• If you are having problems logging in please use the Contact Us in the lower right hand corner of the forum page for assistance.

Experimental Second Passage of CWD/TME TO CATTLE

Help Support Ranchers.net:

flounder

Well-known member
Joined
Sep 3, 2005
Messages
2,631
Reaction score
0
Location
TEXAS
##################### Bovine Spongiform Encephalopathy #####################


Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: Experimental Second Passage of Chronic Wasting Disease (Cwd-Mule Deer) Agent to Cattle


Authors

Hamir, Amirali
Kunkle, Robert - bob
Miller, Janice - ARS RETIRED
Greenlee, Justin
Richt, Juergen


Submitted to: Journal Of Comparative Pathology
Publication Acceptance Date: July 25, 2005
Publication Date: N/A


Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.
Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.





http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=178318




Research

Title: Experimental Transmission of Chronic Wasting Disease (Cwd Mule Deer) Agent to Cattle by Intracerebral Route

Authors

Hamir, Amirali
Kunkle, Robert - bob
Cutlip, Randall - ARS RETIRED
Miller, Janice - ARS RETIRED
O'Rourke, Katherine
Williams, Elizabeth - UNIVERSITY OF WYOMING
Miller, Michael - COLORADO DIV WILDLIFE
Stack, Mick - VET SERVICES AGENCY, UK
Chaplin, Melanie - VET SERVICES AGENCY, UK
Richt, Juergen


Submitted to: Journal Of Veterinary Diagnostic Investigation
Publication Acceptance Date: January 3, 2005
Publication Date: May 1, 2005
Citation: Hamir, A.N., Kunkle, R.A., Cutlip, R.C., Miller, J.M., Orourke, K.I., Williams, E.S., Miller, M.W., Stack, M.J., Chaplin, M.J., Richt, J. 2005. Experimental Transmission Of Chronic Wasting Disease Agent To Cattle By Intracerebral Route. Journal Of Veterinary Diagnostic Investigation. 17:276-281.

Interpretive Summary: This communication reports final observations on experimental transmission of chronic wasting disease (CWD) from mule deer to cattle. Thirteen calves were inoculated into the brain with brain suspension from mule deer naturally affected with CWD. Three other calves were kept as uninoculated controls. The experiment was terminated 6 years post inoculation (PI). During that time, abnormal prion protein was demonstrated in the brain and spinal cord of 5 cattle by laboratory tests. However, consistent clinical signs and microscopic changes were not seen in any of these cattle. Age related changes were seen in both inoculated and control cattle. Findings of this study show that only 38% of the inoculated cattle were positive for CWD agent. Although inoculation directly into the brain is an unnatural route of exposure, and is the most severe challenge possible, this experiment shows that CWD transmission in cattle could have long incubation periods (up to 5 years). This finding suggests that oral exposure of cattle to CWD agent, a more natural potential route of exposure, would require not only a much larger dose of inoculum, but also, may not result in amplification of CWD agent within brain and spinal cord tissues during the normal lifespan of cattle. It is possible that a second bovine passage of material (cattle brain infected with CWD) from this study may result in a larger incidence of affected cattle with a shortened incubation time, and may produce different clinical and pathological findings. Such a study is now in progress. Also, experimental inoculations of cattle with CWD isolates from white-tailed deer and elk are needed to compare findings with the present study and these studies will be initiated in the near future. Impact: Results of this study show that although cattle inoculated directly into the brain with CWD succumb to the disease, the attack rate was rather small (38%) with this unnatural route of transmission. It is speculated that the oral route of infection may not result in replication of the agent during normal lifespan of cattle.
Technical Abstract: This communication reports final observations on experimental transmission of chronic wasting disease (CWD) from mule deer to cattle by the intracerebral route. Thirteen calves were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD. Three other calves were kept as uninoculated controls. The experiment was terminated 6 years post inoculation (PI). During that time, abnormal prion protein (PrPres) was demonstrated in the central nervous system (CNS) of 5 cattle by both immunohistochemistry (IHC) and Western blot (WB). However, microscopic lesions suggestive of spongiform encephalopathy in the brains of these PrPres positive animals were subtle in 3 cases and absent in 2 cases. The 3 uninoculated control cattle and 8 other inoculated animals euthanized during this time did not have PrPres in their CNS. Degenerative changes indicative of neuroaxonal dystrophy (NAD) were seen in dorsal medulla oblongata and appeared to be related to advancing age in both inoculated and control cattle. Analysis of the gene encoding bovine PRNP revealed homozygosity for alleles encoding 6 octapeptide repeats, serine (S) at codon 46 and S at codon 146 in all samples. Findings of this study show that although PrPres amplification occurred following direct inoculation into the brain, none of the affected animals had classic histopathologic lesions of spongiform encephalopathy. Furthermore, only 38% of the inoculated cattle demonstrated amplification of PrPres. Although intracerebral inoculation is an unnatural route of exposure, and is the most severe challenge possible, this experiment shows that CWD transmission in cattle could have long incubation periods (up to 5 years). This finding suggests that oral exposure of cattle to CWD agent, a more natural potential route of exposure, would require not only a much larger dose of inoculum, but also, may not result in amplification of PrPres within CNS tissues during the normal lifespan of cattle.





Page Modified: 09/05/2005



http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=166311


TSS

#################### https://lists.aegee.org/bse-l.html ####################



##################### Bovine Spongiform Encephalopathy #####################


Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: First and Second Cattle Passage of Transmissible Mink Encephalopathy (Tme) by Intracerebral Inoculation


Authors

Hamir, Amirali
Kunkle, Robert - bob
Miller, Janice - ARS RETIRED
Bartz, J - CREIGHTON UNIVERSITY
Richt, Juergen


Submitted to: Veterinary Pathology
Publication Acceptance Date: August 12, 2005
Publication Date: N/A


Interpretive Summary: Transmissible mink encephalopathy (TME) is a fatal neurologic disease. It is similar to bovine spongiform encephalopathy (BSE) or mad cow disease. To compare TME infection with other similar diseases in cattle, 2 groups of calves were inoculated in the brain with TME agents from 2 different sources. Two uninoculated calves served as controls. Within 15.3 months post inoculation, animals from both inoculated groups developed clinical signs of central nervous system (CNS) abnormality. Laboratory tests revealed lesions and presence of the TME agent in their tissues. Both findings could not be differentiated from those seen in BSE. Our findings also demonstrated that the laboratory tests that are currently used for BSE surveillance would detect TME in cattle should it occur naturally. However, it would be a diagnostic challenge to differentiate TME in cattle from BSE by clinical signs or laboratory tests that are currently available. Results of this study will have an impact on directing future research on TSEs to search for specific laboratory tests to differentiate BSE from TME in cattle.
Technical Abstract: To compare clinicopathological findings of transmissible mink encephalopathy (TME) with other transmissible spongiform encephalopathies (TSE, prion diseases) that have been shown to be experimentally transmissible to cattle (sheep scrapie, and chronic wasting disease, CWD), 2 groups of calves (n = 4 each) were intracerebrally inoculated with TME agents from 2 different sources (mink with TME and a bovine with TME). Two uninoculated calves served as controls. Within 15.3 months post inoculation (PI), animals from both inoculated groups developed clinical signs of central nervous system (CNS) abnormality; their CNS tissues had microscopic spongiform encephalopathy (SE); and PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify TME PrPres but also develop clinical CNS signs and extensive lesions of SE. The latter has not been shown with other TSE agents (scrapie and CWD) similarly inoculated into cattle. The findings also demonstrate that the diagnostic techniques currently used for bovine spongiform encephalopathy (BSE) surveillance would detect TME in cattle should it occur naturally. However, it would be a diagnostic challenge to differentiate TME in cattle from BSE by clinical signs, neuropathology, or the presence of PrPres by IHC and WB.




http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=173819


TSS

#################### https://lists.aegee.org/bse-l.html ####################
 

flounder

Well-known member
Joined
Sep 3, 2005
Messages
2,631
Reaction score
0
Location
TEXAS
roll your eyes all you want, it will not change things tim. you cannot wish this agent away. this has been tried for the last 30 years or so. the only people that can help us here and stop this agent are the ranchers and farmers. as you can see, the USDA et al were a big part of the problem. i do not accept stupidity as an excuse anymore. ...tss
 

Mike

Well-known member
Joined
Feb 10, 2005
Messages
28,480
Reaction score
0
Location
Montgomery, Al
flounder said:
roll your eyes all you want, it will not change things tim. you cannot wish this agent away. this has been tried for the last 30 years or so. the only people that can help us here and stop this agent are the ranchers and farmers. as you can see, the USDA et al were a big part of the problem. i do not accept stupidity as an excuse anymore. ...tss

TS, You're preaching to the choir here. Although there are disagreements on transmission, etc. among us, we know the ramifications that the media can do to our livlihoods and are disappointed in some efforts of the governmental agencies involved with protecting the beef producers and consumers.

The postings allowed by you here will only solidify the opinions on both sides of the spectrum, and will do nothing to diminish the chances of BSE in North America. We are in the cattle and beef business, not politicians, and are at the mercy of the policy makers.

In other words, you're barking up the wrong tree.
 

rkaiser

Well-known member
Joined
Feb 14, 2005
Messages
1,958
Reaction score
0
Location
Calgary Alberta
roll your eyes all you want, it will not change things tim. you cannot wish this agent away. this has been tried for the last 30 years or so. the only people that can help us here and stop this agent are the ranchers and farmers. as you can see, the USDA et al were a big part of the problem. i do not accept stupidity as an excuse anymore. ...tss

That a boy flounder, start calling people stupid. That will certainly get you respect on ranchers.net.

Why don't you come right out and call your AGENT, the INFECTIOUS AGENT flounder. Or are we missing something in your lenghty posts that you yourself believe?
 

flounder

Well-known member
Joined
Sep 3, 2005
Messages
2,631
Reaction score
0
Location
TEXAS
i think i am barking up the right tree here. just have to get you folks to understand this agent better. politics is a big part of the problem here.
nothing i would like better to do than sit down with you guys and gals,
have a thick porter house (minus feces, srms and prions) and a cold lone star. we must get this correct though.

i did not call anyone stupid, i simply said;

> i do not accept stupidity as an excuse anymore.


it's time for the ranchers and farmers to get as mad as we are at the federal gov. this is and was there fault. hell, the farmers are at more of a risk factor to sporadic CJD than we are. but you will not read this either on the USDA/APHIS site;


CJD FARMERS WIFE 1989

http://www.bseinquiry.gov.uk/files/yb/1989/10/13007001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/10/13003001.pdf

20 year old died from sCJD in USA in 1980 and a 16 year
old in 1981. A 19 year old died from sCJD in
France in 1985. There is no evidence of an iatrogenic
cause for those cases....

http://www.bseinquiry.gov.uk/files/yb/1995/10/04004001.pdf

cover-up of 4th farm worker ???

http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf

http://www.bseinquiry.gov.uk/files/yb/1995/10/20006001.pdf

CONFIRMATION OF CJD IN FOURTH FARMER

http://www.bseinquiry.gov.uk/files/yb/1995/11/03008001.pdf

now story changes from;

SEAC concluded that, if the fourth case were confirmed, it would be
worrying, especially as all four farmers with CJD would have had BSE
cases on their farms.

to;

This is not unexpected...

was another farmer expected?

http://www.bseinquiry.gov.uk/files/yb/1995/11/13010001.pdf

4th farmer, and 1st teenager

http://www.bseinquiry.gov.uk/files/yb/1996/02/27003001.pdf

2. snip...
Over a 5 year period, which is the time period on which the advice
from Professor Smith and Dr. Gore was based, and assuming a
population of 120,000 dairy farm workers, and an annual incidence
of 1 per million cases of CJD in the general population, a
DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN
an individual in the general population to develop CJD. Using the
actual current annual incidence of CJD in the UK of 0.7 per
million, this figure becomes 7.5 TIMES.

3. You will recall that the advice provided by Professor Smith in
1993 and by Dr. Gore this month used the sub-population of dairy
farm workers who had had a case of BSE on their farms -
63,000, which is approximately half the number of dairy farm
workers - as a denominator. If the above sums are repeated using
this denominator population, taking an annual incidence in the general
population of 1 per million the observed rate in this sub-population
is 10 TIMES, and taking an annual incidence of 0.7 per million,
IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than
that in the general population...

http://www.bseinquiry.gov.uk/files/yb/1995/01/31004001.pdf

whether it be nvCJD or sCJD your are 100% dead either way.
sCJD IS NOT A STRAIN, but potentially multiple strains from many different routes and sources.


i am not here as the enemy. i am simply here to tell the rest of the story.
many here will not want to hear it. but it must be told...


TSS
 

Kathy

Well-known member
Joined
Feb 11, 2005
Messages
837
Reaction score
0
Location
Home on the Range, Alberta
Terry people might be more willing to listen to things you have to show us, if you were listening to some of the things we show you.

You refuse to acknowledge threads which dispute the infectious hypothesis vs. metal contamination, and induction vs. infection (Parish). Debating our stand, is what we are doing here. Not just throwing papers at each other.

The majority of papers I have seen, that relate the incidents of CJD, Parkinson's and other neurological symptoms to chemicals (mostly Ag chemicals).

A farmer may have never treated his cattle with OPs or other various chemicals, but that does not mean they were not exposed to them. If the farmer fed MBM he was unwittingly feeding his animals the bio-accummulated lipophilic chemicals, like Phosmet (UK BSE epidemic). Fish meal has the potential to be laiden with toxic chemicals as well. Yet, we still allow its use.

Ranchers are working to sort this out. Common sense tells us that if it were an infectious organism the results of infection would be more rampant and much faster. All this crap about 40-50 year incubation periods, is just a deceiptful way of telling people that these metallomicrocrystals are growing slowly, as the right conditions for growth come and go with time/exposures to oxidative stresses. Arthritis is a similar disease affecting bones and joints.

You may continue to bring your points forward here, but I truely wonder who has the closed mind. Some of us look at these transmission/passage experiments and see flaws, you don't. Some of us look at the other options, gathering info from many sources and forming our own opinions, you don't (so it appears). You will take the word of reports which I have time and again, shown to be lying and misleading (Horne Report, Harvard Risk Assessment, AARI Report).

It is truely the debate of the issues which will bring forth knowledge. Not the promulgating of positions. But, the wheels move slowly everywhere.
 

Latest posts

Top