Microcosm (9 page)

Biofilms may be everywhere, but studying them is not a simple matter. Scientists have had to ditch their flasks and petri dishes and think of new kinds of experiments. Some have built special chambers with warm flowing water to mimic the human gut. Under the right conditions,
E. coli
will settle down inside them and begin to build its biofilm. As the bacteria drift through the chamber, some alight on the bottom. Normally the microbes immediately let go and swim on, but sometimes they settle down instead. Some experiments suggest that
E. coli
make this decision if they detect other
E. coli
nearby. They sense their fellow microbes by the chemicals they release—not just serine and other sorts of waste but special molecules that serve as signals and can change the way other
E. coli
behave.

Once a group of
E. coli
has committed itself to forming a biofilm, the microbes start to build sticky fibers to snag one another and pull together into a tight cluster. They’re joined by more floating
E. coli,
and the cluster grows. They begin to squirt a rubbery slime from their pores, entombing themselves in a matrix. As the biofilm takes shape, it does not form a flat sheet. It grows looming towers, broad pedestals, and a network of crisscrossing avenues. All of these changes require each microbe to switch hundreds of genes on and off in a complicated, coordinated fashion.
E. coli
biofilms are in some ways like our bodies. A biofilm may not get up and walk around on two legs. But, like our cells, it forms collectives in which different cells take on different jobs and work together to promote their shared survival.

A biofilm of E. coli

Scientists are still trying to figure out exactly why
E. coli
bothers to build biofilms. An individual microbe must make a great sacrifice to join the effort, spending a lot of its precious energy to build the glue that will join it to other microbes. If an individual
E. coli
should happen to get stuck deep inside the biofilm, it will have a harder time getting food than it would have if it remained floating free. These costs may be outweighed by benefits. Biofilms may provide
E. coli
with sustenance and protection. Biofilms can withstand harsh swings of the environment. Viruses may have a harder time penetrating biofilms than infecting single cells. Antibiotics are a thousand times weaker against biofilms than against individual microbes.

Biofilms may also allow bacteria to work together to catch food. Nutrients may get caught in the rubbery slime of biofilms and flow down canals to reach out-of-the-way microbes. Bacteria can also work cooperatively in biofilms by dividing their labors. The ones near the surface can get more food and oxygen than the ones buried deep inside. But they also face more stress. The
E. coli
nestled at the base of a biofilm may slip into a state of suspended animation, a kind of microbial seed bank. From time to time they may break off from the biofilm and drift away, becoming free-floating individuals or settling back down on the gut to build a new biofilm.

Humans, the supremely social species, don’t cooperate just to build cities and help their fellow humans. They also cooperate to wage war. And here again
E. coli
mirrors our social life. We build missiles and bombs.
E. coli
builds chemical weapons. Known as colicins, these deadly molecules kill in many ways. Some pierce the microbe’s membrane like a spear, forcing its innards to spill out. Others block
E. coli
from building new proteins. Others destroy DNA.

In order to launch a colicin attack, some
E. coli
must make the ultimate sacrifice. A few microbes in a population will build hundreds of thousands of colicin molecules in a matter of seconds, until they swell with weaponry. The microbes do not have channels through which they can neatly pump out their colicins. Instead, they make suicide enzymes that cut open their membranes. As they explode, the colicins blast out and hit neighboring
E. coli.
Their close relatives are spared the attack, however, because they carry genes that produce a colicin-disabling antidote. The sacrifice of a few
E. coli
clears away the competition, and their fellow clones prosper. The social life of
E. coli,
it seems, extends beyond life itself.

FAREWELL, MY HOST

Once a strain of
E. coli
establishes itself in our guts, it can remain there for decades. But the bacteria also escape their hosts, by a route that’s so obvious there’s no need to dwell on it. Suffice it to say that every day the world’s human population releases more than a billion trillion
E. coli
into the environment. Countless more escape from other mammals and from birds. They are swept down sewer pipes and streams, sowed upon the ground and sea. They must withstand summers and winters, droughts and floods. They must eke out an existence without a luxurious diet of half-digested sugar. For long stretches they may have to survive with no food at all. In soil and water there are many predators waiting to devour
E. coli,
including nematode worms and creeping amoebas. Some predators overpower
E. coli
by sheer size. Others, such as the bacteria
Bdellovibrio,
push their way into
E. coli’
s periplasm and destroy it from within. The bacteria
Myxococcus xanthus
release molecules that smell to
E. coli
like the whiff of food. The unlucky microbe swims to its own destruction.

Leaving their hosts is probably a quick trip to death for most
E. coli.
But life can handle bad odds. Oaks shower the ground with acorns, almost none of which survive to become saplings. Our own bodies are made of trillions of cells, only a few of which may escape our own death by giving rise to children. Even if only a tiny fraction of
E. coli
in the wild survives and manages to find a new host, its life cycle will continue. And
E. coli
has several tricks for surviving on the outside. Its versatile metabolism lets it feed on many carbon-bearing molecules—even TNT. If a soil predator tries to eat it, the microbe can avoid being digested and instead thrive as a parasite. And if worse comes to worst,
E. coli
can fold down its DNA into a rugged crystal, slip into the stationary phase, and survive for years.

Or, just perhaps,
E. coli
can abandon hosts altogether. From time to time, scientists discover populations of
E. coli
that appear to be thriving as full-time outdoor microbes. In Australia, for example, researchers have discovered huge blooms of
E. coli
in lakes where none had been expected. The lakes are free of fecal matter, receiving no sewage or farm runoff. Yet on a warm day they are loaded with millions of billions of
E. coli.
The bacteria seem different from more familiar strains. For one thing they make an unusually tough capsule, which may act as a microbial wet suit, allowing them to survive year-round in the lakes. They no longer need hosts to avoid extinction. They have broken free.

A DAY AT THE FAIR

In central Connecticut, where I live, agricultural fairs are serious business. Every summer one town after another—Goshen, Durham, Haddam Neck—raises tents and Ferris wheels. Trailers arrive, rattling along the rocky paths, full of oxen ready to drag concrete blocks. Mayors and selectmen are summoned for cow-milking contests. The fairs have survived long after the agricultural communities that produced them wilted away. Yet they still swarm with thousands of people who come to see prize goats, delicately wrought pies, and flouncing roosters.

I go with my wife and two daughters to a few fairs each summer, and each time we go, I lose my sense of time. I feel as if I’m back in an age when a typical ten-year-old would know how to shear a sheep. But just when I’ve almost completely lost my moorings in a tent full of livestock, I notice a wooden post staked in the ground by the entrance, holding a box of soap. It snaps me back to the twenty-first century, and when we leave the tent I make very sure my daughters scrub their hands.

These tents are home to some exquisitely vicious bacteria. The microbes live in the animals winning the ribbons at the fairs, and they fall with the droppings into the hay, float off on motes of dust, hitchhike on the bristles of flies. They spread through the tents, sticking to floors and fences and wool and feathers. It takes a tiny dose of them—just a dozen entering the mouth—to make a person hideously ill. The intestines bleed; kidneys fail. Antibiotics only make the attack worse. All doctors can do is hook their patients to an intravenous line of saline solution and hope for the best. Most people do eventually recover, but some will suffer for the rest of their lives. A few will die.

When pathologists test the fatal bacteria, they meet up with a familiar friend:
E. coli.

E. coli
comes in many strains. All of them share the same underlying biology, but they range enormously in how they make a living. Most are harmless, but outside laboratories,
E. coli
also comes in forms that can sicken or kill. To know
E. coli,
to know what it means for it to be alive, it’s not enough to study a tame strain such as K-12. The deadly strains are members of the species as well.

Scientists did not appreciate how dangerous
E. coli
could be for decades after Theodor Escherich discovered the bacteria. The first clear evidence that not all strains of
E. coli
were harmless bystanders came in 1945. John Bray, a British pathologist, had been searching for the cause of “summer diarrhea,” a deadly childhood disease that swept across Britain and many other industrialized countries every year. Bray hunted for bacteria that were common in sick children and missing from healthy ones.

Bray searched for the bacteria with antibodies, the best tools of his day. Antibodies are made by our immune cells when they encounter proteins from a pathogen. The antibodies can then attack the pathogen by recognizing its protein. Because antibodies are so exquisitely specific to their targets, they will ignore just about any other protein they encounter. Bray created antibodies to pathogens such as
Salmonella
by injecting the bacteria into a rabbit. Once the rabbit’s immune system had mounted an attack, Bray extracted the antibodies from its blood. He then added the antibodies to cultures of bacteria he reared from the diarrhea of sick children. He wanted to see if they would reveal any pathogens. They did not.

As Bray puzzled over what kind of antibodies to make next, a pediatrician mentioned to him that children sick with summer diarrhea give off a semen-like smell. Bray knew that was also the smell of certain strains of
E. coli.
So he made antibodies to
E. coli
and added them to his cultures. They immediately found their targets. Bray found that 95 percent of the sick children responded to his antibody test. Only 4 percent of the healthy children did.

Bray had identified only a single strain of disease-causing
E. coli,
but in later years scientists would identify many others. Some had long been known to medicine, but under different names. In 1897, Kiyoshi Shiga, a Japanese bacteriologist, discovered the cause of a form of bloody diarrhea called bacillary dysentery. It had
E. coli’
s basic rod-shaped anatomy, but Shiga did not call it
E. coli.
After all, many other species were rod shaped as well. And Shiga’s microbe produced a cell-killing toxin that no one had ever observed
E. coli
make. In addition,
E. coli
could digest lactose, the sugar in milk, but Shiga’s bacteria could not. These differences and others like them caused Shiga to declare it a species of its own, which later scientists named in his honor:
Shigella.
Only in the 1990s, when scientists could examine
Shigella’
s genes letter by letter, did they realize that it was just a strain—actually, several strains—of
E. coli.

As the years passed, scientists discovered still more strains of
E. coli
that could cause diseases. Some strains attacked the large intestine. Others attacked the small intestine. Some lived harmlessly in the gut but could cause painful infections if they got into the bladder, sometimes creeping all the way up to the kidneys. Other strains cause lethal blood infections, and still others reach the brain and cause meningitis. The scale of their cruelty is hard to fathom.
Shigella
alone strikes 165 million people every year, killing 1.1 million of them. Most of the dead are children. I can only wonder what Theodor Escherich would have thought if he had discovered that many of the bacteria killing his young patients were actually his
Bacterium coli communis.

Although many strains of
E. coli
are deadly, one has earned more headlines in recent years than all the rest combined. It goes by the name of O157:H7, a code for the molecules on its surface.
E. coli
O157:H7 is the strain that makes petting zoos hot zones, that can turn spinach or hamburger into poison, that can cause organ failure and death. For all its notoriety, though, it’s relatively new to science.