timh wrote;
News Flash for ya Econo-stud......... Flounder can't present the direct, proven , scientific link either.........because it DOES NOT EXIST.
=======================
news flash for tim, sticking ones head the sand will not make this go away, neither will ignoring 'science' to date :roll:
this is what i am talking about. one must post long posts sometimes in order to properly prove others wrong, as wrong as one can with present science i.e. 'sound science'. but just what is sound science? remember, it is against all ethical law to do TSE transmission studies on humans (however, i could think of a few to do them on, as opposed to animals :shock: so, the next best thing are primates or mice, or other animals. from there, as econ kindly said, one must make there own mind up. AS a producer, one might expect 'industry' based science, or what GW et al now call 'sound science' for some, but i find here that there are indeed some producers that want to know what is going on in the real world of science, while others simply dont want to hear nothing about it, i think thats the most frightening factor, especially in 2006, where science has already told us that this agent can indeed spread around the globe by feeding practices and other routes that have been proven, and that indeed those countries that went by those flimsy OIE BSE guidelines, most all went down with BSE ;
Wed, May. 03, 2006
`Sound science' isn't just a catch phrase - it's a real persuader
By Iris Kuo
Knight Ridder Newspapers
WASHINGTON - The Bush administration, senators, industrialists and farmers repeatedly invoke the term "sound science" to delay or deep-six policies they oppose and dismiss criticism of those they favor.
The administration has waved it at such diverse issues as global warming, beef imports, air pollution and arsenic in drinking water. Last Thursday, Transportation Secretary Norman Mineta used the phrase to slow a congressional bid to raise the U.S. passenger vehicle mileage standard. "An administrative process based on sound science" should precede any change, Mineta said.
No one, however, is sure what "sound science" means.
The phrase has more to do with anti-regulatory lobbying than with laboratory results, said Donald Kennedy, the former head of the Food and Drug Administration and now the editor in chief of the influential magazine Science.
"Sound science is whatever somebody likes," Kennedy said. "It's essentially a politically useful term, but it doesn't have any normative meaning whatsoever. My science is sound science, and the science of my enemies is junk science." .......snip.........end
http://www.macon.com/mld/macon/news/nation/14492214.htm
http://www.thestate.com/mld/thestate/news/nation/14492214.htm
http://www.realcities.com/mld/krwashington/14492214.htm
a few transmission studies to digest for those interested. note, oral route and inoculation;
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
http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf
http://www.bseinquiry.gov.uk/files/yb/1976/10/12002001.pdf
SCRAPIE USA UPDATE AS of March 31, 2006
2 NEW CASES IN GOAT, 82 INFECTED SOURCE FLOCKS, WITH 4 NEW INFECTED SOURCE
FLOCKS IN MARCH, WITH 19 SCRAPIE INFECTED RSSS REPORTED BY NVSL
http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html
Brain and buffy coat transmission of bovine spongiform encephalopathy to the primate Microcebus murinus.
Bons N, Lehmann S, Mestre-Frances N, Dormont D, Brown P.
Laboratory of Functional Neuropathology, School of Advanced Studies, University of Montpellier II, Montpellier, France.
BACKGROUND: More than 100 cases of variant CJD resulting from infections with bovine spongiform encephalopathy (BSE) have accumulated in the United Kingdom since 1995. Concern about the possibility of secondary transmissions via blood and blood components donated by infected individuals has prompted a variety of international donor deferral policies that will continue until laboratory and epidemiologic evidence provides a consensus about potential risk. STUDY DESIGN AND METHODS: BSE was passaged through macaque monkeys and then adapted to the prosimian microcebe (Microcebus murinus). Brain homogenate and buffy coat from an affected microcebe were separately inoculated intracerebrally into three healthy microcebes (two animals received brain and one received buffy coat). RESULTS: All three inoculated microcebes became ill after incubation periods of 16 to 18 months. Clinical, histopathologic, and immunocytologic features were similar in each of the recipients. CONCLUSION: Buffy coat from a symptomatic microcebe infected 17 months earlier with BSE contained the infectious agent. This observation represents the first documented transmission of BSE from the blood of an experimentally infected primate, which in view of rodent buffy coat infectivity precedents and the known host range of BSE is neither unexpected nor cause for alarm.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12084158&dopt=Abstract
IN fact, we are now finding that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE ;
Published online before print March 20, 2001
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.041490898
Abstract of this Article
Reprint (PDF) Version of this Article
Similar articles found in:
PNAS Online
PubMed
PubMed Citation
Search Medline for articles by:
Lasmézas, C. I. || Deslys, J.-P.
Alert me when:
new articles cite this article
Download to Citation Manager
Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*, Virginie Nouvel*,
Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger
] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique
Dormont*, and Jean-Philippe Deslys*
* Commissariat à l'Energie Atomique, Service de Neurovirologie,
Direction des Sciences du Vivant/Département de Recherche Medicale,
Centre de Recherches du Service de Santé des Armées 60-68, Avenue du
Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; [Dagger
] Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003
Lyon, France; § Laboratoire de Neuropathologie, Hôpital de la
Salpêtrière, 83, Boulevard de l'Hôpital, 75013 Paris, France; ¶
Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital,
Crewe Road, Edinburgh EH4 2XU, United Kingdom; and [||] Institute for
Animal Health, Neuropathogenesis Unit, West Mains Road, Edinburgh EH9
3JF, United Kingdom
Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)
Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
References
There is substantial scientific evidence to support the notion that
bovine spongiform encephalopathy (BSE) has contaminated human beings,
causing variant Creutzfeldt-Jakob disease (vCJD). This disease has
raised concerns about the possibility of an iatrogenic secondary
transmission to humans, because the biological properties of the
primate-adapted BSE agent are unknown. We show that (i) BSE can be
transmitted from primate to primate by intravenous route in 25 months,
and (ii) an iatrogenic transmission of vCJD to humans could be readily
recognized pathologically, whether it occurs by the central or
peripheral route. Strain typing in mice demonstrates that the BSE agent
adapts to macaques in the same way as it does to humans and confirms
that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. The agent responsible for French iatrogenic
growth hormone-linked CJD taken as a control is very different from vCJD
but is similar to that found in one case of sporadic CJD and one sheep
scrapie isolate. These data will be key in identifying the origin of
human cases of prion disease, including accidental vCJD transmission,
and could provide bases for vCJD risk assessment.
Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
References
The recognition of a variant of the human transmissible spongiform
encephalopathy (TSE) Creutzfeldt-Jakob Disease (vCJD) in the U.K. in
1996 raised the major concern that it would correspond to human
infection with the agent responsible for bovine spongiform
encephalopathy (BSE; ref. 1). Transmission of BSE to macaques provided
the first experimental evidence as it produced a disease close to vCJD
in humans (2). Strain typing in inbred mice (consisting of measuring the
incubation period and establishing lesion profiles corresponding to the
strain-specific distribution of brain vacuolation) allows reliable
identification of TSE strains (3). This method, together with
biochemical methods, has revealed a single phenotype for the agents of
BSE and the British cases of vCJD (4-6). Mice expressing only the bovine
prion protein (PrP) were highly susceptible to vCJD and BSE, which
induced the same disease (7). Thus, it is now well established that BSE
has caused vCJD, probably by alimentary contamination. In this respect,
the finding of abnormal PrP labeling in the gastrointestinal tract and
lymphatic tissues of orally BSE-contaminated lemurs shows that the BSE
agent can infect primates by the oral route . About 1 million
contaminated cattle may have entered the human food chain, and the
future number of vCJD cases could range from 63 to 136,000 depending on
the incubation period of BSE in humans (9). Unlike sporadic CJD (sCJD)
and iatrogenic CJD (iCJD) linked to the administration of contaminated
growth hormone extracted from human hypophyses, in vCJD, the infectious
agent seems to be widely distributed in lymphoid organs, as pathological
PrP (PrPres) can be detected in tonsils, lymph nodes, spleen, and
appendix even in the preclinical phase of the disease (10, 11). This
raises a public health issue with regard to the risk of iatrogenic
transmission of vCJD through surgical instruments, grafts, blood
transfusion, or parenteral administration of biological products of
human origin. However, this risk is difficult to assess, because it
largely depends on factors such as the virulence of the BSE agent
adapted to primates and the efficiency of secondary transmission to
humans by a peripheral route such as the i.v. one. A further issue is
whether vCJD accidentally acquired from humans would be recognized. The
latter poses the question of a phenotypic variation of the BSE agent
after successive transmissions in humans: does it retain its strain
characteristics, and does it induce a pathology similar to that observed
in the previous host? A 9-year history of transmission of BSE to
primates and mice enables us today to clarify a number of these
important points.
Although BSE has mainly affected the U.K., two definite cases and one
probable case of vCJD have now been reported in France in people who
have never resided in the U.K. (12, 13). We strain-typed the first of
these cases to establish its origin. Strain typing in C57BL/6 mice of
BSE, French, and British vCJD was compared with that of BSE passaged in
nonhuman primates, thus allowing us to study the effect of serial
passages in primates. Comparisons were also made with French cases of
sCJD and iCJD and two strains of scrapie (one of French and one of U.S.
origin). Our findings provide experimental demonstration that the same
agent, namely that responsible for the cattle disease BSE, has caused
vCJD both in France and in the U.K., in line with biochemical data and
with the fact that, until 1996, about 10% of the beef consumed in France
was imported from the U.K. We found that the BSE agent in nonhuman
primates is similar to that causing vCJD in humans and tends to evolve
rapidly toward a primate-adapted variant. Furthermore, we showed that
the strain responsible for iCJD is closely related to that of one
patient with sCJD, and, more unexpectedly, that these agents were
similar to the French scrapie strain studied (but different from the
U.S. scrapie strain). This finding requires a cautious interpretation
for several reasons, not least because of the inevitably limited number
of TSE strains that can be studied by such a cumbersome method as strain
typing. Nonetheless, it also prompts reconsideration of the possibility
that, in some instances, sheep and human TSEs can share a common origin.
snip...
http://www.pnas.org/cgi/content/full/041490898v1
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
1: Vet Rec 1993 Apr 17;132(16):403-6
Experimental transmission of BSE and scrapie to the common marmoset.
Baker HF, Ridley RM, Wells GA.
Division of Psychiatry, Clinical Research Centre, Harrow, Middlesex.
Two young male common marmosets (Callithrix jacchus) were injected intracerebrally and intraperitoneally with a crude brain homogenate prepared from a cow with bovine spongiform encephalopathy (BSE). Two other marmosets were similarly injected with brain homogenate from a sheep with natural scrapie. The two animals injected with scrapie material developed neurological signs 38 and 42 months after injection and the two animals injected with BSE material developed neurological signs after 46 and 47 months. Post mortem examination of the brains revealed spongiform encephalopathy especially in the basal nuclei and diencephalon of all the animals and, in addition, involvement of the cerebral cortex of the marmosets injected with scrapie material. The experiment extends the host range of experimental BSE to include a primate species.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8488658&dopt=Abstract
1: J Gen Virol 1991 Mar;72 ( Pt 3):589-94
Epidemiological and experimental studies on a new incident of transmissible mink encephalopathy.
Marsh RF, Bessen RA, Lehmann S, Hartsough GR.
Department of Veterinary Science, University of Wisconsin-Madison 53706.
Epidemiological investigation of a new incident of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin, U.S.A. in 1985 revealed that the mink rancher had never fed sheep products to his mink but did feed them large amounts of products from fallen or sick dairy cattle. To investigate the possibility that this occurrence of TME may have resulted from exposure to infected cattle, two Holstein bull calves were injected intracerebrally with mink brain from the Stetsonville ranch. Each bull developed a fatal spongiform encephalopathy 18 and 19 months after inoculation, respectively, and both bovine brains passaged back into mink were highly pathogenic by either intracerebral or oral inoculation. These results suggest the presence of a previously unrecognized scrapie-like infection in cattle in the United States.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1826023&dopt=Abstract
1: Ital J Neurol Sci 1983 Apr;4(1):61-4
Creutzfeld-Jakob disease in the province of Siena: two cases transmitted to monkeys.
Fieschi C, Orzi F, Pocchiari M, Nardini M, Rocchi F, Asher D, Gibbs C, Gajdusek D.
Two cases of histopathologically documented Creutzfeldt-Jakob disease were observed in the same area of the province of Siena in 1974-1975. The transmission of the disease was obtained through brain homogenates and lymphnodes in one of the two cases. This confirms that the agent is present in other tissues besides the brain and underlines further the analogies between Creutzfeld-Jakob disease and scrapie.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6345460&dopt=Abstract
1: Dev Biol Stand 1993;80:9-13
Transmission of human spongiform encephalopathies to experimental animals: comparison of the chimpanzee and squirrel monkey.
Asher DM, Gibbs CJ Jr, Sulima MP, Bacote A, Amyx H, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20992.
The agents of kuru and Creutzfeldt-Jakob disease have been consistently transmitted from patients with those diseases to chimpanzees and squirrel monkeys, as well as to other new-world primates, with average incubation periods of two or three years. No other animals have been found so consistently susceptible to the agents in human tissues. More rapid and convenient assays for the infectious agents would greatly facilitate research on the spongiform encephalopathies of humans.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8270119&dopt=Abstract
1: Dev Biol Stand 1993;80:9-13
Transmission of human spongiform encephalopathies to experimental animals: comparison of the chimpanzee and squirrel monkey.
Asher DM, Gibbs CJ Jr, Sulima MP, Bacote A, Amyx H, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20992.
The agents of kuru and Creutzfeldt-Jakob disease have been consistently transmitted from patients with those diseases to chimpanzees and squirrel monkeys, as well as to other new-world primates, with average incubation periods of two or three years. No other animals have been found so consistently susceptible to the agents in human tissues. More rapid and convenient assays for the infectious agents would greatly facilitate research on the spongiform encephalopathies of humans.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8270119&dopt=Abstract
i recieved the 1947 report of the Louping-ill vaccineincident and posted on www here;Louping-ill vaccine (scrapie transmission by vaccine)THE VETERINARY RECORD516 No 47. Vol. 58November 23rd, 1946NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELANDANNUAL CONGRESS, 1946snip...The enquiry made the position clear. Scrapie was developing inthe sheep vaccinated in 1935 and it was only in a few instancesthat the owner was associating the occurrence with louping-illvaccination. The disease was affecting all breeds and it wasconfined to the animals vaccinated with batch 2. This was clearlydemonstrated on a number of farms on which batch 1 had beenused to inoculate the hoggs in 1935 and batch 2 to inoculatethe ewes. None of the hoggs, which at this time were three-year-old ewes. At this time it was difficult to forecast whether allof the 18,000 sheep which had received batch 2 vaccine woulddevelop scrapie. It was fortunate, however, that the majority ofthe sheep vaccinated with batch 2 were ewes and therfore allthat were four years old and upwards at the time of vaccinationhad already been disposed of and there only remained the eweswhich had been two to three years old at the time of vaccination,consequently no accurate assessment of the incidence of scrapiecould be made. On a few farms, however, where vaccination wasconfined to hoggs, the incidence ranged from 1 percent, to 35 percent,with an average of about 5 percent. Since batch 2 vaccinehad been incriminated as a probable source of scrapie infection,an attempt was made to trace the origin of the 112 sheep whosetissues had been included in the vaccine. It was found that theyhad been supplied by three owners and that all were of theBlackface or Greyface breed with the exception of eight whichwere Cheviot lambs born in 1935 from ewes which had been incontact with scrapie infection. Some of these contact ewesdeveloped scrapie in 1936-37 and three surviving fellow lambs tothe eight included in the batch 2 vaccine of 1935 developedscrapie, one in September, 1936, one in February, 1937, and onein November, 1937. There was, therefore, strong presumptiveevidence that the eight Cheviot lambs included in the vaccinealthought apparently healthy were, in fact, in the incubative stageof a scrapie infection and that in their tissues there was aninfective agent which had contaminated the batch 2 vaccine,rendering it liable to set up scrapie. If that assumption wascorrect then the evidence indicated that:-(1) the infective agent of scrapie was present in the brain, spinalcord and or spleen of infected sheep
2) it could withstand a concentration of formalin of 0-35 percent,which inactivated the virus of louping-ill
3) it could be transmitted by subcutaneous inoculation;(4) it had an incubative period of two years and longer.Two Frenchmen, Cuille & Chelle (1939) as the result of experimentscommenced in 1932, reported the successful infection ofsheep by inoculation of emulsions of spinal cord or brain materialby the intracerebral, epidural, intraocular and subcutaneous routesThe incubation period varied according to the route employed,being one year intracerebrally, 15 months intraocularly and 20months subcutaneously. They failed to infect rabbits but succeededin infecting goats. Another important part of their workshowed that the infective agent could pass throught a chamberland1.3 filter, thus demonstrating that the infective agent was afiltrable virus. It was a curious coincidence that while theywere doing their transmission experiments their work was beingconfirmed by the unforeseeable infectivity of a formalinized tissuevaccine.As a result of this experience a large-scale transmision experimentinvolving the ue of 788 sheep was commenced in 1938 on afarm specially taken for the purpose by the Animal DiseasesResearch Association with funds provided by the AgriculturalResearch Council. The experiment was designed to determine thenature of the infective agent and the pathogenesis of the disease.It is only possible here to give a summary of the result whichshowed that (1) saline suspensions of brain and spinal cord tissueof sheep affected with scrapie were infective to normal sheepwhen inoculatted intracerebrally or subcutaneously; (2) the incubationperiod after intracerebral inoculation was seven months andupwards and only 60 percent of the inoculated sheep developedscrapie during a period of four and a half years; (3) the incubationperiod after subcutaneous inoculation was 15 months and upwardsand only about 30 percent of the inoculated sheep developedthe disease during the four and a half years: (4) the infectiveagent was of small size and probably a filtrable virus.The prolonged incubative period of the disease and the remarkableresistance of the causal agent to formalin are features ofdistinct interest. It still remains to determine if a biological testcan be devised to detect infected animals so that they can bekilled for food before they develop clinical symptoms and toexplore the possibilities of producing an immunity to the disease...
USA IMPORTS VACCINE PRODUCTS FROM BSE COUNTRIES
http://www.mad-cow.org/00/may00_news.html
confindentialpigs & pharmaceuticals http://www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf http://www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf http://www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf http://www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf Subject: DURA MATER-ASSOCIATED CJD: FIRST REPORTED CASE FROM PORCINE SOURCE DURADate: April 19, 2006 at 4:56 pm PSTSHORT REPORTDura mater-associated Creutzfeldt–Jakob disease:experience from surveillance in the UKC A Heath, R A Barker, T F G Esmonde, P Harvey, R Roberts, P Trend, MWHead, C Smith, J E Bell,J W Ironside, R G Will, R S G Knight. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .J Neurol Neurosurg Psychiatry 2006;000:1–4. doi: 10.1136/jnnp.2005.073395Between 1970 and 2003, seven cases of human dura materassociatedCreutzfeldt–Jakob disease (CJD) were identified inthe UK. Furthermore, we identified a case of CJD in a porcinedura graft recipient. The mean incubation period of thehuman dura mater cases was 93 (range 45–177) months.The clinico-pathological features of the cases are describedand compared with cases previously reported in the worldliterature.Creutzfeldt–Jakob disease (CJD) exists in four clinicalforms: sporadic, genetic, iatrogenic and variant. Thecause of sporadic CJD, the most common form worldwide,is unknown and case–control studies have failed toidentify any consistent risk factor, although two studies haveimplicated previous surgical interventions.1 2 Genetic forms ofthe disease are associated with underlying mutations of theprion protein gene (PRNP), which are generally considered tobe directly causative.Mutations, however, possibly increaseliability to some, as of yet unrecognised, source of infection.The two remaining forms of CJD are acquired. Variant CJD isconsidered to be caused by bovine spongiform encephalopathy,3–5 through contaminated food products; iatrogenic CJDresults from the inadvertent transmission of CJD during thecourse of medical or surgical treatment. The two mostnumerically significant instances of iatrogenic CJD resultedfrom treatment with cadaveric human growth hormone andthe use of dura mater grafts in surgery. Corneal grafts, depthelectrodes and neurosurgical instruments have also rarelybeen implicated.6 7The first report of dura mater-associated CJD waspublished in 1987,8 with a more detailed report appearingthe following year;9 to date, 164 cases have been recognisedworldwide (P Brown, personal communication) ; . This paperreports and describes the seven cases of human dura matergraft-associated CJD identified during surveillance in the UKand also, for the first time, reports a case of CJD in a porcinedura graft recipient.METHODS
SNIP...END
http://press.psprings.co.uk/jnnp/may/jn73395.pdf
Research Project: Transmission, Differentiation, and Pathobiology ofTransmissible Spongiform EncephalopathiesLocation: Virus and Prion Diseases of LivestockTitle: Evaluation of a Diet Free of Animal Protein in Germfree SwineAuthorsitem Loynachan, A - IOWA STATE UNIVERSITYitem Pettigrew, J - UNIVERSITY OF ILLINOISitem Wiseman, B - NEXTRAN, INCitem Kunkle, Robertitem Harris, D - IOWA STATE UNIVERSITYSubmitted to: XenotransplantationPublication Type: Peer Reviewed JournalPublication Acceptance Date: January 5, 2005Publication Date: March 1, 2005Citation: Loynachan, A.T., Pettigrew, J.E., Wiseman, B.S., Kunkle, R.A.,Harris, D.L. 2005. Evaluation of a Diet Free of Animal Protein in GermfreeSwine. Xenotransplantation. 12:149-155.Interpretive Summary: Basic research into the potential to use organsharvested from swine for the purpose of transplantation to save human liveshas identified potential immunological and transmissible infectious diseaseobstacles. BSE has been transmitted to swine following intracerebellarinoculation, indicating the potential susceptibility of pigs to prioninfections. Although neither natural nor experimental oral transmission ofspongiform encephalopathies has been recorded in pigs, concerns about thetransmission of prion proteins in feed have led to the development of a dietfree of animal protein (DFAP). This study describes a method to rearneonatal pigs in a manner that precludes exposure to environmentalmicroorganisms and animal-derived proteins. Twenty pigs were derived byCesarian-section and housed in sterile bubble-pens. Duplicate trials wereconducted in which germ-free pigs or pigs intentionally colonized exclusively with the bacterium Lactobacillus paracasei subspecies paracasei were fedeither a traditional milk-based diet (Esbilac) or the experimental DFAP. Onthe whole, the pigs in all groups remained healthy, however, two pigs fedthe DFAP developed mild diarrhea and gained less weight. The pigs wereeuthanized at 16 days of age. Examinations revealed no evidence ofcontamination or disease. The use of the probiotic, Lactobacillus paracasei,did not confer any measurable growth advantage to pigs fed either diet. Theexperimental DFAP was capable of sustaining life, but was not as efficaciousas the conventional milk-based diet as based upon weight gain andfeed-conversion.Technical Abstract: Two experiments were conducted in which germfree pigs orpigs monoassociated with Lactobacillus paracasei subspecies paracasei werefed either a traditional milk-based diet (Esbilac) or an experimental dietfree of animal protein (DFAP). Throughout the 16-day study, animals' generaldisposition, total weight gain, feed conversion, and bacterial contaminationwere monitored. At the conclusion of the study the animals were euthanized,necropsied and tissues sampled for L. paracasei isolation. General pigdisposition remained consistent between treatment groups and trials, exceptfor two animals that developed mild diarrhea during trial 1. All pigsremained viable during the study irrespective of the diet fed or probioticinoculation. Germfree pigs fed the Esbilac diet gained on average a total of1034 (+/- 63.0) g, and had a feed conversion ratio of 0.17 (+/- 0.01) g ofgain per 1 ml of diet. Germfree pigs fed the experimental diet gained onaverage a total of 599 (+/- 151) g, and had a feed conversion ratio of 0.10(+/- .02) g of gain per 1 ml of diet. Monoassociated pigs fed the Esbilacdiet gained on average a total of 862 (+ 70.3) g, and had a feed conversionratio of 0.14 (+/- 0.01) g of gain per 1 ml of diet. Monoassociated pigs fedthe experimental diet gained on average a total of 563 (+/- 96.8) g, and hada feed conversion ratio of 0.09 (+/- 0.02) g of gain per 1 ml of diet. L.paracasei established extensively in pigs fed either the Esbilac orexperimental diets. L. paracasei had no effect (p>0.05) on piglet growth anddid not display any interactions based on the diet fed. Statisticaldifferences (p<0.05) were noted on measured growth parameters between trial1 and 2, and on measured growth parameters based on the diet fed. Inconclusion, a diet free of animal protein has been developed and has beenshown to be capable of sustaining life in piglets up to 16 days of age.http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=170002
MAYBE these farmers had BaSEcjd ???
provides information on a probable case of CJD in a farmer,if confirmed, would bring the total number of cases in farmersin the UK to four-all with BSE in their herds...
http://www.bseinquiry.gov.uk/files/yb/1995/09/29001001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/09/29008001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/09/29009001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/09/29012001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/09/29013001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/04003001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/04004001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/04005001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/04006001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/05004001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/10004001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/19002001.pdf
CAUSE FOR CONCERN IN 3RD FARMER WITH CJD
http://www.bseinquiry.gov.uk/files/yb/1995/01/13001001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/01/19002001.pdf
6. Members were reminded that, after the death from CJD of thesecond dairy farmer in 1993, Professor Peter Smith had advised thatIF FOUR CASES AROSE in the first five years of the surveillancescheme the possibility of an association which was NOT DUE TOCHANCE HAD TO BE GIVEN VERY SERIOUS CONSIDERATION...
http://www.bseinquiry.gov.uk/files/yb/1995/01/13001001.pdf
cover-up 4th farmer from cjd
http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/23007001.pdf
Government experts hold secret inquiry as fourth farmer withinfected cattle falls victim to deadly brain disease
http://www.bseinquiry.gov.uk/files/yb/1995/10/23010001.pdf
FOURTH FARMER CONFIRMEDshould there be any further press enquiries specifically about the diagnosisin this case, I therfore suggest that we say that the diagnosis has beenconfimred but that there is nothing to add to SEACs earlier advice.
http://www.bseinquiry.gov.uk/files/yb/1995/11/03008001.pdf
IT WAS ALSO AGREED THAT IF A THIRD CASE OF CJD INA FARMER WITH BSE IN THEIR HER OCCURED, AN IMMEDIATEFULL COMMITTEE MEETING WOULD BE REQUIRED...
http://www.bseinquiry.gov.uk/files/yb/1993/10/07002001.pdf
10. Dr. Will presented information on CJD in farmers in otherEuropean countries - three cases in France in 1992 and 1993,two of which were dairy farmers, and two cases in dairy farmersin Germany since October 1993.
http://www.bseinquiry.gov.uk/files/yb/1995/01/13001001.pdf
IF this new strain of TSE in cattle aBSE or BaSE is in older cattle.IF this new strain of TSE in cattle looks IDENTICAL to sporadic CJD.WHY is it so hard to believe that these sporadic CJD deaths in farmerswe not related to this Base or BaSE?...TSS
Medical SciencesIdentification of a second bovine amyloidotic spongiformencephalopathy: Molecular similarities with sporadicCreutzfeldt-Jakob disease
Cristina Casalone *{dagger} , Gianluigi Zanusso {dagger} {ddagger} ,Pierluigi Acutis *, Sergio Ferrari {ddagger} , Lorenzo Capucci § ,Fabrizio Tagliavini ¶, Salvatore Monaco {ddagger} ||, and Maria Caramelli **Centro di Referenza Nazionale per le Encefalopatie Animali, IstitutoZooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, ViaBologna, 148, 10195 Turin, Italy; {ddagger} Department of Neurologicaland Visual Science, Section of Clinical Neurology, Policlinico G.B.Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; § IstitutoZooprofilattico Sperimentale della Lombardia ed Emilia Romagna, ViaBianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico"Carlo Besta," Via Celoria 11, 20133 Milan, ItalyEdited by Stanley B. Prusiner, University of California, San Francisco,CA, and approved December 23, 2003 (received for review September 9, 2003)
Transmissible spongiform encephalopathies (TSEs), or prion diseases, aremammalian neurodegenerative disorders characterized by aposttranslational conversion and brain accumulation of an insoluble,protease-resistant isoform (PrPSc) of the host-encoded cellular prionprotein (PrPC). Human and animal TSE agents exist as differentphenotypes that can be biochemically differentiated on the basis of themolecular mass of the protease-resistant PrPSc fragments and the degreeof glycosylation. Epidemiological, molecular, and transmission studiesstrongly suggest that the single strain of agent responsible for bovinespongiform encephalopathy (BSE) has infected humans, causing variantCreutzfeldt-Jakob disease. The unprecedented biological properties ofthe BSE agent, which circumvents the so-called "species barrier" betweencattle and humans and adapts to different mammalian species, has raisedconsiderable concern for human health. To date, it is unknown whethermore than one strain might be responsible for cattle TSE or whether theBSE agent undergoes phenotypic variation after natural transmission.Here we provide evidence of a second cattle TSE. The disorder waspathologically characterized by the presence of PrP-immunopositiveamyloid plaques, as opposed to the lack of amyloid deposition in typicalBSE cases, and by a different pattern of regional distribution andtopology of brain PrPSc accumulation. In addition, Western blot analysisshowed a PrPSc type with predominance of the low molecular massglycoform and a protease-resistant fragment of lower molecular mass thanBSE-PrPSc. Strikingly, the molecular signature of this previouslyundescribed bovine PrPSc was similar to that encountered in a distinctsubtype of sporadic Creutzfeldt-Jakob disease.------------------------------------------------------------------------{dagger} C.C. and G.Z. contributed equally to this work.||To whom correspondence should be addressed.E-mail:
[email protected]./cgi/doi/10.1073/pnas.0305777101
http://www.pnas.org/cgi/content/abstract/0305777101v1
BSE prions propagate as either variant CJD-like or sporadic CJD-likeprion strains in transgenic mice expressing human prion proteinEmmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, SusanJoiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, SarahE. Lloyd, Jonathan D.F. Wadsworth and John Collinge1MRC Prion Unit and Department of Neurodegenerative Disease, Institute ofNeurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail:
[email protected]. August 1, 2002; revised September 24, 2002; accepted October17, 2002AbstractVariant CreutzfeldtJakob disease (vCJD) has been recognized to dateonly in individuals homozygous for methionine at PRNP codon 129. Here weshow that transgenic mice expressing human PrP methionine 129,inoculated with either bovine spongiform encephalopathy (BSE) or variantCJD prions, may develop the neuropathological and molecular phenotype ofvCJD, consistent with these diseases being caused by the same prionstrain. Surprisingly, however, BSE transmission to these transgenicmice, in addition to producing a vCJD-like phenotype, can also result ina distinct molecular phenotype that is indistinguishable from that ofsporadic CJD with PrPSc type 2. These data suggest that more than oneBSE-derived prion strain might infect humans; it is therefore possiblethat some patients with a phenotype consistent with sporadic CJD mayhave a disease arising from BSE exposure...
http://embojournal.npgjournals.com/cgi/content/full/21/23/6358
ROUND TABLE ON BSE -- WASHINGTON -- 27-28 JUNE 1989 snip...
The summary does tend to give a particular slant to the epidemiology of BSE
which is not totally sound. It is a possibility that the agent of BSE may be in the
cattle population in a number of countries already apart from the USA and that
clinical cases are occurring on rare occasions. It is also important to off the possibility
of the relationship between BSE and certain low-temperature rendering systems.
For that reason a number of other countries apart from the USA and France are at
risk and, in particular, the Netherlands, Denmark, Germany and Belgium. For these
reasons it would be wise to move to an international ban on the feeding of ruminant
protein to ruminants. Clearly the summary also needs to refer to the incidence of BSE
in the UK and not solely to Great Britain. No doubt this has been tidied up in your
comments on the summary conclusions. It is a pity that more of the comments
put forward by Dr. Kimberlin have not been included in the summary since his
views on page 13 are succinct and valuable...
snip...
http://www.bseinquiry.gov.uk/files/yb/1989/08/29003001.pdf
Is there a Scrapie-like disease in cattle ?
IN CONFIDENCE R.F. MARSH
snip...
re-mink rancher 'Wisconsin' dead stock feeder using
>95% downer or dead dairy and a few horses...
http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf
one must not ignore these findings, and i hope i am wrong. ...TSS
