New Timely Information Sheet: BSE (fwd)

James L. Novak (jnovak@acenet.auburn.edu)
Wed, 27 Mar 1996 09:01:26 -0600 (CST)

Jim Floyd is a veterinarian with the Alabama Cooperative Extension
System. BSE seems to be "the" topic in the press these days. I thought
Jim's article does a good job of laying out the facts.

---------- Forwarded message ----------
Date: Tue, 26 Mar 1996 22:59:44 -0600 (CST)
From: James G. Floyd <jfloyd@ag.auburn.edu>
To: cac@acenet.auburn.edu, specoff@acenet.auburn.edu,
specon@acenet.auburn.edu, ala-am@acenet.auburn.edu
Subject: New Timely Information Sheet: BSE


26 March, 1996

Don't Call It "Mad Cow Disease"
or
Bovine Spongiform Encephalopathy (BSE) - "Just the Facts"

Jim Floyd, DVM - Extension Veterinarian, Auburn University

Anyone who has not heard of "BSE" must not be watching the
news. Since March 21 the TV and papers have been full of stories
claiming that consumption of beef from diseased cattle in Britain
may have caused a fatal human brain disease.

Consumers can be assured that beef and dairy products in the
United States are safe. The following information should provide
sufficient background to substantiate this point of view.

The condition in British cattle has been called "Mad Cow
Disease," an unfortunate substitute for its real name: Bovine
Spongiform Encephalopathy, or BSE. "Mad Cow Disease" is a poor
term because it fails to differentiate BSE from the many other
nervous system disorders in cattle in which cattle might be
described as "mad." These include rabies, ketosis, lead poisoning,
listeriosis, polio, anaplasmosis, and others.

Cattle with BSE have a degenerative brain condition which
develops slowly over a 5 to 8 year period. When cattle develop
clinical signs of the disease near the end of its course they have
abnormal gaits, high stepping, itching, go off feed, lick
excessively, may become aggressive, and die if they are not
humanely euthanized.

BSE is similar in its effects on the cattle brain to other
spongiform encephalopathy (SE) diseases in the brains of other
animals. These include Kuru and Creutzfeldt-Jacob disease (CJD) in
humans, scrapie in sheep, Transmissible Mink Encephalopathy (TME),
chronic wasting disease of mule deer and elk, Feline Spongiform
Encephalopathy (FSE), and a few others. Experimental studies have
demonstrated that some of the SE diseases could be caused in
animals by feeding them nervous system tissues (brain, spinal cord,
etc.) from affected animals. For example, Kuru was seen in natives
of Papua New Guinea who practiced brain cannibalism. Non-human
primates (i.e. monkeys) have developed SE disease by experimental
exposure to nervous tissue from BSE-infected cattle.

The causative agent in the SE diseases may be a prion, or a
filterable glycoprotein devoid of detectable nucleic acid that is
resistant to typical means of sterilization. These agents have
survived three years burial outside in soil and heating to 360
degrees C. Prions may be able to induce the production of a
special type of protein in the central nervous system of mammals.
Although the prion theory is currently most favored, there is still
debate about the nature of the causative agent in BSE. An
unidentified virus is also theorized as a cause.

BSE was first seen and diagnosed in Britain in 1986. It may
have arisen as a result of feeding rendered sheep by-products to
cattle as protein supplements. Some of these sheep may have been
infected with scrapie, an SE disease which has been known for over
200 years. The number of BSE cases increased to a peak of about
1,000 new cases per weak by January, 1993, and then began to
decrease. The epidemic may have worsened because of feeding
rendered cattle which had been affected with BSE. The British
government banned feeding of ruminant-derived animal proteins to
other ruminants in 1989. Because of the five to eight year
"incubation" period of development of BSE, cases continued to occur
after this ban. The number of cases now seen is a few hundred a
week, some in cattle born after the 1989 feeding ban. These
animals may have been exposed to protein supplements still in the
pipeline after the ban, or due to incomplete compliance with the
ban. In any event, the number of cases has decreased significantly,
and continues to decrease as a result of regulatory interventions
such as the offal feeding ban which is now effectively applied.

Until March 21, 1996 the British government maintained that
there was no danger of transmission of SE disease from cattle to
people. On that day the government announced that a scientific
advisory panel had considered ten human cases diagnosed as a rare,
fatal, and slowly developing degenerative brain condition called
Creutzfeldt-Jacob Disease (CJD). This disease occurs at the rate
of about .5 to 1 cases per million people. The rate of cases of
CJD in Britain is not higher than expected for the population;
however, these ten cases occurred in younger people than usual and
whose symptoms were not typical of CJD. This caused the advisory
committee to conclude that the cause of these unusual cases of CJD
was unknown and that there might be a link with BSE. This
announcement created a furor, which continues.

Muscle tissue and milk have not been demonstrated to transmit
BSE, but brain and spinal cord have. Therefore, steps taken in
Britain to insure that nervous tissues from cattle do not enter the
human food supply should effectively prevent any transmission, if
it ever occurred in the first place. These steps have also been
taken in the U.S., even though BSE has never occurred here.

No case of BSE has been diagnosed in the United States, and
plenty of people have been looking for it. In 1990 the U.S.
Department of Agriculture initiated an aggressive and thorough
surveillance program for BSE. This includes examination at the
National Services Veterinary Laboratory of the brains of nearly
3,000 cattle diagnosed with nervous system disease, and the
periodic examination of all live cattle in the U.S. which came from
the U.K. before the import ban. In 1993 a single BSE case occurred
in Canada in a calf which had been imported from Britain. No other
cases have occurred in Canada. In the U.S., state veterinary
diagnostic labs and practicing veterinarians have been alerted to
watch for nervous system disease in cattle and to always consider
BSE as a potential diagnosis. BSE can be definitively diagnosed
only by a post-mortem microscopic exam of brain tissue.

To prevent the possibility of BSE entering the country, in
1989 the U.S. banned imports of live cattle and zoo ruminants from
the United Kingdom and from any country with BSE. Sheep and goat
imports from the U.K. had been banned for years previously because
of scrapie. In 1989 the U.S. rendering industry voluntarily
adopted the policy that sheep greater than one-year old should not
be rendered into protein supplements for animal consumption. The
voluntary ban on rendering sheep has been largely effective,
although some questions have been raised about its effectiveness in
sheep-dense areas. The U.S. Food and Drug Administration in 1994
proposed a rule that would prohibit adult sheep and goat tissues
from brain, spinal cord, spleen, thymus, tonsil, lymph nodes, or
intestines (i.e. any tissue which would contain even small amounts
of nervous system material) for use in ruminant feed. To date this
rule has not been formally adopted.

In the U.S., the reaction to the threat of BSE by the
responsible governmental agencies and industry associations have
been appropriate and effective by all indicators. Because of the
current heightened public awareness of the potential problem, more
regulatory actions may occur in the near future. In the meantime,
the public can be assured that meat and dairy products in the U.S.
are safe.

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* Jim Floyd, DVM *
* Extension Veterinarian *
* Auburn University *
* *
* e-mail: jfloyd@ag.auburn.edu *
* voice: (334) 844-1501 *
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