Original subtitles

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 2� 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.

Visit www.pbs.org.

The seven-part Evolution boxed set and the companion book

are available from WGBH Boston Video.

To place an order, please call: