Every pathogen has a story, but the biography of E. coli O157:H7 is
especially instructive because it shows how chance favors the prepared germ --
and how we are giving certain disease-causing organisms more chances than a
rigged roulette wheel. Though E. coli O157:H7 has turned up in
unpasteurized apple cider in 1991, 1996, and nearly every year since the
Odwalla outbreak [in 1996], it is best known as the agent behind "hamburger
disease." Hamburgers, in fact, are Rolls-Royce conveyances for O157. Think of
your next Big Mac as the end product of a vast on-the-hoof assembly line. The
story begins on hundreds of feedlots in different states and foreign countries.
The animals are shuttled to slaughterhouses, where they become carcasses. The
carcasses go to plants that separate meat from bone. The boning plants ship
giant bins of meat to hamburger-making plants. The hamburger-making plants
combine meat from many different bins to make raw hamburgers. At this point,
your burger is more fluid than solid, because ground beef continually mixes and
flows as it's made, its original ingredients indistinguishable. Grinding also
multiplies surface area, so that the meat becomes a kind of soup or lab medium
for bacteria. Finally, from the hamburger-making plants, these mongrel patties
are frozen and sent to restaurants. A single patty may mingle the meat of a
hundred different animals from four different countries. Or, looked at from
another perspective, a single contaminated carcass shredded for hamburger can
pollute eight tons of finished ground beef. Finding the source of contamination
becomes impossibly daunting. (Making juice is also like making hamburgers: one
bad apple can ruin a huge batch.) In the Jack in the Box outbreak,
investigators found that the ground beef from the most likely supplier
contained meat from 443 different cattle that had come from farms and auction
in six states via five slaughterhouses. As the meat industry consolidates and
the size of ground beef lots grows, a single carcass may have even more deadly
potential. In 1997, Hudson Foods was forced to recall 25 million pounds of
ground beef for this very reason: a small part of one day's contaminated beef
lot was mistakenly mixed with the next day's, vastly spreading the risk.
E. coli O157:H7, the organism that this endless mixing amplifies, is a
quiet tenant in the intestines of the 50 percent or so of feedlot cattle it
infects, but a vicious hooligan in the human gut. In the bowel, Escherichia
coli, rod-shaped bacteria first described by German pediatrician Theodore
Escherich in 1885, perform a vital task by keeping disease-causing bacteria
from taking over. For many decades, that knowledge obscured the fact that some
forms of E. coli trigger violent disease. E. coli O157:H7 (the
letters and numbers refer to immune system-provoking antigens on the body and
on the whiplike flagella of the organism) was discovered in 1982, during an
epidemic spread by undercooked patties from McDonald's restaurants in Oregon
and Michigan. The outbreak wasn't highly publicized; even some scientists
perceived O157 as more of an academic curiosity than a harbinger of bad things.
Eleven years later, the Jack in the Box hamburger chain promoted its "Monster
Burgers" with the tag line: "So good it's scary." These large,
too-lightly-grilled patties killed four children and sickened more than 700
people -- bringing the exotic-sounding bacterium out of the lab and into public
consciousness. In fact, however, by the time of the Jack in the Box tragedy, 22
outbreaks of E. coli O157:H7, killing 35 people, had already been
documented in the United States. Suddenly, fast food hamburgers -- a staple of
American culture -- were potentially lethal.
What makes E. coli O157:H7 so fearsome is the poison it churns out --
the third most deadly bacterial toxin, after those causing tetanus and
botulism. Known as a Shiga toxin, because it is virtually identical to the
toxin produced by Shigella dysenteriae type 1, it is a major killer in
developing nations. The distinctive symptoms of E. coli O157:H7 are
bloody diarrhea and fierce abdominal cramps; many victims say it's the worst
pain they ever suffered, comparing it to a hot poker searing their insides.
Between 2 and 7 percent of patients -- mostly young children and the elderly
-- develop hemolytic uremic syndrome, which can lead to death. HUS sets in
when Shiga toxins ravage the cells lining the intestines. The bleeding that
ensues permits the toxins to stream into the circulatory system, setting up a
cascade of damage similar to that of rattlesnake venom. The toxins tear apart
red blood cells and platelets, leaving the victim vulnerable to brain
hemorrhaging and uncontrolled bleeding. Clots form in the bloodstream, blocking
the tiny blood vessels around the kidneys, the middle layer of the heart, and
the brain. As the kidneys give out, the body swells with excess waste fluids.
Complications ripple through all major organ systems, leading to strokes,
blindness, epilepsy, paralysis, and heart failure. Though doctors can manage
HUS symptoms, and are working on new ways to stymie the toxin, they currently
can offer no cure or even effective treatment.
For public health officials, the emergence of E. coli O157:H7 is an
object lesson in how a new pathogen can lie low in the environment, biding its
time until humankind changes a certain activity and in so doing rolls out a red
carpet. Like other emerging pathogens, such as the AIDS virus, 0157 had struck
long before it caught the attention of public health officials. In 1955, a
Swiss pediatrician in a dairy farm area first described HUS, which physicians
today consider to be a gauge of E. coli O157:H7 infection. Over the
ensuing years, the number of cases kept rising, suggesting that O157 was
quietly spreading. In 1975, doctors took a stool sample from a middle-aged
California woman with bloody diarrhea, cultured the apparently rare bacterium
and sent it to the CDC, where it sat in storage until the McDonald's outbreak
prompted researchers to scour their records for earlier evidence of the vicious
organism. In other words, for nearly 30 years before the first bona fide
epidemic, E. coli O157:H7 had turned up in scattered, sporadic cases of
bloody diarrhea. It was out in the meat supply, but not in high enough
concentrations to catch health officials' notice.
Where did E. coli O157:H7 come from in the first place? Scientists have
pieced together a long, rather provocative history. Genetic lineages suggest
that about 50,000 years ago, O157 and another closely related serotype --
O55:H7, which causes infant diarrhea in developing nations -- split off from
the same mother cell. Since then, O157 has taken part in a series of biological
mergers and acquisitions that left it as vigorous as one of today's giant
pharmaceutical houses. Indeed, a 2001 study showed that O157, composed of more
than 5,400 genes, picks up foreign DNA at a much faster rate than do other
organisms. At some point, it acquired two deadly Shiga toxin genes after being
infected by a bacteriophage, a tiny virus that insinuates its DNA into the
chromosome of a bacterium. In the microbial world, phages are like squatters in
Amsterdam, casually taking up residence in new bacteria, perhaps as a response
to environmental stresses such as ultraviolet light or toxic chemicals.
Bacteriophages are also the villains behind some of the most deadly human
plagues; the genes coding for the cholera toxin, for instance, were borne on a
phage. So what surrounding pressures compelled the phage carrying the Shiga
toxin genes to light out for a new home in E. coli? In experiments on
mice, Tufts University researcher David Acheson may have found the answer. When
Acheson gave the animals low levels of antibiotics, the phage virus wildly
replicated itself, and its magnified forces were more likely to infect other
bacteria. Antibiotics also spurred the phage to pour out clouds of Shiga toxin.
Acheson speculates that when farmers began the practice of feeding cattle small
doses of antibiotics to spur growth, beginning in the 1950s -- perhaps not
coincidentally, when the first reports of sporadic HUS in children came out --
they may have unleashed O157. More backing for this theory comes from
epidemiological evidence. E. coli O157:H7 is a disease of affluent,
developed nations -- which also happen to be the ones that feed
growth-promoting antibiotics to livestock.
What worries Acheson and other scientists is that the restless phages that
manufacture Shiga toxin may jump to other disease-causing bacteria. Actually,
they've already proven they're disposed to do this, having set up home in about
200 other strains of E. coli. One of these, E. coli O111:H8, in
1999 caused a massive epidemic of nausea, vomiting, bloody diarrhea, and severe
stomach cramps at a high school drill team camp in Texas, sickening dozens of
the 750 teenage girls who attended. Though investigators never did find where
the organism was hiding, they suspect it was either in the ice the girls used
to soothe their parched throats during the drills or somewhere in the salad
bar. Shiga toxin phages have also landed in Enterobacter and
Citrobacter -- other bacteria that stir up intestinal disease. To find
out just how prevalent these mysterious strains of dangerous E. coli may
be, Acheson analyzed ground beef samples from 12 supermarkets in Boston and
Cincinnati. The results came as a shock. He found Shiga toxin in a quarter of
the samples -- toxin produced not by O157:H7, but by other kinds of E. coli.
And this may not be the end of their roving, Acheson warns. "Suppose
something like Salmonella developed the ability to produce Shiga toxins.
That could be an extremely deadly pathogen." Not only is Salmonella
common, but, more than E. coli O157, it has a talent for quickly
invading the bloodstream, meaning it could speedily convey Shiga toxins
throughout the body like tiny poison-tipped missiles. Even more problematic,
the antibiotics normally used to treat E. coli O157:H7 infections may
actually aggravate the illness, by kicking phages into overdrive and stepping
up their production of toxins, leading to hemolytic uremic syndrome.
Along its evolutionary path, E. coli also became acid resistant, so
impervious to a low pH environment that it can survive the incredibly sour bath
in the human stomach. Grain-feeding cattle, which supplanted traditional hay
feeding after World War II, may have made the bacteria more acid resilient.
Because of this acid tolerance, as few as 10 organisms are enough to cause
infection. Having acquired a mean set of toxin genes, acid resistance, and
other virulence properties, all E. coli O157:H7 needed to become a truly
fearsome threat was access. That it acquired by spreading in domesticated
cattle and then entering the gears of modern industrial meat production, all
within the past 25 years. Unfortunately, O157 may have left the door open
behind it. Other strains of E. coli, "if tweaked in the right way" by
phages and the mobile rings of DNA known as plasmids, could negotiate the same
path, says Tom Whittam, a biologist at Pennsylvania State University who has
studied O157 evolution.
Research is under way on vaccines that would prevent cattle from carrying O157,
and on feed additives -- including competing intestinal bacteria -- that would
eliminate the pathogenic organism in livestock. Thoroughly cooking ground beef
to a temperature of 160 degrees Fahrenheit is the proven method of killing
E. coli O157:H7. But in the United States, the organism retains a
fighting chance because of the American love affair with rare burgers, which
practically guarantees that one man's meat will be another man's poison. As a
restaurant menu in suburban Dallas proudly informs its customers: "The
Department of Health suggests MEDIUM-WELL for any ground beef product. Our
burgers are cooked MEDIUM (PINK) unless you request otherwise."
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