Envt.11: Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
Justin Greenlee,† Robert Kunkle and Jodi Smith
National Animal Disease Center, ARS, USDA; Ames, IA USA †Presenting author; Email: justin.greenlee@ars.usda.gov
Transmissible spongiform encephalopathies (TSEs, prion diseases) are chronic neurodegenerative diseases that occur in humans, cattle, sheep, goats, cervids and a number of laboratory animal models. There is no evidence of the natural occurrence of any form of TSE in the pig, but pigs have been shown to be susceptible to Bovine Spongiform Encephalopathy (BSE) infection by multiple-route parenteral challenge. However, pigs orally exposed at eight weeks of age to large amounts of brain from cattle clinically affected with BSE did not support infection after seven years of observation. In the US, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine, mink and poultry still occurs. Although unlikely, the potential for swine to have access to TSE-contaminated feedstuffs exists. The potential for swine to serve as a host for the agent of chronic wasting disease (CWD) is unknown. The purpose of this study was to perform intracerebral inoculation of the CWD agent to determine the potential of swine as a host for the CWD agent and their clinical susceptibility. This study utilized 26 swine randomly divided into controls (n = 6) and intracranial inoculates (n = 20). CWD inoculum was a pooled 10% (w/v) homogenate derived from three white-tailed deer clinically ill with CWD from three different sources (elk, white-tailed deer, mule deer) and was given by a single intracranial injection of 0.75 ml. Necropsies were done on ten animals at six months post inoculation (PI), at approximately the time the pigs were expected to reach market weight. Additional pigs have been necropsied due to intercurrent disease (primarily lameness) over the course of the study (29–64 months). Samples collected at necropsy were examined for spongiform change after routine staining (hematoxylin and eosin) and for immunoreactivity to prion protein (PrPSc) by immunohistochemistry. Further, brain samples from at least two regions were tested by western blot. No results suggestive of spongiform encephalopathy were obtained from animals necropsied at six months PI, but positive results after an incubation period of only six months would be uncharacteristic. A single animal was positive for CWD by IHC and WB at 64 months PI. Two inoculated pigs and one control pig remain alive, so it is not possible to determine the attack rate of CWD in swine at this time. However, lack of positive results in pigs necropsied at 29–56 months PI and the long incubation of the single positive case suggest that swine are unlikely to be affected by CWD if inoculated by a natural route.
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE; 1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,
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The neuropathology of experimental bovine spongiform encephalopathy in the pig.
Ryder SJ, Hawkins SA, Dawson M, Wells GA.
Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.
PMID: 10684682 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract
Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report
Authors
Greenlee, Justin Kunkle, Robert Hamir, Amirali
Submitted to: American Association of Veterinary Laboratory Diagnosticians Publication Type: Abstract Publication Acceptance Date: November 5, 2005 Publication Date: November 5, 2005 Citation: Greenlee, J.J., Kunkle, R.A., Hamir, A.N. 2005. Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report [abstract]. Proceedings of the American Association of Veterinary Laboratory Diagnosticians 48th Annual Conference. P. 38.
Technical Abstract: Transmissible spongiform encephalopathies (TSEs, prion diseases) are chronic neurodegenerative diseases that occur in humans, cattle, sheep, goats, cervids, and a number of laboratory animal models. In a laboratory setting, the host range of a given TSE can be tested by inoculating animals with brain tissue from affected animals through various routes including oral and intracranial. There is no evidence of the natural occurrence of any form of TSE in the pig, but pigs have been shown to be susceptible to bovine spongiform encephalopathy (BSE) infection by multiple-route parenteral challenge. However, pigs orally exposed at eight weeks of age to large amounts of brain from cattle clinically affected with BSE did not support infection after seven years of observation. In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility. This study utilized 26 swine randomly divided into three groups: controls (n=6), oral inoculates (n=8), and intracranial inoculates (n=12). Brain homogenate (10%) derived from scrapie-affected sheep was given by a single intracranial injection of 0.75 ml or by oral inoculation of 15 ml on four consecutive days. Scrapie inoculum was derived from clinically ill sheep inoculated with material derived from 13 sheep in seven source flocks. A sample of this material was also inoculated back into sheep to assure infectivity. Necropsies were planned for six months post inoculation, at approximately the time the pigs were expected to reach market weight. Samples collected were examined microscopically after routine staining (hematoxylin and eosin) and staining by standard immunohistochemical methods for prion protein (PrP**Sc). After approximately six months incubation time, no histologic lesions suggestive of spongiform encephalopathy or immunohistochemical evidence of prion infection were obtained. No evidence of scrapie infection was demonstrated in this short-term study, but positive results after an incubation period of only six months would be uncharacteristic. The only TSE with an incubation of six months or less known at this time is transmissible mink encephalopathy in mink, skunk, or raccoon hosts. However, scrapie in the raccoon model has a two-year incubation period. A replicate of littermate pigs has been inoculated and will be studied after long-term (3-7 years) incubation, and a similar study is underway with pigs inoculated with material derived from elk, mule deer, and whitetail deer affected by chronic wasting disease (CWD).
Last Modified: 03/19/2006
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=180786
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
http://web.archive.org/web/20031026000118/http://www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
http://web.archive.org/web/20040302031004/http://www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf
http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf
http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf
http://web.archive.org/web/20040302050655/http://www.bseinquiry.gov.uk/files/yb/1990/09/14007001.pdf
Since this result shows that pigs can get spongiform encephalopathy, even though there is no evidence that they have done so in the field, we believe that pigs should no longer be fed with protein derived from bovine tissues which might contain the BSE agent, ie, those 'specified' bovine offals that are already excluded from human consumption. It would make sense to extend this prohibition to feed for all species, including household pets, as other species have now developed spongiform encephalopathies. We are aware that many animal feed compounders and pet food manufacturers are already applying such a ban on a voluntary basis.
http://web.archive.org/web/20060625223925/http://www.bseinquiry.gov.uk/files/yb/1990/09/20002001.pdf
4.318 SEAC advised that:
While there was at present no way of assessing the risk that the use of porcine material in cattle feed might lead to the transmission of an SE agent, and while it was reasonable to assume that any risk was low, it was not possible to say there was no risk. The Committee noted that in practice porcine material was not being fed to cattle and felt that it was advisable for this situation to continue.
http://web.archive.org/web/20060926204901/http://www.bseinquiry.gov.uk/files/yb/1992/10/15002001.pdf
4.319 At its next meeting, on 22 April 1993, SEAC was informed that MAFF Ministers had accepted the advice that porcine protein should not be fed to cattle. MAFF felt that a statutory ban was unnecessary but the industry would be told that legislation would be introduced if there were any indications that such material might be used in practice.
http://web.archive.org/web/20040311072017/http://www.bseinquiry.gov.uk/files/yb/1993/04/22002001.pdf
Discussion 4.320 It is not easy to follow the precise nature of risk evaluation that led to Mr Gummer's reaction or SEAC's endorsement of it. We suspect that the former was a broad reaction against reinstituting the 'unnatural practice' of feeding animal protein to ruminants and that SEAC were happy to endorse a precautionary approach that did no more than continue the existing position.
4.296 On 20 August 1990, a positive result was recorded in the CVL's experiment to transmit BSE to pigs. One pig had been diagnosed by post-mortem pathology as having developed a spongiform encephalopathy. A confidential pathology report submitted by Mr Gerald Wells, Head of the CVL's Neuropathology Section, to his colleague Mr Michael Dawson in the Virology Department, included the following remark:
The result, albeit confined to one animal in the experimental challenge group is incontrovertible evidence of the transmissibility of BSE to the pig by simultaneous intracerebral, intravenous and intraperitoneal inoculation routes. 11
IN CONFIDENCE: PATHOLOGY REPORT
SNIP...
REMARKS
The changes are unequivocally those of a scrapie-like encephalopathy. The clinical history of this animal also provides strong supportive evidence of a scrapie-like disease.
snip...
The result, albeit confined to one animal in the experimental challenge group is incontrovertible evidence of the transmissibility of BSE to the pig by simultaneous intracerebral, intravenous and intraperitoneal inoculation routes.
http://web.archive.org/web/20031216035517/http://www.bseinquiry.gov.uk/files/yb/1990/08/20003001.pdf
IN CONFIDENCE
SNIP...
On 23 August 1990, Dr Pickles reported the discovery to Sir Donald Acheson. Her minute noted:
CMO should be aware that a pig inoculated experimentally (i.c., i.v. and i.p.) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there are no previous attempts at experimental inoculation with animal material. The Southwood group had thought pigs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. An urgent meeting is being called of [SEAC] but since key members and the chairman are now overseas at a meeting this may not be until the week beginning the 3rd September. Points for consideration: (i) In view of the long term exposure of pigs to scrapie without ill effect, does this suggest the species range for BSE is wider than that of scrapie, and if so what are the implications? (ii) Should the feeding of ruminant protein including BSE and scrape-infected offal to pigs now be discontinued? (iii) Is any action needed to protect humans, eg extending the offal ban to pigs? For information, there are now 9 cats confirmed with feline spongiform encephalopathy, suggesting this is indeed a new disease and exposure to BSE unlike exposure to scrapie has been hazardous for cats. Mr Maclean was informed last night and has agreed an early meeting of [SEAC] is required to give advice on which decisions will be made. In the meantime, he does not want to go public. Mr Maclean is expected to advise Mr Gummer. In these circumstances, CMO might like to consider whether [Mr Dorrell] should be informed.
SNIP...
http://web.archive.org/web/20040302031004/http://www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf
IN CONFIDENCE
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;
http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf
IN CONFIDENCE
So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...
http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf
BSE TO PIGS NEWS RELEASE
http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf
CONFIDENTIAL
BSE: PRESS PRESENTATION
http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf
http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf
INDUSTRY RESPONSE TYPICAL
http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf
DEFENSIVE BRIEFING
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf
CONFIDENTIAL
pigs & TSE prions & pharmaceuticals & CJD
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf
COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP
There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............
http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf
many questions remained unanswered; for example, would smaller doses cause disease, would large doses given by mouth be effective and would scrapie produce spongiform encephalopathy in pigs under similar conditions?
http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf
It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
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 was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.
http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf
4.303 The minutes of the meeting record that:
It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17
http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf
4.308 SEAC issued formal advice on 20 September 1990, following its meeting on the previous day. The advice stated:
Since this result shows that pigs can get spongiform encephalopathy, even though there is no evidence that they have done so in the field, we believe that pigs should no longer be fed with protein derived from bovine tissues which might contain the BSE agent, ie, those 'specified' bovine offals that are already excluded from human consumption. It would make sense to extend this prohibition to feed for all species, including household pets, as other species have now developed spongiform encephalopathies. We are aware that many animal feed compounders and pet food manufacturers are already applying such a ban on a voluntary basis. 22
http://web.archive.org/web/20060625223925/http://www.bseinquiry.gov.uk/files/yb/1990/09/20002001.pdf
4.309 In a statement to the Inquiry, Dr Tyrrell said:
It was the rapid increase in the BSE epidemic, the occurrence of more cases of FSE and the results of the pig transmission experiment which led SEAC to give the advice we did on the extension of the SBO ban. Before then (September 1990), we were not asked to advise on the extension of the SBO ban. It was important to consider humans before other animals. It should be remembered that prior to the test results of the pig transmission experiment, pigs and poultry were not known to be susceptible to TSEs. Breeding pigs, in particular, were thought to have received a very high exposure to the same type of contaminated MBM as cattle but without any evidence of the occurrence of TSE. The issue of symptom-less hosts was considered very carefully because it could apply to all domestic and farmed animal species. 23
http://web.archive.org/web/20040225164252/http://www.bseinquiry.gov.uk/files/ws/s011b.pdf
Sunday, December 06, 2009
Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer
http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
SNIP...
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089
" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.
http://cshperspectives.cshlp.org/letters/submit
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu
http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.
snip...
http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html
please see CWD potential to humans here ;
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089
"although the infection rate was low (4 of 13 animals [Hamir et al. 2001])."
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
MARCH 1, 2011
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
----- Original Message -----
From: David Colby
To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.
Warm Regards, David Colby
--
David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware
====================END...TSS==============
SNIP...SEE FULL TEXT ;
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html
Title: Transmission of Chronic Wasting Disease of Mule Deer to Suffolk Sheep Following Intracerebral Inoculation
Authors
Hamir, Amirali Kunkle, Robert Cutlip, Randall - ARS RETIRED Miller, Janice - ARS RETIRED Williams, Elizabeth - UNIVERSITY OF WYOMING Richt, Juergen
Submitted to: Conference Research Workers Disease Meeting Publication Type: Abstract Publication Acceptance Date: December 3, 2006 Publication Date: December 3, 2006 Citation: Hamir, A.N., Kunkle, R.A., Cutlip, R.C., Miller, J.M., Williams, E.S., Richt, J.A. 2006. Transmission of chronic wasting disease of mule deer to Suffolk sheep following intracerebral inoculation [abstract]. Conference of Research Workers in Animal Diseases 87th Annual Meeting. Paper No. P34. p. 108.
Technical Abstract: To determine the transmissibility of chronic wasting disease (CWD) to sheep, 8 Suffolk lambs of various prion protein (PRNP) genotype (4 ARQ/ARR, 3 ARQ/ARQ, 1 ARQ/VRQ at codons 136, 154 and 171, respectively) were inoculated intracerebrally with brain suspension from mule deer with CWD (CWD**md). Two other lambs were kept as non inoculated controls. Within 36 months post inoculation (MPI), 2 inoculated animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in this sheep and its tissues were positive for the abnormal prion protein (PrP**res) by immunohistochemistry and Western blot. Three other inoculated sheep were euthanized (36 to 60 MPI) because of conditions unrelated to TSE. The 3 remaining inoculated sheep and the 2 control sheep were non clinical at the termination of the study (72 MPI) and were euthanized. One of the 3 remaining inoculated sheep revealed SE and its tissues were positive for PrP**res. The sheep with clinical prion disease (euthanized at 35 MPI) was of the heterozygous genotype (ARQ/VRQ) and the sheep with the sub clinical disease (euthanized at 72 MPI) was of the homozygous ARQ/ARQ genotype. These findings demonstrate that transmission of the CWD**md agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a significant part in successful transmission and incubation period of CWD**md.
Project Team
Kunkle, Robert NICHOLSON, ERIC GREENLEE, JUSTIN
Publications
Publications
Related National Programs
Animal Health (103)
Patents
Method For Detecting A Gene Linked To Mad Cow Disease
Last Modified: 07/05/2011
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=198158
Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]
http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html
The case for mad pigs in the US
From the Consumer Policy Institute and Consumers Union: March 24, 1997
Stephen F. Sundlof, D.V.M., Ph.D Center for Veterinary Medicine Food and Drug Administration 7500 Standish Place, Room 482, HFV 1 RockvLIle, MD 20855 Dear Dr. Sundlof:
We are writing to you to submit information that has recently come to our attention which suggests that a TSE like disease (transmissible spongiform encephalopathy) might exist in pigs in the U.S. We believe this new informantion calls for intensive research and makes it urgent to ban the use of all mammalian proteins, including swine, in the feed of all food animals, until better answers are found.
The evidence for the potential PSE (porcine spongiform encephalopathy ) is as follows. In 1979, an FSQS veternarian, Dr. Masuo Doi, noticed some unusual central nervous system (CNS) symptoms in young (about 6 months old) hogs coming into a slaughter plant In Albany, New York. Since the plant received hogs from a wide variety of sources (New York, Canada, Indiana, Illinois, Ohio, and other Midwestern states) and was not a plant used to dealing with diseased animals, Dr. Doi thought that the problem might be affecting hogs slaughtered nationwide. So, he decided to conduct a detailed study on central nervous system (CNS) symptoms/disease in young hogs coming into that slaughter plant. The study ran for 15 months (January, 1979 to March, 1980) and consisted of extended observations of the behavior of animals with suspected CNS symptoms at the plant, followed by pathological, histopatholpgical, and microbiological work on tissues from various organs of particular animals after slaughter.
For his behavioral observational work, Dr. Doi extended the usual two day observation period to three to four days, during which he took careful notes on the animals' behavior and other vital signs. During the 15 month period of the study, some 106 animals exhibiting CNS symptoms were retained during antemortem inspection.
A 1980 paper that summarized Dr. Doi's findings on the clinical symptoms and incidence of the 'disease," contained descriptions of these symptoms that sound remarkably similar to the symptoms noted for bovine spongiform encephalopathy (BSE):
"Excitable or nervous temperament to external stimuli such as touch to the skin, handling and menacing approach to the animals is a common characteristic sign among swine affected with the disease.... In the advanced stage of the disease, manifestation of neurological signs are evidenced in the form of general ataxia . . . Many animals have been found to be "downers' at first observation; if the hindquarters of these downers are raised they may be able to walk one or two steps and then fall to the ground" (Doi et al., 1980: 2, 4). Indeed, a table of symptoms includes, for the early stage: "excitability and nervousness (squealing, smacking of lips, grinding of teath, chewing, gnawing ant foaming at mouth); stiffness of limbs . . . 'tic'; weakness of hindquarters; focal tremors of skeletal muscles"; and for the advanced stage: depression; ataxia; crossing over of limbs . . . kneeling posture . . . crawling". In addition to his clinical observations, Dr. Doi also made an 8 mm film of thirteen of the affected animals; film of two of the pigs was shown at the MPI National Pathology Meeting in Seattle, Washington on flay 20, 1979.
Dr. Doi sent tissue samples from suspect cases to the USDA's Eastern Laboratory in Athens, GA for pathological, histopathogical and microbiological work. Known infectious diseases were ruled out. As Dr. Doi points out, "Histopathological studies of tissue collected from the brain and spinal cord of these animals in the early stage of the disease show congestion, hemorrhage and neuronal degeneration. All animals in the advanced stage of the disease have been confined to have Encephalitis or Meningitis by MPI laboratory" (Doi et al., 1980: 5). Eventually some 60 animals were confirmed by the MPI Laboratory to have encephalitis or meningitis, with no ldentifiable cause. As pointed out in a paper presented at the 1979 MPI National Pathology Meetings,
"Since January, a number of hogs in this establishment have been found, in antemortem, to show what appears to be CNS. Sets of tissue samples were sent to the laboratory for examination, various tests were done which include histological study (E H stain), fluorescence antibody technique, virus neutralization and viral and bacteriological isolation. Differential diagnosis was also done to exclude vitamin B deficiency, post vaccination reaction, chlorinated hydrocarbon, arthritis, and transport stress" (Doi et al., 1979). The brains of the 60 animals were examined. The brain of one of these pigs, on histopathological analysis, exhibited signs reminiscent of a TSE. This histopathological work was performed by Dr. Karl Langheinrich, Pathologist-In-Charge at USDA's Eastern Laboratory in Athens, Georgia. According to the USDA FSQS laboratory report, dated early November, 1979, Dr. Langheinrich noted:
"Microscopic examination of the barrow tissues revealed a encephalopathy and diffuse gliosis characterized by vacuolated neurons, loss of neurons and gliosis in a confined region (nucleus) of the brain stem (anterior ventral midbrain). Only an empty sometimes divided vacuole was present instead of the normal morphology of a nerve cell. Occasionally a shriveled neuron was seen. According to . . . Pathology of Domestic Animals, . . . 'The degeneration of neurons, the reactivity of the glia .... are the classical hallmarks of viral infection of the central nervous system' .... Scrapie of sheep, and encephalopathy of mink, according to the literature, all produce focal vacuolation of the neurons similar to the kind as described for this pig. I was unable to locate any lead as to the cause of this interesting phenomenon in other species including swine'' (Langheinrich, 1979). Indeed, Dr. Langheinrich's main diagnosis was, " Encephalopathy and diffuse gliosis of undetermined etiology." Portions of the brain were sent for microbiological testing to a neurologist at the University of Georgia, where they came up negative for pseudo-rabies. The brain was unique enough that USDA scientists, such as Dr. Langheinrich and Or. Dot, mentioned it to student and scientific colleagues over the years.
In 1979-1980, BSE was completely unknown. However, both the behavior of the pigs, as well as the histopathology on at least one pig, both showed sign consistent with a porcine TSE. This raises particular concern became the affected animal was only 6 months old; in an animal this young, one would rust expect to see any physical signs of TSE in the brain. Histopathology of TSEs can be very variable, so that spongiform appearance (i.e. vacuolated neurons) are not always present. Behavioral changes can be seen in TSE-infected animals before any changes in brain morphology are visible. Dr. Clarence Gibbs, in testimony before a Congressional hearing on the TSE issue on January 29, 1997 made just this point:
''In the mid-1960s, we demonstrated with our French and English collaborators that during the early incubation of the TSEs, when the virus titer in the brain was very low, there were already marked functional changes, even though no pathology was yet detectable, even ultrastructurally. A month or hero later, polynucleation of neurons appeared in spider monkeys, incubating kuru, and somewhat later, microvacuolation and membrane changes visible only by electron microscopy. This preceded the pest appearance of astrogliosis and spongiform change. It was only much later that the classical scrapie TSE pathology appeared with virus titers in brain of 10 -5 or higher" (Gibbs, 1997; pg. 4). Given that TSEs can cause behavioral changes in infected animals before any physical changes in the brain can be seen, that the manifestation of TSE in the brain can be quite variable, and that changes in brain morphology are not usually seen in 6 month old animals, we are concerned that the brain of one pig actually showed physical evidence consistent with a TSE.
Following the announcement In March, 1996 of ten cases of new variant CJD (Creutzfeldt-Jakob Disease) in the United Kingdom and their possible connection to BSE, Drs. Doi, Langheinrich and others urged reinvestigation of this case.
In August, 1996, the USDA sent five slides, one of which was a histopathology slide, to Dr. Janice Miller of USDA's Agricultural Research Servicer . Dr. Miller stained four of the slides for prion protein (she didn't stain the H&E slide). Dr. Miller told Consumers Union that Dr. Patrick McCaskey, USDA/FSIS, in charge of the Research Center at Athens, GA, called her, told her that he had five slides that all showed "problems" and asked her to stain four of them. The H&E slide, which clearly show vacuoles in the neurons (one sign of TSE), wasn't stained because to stain for PrP entails removing the slide cover, baking the slide to destain it and then restaining it for PrP; they didn't want to risk destroying the H&E slide.
Dr. Doi had kept frozen samples of the brain and spinal chord of the suspect PSE pig in case the Eastern lab wanted more material for analysis. Unfortunately, these samples were discarded when the packing plant in Albany, NY closed in 1991. It appears that the brain material sent to the Univcrsity of Georgia may have been discarded. [pers com.. Dr. Doi 3/13/97]
Dr. Miller found that the PrP stained in the four pig slides was found only on the inside of neurons, while a positive control slide from a scrapie sheep showed massive amounts of extraneuronal staining. In a letter summarizing her results (copy attached), she concludes that the PrP stained in this pig was normal: "In the pig sections you will see a small particulate type of staining that is confined to neurons and as I indicated on the phone, I would interpret as normal PrP. It is in marked contrast to the massive amount of extraneuronal staining seen in the scrapie section" (Miller, 1996).
Unfortunately, Dr. Miller's finding toes not conclusively rule out a TSE. We are concerned that while British BSE and serapie create a massive amount of extraneuronal staining, there are TSEs where this isn't the case. Three experiments were done in He U.S. -- in Mission, TX (APHIS work), Pullman, Washington (ARS work), and Ames, Iowa (ARS work) -- to see whether sheep scrapie can possibly infect cows. In all the experiments, cattle were inoculated with tissue from scrapie -infected sheep primarily by intra-cranial injection, but in the case of the Texas and Iowa studies also by oral feeding -- to see if cattle were susceptible to scrapie at all. In all three experiments, the majority of cows injected in the brain with scrapie-infected sheep material (usually brains) also developed a fatal spongiform encephalopathy.
However, in all three examples, the symptoms of the spongifonn encephalopathy differed from "mad cow" disease ~ England, as did the appearances of slides from their brains. The brain lesions seen in all these animals were more variable than those seen in England. When Dr. Miller did similar staining for PrP from these brains (what she called "bovine scrapie") she only found PrP stains on the inside of the neurons, not the massive extraneuronal staining seen in BSE (Miller, pers. comm., March 7, 1997). Thus, Dr. Miller's finding of PrP stains only inside the neurons in the suspect pigs is not particularly reassuring.
In November 1996, USDA sent the single histopathology slide to Dr. William Hadlow, one of the foremost spongiform encephalopathy pathologists in the world. (For unknown reasons, Dr. Hadlow was only sent the one slide; he was not told of the existence of the other slides, nor of Dr. Miller's findings, nor was he told or given the behavioral report from Dr. Doi or the morphology work by Dr. Langheinrich, or shown film of the affected pigs [Dr. Hadlow, pers. com., 3/13/97] From this single slide, Dr. Hadlow found some evidence consistent with TSEs but not enough for a conclusive diagnosis. He noted that the slide contained vacuoles inside neurons, one of the signs of a TSE (Dr. Langheinrich had noted this as well).
However, since such vacuoles occasionally occur normally in pigs, he thought that was not something special: "About twelve (12) neurons in the parasympathetic nucleus have unilocular optically empty vacuoles in the perikaryon. This is the site where such vacuolated neurons have been seen in the swine (as well as in cats and sheep) as an incidental finding. So I do not think such cells have any significance in this pig" (Hadlow, 1996). However, he did see evidence, Including changes in astrocytes, that suggested a TSE, but without examining other parts of the brain to look for other evidence of TSE, he couldn't be sure:
"I am impressed, though, with what seems to be an increase in the number of astrocytes in the section. Some astrocytes are in clusters, some are enlarged and vesicular. Where they are most numerous, a few rod cells (activated microglia) are seen. These findings suggest some perturbation of the nervous tissue. Although such a global response occurs in the transmissible spongifonn encephalopathies, I do no! know its significance in this case without examining other parts of the brain for changes characteristic of these diseases. Thus, from looking; at this one (1) section of brain, I cannot conclude that the pig was affected with a scrapie-like spongiform encephalopathy" (Hadlow, 1996). In sum, Dr. Hadlow~s letter does not rule out the possibility of a TSE. He says that there is suggestive evidence, but that he would need to look at other slides/sections of the brain, to make a conclusive diagnosis.
In our view, the implications of this data are extremely serious. Experiments in the United Kingdom have shown that pigs are susceptible to BSE. Pigs inoculated with BSE develop a TSE (Dawson et al., 1990). Feeding experiments are underway in the UK to see if BSE can be orally transmitted to pigs; as of March, 1997, some 6 years after the start of the experiment, none of the pigs fed BSE brain have come down with a TSE. Unfortunately the design of this experiment severely limits what we will learn from it, and will most likely not tell us conclusively if pigs can get BSE from feed. It turns out that the pigs were not fed BSE brain continuously. Rather, the pigs were only fed BSE brain material on three days, over a three week period (i.e.. one day each week). Following these three doses, the pigs were never fed contaminated material again. The total amount of infective material given to the pigs was therefore quite small. Thus, a negative finding would be hard to interpret and would not mean that BSE is not orally active in pigs.
We believe that as a top priority USDA should conduct follow-up studies to look for potential CNS/PSE cases in pigs (we plan to communicate about this to USDA separately). In brief, we feel that the following kinds of studies need to be done:
i) TSE pathology experts should examine all the slides from the suspect pig (2709). To our knowledge, at least 12 separate slides exist.
ii) Determine if any brain material from the suspect pig (2709) still exists at the Unlverslty of Georgia. If so, this material should be retrieved and used for transmission studies. In particular, suckling pigs should be inoculated with the material and then permitted to live unto they die of a disease or old age, at which point their brains should be examined for physical signs of a TSE as well as for immunchistochemical evidence (i.e. staining looking for the abnormal PrP).
iii) Increase antemortem inspection for CNS symptoms at hog facilities. Inspectors should be trained to detect the subtle CNS symptoms seen in the Doi et al. study. At a select number of slaughter facilities, animals exhibiting CNS symptoms should be removed and held for observation until they die, at which time their brains should be examined for evidence of a TSE.
iv) Research on CNS symptoms among Me 6,000 or so breeding sows which are permitted to live for 3+ years. Sows exhibiting CNS symptoms should be removed and held for observation until they die, at which time then brains should be exernined for evidence of a TSE.
While such work is underway, given the above inforrnabon, we believe that as a precutionary measure the FDA must expand the proposed ruminant plus mink-to-ruminnant feed ban to prevent protein from any material, including hogs, being fed to any food animal.
Sincerely,
Michael Hansen, Ph.D Research Associate
Jean Halloran Director
References
Dawson, M., Wells, G.A.H., Parker, B.N;J. and A.C Scott. 1990. Primary parental transmission of bovine spongiform encephalopathy to the pig. Veternary Record, pg. 338.
Doi, M., Matzner, N.D. and C. Rothaug. 1979. Observation of CNS disease in market hogs at Est. 893 Tobin Packing Co., Inc. Albany, New York. United States Department of Agriculture, Food Safety and Quality.Service, Meat and Poultry Inspection Service. 7pp.
Doi, M, Langheinrich, K. and F. Rellosa. 1980. Observations of CNS signs in hogs at Est. 893 Tobin Packing C:o., Inc. Presented by Dr. Lngheinrich at the MPI National Pathology Meeting in Seattle, Washington on July 20, 1979.
Gibbs, C. 1997. Statement to the Committee on Governnent Reform and Oversight, Subcommittee on Human Resources and Intergovernmental Relations, U.S. House of Representatives. January 29,1997.
Hadlow, WJ. 1996. Letter to Patrick McCaskey, USDA/FSIS/Eastem Lab, dated November 13, 1996.
Langheinrich, KA. 1979. USDA/FSQS Laboratory report on specimen 2709. Dated November 8, 1979
Miller, J. 1996. Letter to Patrick McCaskey, USDA/ESIS/Eastern Lab, dated September 6, 1996.
Dr. Janice Miller, ARS
http://www.mad-cow.org/~tom/mad_pigs.html
Subject: EXPERIMENTAL INTRACEREBRAL AND ORAL INOCULATION OF SCRAPIE TO SWINE: PRELIMINARY REPORT Date: February 6, 2006 at 12:33 pm PST Title: EXPERIMENTAL INTRACEREBRAL AND ORAL INOCULATION OF SCRAPIE TO SWINE: PRELIMINARY REPORT
SEE MORE HERE ;
PORCINE SPONGIFORM ENCEPHALOPATHY PSE
http://madporcinedisease.blogspot.com/
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov
http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html
Wednesday, July 6, 2011
Mad cow disease: EU must maintain strict controls, says Parliament
snip...
but the ban on feeding animal protein to non-ruminants, such as pigs, could gradually be lifted if further safeguards are put in place, they add.
snip...
http://efsaopinionbseanimalprotein.blogspot.com/2011/07/mad-cow-disease-eu-must-maintain-strict.html
WHAT HAPPENS WHEN YOU RENDER UNTO FEED, AND FEED EVERY LIVESTOCK SPECIES, GAME SPEICIES, ALL STRAINS OF TSE THERE FROM, AND THEN FEED THERE FROM, TO HUMANS AND ANIMALS ???
WE WILL KNOW IN DUE TIME, BECAUSE THIS IS AN ONGOING LONG TERM STUDY FOR THE NORTH AMERICAN CONSUMER $$$
BE WARNED, YOU HAVE, AND CONTINUE TO BE EXPOSED $$$
LET'S LOOK AT A FEW SPECIES THAT HAVE BEEN FED BANNED SUSPECT MAD COW FEED IN THE USA OVER THE DECADES ;
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
NOW, LET'S LOOK AT A FEW 100S OF TONS OF THESE BANNED SUSPECT MAD COW FEED IN COMMERCE IN THE USA ;
BANNED SUSPECT MAD COW FEED IN COMMERCE 2006-2007, SOME 10 YEARS AFTER THE INFAMOUS PARTIAL AND VOLUNTARY MAD COW FEED BAN or August 4, 1997, that was nothing more than ink on paper, so really, there was no BSE triple fire wall at all, and this was improving ???
*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
see Alabama banned suspect mad cow feed in commerce ;
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE
Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
NOW, what about that mad cow feed from atypical BSE in commerce and SRM regulations ???
Research Project: Study of Atypical Bse Location: Virus and Prion Research Unit
Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement
Start Date: Sep 15, 2004 End Date: Sep 14, 2009
Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate.
Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.
http://www.ushrl.saa.ars.usda.gov/research/projects/projects.htm?accn_no=408490
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010
http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html
Friday, October 8, 2010
Scientific reasons for a feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food
http://madcowfeed.blogspot.com/2010/10/scientific-reasons-for-feed-ban-of-meat.html
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these countries.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
snip...
To minimise the risk of farmers' claims for compensation from feed compounders.
To minimise the potential damage to compound feed markets through adverse publicity.
To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.
snip...
THE FUTURE
4..........
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...
SEE full text ;
http://web.archive.org/web/20060517074958/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
Monday, June 20, 2011 2011
Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA
http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html
Monday, June 27, 2011
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease
http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html
Monday, June 27, 2011
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html
Sunday, July 03, 2011
Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Naturally/Experimentally Infected Scrapie Sheep and Preclinical/Clinical CWD Deer
http://chronic-wasting-disease.blogspot.com/2011/07/prion-disease-detection-pmca-kinetics.html
Saturday, June 18, 2011
Self-propagation and transmission of misfolded mutant SOD1 Prion or Prion-like phenomenon?
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/self-propagation-and-transmission-of.html
Wednesday, June 29, 2011
TSEAC Meeting August 1, 2011 donor deferral
http://tseac.blogspot.com/2011/06/tseac-meeting-august-1-2011-donor.html
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html
Monday, May 23, 2011
Atypical Prion Diseases in Humans and Animals 2011
Top Curr Chem (2011)
DOI: 10.1007/128_2011_161
# Springer-Verlag Berlin Heidelberg 2011
Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar
http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html
FELINE SPONGIFORM ENCEPHALOPATHY FSE
http://felinespongiformencephalopathyfse.blogspot.com/
CANINE SPONGIFORM ENCEPHALOPATHY
http://caninespongiformencephalopathy.blogspot.com/
IN CONFIDENCE
SUSPECT BSE IN A HORSE
CYO BSE 1 9
IN CONFIDENCE
SUSPECT BSE IN A HORSE
The Parliamentary Secretary (Mr Maclean) will wish to be aware that, in making his differential diagnosis, a veterinary surgeon in the Reading area has included the possibility of BSE in a horse under his care. Although it is unlikely to be BSE, because of the symptoms exhibited the veterinarian believes that he cannot exclude the possibility. The case was brought to the notice of one of the veterinary staff at the CVL by the owner's veterinary surgeon and liaison is being maintained.
The horse in question is a five-year old eventing gelding which was purchased by the present owner about four months ago. Approximately two months after purchase the animal became a little apprehensive, developed mild nervous symptoms and became over-sensitive to noise. The nervous symptoms have increased and the horse is now practically impossible to ride. Investigations by the owner's private veterinary surgeon are continuing but it is likely that the animal will have to be destroyed.
If the horse should die or be destroyed, a full post-mortem examination will be required for insurance purposes and will probably be carried out at a non-Ministry laboratory. However, Mr Bradley of the Pathology Department, CVL, has informed the private veterinary surgeon that he is willing to provide a second opinion on the brain histology if requested.
I will keep the Parliamentary Secretary informed of any further developments in the case.
I CRAWFORD
14 May 1990
Mr M P H Hill, PS/Parliamentary secretary (Mr Maclean) - by FAX
cc:
Private Offices
Mr K C Meldrum
Mrs E A J Attridge D J Evans Mr K C Taylor Mr R Lawson Mr R Bradley. CVL
(hand written notes i cannot read all (cut short) as follows...tss)
The Parliamentary Secretary (Mr Maclean was grateful for this. He said that we must keep very close to ...on it, and when the horse dies, or is put down we must be told immediately. He also feels it is very important that our veterinary staff be involved in the brain examination. .........(cannot read the rest .............TSS)
90/05.14/10.1
http://collections.europarchive.org/tna/20080102214337/http://www.bseinquiry.gov.uk/files/yb/1990/05/14010001.pdf
see history ;
Equine Spongiform Encephalopathy
http://equinespongiformencephalopathy.blogspot.com/
PORCINE SPONGIFORM ENCEPHALOPATHY PSE
http://madporcinedisease.blogspot.com/
Transmissible Mink Encephalopathy TME
http://transmissible-mink-encephalopathy.blogspot.com/
ALSO; in Harash Narang's book THE LINK (i believe he went to work for NIH on TSEs, not sure if he is still there) there is a part about BSE IN HENS (page 135), that a farmer in kent in Nov. 1996 noticed that one of his 20 free range hens the oldest, aged about 30 months, was having difficulty entering its den and appeared frightened and tended to lose its balance when excited. Having previously experiencing BSE cattle on his farm, he took particular notice of the bird and continued to observe it over the following weeks. It lost weight, its balance deteriorated and characteristic tremors developed which were closely associated with the muscles required for standing (Fig. 15). In its attempts to maintain its balance it would claw the ground more than usual and the ataxia progressively developed in the wings and legs, later taking a typical form of paralysis with a clumsy involuntary jerky motion. Violent tremors of the entire body, particularly the legs, similar to those seen in BSE, became common sparked off by the slightest provocation. Three other farmers from the UK are known to have reported having hens with similar symptoms...
with this agent, i would not rule out anything or any species...TSS
From: TSS
Subject: TRANSMISSION STUDIES OF DOMESTIC FOWL AND OSTRICH......
Date: May 9, 2002 at 7:36 am PST
######## Bovine Spongiform Encephalopathy #########
Greetings List Members,
just reading over a few old documents, i am pondering a few things out loud here, hope some find them interesting...TSS
snip...
SE1806
TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN HOMOGENATE
1 challenged cock bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any significant lesions of the central or peripheral nervous systems...
snip...
94/01.19/7.1
(updated url, you better download this while it is still available...tss)
http://tna.europarchive.org/20080609145105/http://www.bseinquiry.gov.uk/files/yb/1994/01/19007001.pdf
also,
TRANSLATION
F437/91
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY -
* The Red-Neck Ostrich 'THE AUTOPSY' & TSEs
THE AUTOPSY
Date: Mon, 11 Jun 2001 16:24:51 -0700
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY'
######## BSE #########
TRANSLATION
F437/91
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY -
H A Schoon, Doris Brunckhorst and J Pohienz Institute of Pathology, Veterinary University of Hannover
Introduction
Since the first appearance of BSE in Great Britain in l985 {review in TRUYEN & KAADEN, l990), research into the incidence, diagnosis, differential diagnosis and epidemiology of spongiform encephalopathies in humans and animals has been a focus of medical and public interest. In view of the growing number of reports of "new" spontaneously or experimentally susceptible species (cats: WYATT et al, l990; pigs: DAWSON et al, 1990), and of the associated questions with regard to the causal agent and in particular its transmissibility, it seems essential that agnopathogenetic individual cases should also be described. We therefore report below the preliminary findings of morphological examinations of three red-necked ostriches in 1986, 1988 and 1989, taking account of differential diagnostic factors.
History/subjects
The three ostriches (Flock A: Ostrich 1, female, adult, 150 kg; Flock B: Ostrich 2, female, adult, 80 kg; Ostrich 3: male, juvenile, 60 kg) came from two zoos in North West Germany and were euthenised because of their hopeless prognosis. Preliminary reports indicated that all three birds had presented protracted central nervous symptoms with ataxia, disturbance of balance and discoordinated feeding behaviour. Ostrich 2 had also exhibited pronounced lameness of the left lower limbs and the juvenile bird was suffering from perosis. The birds were fed on vegetable material, supplemented by commercial compound poultry feed and ''raw meat'', some of which was ''obtained from local small emergency slaughterers''. Comparable clinical pictures with fatal outcome in individual birds had occurred in both flocks: in a male bird at the same time (Flock A) and in several ostriches over recent years (Flock B).
Methods
Autopsy was followed in all three cases by histopathological examination of the following tissues: heart (several locations including coronary arteries and aorta), right and left pulmonary lobes, liver, kidneys, limb musculature, peripheral nerves (brachial plexus, sciatic nerve, in each case both left and right) and brain (left and right cerebral hemispheres, two samples each from the cranial/caudal third, two sagittal sections of the cerebellum, two cross-sections of the brain stem at the level of the optical lobes, four cross-sections from the medulla oblongata). The tissue material was fixed in formalin and embedded in Paraplast by the conventional method and the sections were evaluated using the following staining techniques and histochemical reactions: all organs: haematoxylin eosin staining; brain: PAS reaction (McManus), Ziehl/Neelsen staining (mod. Pearse), iron method (Lillie) for detection of neuromelanin, Turnbull's reaction (Bancroft & Stevens), alkaline Congo red method (Puchtler) (of SCOON & SCHINKEL, 1986), myelin sheath staining (Spielmeyer) (ROMEIS, 1968). In addition, unstained sections were examined by fluorescence microscopy (to detect autofluorescing lipofuscin granula) and the following lipid stains were applied to cryostat sections of liver, and of heart and skeletal musculature: Sudan III, Sudan black, oil red.
Findings
Ostrich 1
Brain: whilst only middle grade oedematisation of the neuropil was noted in the cerebral and cerebellar region, major changes were detected in the brain stem and medulla oblongata (Figures 1-3): in addition to pronounced vacuolation of the grey matter, optically vacant, ovoid to spherical vacuoles of differing sizes occurred bilaterally symmetrically in numerous neurons of the brain centres nucleus ruber, vestibular nucleus and reticular formation, in certain cases compressing the Nissl substance into a narrow fringe. In addition, fine granular pigments were found in the perikaryon of the neurons (with and without vacuoles), which showed a golden brown coloration in the haematoxylin eosin specimen, gave positive reactions to both PAS and Ziehl-Neelsen and also exhibited a yellowish-green spontaneous autofluorescence. Lillie staining to detect neuromelanin gave a negative result. The pigments thus exhibited the characteristics of lipofuscin (SCHOON & SCHINKEL, 1986). Ferruginous pigments and histochemically detectable amyloids were absent. Mild gliosis, isolated necrotic neurons and neuronophagia were observed only in the cranial locations of the brain stem.
Other findinqs: The ostrich exhibited marked adiposity and multiple pressure sores of both lower limbs. Moderate steatosis was found in the heart and skeletal musculature and in the liver. Multifocal arteriosclerotic plaques were also noted in the coronary and limb arteries.
Ostrich 2
Brain: Histopathological changes in the brain of this ostrich were limited to the medulla oblongata and were qualitatively consistent with those found in Ostrich 1, although confined, bilaterally symmetrically, to small localised areas and affecting only individual neurons. Gliosis reaction was almost entirely absent.
Other findinqs: The carcase was moderately well nourished and exhibited multifocal dermal and muscular necroses on both lower limbs in conjunction with lateral chronically destructive tarsitis and coxitis. In the internal organs, parenchymatous degeneration of the liver and kidneys and multifocal arteriosclerotic plaques in the coronary arteries were noted.
Ostrich 3
Brain: Whilst no histopathological changes were found in the cerebrum and cerebellum of this ostrich, a high grade spongious dispersion of the neuropil existed in all locations examined in the brain stem and medulla oblongata (status spongiosus, Figure 4). Individual neurons contained optically vacant vacuoles of varying size, whilst numerous nerve cells exhibited clear signs of nuclear degeneration, in particular in the form of nuclear pyknosis. Low grade gliosis was also noted in all locations.
Other findinqs: The left lower limb of this bird exhibited defective positioning of the tarsal joint resulting from axial distortion of the long bones with applanation of the lateral [Rollkamm - word not found] and resultant instability of the tendons and inward turning of the tarsus.
Discussion
Although ostriches are widely kept in zoos, there are virtually no detailed descriptions of central nervous disorders with associated locomotor disfunction in this species. Neurological symptoms have been reported in connection with an outbreak of Newcastle Disease (KLOPPEL, 1969) and bacterial meningitis has been described (GRZIMEK, 1953), whilst other, sporadic cases have remained etiologically unexplained (ZUKOWSKY, 1959; LANDOWSKI, 1965). Disfunctions of the locomotor system of extracerebral origin occur predominantly in juvenile ostriches, emus and rheas in connection with muscular disease, perosis and trauma (FROIKA, 1982, 1983; MIHALIK & SRANK, 1982; SCHRODER & SEIDEL0 1989). One of the ostriches we examined was suffering from perosis, another from unilateral tarsitis and coxitis. All three, however, exhibited neuropathological findings consisting of a gradual, bilaterally symmetrical, spongiform encephalopathy of varying degree in the brain stem and medulla oblongata. No descriptions of such findings in this species appear in any of the literature we have been able to obtain.
These histopathologically confirmed brain changes are not consistent either with those caused by the classic viral infections in domesticated and wild birds or with those described by GRATZL & KOHLER (1957) and CHEVILLE (1966) as typical of Vitamin E deficiency-related encephalopathy in chicks. Instead, at the light microscopy level, both in qualitative terms and in the pattern of distribution in the central nervous system, there is a high degree of coincidence with findings which occur in transmissible spongiform encephalopathies in mammals (scrapie, BSE, transmissible mink encephalopathy, chronic wasting disease of captive mule deer and elk) (HADLOW, 1961; BURGER & HARTSOUGH, 1965; HARTSOUGH & BURGER, 1965; WILLIAMS & YOUNG, 1980; WELLS et al, 1987, 1989).
The sporadic occurrence of vacuoles in individual neurons of the nucleus ruber in cattle was interpreted species-specifically as an artefact by FRANKHAUSER et al (1972). We are unable to judge whether a similar conclusion is also appropriate in the case of the ostrich, since our experience is based on only a small number of neuropathologically investigated cases. However, examination of the brains of twelve other ostriches which came to autopsy after death from extracerebral causes did not reveal any such findings. FRANKENHAUSER et al (1972) also emphasise that none were observed by them either in small ruminants or in the horse or the dog.
It is not possible at this time to determine whether and to what extent our neuropathological findings in an omnivorous bird, the ostrich, are etiopathogenetically consistent with those of the spongiform encephatopathies of mammals. There are no indications whatever in the relevant literature of even a hypothetical susceptibility in birds, although it must be said by way of qualification that clinical manifestations would be most unlikely in short-lived farm poultry, given the long incubation period. Moreover, Germany was officially free of scrapie and BSE at the time the condition appeared in the ostriches. The question of possible contamination of carcase meal is discussed in the work of TRUYEN & KAADEN (1990).
Conclusive diagnosis, especially in these cases, and in spite of the certainty ascribed by WELLS et al (1989) to histopathological diagnosis in cattle, also requires electron microscopic detection of so-called scrapie-associated fibrils (SCOTT et al, 1987; HOPE et al, 1988) and attempts, by inoculation of suspect brain material, to transmit the disease to the mouse (TRUYEN & KAADEN, 1990). Both of these procedures are normally carried out using fresh material, whereas we now have only tissue fixed in formalin and embedded in Paraplast.
Etiological consideration must also be given retrospectively to unidentified toxic influences, unknown species-specific deficiency diseases and unexplained predisposing metabolic conditions.
The etiologically unexplained neuropathological findings reported here, together with the multitude of unanswered questions in this connection, underline the need for further, systematic, standardised studies in this species, based on a larger sample of birds.
Summary and Literature
[Not translated]
Figures
Figure 1: Spongiform encephalopathy with oedematisation and vacuolation of the neuropil and "ballooning" degeneration of virtually all neurons in this area of the brain - brain stem. (H,-E.-Frgb., magnification x 120)
Figure 2: Detail of Figure 1. In 'addition to oedematisation of the neuropil, numerous, optically vacant vacuoles in the neurons, with partial displacement of the Nissl substance - brain stem. (H.-E.-Frgb., magnification x 480)
Figure 3: Medulla oblongara with high grade spongiform dissociation of the neuropil. (H.-E.-Frgb., magnification x 300)
Figure 4: Medulla oblongata. Status spongiosus with neuron degeneration. (H.-E.-Frgb., magnification x 300).
-----------------------------------------------------
even the late great Dr. Gibbs once told me personally that even if the Chicken did not contract a TSE, IF the chicken had been fed the TSE tainted feed and then slaughtered, the agent survives the digestinal tract to pass on to other species through feed...
TSS
Date: Tue, 27 May 2003 08:07:58 -0500 Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr." Subject: FDA BSE Update - Pet Food from Canadian Manufacturer & MAD DOG DATA
######## Bovine Spongiform Encephalopathy #########
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY
http://web.archive.org/web/20060218170908/http://www.bseinquiry.gov.uk/files/sc/Seac10/tab06.pdf
OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002
OPINION
1. Necrophagous birds as possible transmitters of BSE. The SSC considers that the evaluation of necrophagous birds as possible transmitters of BSE, should theoretically be approached from a broader perspective of mammals and birds which prey on, or are carrion eaters (scavengers) of mammalian species. Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons, eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could be considered possible vectors of transmission and/or spread of TSE infectivity in the environment. In view also of the occurrence of Chronic Wasting Disease (CWD) in various deer species it should not be accepted that domestic cattle and sheep are necessarily the only source of TSE agent exposure for carnivorous species. While some information is available on the susceptibility of wild/exotic/zoo animals to natural or experimental infection with certain TSE agents, nothing is known of the possibility of occurrence of TSE in wild animal populations, other than among the species of deer affected by CWD in the USA.
1 The carrion birds are animals whose diet regularly or occasionally includes the consumption of carcasses, including possibly TSE infected ruminant carcasses.
C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc
http://ec.europa.eu/food/fs/sc/ssc/out295_en.pdf
FDA asked to ban poultry litter from feed AGAIN 17 Aug 2009 Posted Aug 17 2009 11:07pm
http://stanford.wellsphere.com/cjd-article/fda-asked-to-ban-poultry-litter-from-feed-again-17-aug-2009/772893
Tuesday, October 27, 2009
Petition to Declare Poultry Litter as a Food Additive and to Ban Its Use as Cattle Feed August 12, 2009 UNITED STATES
DEPARTMENT OF HEALTH AND HUMAN SERVICES FOOD AND DRUG ADMINISTRATION
http://madcowfeed.blogspot.com/2009/10/petition-to-declare-poultry-litter-as.html
2011 Creutzfeldt Jakob Disease
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Tuesday, April 26, 2011
sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)
http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html
THIS is what happens when you have the industry run the government.
THEY have learned nothing from this mad cow/cjd blunder.
stupid is, as stupid does, and some times, you just can't fix stupid $$$
TSS
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net
Labels: Swine Susceptible CWD Prion feed
