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From: TSS ()
Subject: New twist in tale of BSE's beginnings or old news finally brought forth
Date: March 18, 2007 at 7:09 pm PST

New twist in tale of BSE's beginnings
10:27 18 March 2007
NewScientist.com news service
Debora MacKenzie


THE discovery that a rare brain disease in cows can mutate into BSE has given new life to the theory that mad cow disease started out in cattle, rather than crossing over from sheep.

When BSE emerged in British cattle in the mid-1980s, the leading theory was that they had initially contracted the disease by eating feed containing the remains of sheep infected with scrapie. Both BSE and scrapie are caused by infectious prions, misshapen forms of a normal brain protein. Having made this species jump, BSE would have spread as cattle carcasses were processed into animal fodder and fed back to cows.

Yet attempts to duplicate BSE by deliberately giving scrapie to cows have failed, and many countries included sheep remains in cattle feed without creating BSE. This has led some scientists to speculate that BSE arose as a rare spontaneous condition in cattle, which spread to other cows when they ate these animals' remains.

The new twist to the story comes from studies of a disease called bovine amyloidotic spongiform encephalopathy, or BASE. It was discovered in 2003, when two Italian cows, out of tens of thousands of European cattle screened for BSE at slaughter, were found to have a prion disease that seemed different from BSE. The BASE prion had a lower molecular weight and one, rather than two, sugars bound to it. The brains of cows with BASE were also damaged in different places from those with BSE, and had dense protein deposits called amyloid that are not seen in BSE. Similar prions have also turned up in France, Germany and Japan.

“Two Italian cows being screened at slaughter were found to have a prion disease that seemed different from BSE”
Fabrizio Tagliavini and his colleagues at the Carlo Besta Neurological Institute in Milan, Italy, have now injected material from the brains of cows with BSE or BASE into mice. In animals genetically altered to make cow PrP - the normal form of the prion protein - BSE and BASE produced different symptoms and brain damage, confirming that BASE is a different disease.

When Tagliavini injected material from the brains of cows with BASE into mice with normal mouse PrP, none developed symptoms and only one tested positive for a prion - which looked like BSE, not BASE. When brain material from this first groups of mice was injected into a second round of mice, all of them developed typical BSE (PLoS Pathogens, DOI: 10.1371/journal.ppat.0030031). In unpublished experiments, Tagliavini has shown that the conversion of BASE prion to BSE can also occur in the spleens of mice engineered to carry cow PrP.

If BASE can mutate into BSE, this could well be how mad cow disease emerged. "I think BASE is a natural prion disease of older cattle, which turned into BSE," says Tagliavini.

Another possibility is that BASE turned into BSE after cattle remains were fed to sheep. In preliminary research, Hubert Laude of INRA, the French national agricultural research agency, in Jouy-en-Josas says that he has got BASE to turn into BSE in mice engineered to carry sheep PrP, but not in mice with cow or human PrP.

http://www.newscientist.com/article/dn11395-new-twist-in-tale-of-bses-beginnings.html


seems this brings us back to the old studies of the late Richard Marsh. those mad mink i.e. TME were fed 95%+ dead stock DOWNER CATTLE, so why is it so hard to imagine that BASE could not transmit the same way, orally, as did with BSE. ...tss


To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf


TSS



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