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THE P OLIT I C S O F
Mad Cow Disease
Government officials in the United Kingdom initially sought
to downplay reports of a widespread “mad cow” disease
outbreak to protect the British beef industry, and a
government-sponsored report in 1989 concluded “it was
most unlikely that BSE would have any implications for
human health.” Ultimately, health officials ordered the
slaughter of millions of potentially affected cattle to stop
the disease “once and for all” and restore confidence in
British beef. Ironically, this move prevented scientific study
of how widespread the epidemic had become.
Meanwhile, other governments banned British beef,
purportedly out of concern for their citizens, although cynics
suspected the embargoes may have been imposed to help
those countries’ domestic beef industries. For a while, the
situation took on the appearances of a typical trade dispute—
until people began to die.
As a result of the outbreak, health officials in the U.K.
banned restaurants, supermarkets, and butchers from serving
beef on the bone, reasoning the ban would decrease the
likelihood of variant Creutzfeldt-Jakob disease by preventing
people from eating susceptible marrow and nerve tissue
attached to the bone. No scientific evidence existed at the
time (or since) to confirm that the same piece of meat would
be safer off the bone than on it. Among the tissues at high risk
for BSE contamination, however, the FDA lists a cow’s skull,
brain, part of the small intestine, and nerves attached to the
spinal cord, brain, eyes, and tonsils. So far, milk and cow meat
that haven’t contacted the animal’s central nervous system
tissue have shown no infectivity in laboratory animals.
Health officials eventually pronounced British beef safe for
consumption because the harmful conformation of the
protein was not found in muscle tissue or blood. That negative
finding, however, was subsequently shown to be meaningless
because the tests available at the time were insufficiently
sensitive. We now know that the dangerous
conformation does exist in both blood and muscle.
Since the British epidemic, almost every new discovery of
BSE elsewhere has been accompanied by political posturing—and,
typically, by banning all beef from the home country
of the BSE-affected cow. The contaminated cattle feed
that may have contributed to BSE is largely a thing of the past
thanks to new rules against feeding mammalian protein to
ruminants. These rules were designed to prevent the perpetuation
of the cannibalism cycle. Strangely, feed intended for
pigs and chickens is not subject to such rules, provoking
concern from consumer groups that we are risking the rise of
future prion diseases. Could a massive scare over “mad pig”
disease be next? The refusal to learn permanent lessons from
the BSE crisis seems deeply ingrained in the agricultural
system and its politics.
The best example of this refusal to learn can be found in
the political posturing over testing. New technology enables
rapid testing for BSE at the relatively nominal cost of $20 to
$30 per animal carcass, or only a few pennies per pound of
beef. Yet when several U.S. meat-packing companies began
doing such tests, in part to become eligible to export beef to
Japan, the U.S. Department of Agriculture (USDA) responded
by outlawing them! The USDA argues that the testing is
“unnecessary” because “no scientific proof” that it is required
exists, but how can proof be obtained unless you look? We
believe the real motive for preventing testing is likely to be
political pressure from the beef industry. Perhaps beef
lobbyists oppose the cost, nominal though it may be. More
likely, beef-industry advocates suspect that widespread
testing would turn up some sporadic cases (as it has in other
countries) and undermine confidence in the U.S. beef supply.
Nevertheless, new elk brought to the facility still
developed CWD. The facility remains shuttered
because of the presumption that contamination
persists in some forma scenario that bears
a striking similarity to the results of the Icelandic
scrapie experiments. As with scrapie, no one knows
for sure how CWD is transmitted between the
animals or what transmissible agent has contaminated
the facility, although prions are the prime
suspects, and other studies suggest the particles
can persist in the soil for at least three years.
As of mid-2010, health authorities have found
CWD in 16 U.S. states and two Canadian provinces.
Ironically, CWD-infected deer lose their fear of
humans, which makes them more likely to be shot
by a hunter. CWD may yet be a human health issue;
so far, a number of cases of a CJD-like disease have
been reported among avid deer and elk hunters.
Although this link remains controversial and no
transmission has yet been confirmed in humans,
eating deer, elk, or moose meatand especially the
internal organs, spinal cord, or lymph nodesof
animals shot in affected areas is not recommended
unless they test negative for CWD.
The bad news is that few food-safety recommendations
can be made for prion diseases
because no amount of cooking or sanitation can
eliminate the risk. The large gaps in our understanding
are bound to make these diseases sound
scary. The good news is that the tally of human
cases even tentatively linked to vCJD or CWD
remains quite low, especially when compared
with those attributed to other foodborne pathogens.
Although prions deserve our continued
attention, then, it’s important to remember that
the likelihood of contracting a prion disease is
still remote.
difference in your and others’ health. Diseases like
trichinellosis and botulism may still have fearsome
reputations, but safe kitchen practices can help
ward off even far more threatening bugs, whether
notorious noro viruses, vicious listeria bacteria, or
toxic toxoplasmas.
Further Reading
Debré, P. Louis Pasteur. Johns Hopkins University
Press, 1998.
Friedman, M., et al. “Recipes for Antimicrobial
Wine Marinades Against Bacillus cereus,
Escherichia coli O157:H7, Listeria monocytogenes,
and Salmonella enterica,” Journal of Food Science,
6:72, M207–M213; August 2007.
Mead, P., et al. “Food-Related Illness and Death in
the United States,” Emerging Infectious Diseases,
6:5, 607–625; September –October 1999.
Prusiner, S. Prion Biology and Diseases.
CSHL Press, 2004.
Robinson, R., et al. (editors). Encyclopedia of Food
Microbiology. Academic Press, 1999.
Sompayrac, L. How Pathogenic Viruses Work. Jones
and Bartlett, 2002.
Todar, K. Todar’s Online Textbook of Bacteriology.
Available online at textbookofbacteriology.net
U.S. Food and Drug Administration. Bad Bug
Book. Available online at www.fda.gov/Food/
FoodSafety/FoodborneIllness/FoodborneIllness-
FoodbornePathogensNaturalToxins/
BadBugBook/
Villarreal, L. “Are Viruses Alive?” Scientific
American, 97–102; December 2004.
Yam, P. The Pathological Protein: Mad Cow,
Chronic Wasting, and Other Deadly Prion Diseases.
Springer, 2003.
Cooking beef until it’s well done will not reduce the risk of “mad
cow” disease; better safety rules for cattle feed, however, have
greatly reduced the incidence of BSE over the past decade.
Take Culinary Risks, Safely
Taking risks at the table should be a matter of
trying new dishes and sampling unusual flavors,
rather than chancing the ingestion of any of the
numerous tiny pathogens that can stalk unwary
chefs and their guests. Attempting to rid your
kitchen of all dangerous microbes is futile, of
course. But now you know which ones can wreak
the most havoc and how they do their damage.
Applying that knowledge in practical ways
the subject of the next chaptercan make a huge
160 VOLUME 1 · HISTORY AND FUNDAMENTALS
MICROBIOLOGY FOR COOKS 161