Monday, November 23, 2015

Dynamics of the natural transmission of bovine spongiform encephalopathy within an intensively managed sheep flock

Vet Res. 2015; 46: 126.

 

Published online 2015 Oct 28. doi: 10.1186/s13567-015-0269-x

 

PMCID: PMC4625529

 

Dynamics of the natural transmission of bovine spongiform encephalopathy within an intensively managed sheep flock

 

Martin Jeffrey, Janey P. Witz, Stuart Martin, Steve A. C. Hawkins, Sue J. Bellworthy, Glenda E. Dexter, Lisa Thurston, and Lorenzo Gonzálezcorresponding author

 

Abstract

 

Sheep are susceptible to the bovine spongiform encephalopathy (BSE) agent and in the UK they may have been exposed to BSE via contaminated meat and bone meal. An experimental sheep flock was established to determine whether ovine BSE could be naturally transmitted under conditions of intensive husbandry. The flock consisted of 113 sheep of different breeds and susceptible PRNP genotypes orally dosed with BSE, 159 sheep subsequently born to them and 125 unchallenged sentinel controls. BSE was confirmed in 104 (92%) orally dosed sheep and natural transmission was recorded for 14 of 79 (18%) lambs born to BSE infected dams, with rates varying according to PRNP genotype. The likelihood of natural BSE transmission was linked to stage of incubation period of the dam: the attack rate for lambs born within 100 days of the death of BSE infected dams was significantly higher (9/22, 41%) than for the rest (5/57, 9%). Within the group of ewes lambing close to death, those rearing infected progeny (n = 8, for 9/12 infected lambs) showed a significantly greater involvement of lymphoid tissues than those rearing non-infected offspring (n = 8, for 0/10 infected lambs). Horizontal transmission to the progeny of non-infected mothers was recorded only once (1/205, 0.5%). This low rate of lateral transmission was attributed, at least partly, to an almost complete absence of infected placentas. We conclude that, although BSE can be naturally transmitted through dam-lamb close contact, the infection in this study flock would not have persisted due to low-efficiency maternal and lateral transmissions.

 

snip...

 

Discussion

 

This study provides compelling evidence that sheep BSE is naturally transmissible and contagious. This is in contrast to the report by Foster et al. [28], who did not find evidence of maternal transmission in nine susceptible offspring from four BSE-infected dams. In the present study, 14 lambs born to BSE infected dams and another born to a non-infected dam either developed clinical BSE or were positive for PrPd when culled. Moreover, since the relative risk of infection was much higher (around 35 times) for the progeny of infected dams (~18%) than for the offspring of non-infected ewes (~0.5%), we conclude that, within the context of the experimental design of this study, natural BSE transmission occurs mostly from dam to offspring, that is, through a maternal or vertical route. The importance of maternal transmission as a means of maintaining endemic infection has previously been well documented for classical scrapie [20, 29–31], but there is neither epidemiological nor experimental evidence for maternal transmission of cattle BSE [32, 33].

 

It has recently been suggested that sheep foetuses may be infected with classical scrapie in utero [12–14]. In the present experiment, the lack of PrPd detection in the placentas of the offspring that went on to develop BSE (Figure 4) and the fact that in some twin births only one lamb became infected (Table 3), do not suggest that maternal transmission occurred in utero. However, the relatively small SDs in the ST of the infected Suffolk and Romney F1 progeny, which were comparable to that in the corresponding orally dosed parental stock (Table 1; Figure 2), suggest that all those offspring became infected with similar infectious doses and at a similar time. Since STs of the offspring did not differ from that of the parental stock (Table 1; Figure 2), it is likely that infection occurred shortly after birth, and certainly before 3 months of age when lambs were separated from their dams. The precise maternal source of infectious agent for the progeny cannot be determined in this study. By comparison with classical scrapie, blood and other birth fluids, saliva [34] and milk [18, 19] are all potential sources of BSE agent. Infectivity in the last two secretions most probably reflects presence of the infectious agent in blood (prionaemia) rather than true replication of the agent in the salivary and mammary glands. This possibility is further suggested by the higher levels of PrPd found in the LRS of dams with infected progeny compared to those with uninfected offspring (Table 3) and by the increased probability of infection in lambs born to ewes that lambed close to their death from BSE (Figure 3), that is, in advanced stages of the incubation period. This late preclinical disease stage is when dissemination of the infectious agent throughout the LRS is at its peak, as shown by studies on sheep BSE [7, 8, 10] and on sheep scrapie [35–38] and when prionaemia reaches highest levels, as demonstrated by blood transfusion experiments [39].

 

Lambs that were naturally infected from their dams, survived significantly longer than lambs receiving 1 g oral dose at 6–10 days of age (Figure 2). On one hand, this could be due to natural infection occurring at an older age than 10 days but still before weaning. On the other hand, it could suggest that the infection passed from dams to lambs was less that the equivalent titre represented by a 1 g oral infectious dose. This relatively low maternal infectious dose would also be in agreement with the significantly lower AR observed in the offspring compared to the orally dosed dams and with the fact that in some twin parturitions one lamb became infected and the other did not (Figure 4). However, a low infectious maternal dose may be difficult to reconcile with the fact that the survival times of the naturally infected progeny were actually no longer than those observed in their dams, which were given a 5 g dose. The explanation may lie in the age difference at infection between naturally infected offspring (pre-weaning) and their dams (average 5 months for Suffolk and 10 months for Romney sheep), which would make young lambs significantly more susceptible to BSE than weaned lambs and young adults, as has already been shown in a different study [9].

 

The results of this study thus show that BSE infected dams can transmit infection to their progeny. However, the excretion of the infectious agent is either discontinuous and/or its level variable. Thus, only some lambs –particularly those born at late preclinical stage of the dams—would receive an efficient dose and develop disease with relatively short incubation periods, while others would remain uninfected (at least as shown by PrPd detection within the context of the study). Husbandry factors may also be important to explain the lack of transmission to some of the uninfected offspring. Dams incubating BSE were often poor mothers and, as is common practice in commercial farming, poorly mothered newborn lambs were often reared by other ewes, including sentinel controls and ewes at early BSE incubation stages. Efforts to trace back information about each individual lamb were unsuccessful because of the large scale of the study and its duration.

 

One sheep that was the progeny of a non-infected Romney F1 ewe was found to be BSE-infected. Assuming that there were no confounding management factors (e.g. that this lamb suckled from an infected ewe), this finding is indicative of the occurrence of horizontal or lateral BSE transmission. However, despite the flock being kept indoors for the duration of the study, the level of true horizontal transmission found in this study was very low (~0.5%) and certainly much lower than that observed for classical scrapie, where a high proportion of sheep of susceptible genotypes born to non-infected dams can become infected in a heavily contaminated environment [20]. A possible explanation for the difference between scrapie and sheep BSE in this respect lies in placental infectivity. In classical scrapie, a high proportion of placentas from infected ewes harbouring foetuses of susceptible genotype are infectious and/or contain detectable PrPd/PrPres [16, 17, 40–43] and such infected placentas are regarded as one of the most important, if not the main, sources of environmental contamination and horizontal transmission [20, 44]. In contrast, in this study, where BSE infected dams had foetuses and placentas of the same susceptible genotypes, only one placenta was found to be PrPd positive. This was despite many placentas corresponding to lambs that went on to develop BSE or others being collected once the dam had shown peripheral prion replication as demonstrated by PrPd positive biopsy. Arrival of infectivity in the placenta is most likely through the haematogenous route and, since a high number of BSE infected dams showed LRS involvement around gestation, their placentas are likely to have been exposed to the infectious agent. This would therefore suggest that there is a difference between the scrapie and BSE agents’ ability to replicate in the placenta, although without proper comparative kinetics data between scrapie and BSE infected sheep such a possibility cannot be ascertained. Nevertheless, regardless of the pathogenetic mechanism, the almost complete lack of placental PrPd detected in this study is probably a significant factor in the low rate of horizontal transmission observed.

 

In addition to placentas, environmental contamination at lambing time may be due to birth excreta such as blood and amniotic fluid from infected dams, which were not tested in the course of this study. Even if those fluids were infectious, the level of environmental contamination would have been low, since only a few (50 in 7 years) BSE infected dams lambed each year and even fewer (between 0 and 4 per year for a total of 13 in 7 years) lambed offspring that went on to develop BSE. In other words, pressure of infection at lambing time, which has been recognised as an important factor for sheep scrapie [20], would have been low in the experimental set up of this study. This would have contributed to low environmental contamination and negligible horizontal transmission, as observed.

 

In order to achieve endemic BSE within a flock, horizontal and/or maternal transmission of infection must be efficient. This was not the case in the present study. Only a single lamb became infected by putative horizontal transmission. Of 99 BSE orally infected ewes, 49 succumbed to BSE before lambing or had progeny that died at young age (without having lambed) and 50 lambed viable offspring. Thirty-seven of these dams, most of which lambed only once before succumbing to BSE, had an uninfected progeny. Of the remaining 13, one (C1 in Figure 4) had multiple parturitions with only one of six lambs becoming infected, one (R5) had two parturitions with only one of two lambs becoming infected and the remaining 11 ewes had only one lambing, with 12/14 lambs developing BSE. Only one of these ewes (R7) produced a set of twins both of which developed infection; the rest only reared single infected progeny. Moreover, of the 14 F1 progeny that developed BSE, only 6 sheep (2 each of ARQ Suffolk, ARQ Romney and VRQ Cheviot sheep) were females. In other words, out of almost a hundred infected ewes of the parental stock only slightly more than 6% of the sheep of the F1 generation were in a situation of transmitting infection to the next generation and the only one that lambed did not transmit. Thus, although the results of this study clearly indicate that natural transmission of BSE can occur, they do not provide strong evidence for multigenerational maintenance of infection. This conclusion would agree with the absence of any BSE-like case in a retrospective study on more than 2000 natural ovine TSEs diagnosed between 1998 and 2004 [45]. However, a perhaps important caveat of the present experiment is the rapidity with which orally dosed dams succumbed to BSE. In a different scenario, perhaps with a lower oral dose, infected dams could have had the opportunity to lamb in several successive seasons and this could have led to a higher opportunity to raise infected progeny and/or to increase environmental contamination at lambing time. Therefore, the possibility that ovine BSE may show greater trans-generational spread of infectivity under conditions of high infectivity pressure, which was not the case in this experiment, cannot be ruled out.

 

This study has also provided some additional information regarding the pathogenesis of sheep BSE after oral infection. Firstly, the resistance of M112T ARQ Suffolk sheep to oral BSE, which confirms previous reports [10, 22]; in this respect BSE differs from oral scrapie, for which the threonine polymorphism at codon 112 confers only partial resistance, both in terms of AR and ST [23]. Secondly, the poor correlation between clinical disease, magnitude of PrPd in the brain and survival time (Figure 5A); this is in agreement with previous reports on experiments done by the oral [10] and the intracerebral [25] routes. Thirdly, that non-PrP genetics may be involved in the relative proportion of PrPd in the brain and LRS tissues. Thus, when pooling data from parental stock and F1 together, ARQ Romney sheep showed higher brain PrPd for lower LRS PrPd compared with Suffolk sheep of the same genotype, which showed the reverse pattern (results not shown but can be inferred from Figures 5A and B); this is in agreement with the findings of other sheep BSE experiments [10, González et al., unpublished observations). Fourthly, that VRQ sheep appear to be, in terms of survival time, less susceptible to cattle BSE than to some forms of classical sheep scrapie, which might be related to low replication of the agent in the LRS (Figure 5B) of BSE- compared to scrapie-infected sheep (for review see [46]); however, long incubation periods in VRQ sheep have also been reported for sheep scrapie, when the infectious source is of a heterologous ARQ genotype [23]. Finally, that both in terms of truncation site of intracellular PrPd and of brain PrPd profile, BSE in the naturally infected animals is indistinguishable from that in the donor ewes; this finding is in agreement with those obtained on serial experimental passage of BSE in sheep [47].

 

In conclusion, the results of the present study show that transmission of BSE from dam to offspring may occur. However, the low efficiency of maternal transmission and the almost complete lack of horizontal transmission do not suggest that BSE infectivity is likely to be self-sustaining within sheep flocks, at least within the context of the experimental design reported here and the caveats already expressed.

 

Go to: Authors’ contributions MJ participated in the design of the study, in the immunohistochemical (IHC) examinations, in data analysis and interpretation and drafted the manuscript. JPW carried out statistical analyses. SM coordinated IHC processing and quality control and participated in the IHC examinations. SACH coordinated and participated in post-mortems and sample collection. SJB conceived and designed the study. GED carried out biopsies and participated in post-mortems and sample collection. LT participated in post-mortems and sample collection. LG participated in data analysis and interpretation and helped in drafting the manuscript. All authors read and approved its final manuscript.

 

Acknowledgements This study was funded under Defra project SE1946. The authors wish to thank H. Simmons and the staff at the ARSU (APHA) for provision and husbandry of New Zealand-derived, TSE-free sheep, Y. Spencer and the histology laboratory (APHA-Weybridge) for tissue sample preparation, L. Algar, A. Dunachie and M. Oliva (APHA-Lasswade) for technical support with immunohistochemistry. J. Hope’s (APHA) appraisal of the manuscript is also acknowledged.

 

Competing interests The authors declare that they have no competing interests.

 


 

*** This study provides compelling evidence that sheep BSE is naturally transmissible and contagious

 


 

Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission

 

Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats

 

SUMMARY: We are reopening the comment period for our proposed rule that would revise completely the scrapie regulations, which concern the risk groups and categories established for individual animals and for flocks, the use of genetic testing as a means of assigning risk levels to animals, movement restrictions for animals found to be genetically less susceptible or resistant to scrapie, and recordkeeping requirements. This action will allow interested persons additional time to prepare and submit comments.DATES: The comment period for the proposed rule published on September 10, 2015 (80 FR 54660-54692) is reopened. We will consider all comments that we receive on or before December 9, 2015. ...

 


 


 


 

COMMENT SUBMISSION TERRY S. SINGELTARY SR.

 

WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I kindly submit the following ;

 

>>>The last major revision of the scrapie regulations occurred on August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket No. 97-093-5) a final rule amending part 79 by imposing additional restrictions on the interstate movement of sheep and goats.<<<

 

Indeed, much science has changed about the Scrapie TSE prion, including more science linking Scrapie to humans. sadly, politics, industry, and trade, have not changed, and those usually trump sound science, as is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing animals and the OIE. we can look no further at the legal trading of the Scrapie TSE prion both typical and atypical of all strains, and CWD all stains. With as much science of old, and now more new science to back this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE, and all trading partners to take heed to the latest science on the TSE prion disease, all of them, and seriously reconsider the blatant disregards for human and animal health, all in the name of trade, with the continued relaxing of TSE Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set up to fail in the first place. If the world does not go back to the ‘BSE RISK ASSESSMENTS’, enhance, and or change that assessment process to include all TSE prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’ PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they will continue to mutate and spread among species of human and animal origin, and they will continue to kill. ...

 

please see ;

 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

 

***is the third potentially zoonotic PD (with BSE and L-type BSE),

 

***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

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

 

***thus questioning the origin of human sporadic cases***

 

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

 


 

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

Monday, November 16, 2015

 

Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission

 


 


 


 

Friday, April 24, 2015

 

The placenta shed from goats with classical scrapie is infectious to goat kids and lambs

 


 

*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***

 

THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.

 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. ***We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. ***Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

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

 

***thus questioning the origin of human sporadic cases...

 

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

 


 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 

*** Title: Transmission of scrapie prions to primate after an extended silent incubation period Authors

 

item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -

 

Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573. Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.

 

***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 

Title: Transmission of the agent of sheep scrapie to deer results in PrPSc with two distinct molecular profiles Authors

 

item Greenlee, Justin item Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Kunkle, Robert

 

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: March 31, 2015 Publication Date: May 25, 2015 Citation: Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015.

 

Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum. Prion 2015. p. S62. Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes reveal PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile type readily passes to deer.

 


 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 

Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease Authors

 

item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -

 

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A

 

Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.

 


 

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

 

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***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

 

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PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

 

*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

 

O18

 

Zoonotic Potential of CWD Prions

 

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

 

*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.

 

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

 

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

 

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

 

P.105: RT-QuIC models trans-species prion transmission

 

Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

 

Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.

 

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

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

 

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

 


 

Thursday, July 24, 2014

 

*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations

 


 

***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.

 

***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

 

IBNC Tauopathy or TSE Prion disease, it appears, no one is sure

 

Posted by flounder on 03 Jul 2015 at 16:53 GMT

 


 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

Singeltary et al

 

31 Jan 2015 at 20:14 GMT

 


 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

*** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.

 

*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

 

*** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

see page 176 of 201 pages...tss

 


 

Monday, October 26, 2015

 

*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015

 


 


 

In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.

 


 

 4.2.9 A further hypothesis to explain the occurrence of BSE is the emergence or selection of a strain or strains of the scrapie agent pathogenic for cattle. Mutations of the scrapie agent. which can occur after a single passage in mice. have been well documented (9). This phenomenon cannot be dismissed for BSE. but given the form of the epidemic and the geographically widespread occurrence of BSE, such a hypothesis" would require the emergence of a mutant scrapie strain simultaneously in a large . number of sheep flocks, or cattle. throughout the country. Also. if it resulted "from a localised chance transmission of the scrapie strain from sheep to cattle giving rise , . to a mutant. a different pattern of disease would have been expected: its range would '. have increased with time. Thus the evidence from Britain is against the disease being due to a new strain of the agent, but we note that in the United States from 1984 to 1988 outbreaks of scrapie in sheep flocks are reported to have Increased markedly. now being nearly 3 times as high as during any previous period (18).

 


 

 If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...

 


 


 

EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE

 

This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........

 


 

RISK OF BSE TO SHEEP VIA FEED

 


 

OPII-1

 

Disease incidence and incubation period of BSE and CH1641 in sheep is associated with PrP gene polymorphisms.

 

Goldman WI, Hunter N., Benson G., Foster J. and Hope J. AFRC&MRC Neuropathogenesis Unit, Institute for Animal Health, West Mains Rd. Edinburgh EH9 3JF. U.K.

 

The relative survival periods of mice with different Sine genotype have long been used for scrapie strain typing. The PrP protein. a key molecule in the pathogenesis of scrapie and related diseases, is a product of the Sine locus and homologous proteins are also linked to disease-incidence loci in sheep and man. In sheep alleles of this locus (Sip) encode several PrP protein variants, of which one has been associated with short incubation periods of Cheviot sheep infected with SSBP/1 scrapie. Other isolates, i.e. BSE or CH1641. cause a different pattern of incubation periods and a lower disease incidence in the same flock of Cheviot sheep. Using transmission to sheep of known PrP genotype as our criterion for agent strain typing. we have found a link between BSE and CH1641. a C-group strain of scrapie. Disease susceptibility of sheep to these isolates is associated with different PrP genotypes compared to SSBP/1 scrapie.

 

OPII –2

 

Transmission of Bovine Spongiform Encephalopathy in sheep, goats and mice.

 

Foster J., Hope J., McConnell I. and Fraser H. Institute for Animal Health, AFRC and MRC Neuropathogenesis Unit, Kings Buildings, West Mains Road, Edinburgh EH9 3JF

 

Bovine Spongiform Encephalopathy (BSE) has been transmitted in two lines of genetically selected sheep [differing in their susceptibilities to the SSBP/1 source of scrapie), and to goats by intracerebral injection and by oral dosing. Incubation periods in sheep for both routes of challenge ranged from 440-994 days. In goats this range was 506-1508 days. Both routes of infection in sheep and goats were almost equally efficient. In mice, primary transmission of BSE identified a sinc-independant genetic control of incubation period. Also, intermediate passage of BSE in sheep or goats did not alter these primary transmission properties. Hamsters were susceptible to BSE only after intervening passage through mice.

 


 

RESEARCH ARTICLE

 

Phenotype Shift from Atypical Scrapie to CH1641 following Experimental Transmission in Sheep

 

Marion M. Simmons*, S. Jo Moore¤a, Richard Lockey¤b, Melanie J. Chaplin, Timm Konold, Christopher Vickery, John Spiropoulos

 

Animal and Plant Health Agency—Weybridge, Woodham Lane, Addlestone, Surrey, KT15 3NB, United Kingdom

 

¤a Current address: School of Veterinary and Biomedical Sciences, Murdoch University, South Street, Murdoch, Western Australia, 6150, Australia

 

¤b Current address: University of Southampton, Southampton, SO17 1BJ, United Kingdom * marion.simmons@apha.gsi.gov.uk

 

Abstract

 

The interactions of host and infecting strain in ovine transmissible spongiform encephalopathies are known to be complex, and have a profound effect on the resulting phenotype of disease. In contrast to classical scrapie, the pathology in naturally-occurring cases of atypical scrapie appears more consistent, regardless of genotype, and is preserved on transmission within sheep homologous for the prion protein (PRNP) gene. However, the stability of transmissible spongiform encephalopathy phenotypes on passage across and within species is not absolute, and there are reports in the literature where experimental transmissions of particular isolates have resulted in a phenotype consistent with a different strain. In this study, intracerebral inoculation of atypical scrapie between two genotypes both associated with susceptibility to atypical forms of disease resulted in one sheep displaying an altered phenotype with clinical, pathological, biochemical and murine bioassay characteristics all consistent with the classical scrapie strain CH1641, and distinct from the atypical scrapie donor, while the second sheep did not succumb to challenge. One of two sheep orally challenged with the same inoculum developed atypical scrapie indistinguishable from the donor. This study adds to the range of transmissible spongiform encephalopathy phenotype changes that have been reported following various different experimental donor-recipient combinations. While these circumstances may not arise through natural exposure to disease in the field, there is the potential for iatrogenic exposure should current disease surveillance and feed controls be relaxed. Future sheep to sheep transmission of atypical scrapie might lead to instances of disease with an alternative phenotype and onward transmission potential which may have adverse implications for both public health and animal disease control policies.

 

snip...

 

Despite naturally-occurring atypical scrapie being observed in a range of genotypes, successful experimental transmissions of clinical disease have so far only been reported within a particular homologous donor-recipient genotype model using sheep which are AHQ/AHQ homozygous [8,15,16]. These published transmissions represent part of a large study at APHA which has been running since 2004, investigating the potential transmissibility of atypical scrapie in a range of both homologous and cross-genotype combinations. Here we describe an unexpected and interesting finding from that study where one experimental challenge in which atypical scrapie from an ARR/ARR donor was inoculated intracerebrally into two AHQ/AHQ recipient sheep, and in one of them the resulting disease had a phenotype that was indistinguishable from CH1641 [29], a classical scrapie strain which has some BSE-like Western blot properties.

 


 

Subject: more on scrapie/BSE strain CH1641

 

From: tom

 

Reply-To: Bovine Spongiform Encephalopathy

 

Date: Sun, 10 Jan 1999 21:52:05 -0800

 

Content-Type: text/plain

 

Parts/Attachments: Parts/Attachments text/plain (37 lines) Reply Reply

 

Recall a forthcoming J Gen Virol Jan 1999 v80:1 - 4 says there are similarities between BSE and an experimental isolate of natural scrapie, CH1641. This might then be the long-sought missing scrapie strain that could have given rise to the BSE epidemic. It would raise additional questions about the harmlessness to humans of scrapie.

 

On the other hand, CH1641 happened to be one of the scrapie strains studied very recently by Collinge's group, Neurosci Lett. 1998 Oct 23;255(3):159-62. It did not have the prp-sc type identical to BSE passaged in sheep.

 

The CH1641 strain is mentioned only twice before in Medline abstracts (though there could be many fulltext mentions), one of these being the original naming of the strain in 1988:

 

The unusual properties of CH1641, a sheep-passaged isolate of scrapie.

 

Foster JD, Dickinson AG Vet Rec 1988 Jul 2;123(1):5-8

 

An isolate of scrapie designated CH1641 was identified from a natural case of scrapie in a Cheviot sheep by passage in sheep and goats. It has not been possible to transmit scrapie to mice from this source. The Sip gene which controls the incubation periods of experimental scrapie in Cheviot sheep has two alleles; sA which shortens and pA which lengthens the incubation periods of most strains of scrapie after the first experimental injection in sheep (the A group of strains). The CH1641 isolate differs from them in that the alleles of Sip act in the opposite way, with incubation being shorter in the pA homozygotes. There is some evidence that one or more genes, in addition to Sip, may be implicated in the control of scrapie incubation in sheep and the possibility of a carrier infection with CH1641 is also discussed.

 

Novel polymorphisms in the caprine PrP gene: a codon 142 mutation associated with scrapie incubation period.

 

J Gen Virol 1996 Nov;77 ( Pt 11):2885-91 Published erratum appears in J Gen Virol 1997 Mar;78(Pt 3):697 Goldmann W, Martin T, Foster J, Hughes S, Smith G, Hughes K, Dawson M, Hunter N

 

Age at disease onset and rate of progression of transmissible spongiform encephalopathies in man, sheep and mice are modulated by the host genome, in particular by the PrP gene and its allelic forms. Analysis of the caprine PrP gene revealed several different alleles. Four PrP protein variants were found, three of which were goat specific with single amino acid changes at codons 142, 143 and 240. The fourth was identical to the most common sheep PrP protein variant (Ala136-Arg154-Gln171). The dimorphism at codon 142 (Ile --> Met) appeared to be associated with differing disease incubation periods in goats experimentally infected with isolates of bovine spongiform encephalopathy, sheep scrapie CH1641 or sheep-passaged ME7 scrapie.

 


 


 

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

 

JOURNAL OF VIROLOGY, June 2004, p. 6243–6251 Vol. 78, No. 120022-538X/04/$08.00 0 DOI: 10.1128/JVI.78.12.6243–6251.2004

 

Copyright © 2004, American Society for Microbiology. All Rights Reserved.Molecular Analysis of the Protease-Resistant Prion Protein in Scrapieand Bovine Spongiform Encephalopathy Transmitted toOvine Transgenic and Wild-Type MiceThierry Baron,1* Carole Crozet,1† Anne-Gae¨lle Biacabe,1 SandrinePhilippe,2 Je´re´mie Verchere,1Anna Bencsik,1 Jean-Yves Madec,1 Didier Calavas,2 and Jacques Samarut3Unite´ Agents Transmissibles Non Conventionnels1 and Unite´Epide´miologie,2 Agence Franc¸aise de Se´curite´ Sanitairedes Aliments—Lyon, and Laboratoire de Biologie, Ecole Normale Supe´rieure de Lyon,3 Lyon, France Received 27 October 2003/Accepted 4 February 2004

 

The existence of different strains of infectious agents involved in scrapie, a transmissible spongiform encephalopathy (TSE) of sheep and goats, remains poorly explained. These strains can, however, be differentiated by characteristics of the disease in mice and also by the molecular features of the protease-resistant prion protein (PrPres) that accumulates into the infected tissues. For further analysis, we first transmitted the disease from brain samples of TSE-infected sheep to ovine transgenic[Tg(OvPrP4)] and to wild-type(C57BL/6) mice. We show that, as in sheep, molecular differences ofPrPres detected by Western blotting can differentiate, in both ovine transgenic and wild-type mice, infection bythe bovine spongiform encephalopathy(BSE) agent from most scrapie sources. Similarities of an experimental scrapie isolate (CH1641) with BSE were also likewise found following transmission in ovine transgenic mice. Secondly, we transmitted the disease to ovine transgenic mice by inoculation of brain samples of wild-type mice infected with different experimental scrapie strains (C506M3, 87V, 79A, and Chandler) or with BSE. Features of these strains in ovine transgenic mice were reminiscent of those previously described for wild-type mice,by both ratios and by molecular masses of the different PrPres glycoforms. Moreover, these studies revealed the diversity of scrapie strains and their differences with BSE according to labeling by a monoclonal antibody(P4). These data, in an experimental model expressing the prion protein of the host of natural scrapie,further suggest a genuine diversity of TSE infectious agents and emphasize its linkage to the molecular features of the abnormal prion protein.

 


 

snip...

 


 


 

BSE and Scrapie

 


 

TSE PRION UPDATE USA 2012

 

re-BSE in goats can be mistaken for scrapie

 


 

Wednesday, January 18, 2012

 

BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE

 

February 1, 2012

 


 

Wednesday, January 18, 2012

 

Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie

 

Journal of Neuropathology & Experimental Neurology:

 

February 2012 - Volume 71 - Issue 2 - p 140–147

 


 

Saturday, September 19, 2015

 

*** An interview with Professor John Collinge: VIDEO Director of the MRC Prion Unit Part of the Hayward Gallery's History Is Now ***

 


 

Saturday, September 12, 2015

 

The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014

 

>>>We propose that Canadian policies largely ignored the implicit medical nature of BSE, treating it as a purely agricultural and veterinary issue. In this way, policies to protect Canadians were often delayed and incomplete, in a manner disturbingly reminiscent of Britain’s failed management of BSE. Despite assurances to the contrary, it is premature to conclude that BSE (and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of Canada’s past: BSE remains very much an issue in Canada’s present. <<<

 


 

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

 

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

 

snip...

 

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

 


 

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

 

3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...

 


 

Wednesday, September 23, 2015

 

NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15; 8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE Strains by RT-QuIC

 


 

Thursday, October 1, 2015

 

H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation

 


 

Wednesday, May 27, 2015

 

BSE Case Associated with Prion Protein Gene Mutation

 


 

spontaneous atypical BSE ???

 

don’t let anyone fool you. spontaneous TSE prion disease is a hoax in natural cases, never proven.

 

all one has to do is look at France. France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow disease in numbers they could find any with, after those atypical BSE cases started showing up. shut down the testing to numbers set up by OIE that are so low, you could only by accident find a case of BSE aka mad cow disease. and this brilliant idea by the WHO et al, to change the name of mad cow disease, thinking that might change things is preposterous. it’s all about money now folks, when the OIE, USDA and everyone else went along and made the TSE prion disease aka mad cow type disease a legal trading commodity by the BSE MRR policy, I would say everyone bit off more then they can chew, and they will just have to digest those TSE Prions coming from North America, and like it, and just prey you don’t get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE prion disease in the decades to come, and or pass it to some other poor soul via the iatrogenic medical surgical tissue friendly fire mode of transmission i.e. second hand transmission. it’s real folks, just not documented much, due to lack of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the iatrogenic event is tracked down and documented, and put into the academic and public domain, which very seldom happens. ...

 

As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France.

 


 

FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many spontaneous events of mad cow disease $$$

 

so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS

 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

Saturday, June 14, 2014

 

Rep. Rosa DeLauro (D-CT) Calls for Briefing on Beef Recalled for Mad Cow Potential Rep. Rosa DeLauro (D-CT)

 


 

Sunday, October 25, 2015

 

USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE LIVESTOCK CWD SCRAPIE TSE PRION

 


 

Thursday, October 22, 2015

 

Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened

 


 

Sunday, October 18, 2015

 

World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research

 


 

Friday, May 29, 2015

 

GAO FEDERAL VETERINARIANS US Federal Government Is Unprepared for a Large-Scale Animal Disease Outbreak

 


 

Thursday, September 10, 2015

 

25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015

 


 

Terry S. Singeltary Sr.

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