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http://www.monitor.net/rachel/r607.html

 

RACHEL'S ENVIRONMENT & HEALTH WEEKLY #607 .

 

.. ---July 16, 1998--- .

 

.. HEADLINES: .

 

.. MAD COW DISEASE, PART 2 .

 

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MAD COW DISEASE, PART 2

 

 

 

Mad cow disease appeared for the first time in Britain in 1985.

 

Since that time it has killed roughly 170,000 cows in Britain,

 

and it has spread to humans.[1] In humans the disease is called

 

" new variant Creutzfeld-Jakob disease, " or nvCJD for short. At

 

this point nvCJD has killed 24 people in Britain and one in

 

France. More human deaths are expected in Britain[2] because

 

several million people ate diseased beef before the British

 

government (or the beef industry) acknowledged that mad cow

 

disease could infect people.

 

 

 

From a U.S. perspective, the obvious question is, How can an

 

outbreak of mad cow disease be prevented here?

 

 

 

Mad cow disease is a member of a family of rare diseases called

 

transmissible spongiform encephalopathies, or TSEs. TSEs have

 

different names in different animals (for example, scrapie in

 

sheep, chronic wasting syndrome in deer and elk, and bovine

 

spongiform encephalopathy or BSE in cows). However all TSEs

 

share a few common features: they attack the central nervous

 

system, causing disintegration of the brain; they have a long

 

incubation period between the time when infection first occurs

 

and the appearance of symptoms; TSEs are always fatal; and they

 

are transmitted by the eating of animals or animal parts,

 

especially brains and spinal cords.

 

 

 

TSEs are now thought to be caused by a unique disease agent,

 

called a prion (pronounced PREE-on). A prion is simply a

 

particular kind of protein. All mammals have prions, and some

 

non-mammalian species have them as well. Prions are normal.

 

 

 

According to modern biology, a prion should not be able to

 

reproduce itself, and therefore should not be able to cause

 

disease, because prions contain no DNA. Without DNA,

 

reproduction should not be possible. However, it is now becoming

 

widely accepted that prions do reproduce themselves and do cause

 

disease. Somehow a normal prion goes bad --it gets folded into

 

an abnormal shape and in its abnormal shape it can destroy nerve

 

cells in the central nervous system. The abnormal prions also

 

cause other nearby prions to become folded into the same shape,

 

thus creating more abnormal prions by a domino effect. After a

 

long period of time (months or years, or even decades) the

 

symptoms of disease appear, followed a few weeks or months later

 

by death. Thus animals and humans can be carrying an infectious

 

prion disease for months or years without showing any symptoms.

 

 

 

The prion theory of disease is still not accepted by 100% of the

 

scientific community, but the inventor of the theory, Stanley B.

 

Prusiner of the University of California at San Francisco,

 

received the Nobel Prize for his work in 1997.[3]

 

 

 

In this country, the government agency with primary

 

responsibility for preventing an outbreak of mad cow disease or

 

its human variant, nvCJD, is the U.S. Food and Drug

 

Administration (FDA).

 

 

 

The FDA in 1997 issued a rule declaring it illegal for farmers to

 

feed animal protein from ruminants or mink to other ruminants --a

 

preventive step that had been taken by the British government in

 

1988. Ruminants are animals that chew their cuds, including

 

cattle, sheep, goats, deer and elk. Mink are included in the

 

FDA's ban because they can get a TSE similar to mad cow disease.

 

 

 

When cows, pigs, and chickens are slaughtered, much of the animal

 

cannot be used for food and is sent to a rendering plant to be

 

ground up, boiled down, dried to the consistency of brown sugar

 

and sold as feed for cows, pigs, chickens, and pets. It is this

 

rendered " animal protein " derived from ruminants (and mink) that

 

FDA has banned from feeding to ruminants.

 

 

 

The FDA's ruminant-to-ruminant ban still allows animal protein of

 

all kinds to be fed to pigs and chickens, and it allows animal

 

protein derived from pigs and chickens to be fed to ruminants.

 

The FDA ban also allows blood and gelatin derived from ruminants

 

to be fed to other ruminants. In the U.S., many newborn calves

 

are fed a high-protein diet consisting mainly of dried blood.

 

Blood cells carry prions just as nerve cells do.[4]

 

 

 

A small group of scientists, led by Dr. Michael Hansen of

 

Consumers Union, has challenged the adequacy of FDA's

 

ruminant-to-ruminant rule.[5] They argue that the FDA ban does

 

not go far enough, " does not adequately protect human health, and

 

is not scientifically defensible. " [6] Consumers Union is the

 

publisher of CONSUMER REPORTS magazine.

 

 

 

Scientists on both sides of the controversy agree that mad cow

 

disease probably developed in Britain in one of two ways.

 

Possibly cows ate parts of sheep that had been infected with the

 

TSE called scrapie, and the scrapie, once in cows, evolved into

 

mad cow disease. Or, alternatively, a prion spontaneously went

 

bad (via genetic mutation of the gene that produces normal

 

prions) in a cow, and that cow was fed to other cows, which were

 

fed to other cows until the disease was amplified into an

 

epidemic. In either case, it was cows (which are vegetarians by

 

nature) being forced to eat animals that created the problem.

 

 

 

FDA officials say they are confident that their

 

ruminant-to-ruminant ban has prevented, and will continue to

 

prevent, an epidemic of mad cow disease in this country because

 

(a) mad cow has never been observed in cows in the U.S., and (b)

 

Creutzfeld-Jakob (CJD) disease is not increasing in the U.S.[7]

 

If mad cow were occurring in U.S. cows, some form of CJD should

 

be increasing, and it isn't, the FDA argues.

 

 

 

Michael Hansen of Consumers Union offers evidence that the

 

government may be wrong on both counts. Here are his arguments:

 

 

 

Mad cow may have already appeared in U.S. cows. Hansen offers

 

evidence from seven studies that some " downer " cows may have a

 

form of mad cow disease, though with symptoms somewhat different

 

from those in British cows. Downer cows are cows that cannot

 

stand up, cows that collapse, and cows that die mysteriously.

 

About 100,000 cows die each year in the U.S. with " downer "

 

symptoms, and most of them end up in rendering plants, turned

 

into animal feed.

 

 

 

In 1961, an outbreak of transmissible mink encephalopathy (TME)

 

--a brain-destroying TSE of mink --occurred on six mink farms in

 

Wisconsin. Because all the farms used the same ready-mix feed

 

which came from the same feed plant, investigators assumed that

 

the feed was the source of the infectious agent.[8] Two years

 

later, in 1963, an outbreak of TME occurred on two more Wisconsin

 

mink farms. Based on the 1961 outbreak, scientists suspected

 

feed and they examined the two farms' feed records carefully.

 

They learned that " downer " cows from farm A had been fed to mink

 

on Farm A and Farm B. The researchers wrote, " Since mink on both

 

farms developed the disease almost simultaneously, we believe

 

this feed component has to be incriminated. " [9]

 

 

 

In 1985 an outbreak of TME occurred on a mink ranch in

 

Stetsonville, Wisconsin. Dr. Richard Marsh of the University of

 

Wisconsin investigated and found that the mink had been fed 95%

 

downer cows and 5% horse meat.[10] When brains from infected

 

mink were injected into two calves, within 19 months both calves

 

had a bovine TSE but they did NOT exhibit the symptoms of

 

Britain's mad cows. The Stetsonville cows simply became

 

lethargic and then fell over. In other words, they exhibited

 

typical " downer cow " symptoms. When brains from these cows were

 

injected into mink, the mink got TME, confirming the kind of

 

disease that had killed the cows. Marsh and his colleagues

 

concluded, " These results suggest the presence of a previously

 

unrecognized scrapie-like infection in cattle in the United

 

States. " [10]

 

 

 

Marsh's cattle inoculation experiments have been repeated and,

 

again, mink TME was transmitted to cows and back to mink and the

 

cows exhibited " downer " symptoms, nothing like British mad cow

 

disease.[8] Furthermore, in 1979 U.S. Department of Agriculture

 

researchers in Mission, Texas, inoculated 10 cows with sheep

 

scrapie. Three of the 10 cows developed neurological symptoms,

 

but they were more like " downer cow " syndrome than British mad

 

cow disease: " progressive difficulty in rising, a stiff-legged

 

gait, incoordination, abnormal tail position, disorientation, and

 

terminal recumbency [lying down], " according to Dr. Clarence

 

Gibbs, Acting Chief of the Laboratory of Central Nervous System

 

Studies at the National Institutes of Health.[11] Ten years

 

later, when a test for mad cow disease became available, Dr.

 

Gibbs confirmed a bovine TSE disease in the three cows, whose

 

brains had been preserved.[11] Dr. Gibbs concluded,

 

" Susceptibility of cattle to scrapie further suggests the

 

possibility that sporadic cases of BSE [mad cow disease] may have

 

occurred in the United States under the clinical picture of the

 

downer cow syndrome.... " [11]

 

 

 

After Gibbs confirmed that the Mission, Texas cows had indeed

 

died of a TSE, the U.S. Department of Agriculture repeated the

 

experiments at Ames, Iowa under the direction of Randall

 

Cutlip.[12] Dr. Cutlip described the results: " All calves kept

 

longer than one year became severely lethargic and demonstrated

 

clinical signs of motor neuron dysfunction that were manifest as

 

progressive stiffness, posterior paresis [partial paralysis],

 

general weakness, and permanent recumbency [lying down]. " In

 

other words, cows infected with a sheep TSE had all the signs and

 

symptoms of downer cows.

 

 

 

Thus Hansen argues, there is considerable evidence that a TSE has

 

been present in some U.S. cattle for several decades.

 

 

 

But if mad cow disease is already present in some number of cows

 

in the U.S., where are the human victims? People should be

 

getting some form of CJD [Creutzfeld-Jakob disease], and this

 

disease is thought to be vary rare and not increasing in the U.S.

 

population. So where are the victims?

 

 

 

Hansen argues that CJD may be more prevalent in the U.S.

 

population than is presently thought. The official figures say

 

that CJD is exceptionally rare --one case in every million

 

people. In the U.S. this would mean there are 250 CJD cases at

 

any given time. Hansen points to two studies in which people

 

diagnosed with Alzheimer's were examined after death. In one

 

study, among 54 presumed Alzheimer's victims, 3 (or 5.5%) were

 

found to actually have CJD.[13] A Yale University study of 46

 

victims of Alzheimer's found that 6 (or 13%) actually died of

 

CJD, not Alzheimer's.[14] There are 2 million people with

 

Alzheimer's in the U.S.[8] If 5.5% of them actually have CJD,

 

there are 110,000 cases of CJD in the U.S., not 250 cases. If

 

13% of the 2 million have CJD, then there are 260,000 cases of

 

CJD in the U.S., not 250. If even 1% of the 2 million had CJD,

 

it would mean there was an epidemic of 20,000 cases of CJD

 

masquerading as Alzheimer's. Thus the FDA's argument that CJD is

 

very rare, and not increasing, needs to be re-examined. [To be

 

continued.]

 

--Peter Montague

 

(National Writers Union, UAW Local 1981/AFL-CIO)

 

 

 

===============

 

[1] John Collinge and others, " Molecular analysis of prion strain

 

variation and the aetiology of 'new variant' CJD, " NATURE Vol.

 

383 (October 24, 1996), pgs. 685-690. See also Adriano Aguzzi

 

and Charles Weissmann, " A suspicious signature, " NATURE Vol. 383

 

(October 24, 1996), pgs. 666-667.

 

 

 

[2] S.N. Cousens and others, " Predicting the CJD Epidemic in

 

Humans, " NATURE Vol. 385 (January 16, 1997), pgs. 197-198. See

 

also, David C.G. Skegg, " Epidemic or false alarm? " NATURE Vol.

 

385 (January 16, 1997), pg. 200.

 

 

 

[3] Lawrence K. Altman, " U.S. Scientist Wins Nobel for

 

Controversial Work, " NEW YORK TIMES October 7, 1998, pg. A1.

 

 

 

[4] Elias E. Manuelidis and others, " Transmission to Animals of

 

Creutzfeld-Jakob Disease from Human Blood, " LANCET (October 19,

 

1985), pgs. 896-897.

 

 

 

[5] Marian Burros, " U.S. Is Asked to Take New Steps to Prevent

 

Mad Cow Disease, " NEW YORK TIMES March 28, 1997, pg. A17.

 

 

 

[6] [Michael K. Hansen], " Consumers Union's Comments on Docket

 

No. 96N-0135, Proposed Rule: Substances Prohibited for Use in

 

Animal Food or Feed; Animal Proteins Prohibited in Ruminant

 

Feed, " February 14, 1997. Available from Michael Hansen,

 

Consumer Policy Institute, Consumers Union, 101 Truman Avenue,

 

Yonkers, NY 10703-1057; telephone (914) 378-2000.

 

 

 

[7] Lawrence K. Altman, " U.S. Officials Confident That Mad Cow

 

Disease of Britain Has Not Occurred Here, " NEW YORK TIMES March

 

27, 1996, pg. A12.

 

 

 

[8] Letter from Michael K. Hansen, Consumer Policy Institute, to

 

Thomas Billy, Food Safety Inspection Service, U.S. Department of

 

Agriculture, Washington, D.C. dated May 5, 1997. Available from

 

Michael K. Hansen, Consumer Policy Institute, Consumers Union,

 

101 Truman Avenue, Yonkers, NY 10703-1057; telephone (914)

 

378-2000.

 

 

 

[9] G.R. Hartsough and Dieter Burger, " Encephalopathy of Mink. I.

 

Epizootiological and Clinical Observations, " JOURNAL OF

 

INFECTIOUS DISEASES Vol. 115 (1966), pgs. 387-392.

 

 

 

[10] R.F. Marsh and others, " Epidemiological and experimental

 

studies on a new incident of transmissible mink encephalopathy, "

 

JOURNAL OF GENERAL VIROLOGY Vol. 72, Part 3 (March 1991), pgs.

 

589-594.

 

 

 

[11] C.J. Gibbs, Jr., " Experimental transmission of scrapie to

 

cattle, " LANCET Vol. 335, No. 8700 (May 26, 1990), pg. 1275.

 

 

 

[12] R.C. Cutlip and others, " Intracerebral transmission of

 

scrapie to cattle, " JOURNAL OF INFECTIOUS DISEASES Vol. 169, No.

 

4 (April 1994), pgs. 814-820.

 

 

 

[13] Francois Boller and others, " Diagnosis of dementia:

 

Clinicopathologic correlations, " NEUROLOGY Vol. 39, No. 1

 

(January 1989), pgs. 76-79.

 

 

 

[14] E.E. Manuelidis and L. Manuelidis, " Suggested links between

 

different types of dementias: Creutzfeld-Jakob disease, Alzheimer

 

disease, and retroviral CNS infections, " ALZHEIMER DISEASE AND

 

ASSOCIATED DISORDERS Vol. 3, Nos. 1-2 (1989), pgs. 100-109.

 

 

 

Descriptor terms: mad cow disease; emerging diseases;

 

creutzfeld-jacob disease; new variant creutzfeld-jacob disease;

 

nvcjd; cjd; great britain; consumers union; bse; tse;

 

transmissible spongiform encephalopathies; scrapie; britain;

 

michael hansen; prions; prion theory of disease; fda; stanley

 

prusiner; bans; ruminants; pigs; chickens; cows; consumers union;

 

richard marsh; clarence gibbs; randall cutlip; alzheimer's

 

disease;

 

 

 

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