All language subtitles for Evolution Ep 4 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 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: