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Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting 9/30/13 TSS COMMENTS

Posted Oct 02 2013 6:02pm
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting TSS COMMENTS
 
 
 
Greetings Missouri Wildlife officials and government officials,

 

I kindly wish to comment on the following please ;

 

Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting

 

 


 

 

 

Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;

 

 >>> NO THREAT TO CATTLE HERDS ?

 

>>> COMMINGLING OF CWD cervids WITH CATTLE NO RISK??

 

>>> cwd to humans, no risk ??

 

>>>cwd no risk factor from the world of insects

 

 


 

 

 

THAT IS not exactly correct. same as the assumption that cwd will not affect humans. true, no documented cases to date, of cwd transmission to cattle, or humans. but please let me give you a few factors to a few of these assumptions.

 

first off, the surveillance for human TSE from the many different animal TSE prion disease here in North America, and any iatrogenic event there from, is seriously flawed, and TSEs such as atypical BSE strains, or the different CWD strains, to humans, will not look like nvCJD, of which the nvCJD cases were documented mostly in the UK. however, the risk is very real, and science has shown this. atypical BSE is more virulent than the typical BSE cases, and they do not know if this different TSE in the bovine, will transmit to the cervids, or visa versa. also, what about the shedding of the typical and atypical BSE prions into the environment, and the uptaking there from by cervids? and if you look and compare cwd with scrapie, and recent transmission studies there from, for anyone to state that there has been no risk of transmission to humans or cattle from CWD, or visa versa, especially now that we have more than one strain of CWD, would be (in my opinion) very foolish. the science is there that shows these risk factors. every time some think the prion can’t, it proves them wrong. some of the most famous lines I remember from the past would go like this;

 

>>>BSE mad cow disease will not affect humans...

 

IT DID, IT HAS, AND IS STILL AFFECTING THEM.

 

BSE cannot/will not/has not trasmit to other species;

 

BSE has transmitted to primate, porcine, fowl, and even big bird, i.e. red-tailed ostrich, feline, canine, and many, many species in zoo animals from oral consumption of split carcasses of the bovine, ...and I could go on here, but science has well documented all this. ...in my opinion, this is NOT rocket science. what it IS, is the incubation period, and the fact that industrial and political science has won out over sound peer review science. I remind you all of asbestos and tobacco. just saying...tss

 

>>>sporadic CJD is not related to BSE mad cow disease...

 

SCIENCE HAS NOW SHOWN THAT INDEED SOME SPORADIC CJD CASES ARE LINKED TO ATYPICAL BSE AND ATYPICAL SCRAPIE.

 

>>>nvCJD will not transmit by blood...

 

BLOOD HAS NOW BEEN LINKED TO FOUR nvCJD CASES. ...

 

>>>mad cow disease is not in the USA, our triple mad cow firewall will protect us from any mad cow disease...

 

THERE NOW HAS BEEN TYPICAL C-BSE, ATYPICAL BASE L-TYPE BSE, ATYPICAL H-TYPE BSE, AND ATYPICAL Hg-type BSE DOCUMENTED IN NORTH AMERICA AND THE USA.

 

 

 

P.4.23

 

Transmission of atypical BSE in humanized mouse models

 

Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA

 

Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.

 

Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.

 

Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.*** The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.

 

Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.

 

Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.

 


 

 

Given the quantitative indicators of what seems, in the EU, to be the near-extinction of the animal epidemic and control of cattle-to-human transmission, is there anything left for concern? Unfortunately, there is. With BSE, the global disease burden is far from clear in countries with less well-developed surveillance. In humans, the potential continuing person to person spread by blood and blood products remains a problem as seen with the four cases of transfusion-associated vCJD infection to date (Andrews, 2011). With BSE and other TSEs in animals, the recognition of the wide diversity of prion strains in the field, including three new forms of animal TSEs (L-type Atypical BSE, H-type Atypical BSE and Atypical scrapie), has complicated disease diagnosis and surveillance, as well as scientific assessment of their potential risks to humans. EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential. In particular the L-type Atypical BSE agent might be similarly or even more virulent to humans than the Classical BSE agent. While mankind has been in contact with the major TSE of small ruminants for centuries, there is no epidemiological evidence to suggest that classical scrapie is zoonotic; however, experimental transmission data on humanised mice and non-human primates have been very scarce so far.

 

What does this mean for the future? The decline of the BSE epidemic seen by 2005 led to consideration of some relaxation of costly BSE control measures as depicted in the EU TSE Roadmap (EC, 2005), and will inevitably be followed by further relaxation as already outlined in another EU TSE Roadmap 2 of 2010 (EC, 2010). It remains critical that current levels of consumer protection are maintained and all future changes from well established and highly effective current risk management measures are based upon sound scientific advice that EFSA will continue to provide.

 

Which old issues will remain, and which new issues will become relevant? For Atypical BSE, the most widely accepted hypothesis is that of a spontaneously arising ("sporadic") disease in relatively old bovines. If this holds true, it will be impossible to eradicate such a disease which originates de novo; probably we then have to live forever with a ban on SRMs, in particular the central nervous system (CNS), of older cattle. Given our insufficient knowledge about the true prevalence of atypical animal prion strains in the field, it will be important to continue and improve the systematic surveillance of animal TSEs, and to refine our diagnostic and laboratory methods and experiments. As some scientific data suggest that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011), the issue of a zoonotic potential of prions is likely to remain with us a time. For human TSEs including sporadic CJD, it will be important to continue systematic surveillance that should be able, as clearly shown with vCJD in the past, eventually to identify emerging new phenotypes or new prion strains. In sum, at a time when many scientists and most decision makers are no longer interested in prions and their risk, it will be prudent to stay vigilant, although this must be in a way that is balanced with other risks to human and animal health. In the risk assessment area, this will continue to be a challenge for EFSA in the years to come.

 

 

 

--------------------------------------------------------------------------------

 

 

 

[1] Regulation (EC) No 999/2001 of the European Parliament and of the Council of 22 May 2001 laying down rules for the prevention, control and eradication of certain transmissible spongiform encephalopathies. OJ L 147, 31.05.2001, p. 1-40.

 

 

 

 


 

 

 

 


 

 

 

 

see full text and more here ;

 

 

 


 

 

 

 

believing that a strain or certain genotype of one TSE prion disease, is resistant to any TSE prion disease, EXAMPLE, like the sheep homozygous for the resistant PrPARR allele (A136R154R171),... efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health. ...never say never with the TSE prion disease... http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1276041/

 

 

OR RABBITS, OR CANINE, OR ....SEE LINKS WITH TRANSMISSION STUDIES BELOW.

 

never say never with the tse prion disease.

 

 

ONE PARTICULAR QUESTION, what about tse from typical bse and or the atypical bse TSE STRAINS in the environment, and potential shedding there from, might there be a risk to cervids ?

 

I think by now we should be aware of the risk factors of sheep scrapie to cervids via transmission studies ;

 

 

 

pens, pens, PENS ??

 

 

 

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

 


 

 

now, decades later ;

 

 

2012

 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

 

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 

Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. The purpose of these experiments was to determine susceptibility of white-tailed deer (WTD) to scrapie and to compare the resultant clinical signs, lesions, and molecular profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate. All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer that was necropsied at 15.6 months had widespread distribution of PrPSc highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues prior to the onset of clinical signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of WTD were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

 


 

 

2011

 

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.

 


 

 

Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)

 

Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie and CWD in inoculated deer. Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. We inoculated white-tailed deer intracranially (IC) and by a natural route of exposure (concurrent oral and intranasal inoculation) with a US scrapie isolate. All deer inoculated by the intracranial route had evidence of PrPSc accumulation and those necropsied after 20 months post-inoculation (PI) (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6 months PI did not have clinical signs, but had widespread distribution of PrPSc. This highlights the facts that 1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and 2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile consistent with CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.

 

Committee Business:

 

The Committee discussed and approved three resolutions regarding CWD. They can be found in the report of the Reswolutions Committee. Essentially the resolutions urged USDA-APHIS-VS to:

 

Continue to provide funding for CWD testing of captive cervids

 

Finalize and publish the national CWD rule for Herd Certification and Interstate Movement

 

Evaluate live animal test, including rectal mucosal biopsy, for CWD in cervids

 


 

 

5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man.

 

*** I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough.

 

Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

 

Wednesday, February 16, 2011

 

IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES IN CONFIDENCE

 

reference...

 

RB3.20 TRANSMISSION TO CHIMPANZEES

 

1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.

 

2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :

 

3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.

 

4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.

 

5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

 

6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.

 

R. Bradley 23 September 1990 CVO (+Mr Wells' comments) Dr T W A Little Dr B J Shreeve 90/9.23/1.1.

 


 

 

see more here ;

 

 


 

 

Rabbits are not resistant to prion infection

 

Francesca Chianinia,1, Natalia Fernández-Borgesb,c,1, Enric Vidald, Louise Gibbarda, Belén Pintadoe, Jorge de Castroc, Suzette A. Priolaf, Scott Hamiltona, Samantha L. Eatona, Jeanie Finlaysona, Yvonne Panga, Philip Steelea, Hugh W. Reida, Mark P. Dagleisha, and Joaquín Castillab,c,g,2

 

snip...

 

Discussion

 

Slightly more than 25 y ago, cattle were considered free of prion diseases. No one would have predicted the BSE epidemic with the considerable human and animal health repercussions, and the political and economic impacts that it had in Europe during the 1990s. At that time, the scientific knowledge of prions was too limited to determine its role in the development of spontaneous cases of BSE and their subsequent impact on human health. By 2011, however, several new prion strains, naturally occurring (19, 20) or artificially generated (10), have been described, indicating that their number has increased and that a species should be considered resistant to disease only after careful consideration. The degree of resistance and susceptibility to prion disease(s) differs within species. Animals can be both extremely susceptible to the majority of prion diseases or strains yet remain resistant to others on first passage (21). Therefore, it would be unwise to assume that a species generally resistant to TSEs would represent a minor risk to human health, as new TSEs and strains are continually being detected.

 

It is notoriously difficult to predict how a new TSE or strain will behave in different species, so great caution must be exercised when determining the transmissibility of prions between species. To evaluate the potential risk of transmission, every tool in the prion toolkit is essential, including artificial methods, such as the use of transgenic animals, or secondary in vivo transmission, which can exaggerate the possibility of infection (2, 22).

 

Even these extreme measures, which probably do not reflect the normal mechanisms of infection, have to be considered to avoid future epidemics similar to that observed with the new variant Creutzfeldt-Jakob disease (vCJD). For this reason, we selected PMCA with its associated advantages, including the ability to overcome the transmission barrier (8), as the preferred tool to evaluate the absolute susceptibility of rabbits to TSEs.

 

Using only normal rabbit brain homogenate as a substrate for PMCA, PrPC was efficiently converted to rabbit PrPres when seeded with strains originating from four different species (Table 1), and at least three biochemically distinguishable rabbit PrPres strains were obtained (Fig. 1). This suggests that rabbit PrPC is more readily misfolded than originally thought. However, a prion disease is more than a simple misfolding process, and other factors are probably required for successful disease progression in vivo.

 

To address this point, we inoculated three groups of rabbits, two groups with ME7 based inocula (murine and leporine) and a further group with the de novo rabbit PMCA derived PrPres. Selection of these particular strains was carried out on the basis that ME7 was stable and well characterized and the de novo strain was an unknown entity. The number of strains tested and rabbits challenged were limited because of the necessity of housing these animals in containment level 3 facilities for protracted periods of time that maximized the possibility of transmission and development of disease.

 

Although rabbits were inoculated with prions derived from the same species, a 25-mo period was necessary to observe the standard prion disease. The three animals that died without clinical signs of TSE were all negative by IHC and WB, although the first of these deaths was in a rabbit challenged with ME7 RaPrPSc, which had PrPSc levels in the brain detectable only by PMCA. This result indicates that even though the animal died of a non– TSE-related disease, it might have been at an early preclinical stage of prion disease. However, we cannot rule out the possibility that the limited PrPSc level in the brain sample was due to residual inoculum, as shown previously in PrP knock-out mice (23). To date, the rabbits inoculated with mouse ME7 remain healthy after more than 43 mo, which is in agreement with the experiments performed approximately 35 y ago by Barlow and Rennie (17).

 

In summary, after 3 y postchallenge with three different rabbitderived inocula, we have obtained one positive clinical case, one possible preclinical case, two intercurrent deaths, and six animals that have remained healthy. Although the incubation periods do not directly correlate with the degree of susceptibility, these data might indicate that rabbits are poorly susceptible to prion infection. Although the rabbits used in this study were not inbred, they all had identical full-length PrP sequences and, to date, no difference has been detected in the ORF PrP sequence in any other published rabbit PrP sequence placed in GenBank. To further investigate this, two types of second passage experiment were performed; three raPrPTg mice and 10 rabbits were all intracerebrally inoculated using brain homogenate from the clinically affected rabbit. In contrast to 100% of the de novo RaPrPSc-inoculated transgenic mice having succumbed to a standard clinical prion disease and thereby demonstrating a high rate of transmissibility in vivo, two of 10 rabbits developed a TSE (477 and 540 dpi, respectively) to date. A plausible explanation for the evident differences between these two transmission studies would be the high level of rabbit PrPC expression (4- to 6-fold) in the murine model. In addition, it is well known that even if overexpression does not increase susceptibility, it can significantly reduce the incubation time of disease (2). However, the two positive TSE cases in the second rabbit passage, even though 8 rabbits remained clinically normal at 560 dpi, have led us to conclude that rabbits can no longer be considered a prionresistant species. The long incubation times, even after a second passage, might be due to the presence of some unknown, and probably rare, susceptibility factor in rabbits, which may also be present, for example, in equids and canids.

 

To critically evaluate this risk, several experiments are currently underway to characterize this new prion disease in rabbits and other species to examine its ability to cross the species barrier. In addition, supplementary experiments have been initiated in rabbits and also in transgenic mice that overexpress rabbit PrPC, to evaluate their susceptibilities to other important prion diseases including CWD and BSE. There are several factors that any potential new TSE epidemic would require: (i) the new prion should be efficiently transmitted through the homologous species; (ii) animals should be edible by humans and should be slaughtered at an age at which the disease has developed, thereby increasing the chance that prions have replicated (especially for those prions that require long incubation times); and (iii) the meat and bone meal should be recycled and fed to new members of the same species. In the light of these data and taking into account the previous three factors, it is unlikely there will be an outbreak of “mad rabbit disease,” and consumers of rabbit meat face much less of a risk than consumers of cattle or sheep products.

 


 

 

 

 

> The long incubation times, even after a second passage, might be due to the presence of some unknown, and probably rare, susceptibility factor in rabbits, which may also be present, for example, in equids and canids.

 

 

> equids and canids

 

 

 

TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS

 

 


 

 

 

TSE & HOUNDS

 

GAH WELLS (very important statement here...TSS)

 

HOUND STUDY

 

AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

 

snip...

 


 

 

76 pages on hound study;

 


 

 

The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.

 

38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.

 

39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.

 

40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.

 

41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.

 

Histopathological support to various other published MAFF experiments

 

42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).

 

 


 

 


 

 

It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.

 

snip...

 


 

 

 

2005

 

DEFRA Department for Environment, Food & Rural Affairs

 

Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk

 

GTN: FAX:

 

Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518

 

21 November 2001

 

Dear Mr Singeltary

 

TSE IN HOUNDS

 

Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.

 

As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

 

Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.

 

Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less

 

critical. For more details see- http://www.bseinquiry , gov.uk/files/yb/1995/06/21005001 .pdf

 

As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.

 

Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK

 

You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.

 

I hope this is helpful

 

Yours sincerely 4

 

HUGH MCDONAGH BSE CORRESPONDENCE SECTION

 

 

======================================

 

 

 

FAST FORWARD 2012

 

From: Terry S. Singeltary Sr. Sent: Wednesday, May 30, 2012 12:23 PM To: Terry S. Singeltary Sr. Subject: CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE

 

OR-09: Canine spongiform encephalopathy—A new form of animal prion disease

 

Monique David, Mourad Tayebi UT Health; Houston, TX USA

 

It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.

 

Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.

 

In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.

 

If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).

 

References 1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http:// dx.doi.org/10.1016/S0140-6736(05)67218-2 .

 

2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal . ppat.1000156.

 

3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/ hmg/6.10.1699.

 

4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233 .

 

5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514 .

 

6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.

 

7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317- 75-11-2947.

 

8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102 .

 

9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121 .

 

 


 

 

Monday, March 26, 2012

 

CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE

 

 


 

 


 

 

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

 

 


 

 

 

Mr A Huws Principal WOAD2A CP2

 

SUSPECT BSE IN A HORSE

 

You will wish to be aware that on Thursday afternoon 25 June the T/DVO Powys received a phone call from a veterinary Surgeon reporting his suspicion that a horse had ___contracted BSE after having been fed cattle cake___.

 

The clinical symptoms described were similar to those shown by cattle there ___being a similar case some months ago on the same premises___.

 

The owner' s name and address is:

 

Irene Thomas J Thomas & Company Riding Stables Penybryn Llangorse Brecon

 

The horse is a 12 year old gelding used for pony trekking.

 

By yesterday evening the horse was in a comatose state and on humane grounds was destroyed by the veterinary Surgeon. At his request a full post mortem and laboratory investigation will be carried out at the Carmarthen Veterinary Investigation Centre this morning to ascertain the exact cause; I have been told this will take at least two weeks. Charges to the veterinary Surgeon have been waived in this instance.

 

I will inform you immediately I receive a diagnosis.

 

26 June 1990

 

D SUMMERS DRVO

 

cc

 

Mr D R Williams, RVO

 

Mr A R Hunter, SVIO

 

90/06.26/10.1

 

 


 

 

 

Mr A Huws Principal WOAD2A CP2

 

SUSPECT BSE IN A HORSE

 

You will wish to be aware that on Thursday afternoon 25 June the T/DVO Powys received a phone call from a veterinary Surgeon reporting his suspicion that a horse had contracted BSE after having been fed cattle cake. The clinical symptoms described were similar to those shown by cattle there being a similar case some months ago on the same premises.

 

The owner' s name and address is:

 

Irene Thomas J Thomas & Company Riding Stables Penybryn Llangorse Brecon

 

The horse is a 12 year old gelding used for pony trekking.

 

By yesterday evening the horse was in a comatose state and on humane grounds was destroyed by the veterinary Surgeon. At his request a full post mortem and laboratory investigation will be carried out at the Carmarthen Veterinary Investigation Centre this morning to ascertain the exact cause; I have been told this will take at least two weeks. Charges to the veterinary Surgeon have been waived in this instance.

 

I will inform you immediately I receive a diagnosis.

 

26 June 1990

 

D SUMMERS DRVO

 

cc

 

Mr D R Williams, RVO

 

Mr A R Hunter, SVIO

 

90/06.26/10.1

 

 


 

 

see full text and more here ;

 

 


 

 

 

>>> The most widely accepted hypothesis at this time is that CWD may have originated from an interspecies transmission of scrapie. It is worth noting that experimental transmission of scrapie into elk via IC inoculation is clinically and neuropathologically indistinguishable from CWD with currently available experimental methods.44 <<<

 

 

 

2011 Annual Report

 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit

 

2011 Annual Report

 

In Objective 1, Assess cross-species transmissibility of transmissible spongiform encephalopathies (TSEs) in livestock and wildlife, numerous experiments assessing the susceptibility of various TSEs in different host species were conducted. Most notable is deer inoculated with scrapie, which exhibits similarities to chronic wasting disease (CWD) in deer suggestive of sheep scrapie as an origin of CWD.

 

snip...

 

4.Accomplishments 1. Deer inoculated with domestic isolates of sheep scrapie. Scrapie-affected deer exhibit 2 different patterns of disease associated prion protein. In some regions of the brain the pattern is much like that observed for scrapie, while in others it is more like chronic wasting disease (CWD), the transmissible spongiform encephalopathy typically associated with deer. This work conducted by ARS scientists at the National Animal Disease Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to deer may have been the origin of CWD. This is important for husbandry practices with both captive deer, elk and sheep for farmers and ranchers attempting to keep their herds and flocks free of CWD and scrapie.

 


 

 

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

 

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

 

Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

 

see full text ;

 


 

 

 

Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;

 

>>>animal to animal, prions in urine, deer social animals, environmental contamination, exposed in the environment, why we did the feed and mineral ban. there is no vector for disease other than the social contact or prion in the soil...

 


 

 

 

 

NOT EXACTLY TRUE, oral consumption from animal protein in feed is highly efficient mode of transmission for chronic wasting disease cwd, and the infamous mad cow feed ban was, and is still a seriously flawed system, please see ;

 

 

Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus )

 

Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

 

Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5

 

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail ehoover@lamar.colostate.edu

 

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.

 

snip...

 

These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.

 

snip...

 


 

 

PLEASE SEE FULL TEXT SUBMISSION ;

 


 

 

 

Date: Tue, 24 Apr 2001 09:45:15 –0700

 

From: "Terry S. Singeltary Sr."

 

Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de References: 1 , 2

 

######### Bovine Spongiform Encephalopathy #########

 

Greetings again List Members,

 

''MORE'' violations and warning letters over FDA MAD COW feed ban regulations that have not been complied with since the Aug. 4, 1997 'partial' feed ban was implemented...

 

they implemented something, then forgot to enforce it $$$$$

 

another fine example letter. this one will floor you. 'Jimmy crack corn, and they don't care' no big deal, just flush those mixers with corn, then feed the corn to the deer. NOooooo problem.

 

these people must be brain dead??

 

DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND DRUG ADMINISTRATION

 

April 9, 2001 WARNING LETTER

 

01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED

 

Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT

 

Tel: 215-597-4390

 

Dear Mr. Raymond:

 

Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).

 

Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.

 

In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal. Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.

 

The above is not intended to be an all-inclusive list of deviations from the regulations. As a manufacturer of materials intended for animal feed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. We have enclosed a copy of FDA's Small Entity Compliance Guide to assist you with complying with the regulation... blah, blah, blah...

 


 

 

 

-------- Original Message --------

 

Subject: MAD DEER FEED BAN WARNING LETTER RECALL 6 TONS DISTRIBUTED USA

 

Date: Wed, 20 Oct 2004 14:53:56 –0500

 

From: "Terry S. Singeltary Sr." flounder@WT.NET

 

Reply-To: Bovine Spongiform Encephalopathy BSE-L@UNI-KARLSRUHE.DE

 

To: BSE-L@UNI-KARLSRUHE.DE

 

##################### Bovine Spongiform Encephalopathy #####################

 

 PRODUCT

 

Product is __custom made deer feed__ packaged in 100 lb. poly bags. The product has no labeling. Recall # V-003-5.

 

CODE

 

The product has no lot code. All custom made feed purchased between June 24, 2004 and September 8, 2004.

 

RECALLING FIRM/MANUFACTURER

 

Farmers Elevator Co, Houston, OH, by telephone and letter dated September 27, 2004. Firm initiated recall is ongoing.

 

REASON

 

Feed may contain protein derived from mammalian tissues which is prohibited in ruminant feed.

 

VOLUME OF PRODUCT IN COMMERCE

 

Approximately 6 tons.

 

DISTRIBUTION OH.

 

END OF ENFORCEMENT REPORT FOR October 20, 2004

 


 

 

 

################# BSE-L-subscribe-request@uni-karlsruhe.de #################

 

 

 

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

 

EMC 1 Terry S. Singeltary Sr. Vol #: 1

 


 


 

 

 

Thursday, June 6, 2013

 

BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as at June 5, 2013

 


 

 

 

Friday, July 19, 2013

 

PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED Revised as of April 1, 2013 50# Regular Chicken Feed was found to contain mammalian protein label does not contain the warning statement

 


 

 

 

Tuesday, June 11, 2013

 

Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant deviations from requirements in FDA regulations that are intended to reduce the risk of bovine spongiform encephalopathy (BSE) within the United States

 


 

 

 

Wednesday, September 25, 2013

 

Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE PRION 2013

 


 

 

 

Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;

 

 >>>if you have only one or two not much of a problem, but once the count numbers go up, so does the load of cwd in the environment. ...probably diluted out, it’s all about how many animals infected, before environmental contamination takes over?

 


 

 

 

that’s not completely correct either. ...FEED, captive game farms, and transfer of tainted soil via humans and vehicles, plants, shoes, clothing, etc., don’t believe me, see what the U.K. MAFF/DEFRA are saying ;

 

 

 

Friday, December 14, 2012

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 

snip...

 

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients.

 

*** For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

*** However, this recommendation is guidance and not a requirement by law.

 

Animals considered at high risk for CWD include:

 

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

 

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

 

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

 

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

 

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

 

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

 

snip...

 

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

 

The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

 

Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

 

snip...

 

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

 

snip...

 

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

 

snip...

 

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

 

snip...

 

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

 

 

snip...

 

see full text report here ;

 


 

 

 

see much more here ;

 

Friday, December 14, 2012

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 


 

 

 

Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;

 

>>>> NO THREAT TO CATTLE HERDS ?

 


 

 

 

 

CWD TO CATTLE OR BSE TO CERVIDS, potential risk factors ?? LET’S see what the science says to date ;

 

 

 

 

UPDATED DATA ON 2ND CWD STRAIN

 

Wednesday, September 08, 2010

 

CWD PRION CONGRESS SEPTEMBER 8-11 2010

 


 

 

 

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 ;

 

 

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.

 


 

 

" 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.

 


 

 

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

 


 

 

 

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...

 


 

 

 

----- 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, PhD

 

Assistant Professor Department of Chemical Engineering University of Delaware

 

 

===========END...TSS==============

 

 

SNIP...SEE FULL TEXT ;

 


 

 

 

 

Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;

 

>>> no risk for humans to cwd ?

 


 

 

 

NOW, let’s take a look at what the science is saying on the risk factors of human TSE prion disease from CWD prion disease of cervids.

 

 first, from the cdc/nih et al prion gods, and what they said on human cwd potential, and what that might look like ;

 

 

 

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ??

 

 

 

“Our conclusion stating that we found no strong evidence of CWD transmission to humans”

 

 From: TSS (216-119-163-189.ipset45.wt.net)

 

Subject: CWD aka MAD DEER/ELK TO HUMANS ??

 

Date: September 30, 2002 at 7:06 am PST

 

From: "Belay, Ermias"

 

To:

 

Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

 

Sent: Monday, September 30, 2002 9:22 AM

 

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Dear Sir/Madam,

 

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.

 

That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

 

Ermias Belay, M.D. Centers for Disease Control and Prevention

 

 -----Original Message-----

 

From:

 

Sent: Sunday, September 29, 2002 10:15 AM

 

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

 

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

 

Thursday, April 03, 2008

 

A prion disease of cervids: Chronic wasting disease

 

2008 1: Vet Res. 2008 Apr 3;39(4):41

 

A prion disease of cervids: Chronic wasting disease

 

Sigurdson CJ.

 

snip...

 

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

 

snip...

 

full text ;

 

 


 

 


 

 

 

Monday, February 09, 2009

 

Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD

 

 snip...

 

 Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain

 

Date: August 25, 2007 at 12:42 pm PST

 

our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.

 


 

 

Wednesday, March 18, 2009

 

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

 


 

 

CWD TO HUMAN RISK FACTORS PRION2013

 

 

PRION2013 CONGRESSIONAL ABSTRACTS

 

HD.13: CWD infection in the spleen of humanized transgenic mice

 

Liuting Qing and Qingzhong Kong

 

Case Western Reserve University; Cleveland, OH USA

 

Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.

 

=====

 

Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system

 

Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1

 

1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK

 

Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.

 

Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.

 

Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.

 

Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.

 

=====

 

Invited.16: Studies of chronic wasting disease transmission in cervid and non-cervid species

 

Edward A, Hoover,1 Candace K. Mathiason,1 Davin M. Henderson,1 Nicholas J. Haley,1 Davis M. Seelig,1 Nathaniel D. Denkers,1 Amy V. Nalls,1 Mark D. Zabe,1 Glenn C. Telling,1 Fernando Goni2 and Thomas Wisniewski,2

 

1Prion Research Center; Colorado State University; Fort Collins, CO USA; 2New York University School of Medicine; New York, NY USA

 

How and why some misfolded proteins become horizontally transmitted agents and occasionally cross species barriers are issues fundamental to understanding prion disease. Chronic wasting disease (CWD) of cervids is perhaps a prototype of horizontal prion transmission, encompassing efficient mucosal uptake, lymphoid amplification, neuroinvasion, peripheralization, and dissemination via mucosal excretion. Efficient mucosal transmission of CWD in deer has been demonstrated by oral, nasal, aerosol, and indirect contact exposure. In addition, other studies (Mathiason CK, et al.) reported at the symposium support a significant role for pre- and/or postnatal transmission of CWD from doe to offspring. Accumulating, yet still incomplete, evidence also suggests that the period of relatively covert CWD infection may be longer than originally thought. Given the above, minimally invasive sensitive assays based on body fluids from live animals would aid substantially in understanding the biology of CWD. We have been applying seeded realtirne quaking-induced amplification of recombinant PrP substrates (i.e., RT-QuIC methodology) to: (1) investigate antemortem CWD detection, and (2) model PrP-based species barriers and trans-species adaptation-topics we previously explored using sPMCA and in vivo bioassays. At this symposium, we report sensitive and specific detection CWD prions in saliva, urine, blood (Mathiason lab), and rectal and pharyngeal lymph node samples (Haley NJ, et al.) from pre-symptomatic and symptomatic experimentally and naturally exposed deer. Other ongoing studies are employing RT-QuIC methodology to model amplification barriers among CWD, FSE, BSE, and CJD prions using cervine, feline, bovine, human, and promiscuous rPrP substrates and the above species prion seeds, cellular co-factors, and transgenic mice. Finally, in collaboration with the Wisniewski laboratory, we are conducting of experimental CWD vaccination studies in deer employing oral administration of an attenuated Salmonella vector expressing cervid PrP epitopes.

 

=====

 

AD.06: Detecting prions in the brain and blood of TSE-infected deer and hamsters

 

Alan Elder,1 Davin Henderson,1 Anca Selariu,1 Amy Nalls,1 Byron Caughey,2 Richard Bessen,1 Jason Bartz3 and Candace Mathiason1

 

1Colorado State University; Fort Collins, CO USA; 2NIH Rocky Mountain Laboratories; Hamilton, MT USA; 3Creighton University; Omaha, NE USA

 

While large quantities of protease resistant prion protein (PrPres) can be demonstrated by western blot or IHC in lymphoid biopsies or post-mortem brain tissues harvested from prion-infected animals, these conventional assays are less reliable as means to detect the small quantities of prions thought to be present in bodily fluids or associated with early and asymptomatic phases of TSE disease. The Real Time-Quaking Induced Conversion (RT-QuIC) assay is capable of detecting prions at concentrations below the level of sensitivity of conventional assays and provides a real-time fluorescent readout negating the use of proteases. We have made modifications to the RT-QuIC assay to utilize it for the detection of PrPres in brain and blood harvested from various species infected with prions. In this study, we analyzed CWD-infected deer and CWD/TME-infected hamster whole blood to determine the effect of:

 

(1) various anticoagulants,

 

(2) freezing and

 

(3) NaPTA precipitation.

 

Brain tissue and blood collected from naive deer and hamsters served as negative controls.

 

We were able to demonstrate amplifiable prions in

 

(1) brain and blood samples harvested from CWD/TME-infected animals,

 

(2) heparinized blood,

 

(3) frozen vs. fresh blood and

 

(4) NaPTA treated samples.

 

The RT-QuIC assay is able to detect PrPres in various species of animals and shows promise as an antemortem diagnostic tool for blood-borne TSEs.

 

 =====

 

 

 


 

 


 

 

 Sunday, July 21, 2013

 

*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?

 


 

 

 sCJDMM1-2 should be considered as a separate entity at this time.

 

All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

 


 


 

 

 

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

 


 

 

 

Friday, September 27, 2013

 

Uptake of Prions into Plants

 

Presentation Abstract

 


 

 

 

SEE MORE ;

 

 

Sunday, August 25, 2013

 

***Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

 


 

 

 

Friday, August 09, 2013

 

***CWD TSE prion, plants, vegetables, and the potential for environmental contamination

 


 

 

 

Thursday, August 08, 2013

 

***Characterization of the first case of naturally occurring chronic wasting disease in a captive red deer (Cervus elaphus) in North America

 


 

 

 

Sunday, September 01, 2013

 

***hunting over gut piles and CWD TSE prion disease

 


 

 

 

Wednesday, September 04, 2013

 

***cwd - cervid captive livestock escapes, loose and on the run in the wild...

 


 

 

 

Tuesday, September 10, 2013

 

***Review and Updates of the USDA-APHIS Veterinary Services (VS) National Chronice Wasting Disease (CWD) Program 2012-2013

 


 

 

 

Tuesday, September 17, 2013

 

***USAHA 116TH ANNUAL MEETING October 18 – 24, 2012 CWD, Scrapie, BSE, TSE prion (September 17, 2013)

 


 

 

 

Friday, November 09, 2012

 

*** Chronic Wasting Disease CWD in cervidae and transmission to other species

 


 

 

 

Sunday, November 11, 2012

 

*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012

 


 

 

 

Friday, December 14, 2012

 

***Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012

 


 

 

 

Sunday, June 09, 2013

 

***Missouri House forms 13-member Interim Committee on the Cause and Spread of Chronic Wasting Disease CWD

 


 

 

 

 

Sunday, August 11, 2013

 

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

 

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010

 


 

 

 

 

Thursday, September 26, 2013

 

***Minimise transmission risk of CJD and vCJD in healthcare settings Guidance

 


 

 

 

 

 

Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;

 

>>>cwd no risk factor from the world of insects

 


 

 

 

 

 

Subject: Transmission of TSEs through ectoparasites i.e. P. tenuis and CWD

 

Date: May 3, 2007 at 9:05 am PST

 

 

CONFIDENTIAL SEAC 97/2 Annex 2 UNITED KINGDOM ACCREDITATION SERVICE (UKAS) ASSESSMENT REPORT

 

 

Other organisms

 

 

Transmission of TSEs through ectoparasites has been postulated by Lupi5. Post et al6 fed larvae of meat eating and myiasis causing flies with brain material from scrapieinfected hamsters. Two days after eating infected material, the larvae showed high amounts of PrPSc by Western blot. In further studies, the inner organs of larvae, which had been fed with scrapie brain, were extracted and fed to hamsters. Six out of eight hamsters developed scrapie. Two out of four hamsters fed on scrapie infected pupae subsequently developed scrapie.

 


 

 

 

I AGAIN raise the possibility of that damn brain eating worm in elk and CWD transmission via elk, deer, and other critters eating that worm. ...tss

 

 

 

Immunodiagnosis of experimental Parelaphostrongylus tenuis infection in elk Oladele Ogunremi, Murray Lankester, and Alvin Gajadhar Centre for Animal Parasitology, Canadian Food Inspection Agency, 116 Veterinary Road, Saskatoon, Saskatchewan S7N 2R3 (Ogunremi, Gajadhar); Department of Biology, Lakehead University, 955 Oliver Road, Thunder Bay, Ontario P7B 5E1 (Lankester).

 

 Elk infected with the meningeal worm, Parelaphostrongylus tenuis (Protostrongylidae), do not consistently excrete larvae in feces, making the current method of diagnosing live animals using the Baermann fecal technique unreliable. Serological diagnosis could prove more useful in diagnosing field-infected animals but depends on the identification and availability of good quality antigen. To mimic field infections, 2 elk were inoculated with 6 infective L3 larvae of P. tenuis, and another 2 with 20 L3 larvae. Fecal samples were examined for nematode larvae using the Baermann technique and serum samples taken were tested for anti-P. tenuis antibody with ELISAs by using the excretory-secretory (ES) products of L3, and sonicated adult worms as antigens. One animal passed first-stage larvae in its feces 202 days postinoculation, but passed none thereafter. The remaining 3 inoculated animals did not pass larvae. In contrast to parasite detection, antibodies against larval ES products were detected in all animals starting from 14 to 28 days postinoculation and persisted until the termination of the experiment on day 243 in 2 animals that harbored adult worms. Antibodies against somatic antigens of the adult worm were not detected until day 56 but also persisted until the end of the experiment in the animals with adult worms. In 2 elk that had no adult worms at necropsy, anti-ES antibodies were detected transiently in both, while anti-adult worm antibodies were present transiently in one. These findings confirm the superiority of P. tenuis larval ES products over somatic adult worm antigens as serodiagnostic antigens, as previously observed in studies of infected white-tailed deer, and extend the application of the newly developed ELISA test in diagnosing and monitoring cervids experimentally infected with P. tenuis.

 


 

 

 Subject: TSE & insects as a vector of potential transmission

 

Date: October 26, 2006 at 12:50 pm PST

 

 i try to keep an open mind about any other routes and sources that we may be overlooking. i mean, there is enough TSE protein in circulation now VIA the FDA, just in 2006 alone, and the oral route has been proven with BSE, and the non-forced oral consumption of scrapie to primate, as to not worry about a natural route of a few worms that have maybe been feasting on a deer that's brain is infected with CWD, then excreted out, and then passed on to another worm hungry deer looking for that feast. i suppose maybe just another potential route and source for a TSE, and possibly even a 'double dose' so to speak from not only the worm in the feces (maybe triple with feces), but the soil as well (see soil and prion study as well below) following that are some other studies that may be of interest ;

 

 Myiasis as a risk factor for prion diseases in humans

 

 Journal of the European Academy of Dermatology and Venereology Volume 20 Page 1037 - October 2006 doi:10.1111/j.1468-3083.2006.01595.x Volume 20 Issue 9

 

 REVIEW ARTICLE Myiasis as a risk factor for prion diseases in humans O Lupi *

 

 Abstract

 

 Prion diseases are transmissible spongiform encephalopathies of humans and animals. The oral route is clearly associated with some prion diseases, according to the dissemination of bovine spongiform encephalopathy (BSE or mad cow disease) in cattle and kuru in humans. However, other prion diseases such as scrapie (in sheep) and chronic wasting disease (CWD) (in cervids) cannot be explained in this way and are probably more associated with a pattern of horizontal transmission in both domestic and wild animals. The skin and mucous membranes are a potential target for prion infections because keratinocytes and lymphocytes are susceptible to the abnormal infective isoform of the prion protein. Iatrogenic transmission of Creutzfeldt–Jakob disease (CJD) was also recognized after corneal transplants in humans and scrapie was successfully transmitted to mice after ocular instillation of infected brain tissue, confirming that these new routes could also be important in prion infections. Some ectoparasites have been proven to harbour prion rods in laboratory experiments. Prion rods were identified in both fly larvae and pupae; adult flies are also able to express prion proteins. The most common causes of myiasis in cattle and sheep, closely related animals with previous prion infections, are Hypoderma bovis and Oestrus ovis, respectively. Both species of flies present a life cycle very different from human myiasis, as they have a long contact with neurological structures, such as spinal canal and epidural fat, which are potentially rich in prion rods. Ophthalmomyiases in humans is commonly caused by both species of fly larvae worldwide, providing almost direct contact with the central nervous system (CNS). The high expression of the prion protein on the skin and mucosa and the severity of the inflammatory response to the larvae could readily increase the efficiency of transmission of prions in both animals and humans.

 


 

 

 

International Journal of Dermatology Volume 42 Page 425 - June 2003 doi:10.1046/j.1365-4362.2003.00345.x Volume 42 Issue 6

 

 Review Could ectoparasites act as vectors for prion diseases? Omar Lupi, MD, PhD Abstract

 

 Prion diseases are rare neurodegenerative diseases of humans and animals with a lethal evolution. Several cell types found on the human skin, including keratinocytes, fibroblasts and lymphocytes, are susceptible to the abnormal infective isoform of the prion protein, which transforms the skin to produce a potential target for prion infection. Iatrogenic transmission of Creutzfeldt-Jakob disease was also recognized after corneal transplants in humans, and scrapie was successfully transmitted to mice after ocular instillation of infected brain tissue, confirming that these new routes, as well as cerebral inoculation and oral ingestion, could be important in prion infections. Animal prion infections, such as scrapie (sheep) and "mad cow disease" (cattle), have shown a pattern of horizontal transmission in farm conditions and several ectoparasites have been shown to harbor prion rods in laboratory experiments. Fly larvae and mites were exposed to brain-infected material and were readily able to transmit scrapie to hamsters. New lines of evidence have confirmed that adult flies are also able to express prion proteins. Because ocular and cerebral myiases and mite infestation are not rare worldwide, and most cases are caused by fly larvae or hay mites that usually affect sheep and cattle, it is important to discuss the possibility that these ectoparasites could eventually act as reservoirs and/or vectors for prion diseases.

 


 

 

 

P. tenuis – The White-tailed Deer Parasite

 

 “Brain worms” (meningeal worms) can affect sheep, goats, llamas, alpacas, moose and other exotic small ruminants

 

 M. Kopcha, D.V.M., M.S., J. S. Rook, D.V.M. & D. Hostetler, D.V.M

 

 MSU Extension & Ag. Experiment Station

 

 Michigan State University

 

 College of Veterinary Medicine

 

 Many livestock producers are familiar with internal parasites that invade the digestive system (the abomasum, small or large intestines), liver, and lungs. An internal parasite which may not be so well-recognized is one that invades the central nervous system (brain and spinal cord). Commonly called the “brain worm” or meningeal worm (the meninges are a thin membrane that covers the brain and spinal column), the scientific name for this parasite is Parelaphostroneylus tenuis (P. tenuis), and its natural host is the White-tailed deer. Usually, P. tenuis completes its life cycle in the deer (Figure 1) without causing noticeable problems. ***However, when P. tenuis is ingested by unnatural, or aberrant hosts such as, llamas, sheep, goats, moose, elk, caribou, and other susceptible ruminants, the parasite moves into the brain and/or spinal cord, damaging delicate nervous tissue.

 

 Neurologic problems result.

 

 White-tailed deer may he parasitized by P. tenuis year-round. However, the neurologic disease seen in aberrant hosts has a seasonal occurrence that starts in the late summer and continues until a hard freeze occurs. A cool, moist summer and/or a mild winter may extend the period during which the disease occurs.

 

 How does it occur?

 

 To understand this disease and how to prevent or minimize its occurrence, it is important to understand the life cycle of P. tenuis in the White-tailed deer and what happens when the parasite is ingested by susceptible ruminants. The life cycle is as follows (Figure 1): adult meningeal worms live in the deer's central nervous system (brain and spinal cord) and produce eggs which hatch into larvae. The larvae migrate from the deer's central nervous system to the lungs, where they are coughed into the mouth, swallowed and passed from the intestinal tract with the manure. This portion of the life cycle takes approximately three months (Figure 1 - numbers 1 and 2).

 

 After excreted in the manure, larvae must continue their development in an intermediate host (certain land-dwelling snails and slugs) for another three to four weeks until they reach their infective stage (Figure 1 - numbers 3 and 4).

 

 White-tailed deer become infested with P. tenuis by eating these snails or slugs that contain the infective stage of the larvae (Figure 1 - number 5). Once ingested, the larvae migrate through the deer’s gut and eventually move into their central nervous system where they mature into adults, produce eggs, Figure 2 The Angora goat in the center of the picture had a mild lameness in its left forelimb (arrow). The presumptive diagnosis was meningeal worm infestation. Mild cases such as this one may recover spontaneously.

 

snip...

 

 

 


 

 


 

 

 

other potential vectors for cwd tse prion disease ;

 

 

 

Wednesday, October 17, 2012

 

Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos)

 


 

 

 

Sunday, November 01, 2009

 

AS THE CROW FLIES, SO DOES CWD

 

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

 


 

 

 

 

Monday, July 13, 2009

 

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

 


 

 

 

Sunday, July 07, 2013

 

Could avian scavengers translocate infectious prions to disease-free areas initiating new foci of chronic wasting disease?

 

Prion. 2013 Jul 3;7(4). [Epub ahead of print]

 


 

 

 

 

another fine example letter. this one will floor you. 'Jimmy crack corn, and they don't care' no big deal, just flush those mixers with corn, then feed the corn to the deer. NOooooo problem.

 

 

Subject: ''MORE'' 'VIOLATORS' of Animal Proteins Prohibited in Ruminant Feed--U.S.A. (more and more MAD COW FEED RULES BROKEN IN U.S.A.]

 

Date: Tue, 24 Apr 2001 09:45:15 –0700

 

From: "Terry S. Singeltary Sr."

 

Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de References: 1 , 2

 

######### Bovine Spongiform Encephalopathy #########

 

Greetings again List Members,

 

''MORE'' violations and warning letters over FDA MAD COW feed ban regulations that have not been complied with since the Aug. 4, 1997 'partial' feed ban was implemented...

 

they implemented something, then forgot to enforce it $$$$$

 

another fine example letter. this one will floor you. 'Jimmy crack corn, and they don't care' no big deal, just flush those mixers with corn, then feed the corn to the deer. NOooooo problem.

 

these people must be brain dead??

 

 

 

DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND DRUG ADMINISTRATION

 

April 9, 2001 WARNING LETTER

 

01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED

 

Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT

 

Tel: 215-597-4390

 

Dear Mr. Raymond:

 

Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).

 

Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.

 

In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal. Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.

 

The above is not intended to be an all-inclusive list of deviations from the regulations. As a manufacturer of materials intended for animal feed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. We have enclosed a copy of FDA's Small Entity Compliance Guide to assist you with complying with the regulation... blah, blah, blah...

 


 

 

 

-------- Original Message --------

 

Subject: MAD DEER FEED BAN WARNING LETTER RECALL 6 TONS DISTRIBUTED USA

 

Date: Wed, 20 Oct 2004 14:53:56 –0500

 

From: "Terry S. Singeltary Sr." flounder@WT.NET

 

Reply-To: Bovine Spongiform Encephalopathy BSE-L@UNI-KARLSRUHE.DE

 

To: BSE-L@UNI-KARLSRUHE.DE

 

##################### Bovine Spongiform Encephalopathy #####################

 

 PRODUCT

 

Product is __custom made deer feed__ packaged in 100 lb. poly bags. The product has no labeling. Recall # V-003-5.

 

CODE

 

The product has no lot code. All custom made feed purchased between June 24, 2004 and September 8, 2004.

 

RECALLING FIRM/MANUFACTURER

 

Farmers Elevator Co, Houston, OH, by telephone and letter dated September 27, 2004. Firm initiated recall is ongoing.

 

REASON

 

Feed may contain protein derived from mammalian tissues which is prohibited in ruminant feed.

 

VOLUME OF PRODUCT IN COMMERCE

 

Approximately 6 tons.

 

DISTRIBUTION OH.

 

END OF ENFORCEMENT REPORT FOR October 20, 2004

 


 

################# BSE-L-subscribe-request@uni-karlsruhe.de #################

 

 

 

now, just what is in that deer feed? _ANIMAL PROTEIN_

 

 Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES

 

Date: Sat, 25 May 2002 18:41:46 –0700

 

From: "Terry S. Singeltary Sr."

 

Reply-To: BSE-L

 

To: BSE-L

 

8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed Analysis Ingredients / Products Feeding Directions

 

snip...

 

_animal protein_

 


 

 REFERENCES

 

snip...see full text ;

 

 

 

 -------- Original Message --------

 

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

 

Greetings FDA,

 

i would kindly like to comment on;

 

Docket 03D-0186

 

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

 


 

 

 

 PO-248: TSE infectivity survives burial for five years with little reduction in titer

 

 Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and R(D)SVS; University of Edinburgh; Edinburgh, UK

 

 BSE infected animals, BSE-contaminated materials and other sources of TSE (prion) infection, such as carcasses from scrapie infected sheep, CWD infected deer and cadavers of individuals infected with CJD may all end up in the environment through burial or other methods of disposal. They may continue to act as a reservoir of TSE infectivity if cattle or other susceptible animals were to be exposed to these sources in the future. In order to address these concerns, we performed two large scale demonstration experiments under field conditions which were designed to mimic some of the ways by which TSE infected materials may have been disposed of. The project examined the fate of TSE infectivity over a period of five years in two scenarios; when the infectivity was contained within bovine heads and when the infectivity was buried without any containment. Two soil types were compared: a sandy loam and a clay loam. We used the 301V TSE strain which was derived by serial passage of BSE in VM mice.

 

 TSE infectivity was recovered from all the heads exhumed annually for five years from both types of soil, with little reduction in the amount of infectivity throughout the period of the experiment. Small amounts of infectivity were found in the soil immediately surrounding the heads, but not in samples remote from them. Similarly there was no evidence of significant lateral movement of infectivity from the buried bolus. However large amounts of TSE infectivity were recovered at the site of burial of both boluses. There was limited vertical upward movement of infectivity from the bolus buried in clay soil and downward movement from the bolus buried in sandy soil.

 

 Now that these experiments are completed we conclude that TSE infectivity is likely to survive burial for long periods of time with minimal loss of infectivity and restricted movement from the site of burial. These experiments emphasize that the environment is a viable reservoir for retaining large quantities of TSE infectivity, and reinforce the importance of risk assessment when disposing of this type of infectious material.

 

 

 


 

 

 

see more about soil content and CWD here ;

 


 

 

 

Friday, February 25, 2011

 

Soil clay content underlies prion infection odds Soil clay content underlies prion infection odds

 


 

 

 

Saturday, March 10, 2012

 

CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein feed CUSTOM MADE for deer and elk

 


 

 

 

Thursday, May 31, 2012

 

CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more

 


 

 

 

Friday, February 08, 2013

 

*** Behavior of Prions in the Environment: Implications for Prion Biology

 


 

 

 

Greetings again Missouri et al,

 

 

considering what we have learned about environmental factors, and soil factors of the TSE prion disease with CWD and Scrapie, and other transmission studies in many different species, the new more sensitive TSE prion testing techniques (I am very interested in the atypical BSE strains), as the crows fly and TSE there from, I think we cannot rule the possibility of insects and or the ingestion of insects, that may have been exposed to the TSE prion, that this could be a potential vector of the TSE prion disease. cervids are highly susceptible to oral consumption of the TSE prion disease. whether or not the insect becomes diseased is one thing, but as an instrument of transmission feasting on the brain of a CWD infected cervid, and then consumed by a cervid, or whatever, then this is a real potential vector of transmission. reminds me of the decades old argument of feeding ruminant by-product to fowl or porcine, on the false assumption that the fowl or porcine will not go down with a TSE (which tse prion disease has been proven to transmit to both fowl and porcine, but that’s another day for debate), but the fact on that false assumption, even though, the pigs and or chicken would consume the tainted TSE prion product and even though it may not go clinical with TSE prion disease, even though, the said potential banned TSE prion ruminant protein in feed would survive the digestive tract, thus using said by-products from the fowl or porcine would still be exposed via said potential banned by-products in the digestive tract.Gibbs et al. then you must factor in whether the one dose theory or the accumulation theory, or both (because you have to figure in genetic susceptibility from both ends) , for when a TSE prion disease goes from sub-clincal to clinical disease, or if it will, can ever be proven, only then will these assumptions be proven correct or incorrect. but this continued gamble on if’s and what not’s, potential, could be, might be, might not’s and never’s, today in 2013, so many humans and animals exposed, and when the incubation period hits it’s peak from the highest point of load factors from all the TSEs’ in North America, then you have to hedge your bet with all the failures of the i.e. FDA/USDA/OIE TRIPLE FIREWALLS of proven deceit and fraud over the past 3 decades or so with the many different Transmissible Spongiform Encephalopathy’s TSE aka mad cow type prion disease in the many different species in the USA and North America, the consumer consumption via food, and other products, and the many different iatrogenic potentials there from, only time will tell. but to avoid considering any of these factors until proven otherwise, would not be scientific. . ...if your not confused now, that’s great, because I think I confused myself pondering out loud here. ...

 

 

 

kind regards, terry

 

LAYPERSON!

 

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
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