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Exp. Second Passage of CWD (CWDmule deer) Agent to Cattle

flounder

Well-known member
Subject: Experimental Second Passage of CWD (CWDmule deer) Agent to Cattle
Date: April 25, 2006 at 8:01 am PST

Experimental Second Passage of Chronic Wasting

Disease (CWDmule deer) Agent to Cattle


A. N. Hamir, R. A. Kunkle, J. M. Miller, J. J. Greenlee and J. A. Richt

Agricultural Research Service, United States Department of Agriculture, National Animal Disease Center, 2300 Dayton

Avenue, P.O. Box 70, Ames, IA 50010, USA

Summary

To compare clinicopathological findings in first and second passage chronic wasting disease (CWDmule deer)

in cattle, six calves were inoculated intracerebrally with brain tissue derived froma first-passageCWD-affected

calf in an earlier experiment. Two uninoculated calves served as controls. The inoculated animals began to

lose both appetite and weight 10–12 months later, and five subsequently developed clinical signs of central

nervous system (CNS) abnormality. By 16.5 months, all cattle had been subjected to euthanasia because of

poor prognosis. None of the animals showed microscopical lesions of spongiform encephalopathy (SE) but

PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and rapid Western blot (WB)

techniques. Thus, intracerebrally inoculated cattle not only amplified CWD PrPres from mule deer but also

developed clinicalCNSsigns in the absence of SElesions.This situation has also been shown to occur in cattle

inoculated with the scrapie agent. The study confirmed that the diagnostic techniques currently used for

diagnosis of bovine spongiformencephalopathy (BSE) in theUS would detect CWDin cattle, should it occur

naturally. Furthermore, it raised the possibility of distinguishing CWDfromBSE in cattle, due to the absence

of neuropathological lesions and to a distinctive multifocal distribution of PrPres, as demonstrated by IHC

which, in this study, appeared to be more sensitive than the WB technique.



snip...



The present study and a previous experiment

(Hamir et al., 2005a) have established the biological

characteristics of the CWDmule deer agent in cattle.

However, isolates of CWD from other cervids (e.g.

CWDwhite-tailed and CWDelk) may differ. Transmission

experiments with different CWD isolates

are therefore needed to examine the possibility of

variation in the CWD agent in wild cervids. Such

experiments have recently been initiated at the

National Animal Disease Center (NADC).


Acknowledgments

We thank Dr Katherine I. O’Rourke for providing

the antibody for the IHC procedure. Martha

Church, Kevin Hassall, Dennis Orcutt, Jean

Donald, Sharla Van Roekel, and animal handlers

at the NADC provided expert technical assistance.

This study was carried out under the guidelines of

the institutional Animal Care and Use committee at

NADC. Mention of trade names or commercial

products in this article is solely for the purpose of

providing specific information and does not imply

recommendation or endorsement by the United

States Department of Agriculture.

References.......snip........end..............TSS
 

don

Well-known member
if they injected anything intracrebrally i think you could expect something to happen. these injections don't prove anything except that prions are involved in brain wasting diseases.
 

Mike

Well-known member
don said:
if they injected anything intracrebrally i think you could expect something to happen. these injections don't prove anything except that prions are involved in brain wasting diseases.


From the UK BSE Inquiry:

"3.203 The first successful BSE transmission studies, carried out at the NPU in November 1987, involved the intracerebral inoculation of mice with brain homogenates from BSE-affected cattle. By September 1988 positive results were obtained. 10 This was important in two respects:

1. it established the transmissible nature of BSE, and showed that brain tissue was infective in BSE-affected cattle; and
2. it showed that mice could be used as an experimental model for the disease - hence the establishment of the mouse bioassay."
 

don

Well-known member
mike: From the UK BSE Inquiry:

"3.203 The first successful BSE transmission studies, carried out at the NPU in November 1987, involved the intracerebral inoculation of mice with brain homogenates from BSE-affected cattle. By September 1988 positive results were obtained. 10 This was important in two respects:

1. it established the transmissible nature of BSE, and showed that brain tissue was infective in BSE-affected cattle; and
2. it showed that mice could be used as an experimental model for the disease - hence the establishment of the mouse bioassay."

that makes sense to me too. my point is that if we're to go with the feed transmission theory it's got to be proven. of course if it is valid it has to be shown how much contamination must be ingested and then the normal incubation period must be observed during which other causes must be eliminated. it's not as straightforward or obvious as some want to paint it.
 

flounder

Well-known member
don wrote;

that makes sense to me too. my point is that if we're to go with the feed transmission theory it's got to be proven. of course if it is valid it has to be shown how much contamination must be ingested and then the normal incubation period must be observed during which other causes must be eliminated. it's not as straightforward or obvious as some want to paint it...............




FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT


Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual. ...

snip...


http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html





WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.


look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;


Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa



It is clear that the designing scientists must

also have shared Mr Bradley’s surprise at the results because all the dose

levels right down to 1 gram triggered infection.



http://www.bseinquiry.gov.uk/files/ws/s145d.pdf




2

6. It also appears to me that Mr Bradley’s answer (that it would take less than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise that it

could take as little of 1 gram of brain to cause BSE by the oral route within the

same species. This information did not become available until the "attack rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to ensure

that the actual result was within both a lower and an upper limit within the study

and the designing scientists would not have expected all the dose levels to trigger

infection. The dose ranges chosen by the most informed scientists at that time

ranged from 1 gram to three times one hundred grams. It is clear that the designing

scientists must have also shared Mr Bradley’s surprise at the results because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf




Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]



http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram



http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm




2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)



http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml




SADLY, DEC 2005 SHOWS THAT WE STILL HAVE A SERIOUS PROBLEM WITH BSE/TSE MAD COW DISEASE FEED


GAO


GAO-06-157R FDA Feed Testing Program

October 11, 2005


SNIP...FULL TEXT 29 PAGES ;




http://www.gao.gov/new.items/d06157r.pdf




Mad Cow Disease: An Evaluation of a Small Feed Testing Program FDA Implemented in 2003 With Recommendations for Making the Program a Better Oversight Tool. GAO-06-157R, October 11



http://www.gao.gov/cgi-bin/getrpt?GAO-06-157R




CVM Update
November 2005 Update on Feed Enforcement Activities to Limit the Spread of BSE


Issued by:
FDA, Center for Veterinary Medicine,
Communications Staff, HFV-12
7519 Standish Place, Rockville, MD 20855
Telephone: (240) 276-9300 FAX: (240) 276-9115
Internet Web Site: http://www.fda.gov/cvm




http://www.fda.gov/cvm/5580.htm






TSS
 

don

Well-known member
the time has come to prove the theory by producing results in exactly the manner theorized and not just by saying tests 'indicate'. feed animals of different ages different rates over varying lengths of time and see what it takes to produce an infection in exactly the way infection is postulated to occur by the feed transmission theory. maybe i haven't been reading the right material but i have seen nothing to say definitively that animals fed a realistic amount of known infected material and kept alive to allow for incubation have developed in numbers statistically significant the bse condition. all i see is infection occurs after intracerebral injection and that is a heck of a lot different than an animal eating part of a gram.
 

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