tell the bacteria that it’s time to prepare to make us sick. They build themselves flagella and swim, scanning the molecules floating by for signals released by their fellow
E. coli
O157:H7. They follow the signals and gather together. Once they’ve formed a large enough army, they begin constructing their weapons.
Their most potent weapon is a syringe they use to pierce intestinal cells and inject a cocktail of molecules. The molecules reprogram the cells. The skeleton-like fibers that give the cells structure begin sliding over one another. A pedestal-like cup rises from the top of each cell, giving
E. coli
O157:H7 a place to rest. The cells begin to leak, and the bacteria feed on the passing debris. Along with diarrhea comes bleeding, and
E. coli
O157:H7 snatches up the iron in the blood with siderophores.
It’s at about this point, about three days after ingesting
E. coli
O157:H7, that people start to feel awful. They develop violent diarrhea, which begins to turn bloody. The cramps can feel like knife stabs. Most people infected with
E. coli
O157:H7 can recover within a few days. But for every twenty people who get infected, one or two have much worse in store. Their
E. coli
O157:H7 releases a new kind of toxin. This one invades cells and attacks their ribosomes, the factories that build proteins. The cells die and burst open. The toxins move from the intestines into the surrounding blood vessels and spread to the rest of the body. They trigger blood clots and seizures. They shut down entire organs, particularly the kidneys. For some the toxin is fatal. Even for the lucky ones, recovery can take years. Some will need dialysis for the rest of their lives. Children may suffer brain damage and have to learn how to read again.
E. coli
O157:H7 gets a lot of press because it can create sudden epidemics in industrialized countries, but it is just one of many dangerous strains that can make us sick in many ways.
Shigella,
for example, does not rest on a pedestal the way
E. coli
O157:H7 does. It wanders. Once it reaches the intestines, it releases molecules that loosen the junctions between the cells that make up the gut wall and slips through one of the gaps. The breach draws the attention of nearby immune cells, which crawl after the microbe. But
Shigella
does nothing to camouflage itself. On the contrary, it goes out of its way to produce molecules that provoke a strong attack.
The immune cells chase after
Shigella
and devour it. But instead of killing
Shigella,
the immune cells are killed by their prey.
Shigella
releases molecules that trigger the immune cells to commit suicide and burst open. The dying immune cells draw the attention of living ones, but they are equally helpless to stop
Shigella.
In fact, they only make it easier for more
Shigella
to invade, by opening up more gaps in the intestinal wall as they push their way in.
Having fended off the immune system,
Shigella
chooses a cell in the intestinal wall to invade. It builds itself a syringe very much like the one made by
E. coli
O157:H7 and pierces a cell. The molecules it injects do not cause the cell to form a pedestal but, rather, cause it to open a passageway through which
Shigella
can slither. Once inside, it takes control of the cell’s skeleton. It moves forward by causing one of the cell’s fibers to grow from its back end while it hacks apart the fibers that cross its path. Once
Shigella
has finished feasting on the cell, it pushes its way out through the membrane and invades a neighbor. The dying cell summons more immune cells to the infection, and they open up more gaps through which more
Shigella
invade.
How is it that
E. coli
can be so many different things? We tend to assume that a species is made up of individuals that all share the same essence. In the ways
Shigella
and
E. coli
O157:H7 act, they seem like completely different species from the harmless K-12. Yet a comparison of their DNA shows otherwise.
If you should find yourself
E. coli
O157:H7. They follow the signals and gather together. Once they’ve formed a large enough army, they begin constructing their weapons.
Their most potent weapon is a syringe they use to pierce intestinal cells and inject a cocktail of molecules. The molecules reprogram the cells. The skeleton-like fibers that give the cells structure begin sliding over one another. A pedestal-like cup rises from the top of each cell, giving
E. coli
O157:H7 a place to rest. The cells begin to leak, and the bacteria feed on the passing debris. Along with diarrhea comes bleeding, and
E. coli
O157:H7 snatches up the iron in the blood with siderophores.
It’s at about this point, about three days after ingesting
E. coli
O157:H7, that people start to feel awful. They develop violent diarrhea, which begins to turn bloody. The cramps can feel like knife stabs. Most people infected with
E. coli
O157:H7 can recover within a few days. But for every twenty people who get infected, one or two have much worse in store. Their
E. coli
O157:H7 releases a new kind of toxin. This one invades cells and attacks their ribosomes, the factories that build proteins. The cells die and burst open. The toxins move from the intestines into the surrounding blood vessels and spread to the rest of the body. They trigger blood clots and seizures. They shut down entire organs, particularly the kidneys. For some the toxin is fatal. Even for the lucky ones, recovery can take years. Some will need dialysis for the rest of their lives. Children may suffer brain damage and have to learn how to read again.
E. coli
O157:H7 gets a lot of press because it can create sudden epidemics in industrialized countries, but it is just one of many dangerous strains that can make us sick in many ways.
Shigella,
for example, does not rest on a pedestal the way
E. coli
O157:H7 does. It wanders. Once it reaches the intestines, it releases molecules that loosen the junctions between the cells that make up the gut wall and slips through one of the gaps. The breach draws the attention of nearby immune cells, which crawl after the microbe. But
Shigella
does nothing to camouflage itself. On the contrary, it goes out of its way to produce molecules that provoke a strong attack.
The immune cells chase after
Shigella
and devour it. But instead of killing
Shigella,
the immune cells are killed by their prey.
Shigella
releases molecules that trigger the immune cells to commit suicide and burst open. The dying immune cells draw the attention of living ones, but they are equally helpless to stop
Shigella.
In fact, they only make it easier for more
Shigella
to invade, by opening up more gaps in the intestinal wall as they push their way in.
Having fended off the immune system,
Shigella
chooses a cell in the intestinal wall to invade. It builds itself a syringe very much like the one made by
E. coli
O157:H7 and pierces a cell. The molecules it injects do not cause the cell to form a pedestal but, rather, cause it to open a passageway through which
Shigella
can slither. Once inside, it takes control of the cell’s skeleton. It moves forward by causing one of the cell’s fibers to grow from its back end while it hacks apart the fibers that cross its path. Once
Shigella
has finished feasting on the cell, it pushes its way out through the membrane and invades a neighbor. The dying cell summons more immune cells to the infection, and they open up more gaps through which more
Shigella
invade.
How is it that
E. coli
can be so many different things? We tend to assume that a species is made up of individuals that all share the same essence. In the ways
Shigella
and
E. coli
O157:H7 act, they seem like completely different species from the harmless K-12. Yet a comparison of their DNA shows otherwise.
If you should find yourself
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