotics in animal feeds we have antibiotics running rampantly through hospitals we have antibiotics in the environment.
By developing as many antibiotics that we have over the last 50 years we've essentially accelerated an evolutionary process.
The outcome is that we're going to have more drug-resistant microbes to the point where some of the most dangerous bacteria will not be treatable.
We're racing against the microbe every day and unfortunately we're losing.
NARRATOR: It's an arms race without end.
The more drugs we launch at microbes the more resistance they evolve.
Maybe it's time to change our strategy.
If we can drive microbes to evolve drug resistance then we can also make them evolve in ways that benefit us.
This is the radical proposition of Amherst biologist Paul Ewald.
EWALD: When people are looking at the antibiotic resistance problem they see evolution as sort of the the bad guy.
It's the evolutionary process that's led to antibiotic resistance and that's true.
But, just as easily, we can have evolution being the solution.
In other words, we can have evolutionary processes leading to organisms becoming more mild.
NARRATOR: Disease organisms evolve to be more or less harmful depending on how they are spread.
Microbes that depend on close contact between people tend to be mild.
EWALD: The rhinovirus that causes a common cold is transmitted by people walking around sneezing or coughing on other people.
Since it really does depend on fairly healthy people to be transmitted not surprisingly, it's one of the mildest viruses that we know about.
NARRATOR: But microbes that are transmitted by insects or by tainted food or water tend to make people very sick.
EWALD: The worst of all of the diarrheal bacteria that we know of have been waterborne.
The bacteria that cause cholera and typhoid fever are often waterborne.
So even if the organism is so harmful that the sick person can't move from bed the organism can still be transmitted to large numbers of people.
Once we understand the factors that favor increased harmfulness and decreased harmfulness then we can look at all of the things we do in society and we can ask the question: Are we doing certain things or can we do certain things that would favor organisms evolving towards mildness? We can look at the cholera outbreak in South America as a kind of natural experiment that allows us to evaluate these ideas.
NARRATOR: In 1991, cholera invaded Peru and spread quickly.
Over the next five years, more than one million people were stricken with diarrhea and vomiting, some severely.
Over 10,000 people died.
The disease was transmitted through water contaminated with human waste or through food that was washed or handled by infected people.
Ewald collected strains of cholera bacteria from South America and measured the amount of toxin they produced, an indication of their virulence.
Over time, he would document evolution in action.
EWALD: If you have contaminated water, allowing transmission we expect the cholera organism to evolve to a particularly high level of harmfulness and that's exactly what we see.
We find that the bacteria that had invaded countries with poor water supplies evolved increased harmfulness over time; they've actually become more toxigenic, they produce more toxin than they did at the outset.
If, instead, we clean up the water supplies then we force the bacteria to be transmitted only by routes that require healthy people.
And what we find is that when cholera invaded countries with clean water supplies the organism dropped in its harmfulness.
Those bacteria evolved lower levels of toxin production; they actually became more mild through time.
People would still be getting infected but the infections would be so mild that most people won't even be sick.
So, the cholera outbreak in Latin America suggests that we may need only a few years to change the cholera organism from one that would often kill people to one that hardly ever causes the disease.
What we're suggesting here is that we can domesticate these disease organisms, very much in the same way that we have domesticated other organisms that are potentially harmful.
For example, wolves have been harmful to us throughout our evolutionary history but through domestication some wolves have evolved into dogs that instead of harming us, actually help us.
And I think we can do the same thing with these disease organisms.
NARRATOR: Working with evolution instead of against it we might eventually subdue even the deadliest microbes.
Evolution has already forged such surprising truces.
WOMAN: Okay.
NARRATOR: Most wild cats have evolved a way to live with a virus closely related to one that is decimating humans.
The story was unraveled by Stephen O'Brien, here at the National Zoo to examine a tranquilized cheetah.
Well, we originally became interested in the cats because I was interested in the interplay between infectious diseases and the genes of the species that suffer them.
We began working with cheetahs and subsequently started to study each of the 37 different species in the cat family.
What we're learning from them is that they are mirrors of evolutionary processes in humans.
NARRATOR: It all began in the 1980s when O'Brien became concerned that small populations of endangered cats were especially vulnerable to the ravages of infectious disease.
Then he heard that domestic cats were falling prey to a newly discovered and lethal virus: The Feline Immunodeficiency Virus, or F.
I.
V.
F.
I.
V.
is associated with very skinny and malnourished and wasting disease in house cats.
And that disease was the result of the collapse of the immune system.
So, the parallels with Human Immunodeficiency Virus were very strong.
I was curious as to whether or not the virus had also been able to infect nondomestic cats.
NARRATOR: O'Brien had collected biological specimens from thousands of wild cats around the world.
He began to screen them for the presence of the virus.
O'BRIEN: Well, when we did that in cheetahs from East Africa and the pumas in the Rockies and the ocelots down in the Andes and the lions in the Serengeti, it turned out that virtually every species of cats on the planet had been exposed to and infected with a version of Feline Immunodeficiency Virus.
Well, I was terrified because I thought that we were just a heartbeat away from a epidemic that was going to decimate some of these cats and, since 36 of 37 of these cat species are already considered endangered or threatened then this could be the final wallop.
NARRATOR: For years, O'Brien feared the worst.
He urged zoo keepers and game wardens around the world to test their animals for the virus and to watch for AIDS-like symptoms.
O'BRIEN: What we discovered, though, over time is that these cats were really not getting ill.
It was as if they had somehow come up with a resistance to a fatal virus.
NARRATOR: O'Brien's research suggests F.
I.
V.
first infected the cats' ancestors around one million years ago.
It decimated the animals but a few cats carried mutations that made them resistant to the virus.
These survivors passed on their protective genes to their offspring and to most wild cats alive today.
Over time, the virus may also have evolved into less lethal strains.
Today, wild cats and F.
I.
V.
have reached the end of a long evolutionary process and have adapted to each other.
Humans and H.
I.
V.
only recently embarked on the path that might eventually lead to a truce.
But the example of the wild cats convinced O'Brien there must be people endowed with mutations that protect them from H.
I.
V.
He set out to find them.
O'BRIEN: Over a ten-year period of time I quietly collected blood samples from 10,000 individuals that are high risk.
My colleagues and I extracted the DNA and we were stunned to discover a whopping mutation which protected against H.
I.
V.
infection.
And it was the first gene that we could definitively say was influencing the outcome of exposure to this deadly virus.
NARRATOR: Most people have receptors on their immune cells that allow H.
I.
V.
to dock and gain entry.
But people with the mutation discovered by O'Brien lack some or all of these receptors.
Infection by H.
I.
V.
becomes impossible.
The mutation is present in about ten percent of European Caucasians but completely absent in native African and East Asian peoples.
Something in the evolutionary history of Caucasians must have favored the survival of people with this mutation.
O'BRIEN: We've actually used precise dating techniques to date the last time such a selective pressure took place.
And that came out 700 years ago.
Well, if you look in the history books that was the time of a rather dramatic infectious disease a pandemic, which was the Black Death or the bubonic plague.
And at that time, a third of Europeans were wiped out.
NARRATOR: A mutation that saved people from the plague seven centuries ago may now protect their descendants from infection by H.
I.
V.
O'BRIEN: Today, when we scroll through the genes of cats or humans we discover that they're littered with these footprints of historic epidemics that have defined the survival of today's living species.
NARRATOR: We all bear the marks of our ancestors' struggle for survival but evolution is driven not just by conflict and competition.
Cooperation and teamwork have also ensured the "survival of the fittest.
" Toward the end of the 20th century biologists began to realize that there's another force equally important and responsible for the buildup of a great deal of the magnificent superstructure of the Earth's biodiversity.
And that is cooperation, what we call symbiosis, and, particularly, mutualistic symbiosis; that is, intimate living together of different kinds of organisms in which there's a partnership which benefits both of the partners.
NARRATOR: Nature abounds in symbiosis.
Many species depend on a partner for their very survival.
A grouper enjoys a cleaning as tiny shrimp eat the parasites on its skin.
Anemones give safe harbor to clownfish who bring food and chase off predators.
With nectar and pollen, flowers entice birds and bees to help fertilize them.
Most plants rely on fungi living on their roots to extract nutrients from the soil.
And grazing animals could not digest their diet without the bacteria that live in their gut and break down plant matter.
We, too, are symbiotic creatures.
Beneficial bacteria cover every inch of our skin and the length of our intestines.
They help digest food, produce vitamins and keep dangerous microbes out.
(forest buzzing with insect and animal calls) Symbiosis has deep roots in the history of life.
Some 50 to 60 million years ago just after the age of the dinosaurs two species formed a lasting bond here in the dense thicket that would become the Amazonian rain forest.
MAN: A big mature Atta nest.
NARRATOR: These huge mounds of earth are the product of that partnership, one that brought Ted Schultz and Ulrich Mueller to a remote corner of Brazil.
The unlikely excavators of all this dirt are leaf-cutter ants.
MAN: Look, they're bringing stuff in.
There're some foragers here starting.
Yeah NARRATOR: Leaf-cutter ants make their nests in underground chambers.
They emerge regularly to forage, blazing trails that extend hundreds of feet into the forest.
Most tropical plants are permeated with toxic chemicals, a deterrent against browsers.
The ants cut fresh vegetation, but they don't eat it.
They feed it to another organism.
Foragers carry their cargo down into the nest and turn it over to smaller worker ants.
They clean the leaf fragments and chew them into a pulpy mulch.
Leaf-cutters cultivate a fungus that breaks down the toxins in the leaves and swells with proteins and sugars.
This is the ants' food.
MUELLER: Both the ants and the cultivated fungus are dependent on each other for living.
The ants need the fungus as a food, they're dependent on it; you take away the fungus, they will die.
In reverse, the fungus cannot do without the ants.
So, it's a mutual co-dependency.
SCHULTZ: A mature colony of leaf-cutter ants can consist of as many as eight million individuals and they're the dominant herbivores of the New World tropics.
They take an estimated 15% to 20% of all the fresh vegetation.
A mature colony of Atta leaf-cutter ants are the equivalent of an adult cow sitting in the middle of the rain forest foraging on the vegetation in their immediate area.
NARRATOR: The entire rain forest is affected by the symbiosis of ant and fungus.
To understand how it evolved Schultz and Mueller collect ant nests throughout Latin America.
Here's one.
Where? Oh, yeah.
NARRATOR: An experienced eye can spot the subtle signs of a young nest founded perhaps six months ago when a new queen left home with a bit of fungus in her mouth and burrowed into the ground.
BOTH: There it is.
SCHULTZ: Beautiful.
MUELLER: Opening a nest is a very exciting moment.
Suddenly, the cavity opens and you see the fungus garden and then you may see the queen.
SCHULTZ: There's the queen.
MUELLER: Yes, there she is.
The size of a peanut.
MUELLER: What we've learned from studying the ants is that you can have a long-term existence, over 50 million years as an agriculturist.
There's clear parallels between the ant agriculture and the human agriculture.
Both types of societies are dependent on cultivation of some other organism and have very sophisticated procedures how to promote the growth of these organisms.
NARRATOR: But human farmers are plagued by pests in their crops while the ants' gardens seemed pest-free.
A century of research had concluded that the ants are probably so adept at weeding that no infestation can take hold.
A graduate student in 1998 Cameron Currie just didn't buy it.
I actually had some people tell me that looking at diseases in the ant gardens was kind of a silly project, that the ants maintained their gardens free of diseases and so why would you be going there to look for diseases? So I went out and collected ant colonies and then I isolated pieces of the garden to see what was there other than the fungus the ants cultivated.
NARRATOR: He cultured 1,500 fungus samples and the same aggressive mold kept showing up.
When he removed the ants from a nest he saw the mold devastate the fungus in a matter of days.
So the antsdidhave a pest in their gardens.
But how did they keep it so completely under control? Cameron began to wonder about a white, waxy coating on the body parts of some ants.
What really intrigued him were the ants working deep in the gardens that were covered with the stuff.
He asked the experts about it.
SCHULTZ: In the past people had just considered this to be some sort of nondescript secretion that was produced by the ants for unknown, probably uninteresting reasons.
And Cameron was the first to put this waxy secretion under the microscope and notice it was not inert and lifeless but it was actually alive.
NARRATOR: The "wax" turned out to be tangled mats of bacteria.
But what shocked Cameron was these were the same types of bacteria that produce half the antibiotics used in human medicine.
CURRIE: I remember my graduate advisor and I were laughing thinking that wouldn't this be exciting if these ants had been effectively using these bacteria for production of antibiotics for millions of years when humans only discovered this 60 years ago.
And we thought at the time that this was maybe a bit farfetched.
NARRATOR: Farfetched but true.
It seems the ants have been using antibiotics to control the pest in their gardens for some 50 million years.
So why hasn't the mold evolved antibiotic resistance? SCHULTZ: I think that the answer probably lies in the fact that the ants are using cultures of millions of cells of bacteria to produce these antibiotics.
And so these bacteria are evolving.
Likewise the pathogen that is the target of these antibiotics is also evolving, and it's an evolutionary arms race that has continued for 50 million years.
NARRATOR: And so the symbiosis of ant and fungus also includes the aggressive mold in the fungus garden and the bacteria living on the ants.
Nature is often more complex than it first appears.
WILSON: Scientists have just begun to understand how two species can interact, or three or four.
But they're a long way from understanding how thousands, or tens of thousands of species can interact to create the monumental ecosystems of the world, like rain forests and coral reefs.
And the most remarkable gap in our knowledge is in bacteria and other microorganisms because these make up the base of the living world.
We need them; they don't need us.
NARRATOR: And yet we do everything in our power to avoid microbes.
A barrage of new products states the message loud and clear: The only good germ is a dead one.
Are we making our world too clean? Consider the research of pediatrician Erika von Mutius.
Du musst feste einatmen, bitte.
Stelltest richtig fest Gut, noch mal.
NARRATOR: She treats allergies and asthma, conditions in which the immune system overreacts to harmless substances.
Rates of both disorders are on the rise in affluent, industrialized regions.
Perhaps children are growing up in surroundings too germ-free for their own good.
VON MUTIUS: Microbes do a lot of harmful things to us but they may also be important for our immune system to learn how to deal with the environment and how to tolerate and fight viruses, bacteria and infections.
NARRATOR: To understand the causes of allergies and asthma Von Mutius is conducting research in a place where these conditions are rare The Bavarian countryside.
She wants to sort out exactly which environmental factors may be protecting children who grow up here.
VON MUTIUS: The study we're doing is a comparison within little villages.
So we compare children who live on the farm to children in the same village who do not live on the farm.
NARRATOR: She has enlisted over 800 families with children between the ages of six and 12 to participate in a detailed survey of health and lifestyle.
Dann, wieviel Zeit VON MUTIUS: In each questionnaire, we asked for allergic conditions and then most importantly we asked for the contact to farm animals and farming activities.
(interview proceeding in German) NARRATOR: Her goal is to create a profile of environmental exposures for each child.
Her team analyzes dust samples from carpets and bedding throughout the house for the presence of animal hair, dust mites and microorganisms.
If the family keeps livestock samples from the stables are screened for microbes released in the shedding and droppings of animals.
The study is in progress but preliminary results suggest one very strong correlation.
VON MUTIUS: One of the factors that seems to be important is the contact to the livestock.
These children, the more they are in the stables, um and the earlier they are in the stables that this gives a protection against the development of allergies.
NARRATOR: High levels of microorganisms in the stables may help prime a child's immune system for life.
VON MUTIUS: Microbes have been around us always and probably we need to find a balance between eradicating the harmful effect of bacteria and maybe also taking the beneficial components of this.
But this is really into the future.
(cows mooing) NARRATOR: Our species evolved in a world awash with microbes crowded with other creatures.
We've only begun to understand the value of this heritage.
WILSON: Scientists and medical researchers who have focused on the subject are more and more in agreement that it's a big mistake for humanity to separate itself from the rest of the living world too much.
The vast majority of species out there are our friends; they're not our enemies.
And we not only benefit from them but as a whole, they are essential to our existence.
We're the fortunate heirs of more than three billion years of evolution that created this stupendous diversity.
We need to learn a lot more about the living world and the way that humanity itself is affecting evolution.
NARRATOR: Like all living things, humans are a product of evolution.
But we're the only species that knows it.
We alone can see into the distant past and marvel at the history of life.
We alone are beginning to understand that we can use evolution to shape the future for all of life.
More than anything else this unique vision may be what makes us human.
Continue the journey into where we're from and where we're going at the Evolution web site.
The seven-part Evolution boxed set and the companion book are available from WGBH Boston Video.
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