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Just how little BSE in feed will result in transmission?

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Mike-"I was gonna attempt to show you how the paper you posted proves the feed transmission theory.

Do you understand it yet?"

Well, I'm pretty sure I understand it ,Mike. My position all along has been that .....scientists have, thus far, been unable to infect(confirmed by actual BSE test) another bovine with BSE by FEEDING (not injecting) it a normal dosage(not homogenate) of infective material.
There is nothing in that paper that proves they have. Those calves were drenched with homegenate and then homogenates of their tissues were injected into mice.No mention of how long after they were drenched until the tissues were taken....the next day???How does that equate to proof positive that feeding a normal dose will produce infectivity in a bovine?
I hate to quote an unpublished study, but if you look in that chart there is one in which calves fed an oral dose showed no infectivity after 7 years. But as I said that study ,for whatever reason, is unpublished.
I'll stand behind my position. Scientist have yet to infect a bovine with BSE through normal feeding. :D
 
TimH said:
Mike-"I was gonna attempt to show you how the paper you posted proves the feed transmission theory.

Do you understand it yet?"

Well, I'm pretty sure I understand it ,Mike. My position all along has been that .....scientists have, thus far, been unable to infect(confirmed by actual BSE test) another bovine with BSE by FEEDING (not injecting) it a normal dosage(not homogenate) of infective material.
There is nothing in that paper that proves they have. Those calves were drenched with homegenate and then homogenates of their tissues were injected into mice.No mention of how long after they were drenched until the tissues were taken....the next day???How does that equate to proof positive that feeding a normal dose will produce infectivity in a bovine?
I hate to quote an unpublished study, but if you look in that chart there is one in which calves fed an oral dose showed no infectivity after 7 years. But as I said that study ,for whatever reason, is unpublished.
I'll stand behind my position. Scientist have yet to infect a bovine with BSE through normal feeding. :D
Click to expand...

An actual BSE test is a mouse bioassay. Time consuming, but nevertheless, an actual test. It's all they had until the IHC was used.

The four month old calves were fed by Dawson and Wells dried brain matter from infected cattle. 100 grams, 10 grams, and 1 gram

The calves were harvested in intervals from 6 months to 6 years. Different parts of the calves were injected into mice, intracerebral and also some were injected intraperitoneal. The mice came down with the disease because of the infected material (homogenate)from the calves infected them.

Every calf was positive. The calves fed the lower doses had a longer incubation period.

If there were no prions in the calf material the mice would NOT have become infected.

It was proof positive and still stands today that feed transmission is a fact.

Read that one again about the 7 years and you will see that you are wrong on that one too!
 
Mike, this Tim guy is never going to get it! He refuses to see that which is in front of him. We have tried, but he still refuses to see that any animal that ingests BSE infected material, regardless of whether it is brain or fried eggs, the ingestion process is what transmits the infection to the animal. It is simply put, a fact. Give it up and move on. He will never be satisfied - period! I tried to offer him something and he shoots it down in flames when you and I know it to be a fact. Oh well, I am moving on and will engage in wholesome discussion with those who wish to accept the truth and discuss it reasonably. GOod effort though Mike. He does appear to be well versed in the field of BSE and yet he also appears to be somewhat focused on the absurd reasoning that oral routing is NOT direct ingestion. What is with that hypothesis?
 
They have four confirmed cases of BSE in North America, that should be enough for these scientists to go on. They seem very well versed in hypothetical cases, they have now got some real cases to expand on. Try figuring out where it has come fro, how it was transmitted, how much feed it has taken to infect, etc.

Work with the real world, not hypothetical?
 
1: Dev Biol Stand. 1993;80:157-70. Related Articles, Links


The research programme on transmissible spongiform encephalopathies in Britain with special reference to bovine spongiform encephalopathy.

Bradley R.

Central Veterinary Laboratory, Addlestone, Surrey, UK.

Research into bovine spongiform encephalopathy (BSE) commenced immediately following its discovery in November 1986. Formal epidemiological studies commenced in June 1987 and were part of a large research programme set up mainly at the Central Veterinary Laboratory Weybridge and the Institute for Animal Health, AFRC/MRC Neuropathogenesis Unit in Edinburgh. This programme also covered the clinicopathology of BSE, transmission studies and molecular chemistry. Research results have shown that BSE is a member of the group of diseases known as the sub-acute spongiform encephalopathies caused by unconventional transmissible agents and which includes scrapie of sheep, from which BSE was probably derived, and Creutzfeldt Jakob disease (CJD) of man. The agent causing BSE closely resembles strains of the scrapie agent but is not identical. Spongiform encephalopathy has developed in sheep, goats, pigs, cattle, marmosets and mice but not hamsters following experimental inoculation of brain material from confirmed clinical cases of BSE. BSE agent has been detected by mouse bio-assay in brain from cows from several sources confirmed to have BSE. Infectivity has not been detected in spleen, buffy coat, semen, muscles, placenta and bone marrow (all following parenteral inoculation) nor in milk/mammary gland, spleen, placenta and a variety of lymph nodes following substantial oral exposure. This latter route successfully transmitted disease to mice with brain/cerebrospinal fluid. The introduction of modified rendering systems, which did not employ hydrocarbon solvent extraction, were probably responsible for an increase in exposure of cattle from 1981-1988 sufficient to cause the disease. Experiments are in progress to investigate the effectiveness of different rendering systems used in the European Community and of chemical and physical de-activating procedures for destroying BSE and scrapie infectivity. A clear genetic influence on disease susceptibility has been suggested but is not yet proven. The Agricultural and Food Research Council have set up a large Biology of Spongiform Encephalopathies Research Programme to address some of the more fundamental unknowns of this group of diseases but it is too early to report results. As with scrapie, no epidemiological relationship has been demonstrated between BSE and the human diseases through the monitoring programme that has been established by the Department of Health to detect such an occurrence. BSE research results so far show that controls to protect animal and human health and based initially on scrapie research findings, are sound.(ABSTRACT TRUNCATED AT 400 WORDS)

Publication Types:
Review
Review, Tutorial

PMID: 8270105 [PubMed - indexed for MEDLINE]

************************************************************

Ron, I don't know why these guys don't get it. Maybe the homogenate thing or the mouse bioassay thing is throwing them off?

homogenate:
A chaotic slurry of tissues and cells which results when cell-tissue structure has been mechanically disrupted (as opposed to by chemical means).

The reason for homogenates is simply to prepare the tissue for injection by a syringe. After all, you can't stick a brain in a syringe and inject it.

They are confusing the mouse bioassay in these test methods. All of the early testing used mouse bioassay. It's simply the only method they had at the time.
 
Quote from Mike's above post- "....substantial oral exposure. This latter route successfully transmitted disease to mice with brain/cerebrospinal fluid."

What does "substantial oral exposure mean" to you???


More interesting quotes-"The introduction of modified rendering systems, which did not employ hydrocarbon solvent extraction, were probably responsible for an increase in exposure of cattle from 1981-1988 sufficient to cause the disease."

Are these prions indestructible or not??? Excellent use of the word "probably" in a "scientific" article.

And my favorite- "As with scrapie, no epidemiological relationship has been demonstrated between BSE and the human diseases through the monitoring programme that has been established by the Department of Health to detect such an occurrence."

"no epidemiological relationship has been demonstrated between BSE and the human diseases ...."

NO relationship between BSE and the human diseases, and yet people are led to believe that vCJD is caused by eating contaminated beef.

Tell us R2, would that qualify as a "smokescreen"???? :lol:
 
reader (the Second) said:
Mike - this smokescreen stuff has been going on for as long as I have been posting on Ranchers.net. If something is proven in the lab by scientists, it is disbelieved. There appears to be a basic misunderstanding about what is science and the scientific method.

Purdey is believed because he ASSERTS that he's been everywhere where there are TSEs in the world -- not believable in itself frankly -- and sampled the soil for metals. Even when the facts contradict him, he is believed whereas 15 years of lab work by hundreds of scientists is rejected outright. Any excuse will do.
Click to expand...

I know, R2. A comment was made some time ago about the work with mice and BSE. I could only stand back and snicker. Medicine and research would be in the dark ages were it not for mice experimentation.

The argument about "Homogenates" is a joke too.

This is not really a "smokescreen" as you put it. I think it's the inability to comprehend because of the unwillingness to believe.

Feed transmission in cattle is a fact. No reasonable person could argue it given the information available.

I also believe that Purdey is somewhat correct in some of his metals and/or organophosphates theory in that metals played a part in the immunities of cattle making them more susceptable to prions.
The work on BSE is below a molecular level, it is probably down to the atoms and nano level which means that it may be years before we fully understand it fully.
 
TimH said:
Quote from Mike's above post- "....substantial oral exposure. This latter route successfully transmitted disease to mice with brain/cerebrospinal fluid."

What does "substantial oral exposure mean" to you???


More interesting quotes-"The introduction of modified rendering systems, which did not employ hydrocarbon solvent extraction, were probably responsible for an increase in exposure of cattle from 1981-1988 sufficient to cause the disease."

Are these prions indestructible or not??? Excellent use of the word "probably" in a "scientific" article.

And my favorite- "As with scrapie, no epidemiological relationship has been demonstrated between BSE and the human diseases through the monitoring programme that has been established by the Department of Health to detect such an occurrence."

"no epidemiological relationship has been demonstrated between BSE and the human diseases ...."

NO relationship between BSE and the human diseases, and yet people are led to believe that vCJD is caused by eating contaminated beef.

Tell us R2, would that qualify as a "smokescreen"???? :lol:
Click to expand...
What does "substantial oral exposure mean" to you???

Substantial oral exposure would mean enough to infect the cattle with BSE.
Click to expand...
More interesting quotes-"The introduction of modified rendering systems, which did not employ hydrocarbon solvent extraction, were probably responsible for an increase in exposure of cattle from 1981-1988 sufficient to cause the disease."

Are these prions indestructible or not??? Excellent use of the word "probably" in a "scientific" article.

There was a big argument in the UK about cooking rendered material to a
high enough temperature that was thought at the time to destroy prions.
Remember that this was before much was known about prions. Prions have been proven since to be destructable by certain chemicals AND above certain temperatures.

"no epidemiological relationship has been demonstrated between BSE and the human diseases ...."

NO relationship between BSE and the human diseases, and yet people are led to believe that vCJD is caused by eating contaminated beef.
Click to expand...

Remember also this was before the connection was not made between BSE and vCJD. The subsequent research has proven otherwise.

Tim, you're fighting a losing battle here and making a fool of yourself. You're using old research to try to prove a now known mute point, but on the other hand will not use old research that has not been discredited.
You're out of your element, Jethro.
 
Excellent artcle R2. My personal theory of reductions in copper levels lowering the immunities in cattle are not purely conjecture. However, we are not dealing with bacteria and viruses, as far as known yet.

You are probably correct that DNA is somehow the barrier we are looking for in susceptability to the disease. The Prionic's Test that establishes a DNA model analysis along with the prion test may be the key that determines the future of BSE, as we know it. The sub-atomic ramifications could be part of it also. Nano-technology is a few years down the road.
 
Mike- "Tim, you're fighting a losing battle here and making a fool of yourself. You're using old research to try to prove a now known mute point, but on the other hand will not use old research that has not been discredited.
You're out of your element, Jethro."

Huh??? :? I'm using old research??? You posted the article to try to prove YOUR point, Mike.
You are quoting 10 year-old studies done using now obsolete mouse bioassy methods as proof positive of feed transmission. I'm not the only person in the world who questions the validity of BSE research being done with mouse bioassay.

How could you possibly know what my "element" is? :???: Are you psychic?? :roll:
Gotta run. Just popped in for a quick bite and now back to work.
Maybe we could fight some more, later!! :lol: :lol: :wink:
 
You are quoting 10 year-old studies done using now obsolete mouse bioassy methods as proof positive of feed transmission. I'm not the only person in the world who questions the validity of BSE research being done with mouse bioassay.
Click to expand...

The 10 year old studies of feed transmission still stand as accepted Tim. No more tests of feed transmissibility will probably ever be done because these early ones are accurate. Just try to get funding for research that has already been proven.

You still do not understand the meaning of mouse bioassay. It is a test that can and is still being used as a means for determining BSE in cattle. Before the advent of IHC, it was the only test known. In fact, the accuracy testing of IHC was based on the bioassay as being the "reference" test.

There are no scientists that question mouse bioassay as being accurate or valid. What gives you more credentials to question it?

I know what your "element" is because of your comprehension, or lack of, in what is written. I mean this with no ill feelings.
 
Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update.

Wells GA, Hawkins SA, Green RB, Austin AR, Dexter I, Spencer YI, Chaplin MJ, Stack MJ, Dawson M.

Veterinary Laboratories Agency, Central Veterinary Laboratory, New Haw, Addlestone, Surrey.

Further preliminary observations are reported of an experiment to examine the spread of infectivity and the occurrence of pathological changes in cattle exposed orally to infection with bovine spongiform encephalopathy. Calves were dosed at four months of age and clinically monitored groups were killed sequentially from two to 40 months after inoculation. Tissues were collected for bioassay, for histopathological examinations and for the detection of PrP. Previous reported observations have included the presence of infectivity in the distal ileum of cattle killed after six to 18 months, the earliest onset of clinical signs in an exposed animal after 35 months, and diagnostic histopathological changes in the brain, in association with clinical disease, after 36, 38 and 40 months. In spite of the relative inefficiency of the bioassay of scrapie-like agents across a species barrier the new observations confirm that the onset of clinical signs and pathological changes in the central nervous system (CNS) occur at approximately the same time. The earliest pathological change, the presence of abnormal PrP 32 months after inoculation, coincided with the earliest detected infectivity in the CNS and occurred shortly before there was evidence of typical spongiform changes in the brain 36 months after inoculation. Infectivity has now been demonstrated in the peripheral nervous system, in the cervical and thoracic dorsal root ganglia 32 to 40 months after inoculation and in the trigeminal ganglion 36 and 38 months after inoculation. At the time of writing evidence of infectivity in other tissues is confined to the distal ileum, not only after six to 18 months but also after 38 and 40 months, but these findings may be supplemented by the results of further mouse assays. Nevertheless, they are in general agreement with current knowledge of the pathogenesis of scrapie.

PMID: 9501384 [PubMed - indexed for MEDLINE]
 
And another.

roc Natl Acad Sci U S A. 2002 Dec 10;99 Suppl 4:16378-83. Epub 2002 Aug 14. Related Articles, Links
Click here to read Click here to read
Transmission of prions.

Weissmann C, Enari M, Klohn PC, Rossi D, Flechsig E.

Medical Research Council Prion Unit, Department of Neurodegenerative Disease, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom. [email protected].

The "protein only" hypothesis states that the infectious agent causing transmissible spongiform encephalopathies is a conformational isomer of PrP, a host protein predominantly expressed in brain, and is strongly supported by many lines of evidence. Prion diseases are so far unique among conformational diseases in that they are transmissible, not only experimentally but also by natural routes, mainly by ingestion. A striking feature of prions is their extraordinary resistance to conventional sterilization procedures, and their capacity to bind to surfaces of metal and plastic without losing infectivity. This property, first observed in a clinical setting, is now being investigated in experimental settings, both in animals and in cell culture.

PMID: 12181490 [PubMed - indexed for MEDLINE]
 
Fraser et al managed to bring about BSE infection through the oral routing of BSE infected tissue in cattle, goats and sheep. TimH seems only to want to resead the inoculation section of the Paper and dismiss the oral to suit his lame-brain arguments regarding oral ingestion. I rest my case with this clown. He appears only to want to ridicule the postings of others here and when offered the evidence he seeks, he simply refuses to see it. Mike, give up on this guy. I have. Narang did it while working for MAFF and the Edinburgh team, including Robinson et al, did it in the late 80's and early 90's. THe CFIA and the USDA as well as the EFSA have stated that infected feed was/is the culprit.
 
bse-tester said:
Fraser et al managed to bring about BSE infection through the oral routing of BSE infected tissue in cattle, goats and sheep. TimH seems only to want to resead the inoculation section of the Paper and dismiss the oral to suit his lame-brain arguments regarding oral ingestion. I rest my case with this clown. He appears only to want to ridicule the postings of others here and when offered the evidence he seeks, he simply refuses to see it. Mike, give up on this guy. I have. Narang did it while working for MAFF and the Edinburgh team, including Robinson et al, did it in the late 80's and early 90's. THe CFIA and the USDA as well as the EFSA have stated that infected feed was/is the culprit.
Click to expand...
If you all seem to agree that feed transmition is the only plausable means of transmision, why do we not find herdmates that ate the same feed under the same conditions infected????? Some of the studies sited showed very high transmision rates with low ingestion rates of prions? If feed were the only cause a person would think that you would see clusters caused by bad feed and feeding practises!!!!!!!
 
I do not think anyone mentioned that infected feed was the sole cause of BSE in any of these recent postings. But your comment does raise the question of why the CFIA and the USDA would slaughter all animals in the same herd as a BSE positive animal, when none of them displayed any clinical symptoms?
 
bse-tester said:
I do not think anyone mentioned that infected feed was the sole cause of BSE in any of these recent postings. But your comment does raise the question of why the CFIA and the USDA would slaughter all animals in the same herd as a BSE positive animal, when none of them displayed any clinical symptoms?
Click to expand...

My point is that if the feed is the no. 1 suspect by all the leading experts, why do they not find problems with herdmates of the same age ingesting the same feed under the same conditions? A person using logic and there findings would conclude that there would be some clusters. The lack of any herdmates having bse is one reason that many people are hard to convince :shock: They tell us how easy it is to transmit bse with contaminated feed but can not show us a second case from eating the very same feed that was blamed for the cases that were found?
 
mwj said:
bse-tester said:
Fraser et al managed to bring about BSE infection through the oral routing of BSE infected tissue in cattle, goats and sheep. TimH seems only to want to resead the inoculation section of the Paper and dismiss the oral to suit his lame-brain arguments regarding oral ingestion. I rest my case with this clown. He appears only to want to ridicule the postings of others here and when offered the evidence he seeks, he simply refuses to see it. Mike, give up on this guy. I have. Narang did it while working for MAFF and the Edinburgh team, including Robinson et al, did it in the late 80's and early 90's. THe CFIA and the USDA as well as the EFSA have stated that infected feed was/is the culprit.
Click to expand...
If you all seem to agree that feed transmition is the only plausable means of transmision, why do we not find herdmates that ate the same feed under the same conditions infected????? Some of the studies sited showed very high transmision rates with low ingestion rates of prions? If feed were the only cause a person would think that you would see clusters caused by bad feed and feeding practises!!!!!!!
Click to expand...

Many herdmates that ate the same feed HAVE been infected. Just not in North America. Key here is that you have to have prions in the feed to begin with for it to infect. Since the UK has so many sheep and the infection is believed to have jumped species there, it reciprocated itself through the rendering system. They were incubating it long before they even knew they had it.

DNA types are believed to be a barrier also.
 
My point is that if the feed is the no. 1 suspect by all the leading experts, why do they not find problems with herdmates of the same age ingesting the same feed under the same conditions? A person using logic and there findings would conclude that there would be some clusters. The lack of any herdmates having bse is one reason that many people are hard to convince.

You just have to wait longer on smaller amounts.We use to feed Honneggers MBM back in the eightys and early ninetys as the college's were pushing it in the feed ration,it was even in the Feeds and Feeding book.
Now I hope the FDA gets their act together so it will be removed from all livestock and fowl rations and this whole fiasco will be behind society 50 yrs from now.
 

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