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2

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

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