FEATURE ARTICLE
Mad-Cow Disease in Cattle and Human Beings
Bovine spongiform encephalopathy provides a case study in how to manage risks while still learning the facts
Paul Brown
BSE in North America
Were it not for the international trade in cattle and cattle feed,
BSE would probably have been confined to Great Britain. But cattle
and feed continued to be exported from Britain to countries all over
the globe for several years—throughout the late 1980s and
early '90s—after the cause of BSE had been identified. From
the mid-1990s onwards, cases of the disease began to appear in
Europe and in countries as far afield as Oman and Japan.
Ironically, the discovery of BSE in the United States at the end of
2003 recapitulated what had occurred with scrapie nearly 60 years
before, when infected sheep were imported from Canada, which had
earlier imported infected sheep from Great Britain. This time, at
least one BSE-infected cow (and probably more) was imported to
Canada from Great Britain during the high-risk 1980s. At some point
these cows were probably rendered into feed that infected some
"next generation" cows. The BSE cow that was discovered in
Washington state in December 2003 had been imported to the U.S. in
September 2001 from the same province of Canada (Alberta) in which
the Canadian BSE cow had earlier been identified. Both cows were
born in 1997, just before the ruminant-to-ruminant feed ban was
implemented, and it is now a matter of record that some leftover
feed continued to be used to supplement the diets of newborn calves.
When the two cows were slaughtered in 2003, neither was suspected of
having BSE, so their carcasses were sent to rendering plants for use
in feed supplements. The cows were only discovered to have BSE when
their brains were later tested as part of a routine surveillance
program of "downer" (nonambulatory or disabled) cows, and
beef products from the cow in Washington state had already entered
the human food supply.
Regulatory agencies in Canada and the U.S., primed by the mad-cow
scare in Great Britain and continental Europe, reacted quickly in
response to the discovery of the infected cows. All living cows that
could be traced from both farms, as well as products made from their
tissues, were destroyed. A host of new regulations were also either
implemented or proposed, of which the most important were these:
prohibition of tissues known to be infectious in BSE cows (cranium,
vertebral column, distal ileum, lymphoreticular tissues) for use by
either animals or human beings; elimination of mechanically
recovered meat unless it could be shown by sensitive immunologic
tests to be free of nervous tissue; initiation of a much-increased
BSE immunological testing program for downer cows (which are
henceforth not to be used for food or other products for either
animals or human beings); and a "beefed-up" program of
onsite inspections of rendering plants, feed mills and
slaughterhouses. Along with a strictly enforced ruminant-to-ruminant
feed ban, these measures should prevent the future spread of BSE to
other animals and human beings—even if the disease is
eventually found to occur as a rare spontaneous event.
Given the absence of indigenously infected cattle and the expanded
BSE testing program, the U.S. has both the motivation and resources
to answer, once and for all, the vexing question of whether or not
BSE occurs spontaneously. If it occurs at the same rate as sporadic
CJD in human beings (one case per million per year), several years
of testing hundreds of thousands of cattle will be required to
obtain a statistically significant result. Because other equally
motivated countries are disqualified by the occurrence of cattle
with foodborne BSE, only in the U.S. do we still have this unique,
one-time only opportunity to confirm or refute the thesis that the
BSE outbreak could have resulted from a spontaneous occurrence.
When BSE and its human counterpart, vCJD, pass into
history—which they undoubtedly will—some may believe
that a quarter century of scientific knowledge was gained at the
expense of veterinary and public health. This would be neither fair
nor accurate. Great Britain and indeed the world owe an immense debt
of gratitude to the few key investigators who correctly identified
the basic issues with extraordinary rapidity. The problem was in
translating the evolving scientific knowledge into government
policy, because until public concern forces the issue, governments
are almost always loathe to take a proactive stance in the face of
purely hypothetical risks. This is due in great measure to the fact
that regulations designed to protect public health from imagined
dangers invariably cause real damage to the commercial sectors
involved, and unless the data are undeniable, these interests will
understandably argue against restrictive measures. It is thus not at
all clear that any so-called "lessons" will inform future
situations, because risk-benefit analyses that are based on
incomplete knowledge depend on both scientific and political
considerations and will continue to frustrate scientists and policy
makers alike.
Bibliography
- Brown, P. 2003. Transmissible Spongiform
Encephalopathy as a Zoonotic Disease. ILSI Europe
Report Series. Brussels: International Life Sciences Institute.
- Brown, P., and R. Bradley. 1998. 1755 and all that: A
historical primer of transmissible spongiform encephalopathy.
British Medical Journal 317:1688–1692.
- Brown, P., R. G. Will, R. Bradley, D. L. Asher and L.
Detwiler. 2001. Bovine spongiform encephalopathy and variant
Creutzfeldt-Jakob disease: Background, evolution, and current
concerns. Emerging Infectious Diseases 7:6–16.
- Hadlow, W. J., R. C. Kennedy and R. E. Race. 1982.
Natural infection of Suffolk sheep with scrapie virus.
Journal of Infectious Diseases 146:657–664.
- Prusiner, S. B. 2001. Shattuck
Lecture—Neuro-degenerative diseases and prions. New
England Journal of Medicine 334:1516–1526.
- Stevenson, M. A., et al. 2000. Temporal aspects of the
epidemic of bovine spongiform encephalopathy in Great Britain:
Individual animal-associated risk factors for the disease.
Veterinary Record 147:349–354.
- Taylor, D. M., S. L. Woodgate, A. J. Fleetwood and R. J.
G. Cawthorne. 1997. Effect of rendering procedures on the
scrapie agent. Veterinary Record 141:643–649.
- Wells, G. A. H., et al. 1987. A novel progressive
spongiform encephalopathy in cattle. Veterinary Record 121:419–420.
- Will, R. G., et al. 1996. A new variant of
Creutzfeldt-Jakob disease in the UK. Lancet
347:921–925.
» Post Comment