From: TSS ()
Subject: Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model
Date: November 30, 2007 at 9:58 am PST
Volume 13, Number 12–December 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and
L-type Bovine Spongiform Encephalopathy in a Mouse Model
Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* and
Richard A. Bessen†
*Agence Française de Sécurité Sanitaire des Aliments–Lyon, Lyon, France; and
†Montana State University, Bozeman, Montana, USA
Transmissible mink encepholapathy (TME) is a foodborne transmissible
spongiform encephalopathy (TSE) of ranch-raised mink; infection with a
ruminant TSE has been proposed as the cause, but the precise origin of TME
is unknown. To compare the phenotypes of each TSE, bovine-passaged TME
isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents
(typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine
transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to
infection with bovine-passaged TME, typical BSE, and L-type BSE but not to
H-type BSE. Based on survival periods, brain lesions profiles,
disease-associated prion protein brain distribution, and biochemical
properties of protease-resistant prion protein, typical BSE had a distint
phenotype in ovine transgenic mice compared to L-type BSE and bovine TME.
The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4
mice suggest that L-type BSE is a much more likely candidate for the origin
of TME than is typical BSE.
These studies provide experimental evidence that the Stetsonville TME agent
is distinct from typical BSE but has phenotypic similarities to L-type BSE
in TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely
candidate for a bovine source of TME infection than typical BSE. In the
scenario that a ruminant TSE is the source for TME infection in mink, this
would be a second example of transmission of a TSE from ruminants to
non-ruminants under natural conditions or farming practices in addition to
transmission of typical BSE to humans, domestic cats, and exotic zoo animals
(37). The potential importance of this finding is relevant to L-type BSE,
which based on experimental transmission into humanized PrP transgenic mice
and macaques, suggests that L-type BSE is more pathogenic for humans than
typical BSE (24,38).
Transmissible Mink Encephalopathy TME
Subject: In Confidence - Perceptions of unconventional slow virus diseases
of animals in the USA - APRIL-MAY 1989 - G A H Wells
Gerald Wells: Report of the Visit to USA, April-May 1989
The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...
It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...
3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...
snip...please read this old full text document !
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
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
Transmissible mink encephalopathy (TME) was first reported in 1965 by
and Burger who demonstrated that the disease was transmissible with a long
period, and that affected mink had a spongiform encephalopathy similar to
that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough,
Because of the similarity between TME and scrapie, and the subsequent
finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it
concluded that TME most likely resulted from feeding mink scrapie-infecied
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
evidence that they may be different. Epidemiologic studies on previous
TME indicated that the incubation periods in field cases were between six
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
scrapie which might be highly pathogenic for mink, 21 different strains of
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
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was
by a strain of sheep scrapie not yet tested, or was due to exposure to a
from an unidentified source.
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville,
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
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
neurologic function beginning with locomoior incoordination, long periods of
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
practices, we obtained a careful history of feed ingredients used over the
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or
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
periods of four months. To investigate the possible involvement of cattle in
cycle, two six-week old castrated Holstein bull calves were inoculated
with a brain suspension from affected mink. Each developed a fatal
encephalopathy after incubation periods of 18 and 19 months.
These findings suggest that TME may result from feeding mink infected cattle
we have alerted bovine practitioners that there may exist an as yet
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
relationship to scrapie. Because this new bovine disease in England is
behavioral changes, hyperexcitability, and agressiveness, it is very likely
it would be
confused with rabies in the United Stales and not be diagnosed. Presently,
cattle in the United States which are suspected of rabies infection are only
anti-rabies virus antibody and are not examined histopathologically for
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the
our experimental bovine encephalopathy to mink. Because (here are as yet no
specific proteins or nucleic acids identified for these transmissible
means of distinguishing them is by animal passage and selection of the
grows best in a particular host. This procedure has been used to separate
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The
backpassage of the experimental bovine agent resulted in incubations of only
indicating no de-adaptation of the Stetsonville agent for mink after bovine
Mink fed infected bovine brain remain normal after six months. It will be
demonstrate oral transmission fiom bovine to mink it this proposed
association is to be confirmed.
These studies were supported by the College of Agricultural and Life
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the
States Department of Agriculture. The authors also wish to acknowledge the
encouragement of Robert Hanson who died during the course of these
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II.
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I.
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
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in
Proceedings of the Seventh Annual Western Conference for Food Animal
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform
in cattle. Vet. Rec. 121:419-420.
In Confidence - Perceptions of unconventional slow virus diseases
of animals in the USA - APRIL-MAY 1989 - G A H Wells
SEE FULL TEXT TME
TME hyper/drowsy, INTER-SPECIES TRANSMISSION CWD and strain properties
NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007
Date: Mon, 24 Sep 2007 21:31:55 -0500
I suggest that you all read the data out about h-BASE and sporadic CJD,
GSS,blood, and some of the other abstracts from the PRION2007. ...
*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!!
THE PRICE OF POKER INDEED GOES UP. ...TSS
USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it
today), please note that both the ALABAMA COW, AND THE TEXAS COW, both
were''H-TYPE'', personal communication Detwiler et al Wednesday, August 22,
200711:52 PM. ...TSS
see full text 143 pages ;
full text ;