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Detection of Bovine MBM in Animal Feed at a Level of 0.1%

flounder

Well-known member
Detection of Bovine Meat and Bone Meal in Animal Feed at a Level of 0.1%

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Author(s): Henk J.M. Aarts 1, | El M. Bouw 2, | Jaap B. Buntjer 3, | Johannes A. Lenstra 4, | Leo W.D. van Raamsdonk 5




Print ISSN: 1060-3271
Volume: 89 | Issue: 6
Cover date: November/December 2006
Page(s): 1443-1446



Abstract text


For the control of the transmission of bovine spongiform encephalopathy in cattle via feedstuff, a real-time polymerase chain reaction assay was developed with ruminant-specific Bov-B SINE primers, SYBRGreen fluorescence detection, and melting curve analysis. In formulated cattle and chicken feed samples spiked with pure bovine and sheep meat and bone meal heated at 133°C for 20 min, a contamination level of 0.1% was detected.

Author(s): Henk J.M. Aarts 1, | El M. Bouw 2, | Jaap B. Buntjer 3, | Johannes A. Lenstra 4, | Leo W.D. van Raamsdonk 5


Author(s) affiliations



1RIKILT-Institute of Food Safety, Wageningen UR, Bornsesteeg 45, 6708 PD Wageningen, The Netherlands.
[email protected]
2RIKILT-Institute of Food Safety, Wageningen UR, Bornsesteeg 45, 6708 PD Wageningen, The Netherlands.
3Keygene N.V., PO Box 216, 6700 AE Wageningen, The Netherlands.
4Utrecht University, Faculty of Veterinary Medicine, Yalelaan 8, 3584 CM Utrecht, The Netherlands.
5RIKILT-Institute of Food Safety, Wageningen UR, Bornsesteeg 45, 6708 PD Wageningen, The Netherlands.



http://www.atypon-link.com/AOAC/doi/abs/10.5555/jaoi.89.6.1443


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


[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf


[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)


http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf



THE SEVEN SCIENTIST REPORT ***


http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf


PAUL BROWN M.D.

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf




9 December 2005
Division of Dockets Management (RFA-305)

SEROLOGICALS CORPORATION
James J. Kramer, Ph.D.
Vice President, Corporate Operations

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf



Embassy of Japan
http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm


TSS
 

Kathy

Well-known member
The doc from the French Atomic Energy Commission fed 5 grams of homogenated brain tissue, from a cow with BSE, to 2 macaque monkeys. One developed a neurological disease. The transmissible agent is not identified. There was some component found in the diseased brain which may have resulted in this condition; but it didn't affect both monkeys. What kind of science is this?

You could eat 5 grams of any "food" contaminated with lead, and likely get the same results.

J Comp Pathol. 1984 Apr;94(2):215-31.

Neuropathological lesions in experimental lead toxicosis of dogs.

Hamir AN, Sullivan ND, Handson PD.
Light microscopical examinations were carried out on the central and peripheral nervous systems of 9 dogs maintained on a high-fat-low-calcium diet and dosed orally with a mixture of lead chloride, lead bromide and lead sulphate. Microscopic lesions were present in 7 (78 per cent) of the lead-treated dogs. Cerebrocortical lesions comprising spongiosis, vascular hypertrophy and gliosis predominated. These lesions were bilateral, had a predilection for gyri and were located mainly in the parietal and frontal cortex. There were bilaterally symmetrical spongiform changes in the brain stem. The cerebellum had spongiform changes in the roof nuclei and in the lingula there was spongiosis of the Purkinje cell layer and vacuolation of Purkinje cells. Axonal degeneration was evident in a sciatic nerve of one dog. In a second experiment, designed to study the early ultrastructural changes in the brains of dogs with lead intoxication, 2 groups of dogs, one on a commercial balanced diet and the other fed a high-fat-low-calcium diet, were given similar amounts of lead. Cytoplasmic accumulation of lipid was found in the cerebrovascular pericytes of all dogs treated with lead but vascular changes were otherwise not obvious. Quantitative evaluation of numbers of blood vessels by light microscopy revealed an apparent increase in all dogs receiving lead. This increase in vascularity was greatest in the dogs fed the high-fat-low-calcium diet.

PMID: 6736309


Jean-Philippe Deslys [of the French Atomic Energy Commission]

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.

20 years on, and none of these experts have "characterized the metal content" of the so-called infectious prions.
 

flounder

Well-known member
Kathy said:
The doc from the French Atomic Energy Commission fed 5 grams of homogenated brain tissue, from a cow with BSE, to 2 macaque monkeys. One developed a neurological disease. The transmissible agent is not identified. There was some component found in the diseased brain which may have resulted in this condition; but it didn't affect both monkeys. What kind of science is this?

You could eat 5 grams of any "food" contaminated with lead, and likely get the same results.

J Comp Pathol. 1984 Apr;94(2):215-31.

Neuropathological lesions in experimental lead toxicosis of dogs.

Hamir AN, Sullivan ND, Handson PD.
Light microscopical examinations were carried out on the central and peripheral nervous systems of 9 dogs maintained on a high-fat-low-calcium diet and dosed orally with a mixture of lead chloride, lead bromide and lead sulphate. Microscopic lesions were present in 7 (78 per cent) of the lead-treated dogs. Cerebrocortical lesions comprising spongiosis, vascular hypertrophy and gliosis predominated. These lesions were bilateral, had a predilection for gyri and were located mainly in the parietal and frontal cortex. There were bilaterally symmetrical spongiform changes in the brain stem. The cerebellum had spongiform changes in the roof nuclei and in the lingula there was spongiosis of the Purkinje cell layer and vacuolation of Purkinje cells. Axonal degeneration was evident in a sciatic nerve of one dog. In a second experiment, designed to study the early ultrastructural changes in the brains of dogs with lead intoxication, 2 groups of dogs, one on a commercial balanced diet and the other fed a high-fat-low-calcium diet, were given similar amounts of lead. Cytoplasmic accumulation of lipid was found in the cerebrovascular pericytes of all dogs treated with lead but vascular changes were otherwise not obvious. Quantitative evaluation of numbers of blood vessels by light microscopy revealed an apparent increase in all dogs receiving lead. This increase in vascularity was greatest in the dogs fed the high-fat-low-calcium diet.

PMID: 6736309


Jean-Philippe Deslys [of the French Atomic Energy Commission]

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.

20 years on, and none of these experts have "characterized the metal content" of the so-called infectious prions.


METALS DON'T CAUSE TSE KATHY :roll:


1: J Infect Dis 1980 Aug;142(2):205-8



Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


TSS
 

Kathy

Well-known member
A breakdown in the cellular defense mechanisms causes TSEs.

Gadjusek was proven wrong! no virus(es) exist in the tissue used in these transmission experiments.

Gadjusek even requested Mark Purdey's papers, that was just before he was thrown in jail.

Even Stan the man Prusiner has requested reprints of Mark's papers....

Breakdown in the cellular defense mechanisms would allow for all kinds of opportunistic bacteria and viruses to afflict the host animal. But they are not the original cause of the death of microglial cells, and the breakdown of antioxidants like superoxide dismutase (the Cu/Zn one), etc.
 
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