Saturday, December 12, 2015

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015

 

***********OCTOBER 2015*************

 

*** 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.

 

P.108: Successful oral challenge of adult cattle with classical BSE

 

Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada

 

Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, 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. Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.

 


 

>>>At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, 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.<<<

 

Wednesday, July 15, 2015

 

Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?

 


 

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...

 

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

 


 

***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.

 

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

 


 


 

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

 

***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.

 

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

 

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

 


 

Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

 

Nadine Mestre-Francés, Simon Nicot, Sylvie Rouland, Anne-Gaëlle Biacabe, Isabelle Quadrio, Armand Perret-Liaudet, Thierry Baron, and Jean-Michel Verdier

 

We report transmission of atypical L-type bovine spongiform encephalopathy to mouse lemurs after oral or intracerebral inoculation with infected bovine brain tissue. After neurologic symptoms appeared, transmissibility of the disease by both inoculation routes was confi rmed by detection of disease-associated prion protein in samples of brain tissue.

 

Transmissible spongiform encephalopathies, also known as prion diseases, are fatal neurodegenerative disorders that affect humans and animals. An atypical form of bovine spongiform encephalopathy (BSE) was recently identifi ed in cattle in Europe (1,2), North America (3), and Japan (4). This atypical BSE was designated L-type BSE (L-BSE) because Western blot analysis showed that the disease-associated protease-resistant prion protein (PrPres) was of lower apparent molecular mass than in the agent of classical BSE, which is involved in the major foodborne epizooty in cattle and in variant Creutzfeldt-Jakob disease in humans (5).

 

Evidence from experimental studies in primate models (6,7) and transgenic mice expressing human prion protein (PrP) (8,9) suggests that the rare and putatively sporadic form of L-BSE (10) presents a higher risk than classical BSE for transmission to humans. However, a major unresolved issue is whether L-BSE can be transmitted by the oral route. To address this issue, we inoculated gray mouse lemurs (Microcebus murinus), a nonhuman primate model, by the oral and intracerebral (IC) routes with the agent of L-BSE.

 

Conclusions

 

We demonstrated that the agent of L-BSE can be transmitted by the oral route from cattle to mouse lemurs. As expected, orally inoculated animals survived longer than IC-inoculated animals. Orally inoculated lemurs had less severe clinical signs and symptoms, with no evidence of motor dysfunction. It was previously suggested that the agent of L-BSE might be involved in the foodborne transmission of a prion disease in mink (11,12), a species in which several outbreaks of transmissible mink encephalopathy had been identifi ed, notably in the United States (13).

 

Our study clearly confi rms, experimentally, the potential risk for interspecies oral transmission of the agent of L-BSE. In our model, this risk appears higher than that for the agent of classical BSE, which could only be transmitted to mouse lemurs after a fi rst passage in macaques (14). We report oral transmission of the L-BSE agent in young and adult primates. Transmission by the IC route has also been

 

reported in young macaques (6,7). A previous study of L-BSE in transgenic mice expressing human PrP suggested an absence of any transmission barrier between cattle and humans for this particular strain of the agent of BSE, in contrast to fi ndings for the agent of classical BSE (9). Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.

 


 

P.150: Zoonotic potential of L-type BSE prions: A new prion disease in humans?

 

Emilie Jaumain,1 Stéphane Haïk,2 Isabelle Quadrio,3 Laetitia Herzog,1 Fabienne Reine,1 Armand Perret-Liaudet,3 Human Rezaei,1 Hubert Laude,1 Jean-Luc Vilotte,4 and Vincent Béringue1 1INR A (Institut National de la Recherche Agronomique); UR892; Virologie Immunologie Moléculaires; Jouy-en-Josas, France; 2IN SERM; Equipe maladie d’Alzheimer et maladies à Prions; CRicm; UMRS 1127; CNR S; UPMC. R.; ICM, Hôpital de la Salpêtrière; Paris, France; 3Neurobiologie, CMRR , Gériatrie, Hospices Civils de Lyon, Université Lyon 1-CNR S UMR5292-IN SERM U1028; Lyon, France; 3INR A; UMR1313; Génétique Animale et Biologie Intégrative; Jouy-en-Josas, France

 

Two novel prion strains, referred to as BSE-L and BSE-H, have been recognized in bovines through active prion surveillance programs, both being distinct from the epizootic, ‘classical’, BSE strain (C-BSE). Both H and L-types have been detected worldwide as rare cases occurring in aged animals. Like C-BSE prions, H- and L-types prions can propagate with relative ease in foreign species or in transgenic mouse lines expressing heterologous PrP sequences. A prion exhibiting biological properties similar to C-BSE agent sometimes emerged from these cross-species transmissions. Previously, L-type prions were shown to transmit to transgenic mice expressing human PrP with methionine at codon 129 with higher efficacy than C-BSE prions. Here, we examined whether L-type prions propagate without any apparent transmission barrier in these mice and whether such ‘humanised’ L-type prions share biological properties with CJD prions. L-type prions and a panel of human CJD cases with various genotypes at codon 129 and electrophoretic PrPres signatures were serially transmitted by intracerebral route to human PrP mice. The biological phenotypes induced by these agents were compared by all the standard methods currently used to distinguish between prion strains. At each passage, L-type prions were also transmitted back to bovine PrP mice to assess whether the agent has evolved upon passaging on the human PrP sequence. L-type prions transmitted to human PrP mice at 100% attack rate, without notable alteration in the mean incubation times over 5 passages. At each passage, ‘humanized’ L-type prions were able to transmit back to bovine PrP transgenic mice without apparent transmission barrier, as based on the survival time and the restoration of a L-type BSE phenotype. Comparison of mean incubation times on primary and subsequent passages in human PrP mice showed no overlap between L-type and sporadic CJD agents. While the electrophoretic signature and regional distribution of PrPres in L-type diseased mouse brains resembled that seen after transmission of MM2 CJD strain type, both agents exhibited distinct resistance of the associated PrPres molecules to protease denaturation.

 

In summary, L-type prions can be passaged on the human PrP sequence without any obvious transmission barrier. The phenotype obtained differs from the classical CJD prion types known so far. Careful extrapolation would suggest that the zoonotic transmission of this agent could establish a new prion disease type in humans.

 

========Prion2013==========

 

2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday, August 4, 2012

 

*** Final Feed Investigation Summary - California BSE Case - July 2012

 


 

Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation

 

period in cattle – an update Timm Konold1*, Mark E Arnold1, Anthony R Austin2, Saira Cawthraw1, Steve AC Hawkins1, Michael J Stack3, Marion M Simmons1, A Robin Sayers1, Michael Dawson3, John W Wilesmith4 and Gerald AH Wells5

 

Abstract

 

Background: To provide information on dose–response and aid in modelling the exposure dynamics of the BSE epidemic in the United Kingdom groups of cattle were exposed orally to a range of different doses of brainstem homogenate of known infectious titre from clinical cases of classical bovine spongiform encephalopathy (BSE). Interim data from this study was published in 2007. This communication documents additional BSE cases, which occurred subsequently, examines possible influence of the bovine prion protein gene on disease incidence and revises estimates of effective oral exposure.

 

Findings: Following interim published results, two further cattle, one dosed with 100 mg and culled at 127 months post exposure and the other dosed with 10 mg and culled at 110 months post exposure, developed BSE. Both had a similar pathological phenotype to previous cases. Based on attack rate and incubation period distribution according to dose, the dose estimate at which 50% of confirmed cases would be clinically affected was revised to 0.15 g of the brain homogenate used in the experiment, with a 95% confidence interval of 0.03–0.79 g. Neither the full open reading frame nor the promoter region of the prion protein gene of dosed cattle appeared to influence susceptibility to BSE, but this may be due to the sample size.

 

Conclusions: Oral exposure of cattle to a large range of doses of a BSE brainstem homogenate produced disease in all dose groups. The pathological presentation resembled natural disease. The attack rate and incubation period were dependent on the dose.

 

SNIP...

 

Results and discussion

 

Previously published results of the first phase of the study established BSE in all ten cattle dosed with 3×100 g (IP range: 33–45 mpe) and 100 g (IP range: 31– 60 mpe), in seven of nine cattle dosed with 10 g (IP range 41–72 mpe, the tenth died of an intercurrent disease at 14 mpe), and in seven of ten cattle dosed with 1 g (IP range: 45–72 mpe) [1]. In the second phase interim published results reported BSE in three of four cattle dosed with 1 g (IP range: 58–73 mpe), in seven of fifteen dosed with 100 mg (IP range: 53–98 mpe) and in single cattle from groups of fifteen dosed with 10 mg (IP: 56 mpe) or 1 mg (IP: 68 mpe).

 

After publication of the interim findings, two further cases of BSE were diagnosed in cattle in the second phase, one dosed with 100 mg and the other with 10 mg. For completeness of the data from the second phase the times from exposure to onset of the different clinical stages and cull for all BSE-positive cases are given in Table 1 and for all other cattle where BSE was excluded by postmortem tests in Table 2. Neuropathological examination confirmed a vacuolar profile in the brain of the case dosed with 10 mg consistent with that reported previously in the study and with that of naturally affected cattle [1]. The animal dosed with 100 mg and culled with spastic syndrome did not present with vacuolar changes in the brain but in both cases the diagnosis of BSE was confirmed by detection of PrPd immunohistochemically and PrPres on WB.

 

The clinical duration in confirmed BSE cases (time from onset of possible signs to cull, excluding those animals that were culled prior to displaying definite signs) ranged from 4 months (CM917 dosed with 1 g) to 48 months (CM923 dosed with 1 mg). Although there was a tendency of cattle exposed to extremely high doses (3× or single dose of 100 g) to have a shorter clinical duration compared to lower doses [median (range; standard deviation) for 3×100 g: 9 (5–18, 4.5), for 100 g: 13 (6–33; 8.7), for 10 g: 18 (11–43; 13.0), for 1 g: 18.5 (4–32; 8.9) and for 100 mg: 15 (5–37; 12.8) months; see [1] and Table 1], the difference was not statistically significant (P = 0.08, Kruskal-Wallis test, GraphPad Prism version 5, GraphPad Software, La Jolla, USA). Determination of the exact clinical onset to estimate clinical duration is invariably subjective because it is often based on the display of behavioural changes that may also occur to some extent in “normal” cattle, as observed in undosed controls in this study, even in the absence of another underlying condition. It is for this reason that throughout the study IP has been defined on the basis of onset of definite signs.

 

No novel polymorphisms were detected in the ORF regions of the 86 tested cattle. Variations in the number of N-terminal octapeptide repeats among PrP gene sequences were reported previously [1]. The other ORF DNA polymorphisms detected were silent in that they do not result in an amino acid change. A summary of the results is given in Table 3. The findings were consistent with those reported previously [5]. Five common promoter genotypes were identified in this study, with the sixth (23 bp −/−, 12 bp +/+) being relatively rare (only found in one animal, see Table 3), which is consistent with previous findings [7]. Proportional hazard regression analysis using the data from 76 orally dosed cattle revealed that the dose was the most important predictor of hazard (P < 0.0001), which was expected, whereas none of the genotype parameters were significant predictors (P > 0.3). In other words, the main factor that determined how rapidly orally dosed cattle succumbed to BSE was the dose of inoculum, and the genotype did not appear to have a significant influence. Whilst it has been reported that homozygous carriers of the 12 bp insertion allele (12 bp +/+) have a lower risk of developing natural BSE [7], this promoter genotype did not appear to reduce susceptibility to oral exposure to BSE. This may be due to sample size in the current study: to have a reasonable power (80%) to detect the differences (20.5%) as observed by Juling et al. [7], for UK Holstein cattle sample sizes of 60 (12 bp +/+) and 210 (12 bp +/− or −/−) would have been required.

 

Using the individual IP data for each confirmed BSE case (Table 1 and [1] for phase 1 of the study), the probability of infection given the dose S (d) could be expressed as: S(d) = exp(α+β*d)/(1+exp(α+β*d)) with parameters (and 95% confidence intervals) given by α = −3.01 (−3.59, −2.44) and β = 1.12 (0.93, 1.33) (see Figure 1), which is a slight modification to the parameters reported previously (α = −3.50; β = 1.26 [1]), and the additional data resulted in a revised estimate of one cattle oral ID50 being equivalent to 102.7 mouse i.c./ i.p. ID50/g (with 95% confidence interval of 102.0, 103.4) compared to the previous estimate of 102.8 mouse i.c./i.p. ID50/g (with 95% confidence interval of 102.1, 103.5). This ID50 estimate is equivalent to 0.15 g of the brain homogenate used in the experiment (previous estimate:

 

0.20 g), with a 95% confidence interval of 0.03–0.79 g. As it has been shown that one mouse i.c./i.p. ID50 equals 102.7 cattle i.c. ID50 [8], it can be extrapolated that one cattle oral ID50 equals 105.4 cattle i.c. ID50, (previously estimated at 105.5 cattle i.c. ID50).

 

The IP followed a lognormal distribution with parameters of μ = a−b×log10(dose), with a = 4.66 (4.54, 4.71) and b = 0.14 (0.13, 0.17), and σ = 0.23 (previously: μ = 4.54−0.14×log10(dose), σ = 0.21), where dose is the titre of brain homogenate in terms of mouse i.c./i.p. ID50/g [see Figure 2, which shows the association between mean IP (given by exp(μ+0.5σ2) and the dose].

 

Preliminary findings from the original study contributed to quantitative risk assessment of the exposure of humans to consumption of infected bovine products [9]. An estimate of human ID50 assumed the worst case of a cattle to human species barrier of a factor of one, giving the range of human oral ID50s in 1 g of brain from a clinically affected cow as approximately 0.52 to 5. Data from the previously published interim results revised this estimate to 1.0 to 20 and additional results in the present study indicate that this range should now be revised to 1.3 to 33.3, although, as previously, it could be greater with higher titres of BSE affected brain than used in the present study. These estimates have been used to assess the impact of BSE control measures on potential consumption of BSE infectivity (BSE control model [10]). Although the reduced ID50 based on the present results would increase estimates of the exposure of humans in terms of bovine oral ID50s, the effect would be comparatively small relative to the uncertainty in such risk assessments. Nevertheless, with decline of the BSE epidemic and the potential for relaxation of certain controls, the revised estimate of human oral ID50 is available to revisit risk assessments.

 

The present data do not affect the previous approximation that single doses in the range from 100 mg to 1 g of the brainstem homogenate used correspond to the range of mean IPs of cattle through the BSE epidemic [1]. The observation that a relatively small, single exposure (less than 1 g of high titre brain) can result in infection reinforces the importance of preventing crosscontamination during feed ingredient storage and feed production. This proved to be problematical in feed mills producing ruminant and non-ruminant feedstuffs as is evident from the incomplete effect of the initial statutory control on the feeding of meat and bone meal to ruminants introduced in the UK in 1988. The low dose phenomenon, together with the persistent viability of the BSE agent, has required the removal of specific high risk tissues from cattle at slaughter and the total ban on the use of mammalian meat and bone meal for use in farmed livestock [11].

 

Conclusions

 

The present results concur with the interim findings of this study, that the oral exposure of cattle to BSE brain homogenate produced dose dependent effects on IP and attack rate such that in general the higher the dose the shorter the IPs and the greater the attack rate. In all cases the induced disease closely resembled the pathology of the natural disease. This is in keeping with the analysis of the pathology in orally dosed cattle from another study [12] and reinforces the validity of the oral exposure model for the study of classical BSE in the natural host. The estimate of a cattle oral ID50 is revised to 0.15 g brain material used for the studies. Decline of the BSE epidemic indicates that the use of a revised estimate of human oral ID50 in risk assessments is, in future, likely to contribute mainly to reassessments in relation to possible relaxation of controls.

 

Keywords: Bovine spongiform encephalopathy, BSE, Cattle, Oral dose, Dose–response, Attack rate, Incubation period, Model, Risk of infection, Prion protein gene

 


 

Experimental Classical Bovine Spongiform Encephalopathy: Definition and Progression of Neural PrP Immunolabeling in Relation to Diagnosis and Disease Controls

 

Veterinary Pathology OnlineFirst, published on November 15, 2010 as doi:10.1177/0300985810387072

 

M. M. Simmons1,2, J. Spiropoulos1,2, P. R. Webb1, Y. I. Spencer1, S. Czub3,4, R. Mueller5, A. Davis1,6, M. E. Arnold7, S. Marsh1, S. A. C. Hawkins1, J. A. Cooper1, T. Konold1, and G. A. H. Wells1

 

Abstract

 

Tissues from sequential-kill time course studies of bovine spongiform encephalopathy (BSE) were examined to define PrP immunohistochemical labeling forms and map disease-specific labeling over the disease course after oral exposure to the BSE agent at two dose levels. Study was confined to brainstem, spinal cord, and certain peripheral nervous system ganglia—tissues implicated in pathogenesis and diagnosis or disease control strategies. Disease-specific labeling in the brainstem in 39 of 220 test animals showed the forms and patterns observed in natural disease and invariably preceded spongiform changes. A precise temporal pattern of increase in labeling was not apparent, but labeling was generally most widespread in clinical cases, and it always involved neuroanatomic locations in the medulla oblongata. In two cases, sparse labeling was confined to one or more neuroanatomic nuclei of the medulla oblongata. When involved, the spinal cord was affected at all levels, providing no indication of temporal spread within the cord axis or relative to the brainstem. Where minimal PrP labeling occurred in the thoracic spinal cord, it was consistent with initial involvement of general visceral efferent neurons. Labeling of ganglia involved only sensory ganglia and only when PrP was present in the brainstem and spinal cord. These experimental transmissions mimicked the neuropathology in BSE-C field cases, independent of dose of agent or stage of disease. The model supports current diagnostic sampling approaches and control measures for the removal and destruction of nervous system tissues in slaughtered cattle. Keywords

 

transmissible spongiform encephalopathy, prion, bovine, central nervous system, immunohistochemistry, pathogenesis, diagnosis, peripheral nervous system

 


 

 PRION 2009 CONGRESS BOOK OF ABSTRACTS

 

O.4.3

 

Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission

 

Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany

 

Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).

 

Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.

 

Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.

 

Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.

 

Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.

 


 

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.

 


 

WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.

 

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

 

Risk of oral infection with bovine spongiform encephalopathy agent in primates

 

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

 

snip...

 

BSE bovine brain inoculum

 

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

 

Primate (oral route)* 1/2 (50%)

 

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

 

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

 

PrPres biochemical detection

 

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

 

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

 

Published online January 27, 2005

 


 

Oral infection by the bovine spongiform encephalopathy prion

 

R. G. Will and J. W. Ironside Author Affiliations

 

National Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Edinburgh, EH4 2XU, United Kingdom Extract Full Text Authors & Info Metrics Related Content Related Article PDF The route by which prion infection spreads from peripheral tissues to the brain has been the subject of interest and research for decades. The seminal pathogenesis studies by Hadlow and colleagues (1, 2) demonstrated that in natural scrapie in Suffolk sheep infectivity initially was detected at 10–14 months of age in tonsil, lymph nodes, spleen, and intestine, including ileum and upper colon. The tissue distribution of infectivity was consistent with uptake from the alimentary tract and, by implication, oral exposure as the likely portal of entry of infection. By the time clinical disease developed, peripheral tissues continued to exhibit a similar distribution and titer of infectivity, but there was also evidence of infectivity in the central nervous system, with higher titers of infectivity, initially in the medulla and diencephalon. Laboratory studies of oral scrapie infection in rodents have confirmed these findings and suggest that infection spreads from the lymphoreticular system to the spinal cord, presumptively via the autonomic nervous system, and thence rostrally to the brain (3). The importance of peripheral pathogenesis is underlined by the marked increase in incubation time in mice after splenectomy (4).

 

There is, however, variation in pathogenesis that is determined by factors including the interaction between host genome and agent strain. Some breeds of sheep affected by natural scrapie, for example, Montadales, have no detectable infectivity in peripheral tissues, and the distribution of infectivity in the brain may vary according to the breed of sheep (5). In bovine spongiform encephalopathy (BSE) infectivity has not been detected in peripheral tissues in natural disease, except for dorsal root ganglia and possibly bone marrow, although infectivity has been found in terminal ileum after experimental oral challenge with BSE brain (6). An important implication of this data is that, accepting the limits of the sensitivity of bioassay …

 


 


 

It also appears to Mr MacLean that Mr Bradley’s answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight: particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the “attack rate” experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective

 

2

 

dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.

 

It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

it is clear that the designing scientists must have also shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

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. ...

 


 


 

10 years post mad cow feed ban August 1997

 

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

 

Date: March 21, 2007 at 2:27 pm PST

 

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

 

PRODUCT

 

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

 

CODE

 

Cattle feed delivered between 01/12/2007 and 01/26/2007

 

RECALLING FIRM/MANUFACTURER

 

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

 

Firm initiated recall is ongoing.

 

REASON

 

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

 

VOLUME OF PRODUCT IN COMMERCE

 

42,090 lbs.

 

DISTRIBUTION

 

WI

 

___________________________________

 

PRODUCT

 

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

 

CODE

 

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

 

RECALLING FIRM/MANUFACTURER

 

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

 

REASON

 

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

 

VOLUME OF PRODUCT IN COMMERCE

 

9,997,976 lbs.

 

DISTRIBUTION

 

ID and NV

 

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

 


 

16 years post mad cow feed ban August 1997

 

2013

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

17 years post mad cow feed ban August 1997

 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

Sunday, June 14, 2015

 

Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion

 


 

*** Monday, October 26, 2015 ***

 

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

 


 

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

 


 

Saturday, January 31, 2015

 

European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

 


 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations 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.

 

======

 

31 Jan 2015 at 20:14 GMT

 

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

 

Terry S. Singeltary Sr.

 

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, November 23, 2015

 

Dynamics of the natural transmission of bovine spongiform encephalopathy within an intensively managed sheep flock Vet Res. 2015; 46: 126.

 


 

*** 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.

 


 

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

 

Title: Evaluation of the zoonotic potential of transmissible mink encephalopathy Authors

 

item Comoy, Emmanuel - item Mikol, Jacqueline - item Ruchoux, Marie-Madeleine - item Durand, Valerie - item Luccantoni-Freire, Sophie - item Dehen, Capucine - item Correia, Evelyne - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Torres, Juan Maria - item Brown, Paul - item Deslys, Jean-Philippe -

 

Submitted to: Pathogens Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 30, 2013 Publication Date: July 30, 2013 Citation: Comoy, E.E., Mikol, J., Ruchoux, M., Durand, V., Luccantoni-Freire, S., Dehen, C., Correia, E., Casalone, C., Richt, J.A., Greenlee, J.J., Torres, J.M., Brown, P., Deslys, J. 2013. Evaluation of the zoonotic potential of transmissible mink encephalopathy. Pathogens. 2:(3)520-532.

 

Interpretive Summary: Cases of bovine spongiform encephalopathy (BSE) or mad cow disease can be subclassified into at least 3 distinct disease forms with the predominate form known as classical BSE and the others collectively referred to as atypical BSE. Atypical BSE can be further subdivided into H-type and L-type cases that are distinct from classical BSE and from each other. Both of the atypical BSE subtypes are believed to occur spontaneously, whereas classical BSE is spread through feeding contaminated meat and bone meal to cattle. Transmissible mink encephalopathy (TME) is another prion disease that transmits to cattle and show similarities to L-type BSE when subjected to laboratory testing. The purpose of this study was to use non-human primates (cynomologous macaque) and transgenic mice expressing the human prion protein to determine if TME could represent a potential risk to human health. TME from two sources (cattle and raccoons) was able to infect non-human primates and transgenic mice after exposure by the intracranial route. This result suggest that humans may be able to replicate TME prions after an exposure that allows infectious material access to brain tissue. At this time, it is unknown whether non-human primates or transgenic mice would be susceptible to TME prions after oral exposure. The results obtained in these animal models were similar to those obtained for L-type BSE. Although rare, the existence of TME and that it transmits to cattle, non-human primates, and transgenic mice suggest that feed bans preventing the feeding of mammalian tissues to cattle should stay in place and that regular prion surveillance during the slaughter should remain in place. Parties with interest in the cattle and beef industries and regulatory officials responsible for safe feeding practices of cattle will be interested in this work. Technical Abstract: Successful transmission of Transmissible Mink Encephalopathy (TME) to cattle supports the bovine hypothesis to the still controversial origin of TME outbreaks. Human and primate susceptibility to classical Bovine Spongiform Encephalopathy (c-BSE) and the transmissibility of L-type BSE to macaques assume a low cattle-to-primate species barrier: we therefore evaluated the zoonotic potential of cattle-adapted TME. In less than two years, this strain induced in cynomolgus macaques a neurological disease similar to L-BSE and distinct from c-BSE. TME derived from another donor species (raccoon) induced a similar disease with shorter incubation periods. L-BSE and cattle-adapted TME were also transmissible to transgenic mice expressing human PrP. Interestingly, secondary transmissions to transgenic mice expressing bovine PrP showed the maintenance of prion strain features for the three tested bovine prion strains (cattle TME, c-BSE and L-BSE) regardless of intermediate host. Thus, TME is the third animal prion strain transmissible to both macaques and humanized transgenic mice, suggesting zoonotic potentials that should be considered in the risk analysis of animal prion diseases for human health. Moreover, the similarities between TME and L-BSE are highly suggestive of a link between those strains, and of the presence of L-BSE decades prior to its identification in USA and Europe.

 


 

Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies 2014 Annual Report

 

1a.Objectives (from AD-416): 1. Investigate the pathobiology of atypical transmissible spongiform encephalopathies (TSEs) in natural hosts. A. Investigate the pathobiology of atypical scrapie. B. Investigate the pathobiology of atypical bovine spongiform encephalopathy (BSE). 2. Investigate the horizontal transmission of TSEs. A. Assess the horizontal transmission of sheep scrapie in the absence of lambing. B. Determine routes of transmission in chronic wasting disease (CWD) infected premises. C. Assess oral transmission of CWD in reindeer. 3. Investigate determinants of CWD persistence. A. Determine CWD host range using natural routes of transmission. B. Investigate the pathobiology of CWD.

 

1b.Approach (from AD-416): The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of accumulation, routes of infection, environmental persistence, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include clinical exams, histopathology, immunohistochemistry and biochemical analysis of proteins. The enhanced knowledge gained from this work will help mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.

 

3.Progress Report: Research efforts directed toward meeting objective 1 of our project plan, Investigate the pathobiology of atypical transmissible spongiform encephalopathies (TSEs) in natural hosts, include work in previous years starting with the inoculation of animals for studies designed to address the pathobiology of atypical scrapie, atypical bovine spongiform encephalopathy (BSE), as well as a genetic version of BSE. Animals inoculated with atypical scrapie have not yet developed disease. Atypical BSE animals have developed disease and evaluation of the samples is currently underway. Animals inoculated with a genetic version of BSE have developed disease and the manuscript has been published (2012). In addition, we have investigated the possibility that atypical scrapie was present earlier than previously detected in the national flock by analyzing archived field isolates using methods that were unavailable at the time of original diagnosis. Sample quality was sufficiently degraded that modern methods were not suitable for evaluation. In research pertaining to objective 2, Investigate the horizontal transmission of TSEs, we have initiated a study to determine if cohousing non-lambing scrapie inoculated sheep is sufficient to transmit scrapie to neonatal lambs. At this time, scrapie free ewes have lambed in the presence of scrapie inoculated animals and the lambs are cohoused with these inoculated animals.

 

4.Accomplishments 1. Evaluated enzyme immunoassay for rapid identification of prion disease in livestock. Scrapie of sheep and bovine spongiform encephalopathy of cattle are diseases that cause damage to the central nervous system including the retina in the eye. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state and is resistant to breakdown by the host cells. Current diagnostic methods require the testing of brain material, which can be difficult to collect and may lead to contamination of the environment and exposure of personnel to the infectious agent. Eyes can be readily collected without opening the skull. ARS researchers at Ames, Iowa demonstrated that the enzyme immunoassay results using eyes of negative controls or samples collected from sheep or cattle with clinical signs were in agreement with approved confirmatory assays (western blot or immunohistochemistry). These results indicate the retina is a useful tissue for rapid diagnosis of prion disease in clinically ill sheep and cattle and could be considered to greatly increase the number of samples submitted for prion disease diagnosis with a minimal investment of time and limited exposure of personnel to prion agents.

 

2. Evaluated E211K cattle as a model for inherited human prion disease. Prion diseases cause damage to the central nervous system of animals and humans. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state and is resistant to breakdown by the host cells and thus accumulates and damages those cells. Some forms of prion disease are genetic and can be inherited. Current models of genetic prion disease in humans rely on mouse models expressing either the human prion protein (E200K) or a combination of both mouse and human sequences. In addition to being an entirely artificial system these mouse models have a short lifespan making them a less than ideal system to study a naturally occurring genetic disorder with a long incubation time and late onset of disease. Cattle, however, exhibit a number of similarities to humans with regard to prion disease and perhaps most notable is the late onset of genetic prion disease. ARS researchers at Ames, Iowa have produced cattle containing both 1 and 2 chromosome copies of the cattle prion gene (E211K) and evaluated many aspects of this prion protein from cattle including protein stability, protein expression levels and ratios, as well as evidence of oxidative stress. Taken together, these results highlight the differences between mouse models of genetic prion disease and a naturally occurring prion disease system in cattle and suggest that cattle will provide a more relevant understanding of genetic prion disease in humans than do current rodent models.

 

Review Publications Smith, J.D., Greenlee, J.J. 2014. Detection of misfolded prion protein in retina samples of sheep and cattle by use of a commercially available enzyme immunoassay. American Journal of Veterinary Research. 75(3):268-272. Haldar, S., Beveridge, A.J., Wong, J., Singh, A.J., Galimberti, D., Borroni, D., Zhu, X., Blevins, J., Greenlee, J., Perry, G., Mukhopadhyay, C.K., Schmotzer, C., Singh, N. 2014. A low-molecular-weight ferroxidase is increased in the CSF of sCJD Cases: CSF ferroxidase and transferrin as diagnostic biomarkers for sCJD. Antioxidants & Redox Signaling. 19(14):1662-1675.

 


 

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.

 


 

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

 


 


 

Tuesday, August 4, 2015

 

FDA U.S. Measures to Protect Against BSE

 


 

Saturday, December 21, 2013

 

Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle

 


 

Wednesday, May 2, 2012

 

ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH

 


 

2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday, August 4, 2012

 

*** Final Feed Investigation Summary - California BSE Case - July 2012

 


 

SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012

 

Summary Report BSE 2012

 

Executive Summary

 


 

Saturday, August 4, 2012

 

Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation

 


 

in the url that follows, I have posted

 

SRM breaches first, as late as 2011.

 

then

 

MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007, when they ceased posting them.

 

then,

 

MAD COW SURVEILLANCE BREACHES.

 

Friday, May 18, 2012

 

Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012

 


 

Monday, August 6, 2012

 

TAFS BSE in USA August 6, 2012

 

BSE in USA

 


 

Saturday, May 26, 2012

 

Are USDA assurances on mad cow case 'gross oversimplification'?

 

SNIP...

 

*** What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”

 

*** The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health.

 

*** "(The agency) has no foundation on which to base that statement.”

 

*** “We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.

 

*** In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said

 

*** The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.

 

SNIP...

 


 

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

 


 

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.

 


 

***atypical spontaneous BSE in France LOL***

 

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

 


 

UNITED STATES OF AMERICA USA

 

a review of the mad cow debacle by USDA et al under Agriculture Secretary Ann Veneman ;

 

 US SENATOR AND STAN THE MAN SLAM USDA ''DAMNING TESTIMONY''

 

 Senator Michael Machado from California

 

 ''USDA does not know what's going on''.

 

 ''USDA is protecting the industry''.

 

 ''SHOULD the state of California step in''

 

 Stanley Prusiner

 

 ''nobody has ever ask us to comment''

 

 ''they don't want us to comment''

 

 ''they never ask''

 

 i tried to see Venemon, after Candian cow was discovered with BSE. went to see lyle. after talking with him... absolute ignorance... then thought I should see Venemon... it was clear his entire policy was to get cattle bonless beef prods across the border... nothing else mattered...

 

 his aids confirmed this... 5 times i tried to see Venemon, never worked... eventually met with carl rove the political... he is the one that arranged meeting with Venemon... just trying to give you a sense of the distance... healh public safety...

 

 was never contacted...

 

 yes i believe that prions are bad to eat and you can die from them... END

 

 Dr. Stan bashing Ann Veneman - 3 minutes

 


 

 Recall Authority and Mad Cow Disease: Is the Current System Good for Californians?

 

 Tuesday, February 24, 2004

 

 JOINT HEARING

 

 AGRICULTURE AND WATER RESOURCES HEALTH AND HUMAN SERVICES AND SELECT COMMITTEE ON GOVERNMENT OVERSIGHT - MACHADO, ORTIZ, and SPEIER, Chairs

 

 ALL VIDEOS OF THIS HEARING HAVE BEEN REMOVED FROM THE WWW, LIKE IT NEVER HAPPENED...but we know different...TSS

 

 -------- Original Message --------

 

Subject: Re: Congressman Henry Waxmans's Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW

 

Date: Wed, 9 Jun 2004 16:48:31 –0500

 

From: "Terry S. Singeltary Sr."

 

Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de References: 40A8CD52.1070308@wt.net

 

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

 

 USA BSE RED BOOK

 

 October 1998

 

 BSE Red Book 2.1-36

 

 7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer will advise the READE(3 Director concerning laboratory capabilities and appropriate laboratory examinations to be conducted to provide needed results as rapidly as possible. This individual will assist with interpretation of results.

 

 seems that if the 'enhanced BSE/TSE testing program' is to test some 400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.

 

 BSE Red Book 2.1-39

 

 7.6 Depopulation Procedures

 

 Under no circumstances may BSE suspects be sent fo slaughhter or rendering.

 

 snip...

 

 BSE Red Book 2.1-40

 

 7.7 Disposal Under no circumstances may BSE suspects be sent to slaughter or rendering. Notify FDA, CVM if you suspect that the carcass of a BSE-confirmed animal has moved to rendering or animal feed manufacturing. Field personel should arrange for the carcass to be transported to and examined by a qualified veterinary pathologist or field veterinary medical officer. After the pathologic examination has been completed and the necessary diagnostic specimens have been obtained, field personnel should arrange for disposal of the carcass. Before a method of disposal is selected, there are many factors that must be considered, and often other State and Federal agencies must be consulted. The environmental and legal impacts of the operation must be considered. Upon recommendation of the State or Federal agencies, VS may consider other disposal methods.

 

 snip...

 

 7.7.3 Rendering Because BSE is spread by rendered animal protein, BSE-suspect and confirmed carcasses must not be rendered, unless the rendered material is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or carcasses have moved to rendering or animal feed manufacturing.

 

 snip...

 

 7.10.11 Prevention--Suspects and animals confirmed to have BSE must not be rendered. Producers, feed mills, and rendering establishments should adhere to U.S. State and local rendering policies and FDA regulations concerning the feeding of rendered animal protein to ruminants.

 

 TSS

 

 Terry S. Singeltary Sr. wrote:

 

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

 

 ONE HUNDRED EIGHTH CONGRESS CONGRESS OF THE UNITED STATES HOUSE OF REPRESENTATIVES COMMITTEE ON GOVERNMENT REFORM 2157 RAYBURN HOUSE OFFICE BUILDING WASHINGTON, DC 20515-6143

 

 > www.house.gov/reform > > May 13, 2004 > > The Honorable Ann M. Veneman Secretary of Agriculture Department of Agriculture 1400 Independence Avenue, SW Washington, DC 20250

 

 Dear Madam Secretary:

 

 I am writing to express concern that the recent failure of the U.S. Department of Agriculture (USDA) to test a Texas cow with neurological symptoms for bovine spongiform encephalopathy (BSE) may reflect wider problems in the surveillance program. USDA apparently does not keep track of how many cows condemned for central nervous system symptoms are tested for BSE nor does it require that suspect carcasses be held pending testing. Effective surveillance and control of BSE in the United States require a reliable system for ensuring that potentially infected cows are tested and that no infected materials enter the animal or human food supply.

 

 Under USDA regulations, any cow that exhibits signs of central nervous system (CNS) problems must be condemned by Food Safety Inspection Service (FSIS) personnel at the plant.1 According to a 1997 Animal and Plant Health Inspection Service (APHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "[i]t is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."3

 

 The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5

 

 1 9 CFR 309.4.

 

 2 USDA APHIS, Veterinary Services Memorandum No. 580.16. Procedures/or Investigation of Adult Cattle With Clinical Signs of Central Nervous System (CNS) Disease and Procedures for Surveillance of Downer Cows for Bovine Spongiform Encephalopathy (BSE) (June 11,1997). 3 Id.

 

 4 U.S. Confirms a Failure to Use Mad Cow Test, Wall Street Journal (May 4, 2004).

 

 The Honorable Ann M. Veneman May 13,2004 Page 2

 

 This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:

 

 Based on information provided by the Food Safety and Inspection Service (FSIS), the number of adult cattle (2 years of age or greater) condemned at slaughter due to CNS signs is much greater than the number whose brains have been collected for testing.6

 

 Despite recognizing the problem more than six years ago, however, USDA apparently did not adopt procedures to ensure that these samples would be collected. In March 2004, the Government Reform Committee asked USDA to provide, for each of the last five years, the number of BSE tests performed on cattle condemned by FSIS inspectors on the basis of CNS symptoms.7 In response, USDA provided information on the numbers of cattle condemned for CNS symptoms by FSIS, but replied that "[i]t is not possible to determine, from the data we currently collect, how many of these cattle were tested by APHIS for BSE."8 It thus appears that not only does USDA not routinely track the gap between the number of condemned and tested cattle, but that USDA could not even calculate this gap when requested to do so by Congress.

 

 There also appears to be a lack of clarity regarding the disposition of cattle with CNS symptoms while BSE tests are pending. In the past, companies could send cattle awaiting BSE testing results for rendering, which would allow their remains to be used in feed for animals other than ruminants, such as pigs and chickens. After this incident, both FDA and USDA policy appear to have changed — in different ways.

 

 USDA policy has apparently shifted to requesting that companies not send cattle to rendering while awaiting test results. A May 5, 2004 memo from APHIS states, "it is requested — though not required — that [the cattle] not go to inedible rendering until the sample comes

 

 USDA's San Angelo Vets and Techs Ordered Not to Test Suspect Cow, Meating Place (May 5, 2004).

 

 6 USDA APHIS, supra note 2.

 

 7 Letter from Rep. Tom Davis and Rep. Henry A- Waxman to Secretary of Agriculture Ann M. Veneman (Mar. 8, 2004).

 

 8 Letter from Ronald F. Hicks, Assistant Administrator, Office of Program Evaluation, Enforcement, and Review- FSIS. to Reo. Henrv A. Waxman- Attachment 1 (Mar. 22- 2004).

 

 The Honorable Ann M. Veneman May 13,2004 Page 3

 

 back negative."9 There is no explanation of why this course of action is requested, but not required.

 

 FDA policy also appears to have shifted towards prohibiting the use of carcasses of cattle with CNS symptoms and indeterminate BSE status in certain types of animal feed. On April 30, FDA requested that the rendering company holding the remains of the Texas cow either destroy them or use them exclusively in swine feed. m the case that the remains are included in swine feed, FDA "will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs."10

 

 Any confusion over what to do with cattle condemned for CNS symptoms awaiting testing for BSE seems unnecessary. The obvious approach is to require companies either to destroy the carcasses or hold them until test results become available. Such a policy would avoid any need for complicated traceback procedures after the discovery of a positive result. According to the information provided to the Committee by USDA, the FSIS has condemned only 200 to 250 cows per year because of signs of central nervous system damage." Mandating the destruction or holding of their carcasses would have minimal economic impact.

 

 The experience with the BSE-infected cow in Washington State illustrates the prudence of waiting for the results of BSE tests. Prior to December 2003, USDA permitted cattle that were sampled as part of the BSE surveillance program to enter commerce even while BSE tests were pending. As a result, when the BSE-infected cow was discovered, it had already entered the food supply. This led to a complicated and partially successful traceback procedure in which hundreds of thousands of pounds of beef had to be destroyed. Because of this debacle, USDA quickly developed a new policy to require holding all carcasses from the human food chain during BSE testing.

 

 I appreciate that you have taken steps to enhance the safety of the U.S. food supply since the discovery of BSE in the United States. I urge you to consider the lessons of this latest

 

 9 Memo from John R. Clifford, Acting Deputy Administrator, Veterinary Services, and William Smith, Assistant Administrator, Office of Field Operations, Food Safety and Inspection Service, to VSMT, Regional Directors, Area Veterinarians in Charge, and Veterinary Services, Subject: Policy Statement Regarding BSE Sampling of Condemned Cattle at Slaughter Plants - for Immediate Implementation (May 5, 2004) (online at http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf).

 

 10 FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. 20, 2004) (online at http://www.fda.gov/bbs/topics/news/2004/NEW01061.html).

 

 11 The yearly totals of FSIS antemortem CNS condemnation for all adult cattle were 233 (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003). The database for 2003 had not yet closed.

 

 The Honorable Ann M. Veneman May 13,2004 Page 4

 

 incident. USDA should develop a process that ensures the tracking of cattle condemned for CNS signs and should institute a policy requiring all carcasses with pending BSE tests to be destroyed or held. If there are any statutory barriers to these steps, please do not hesitate to let me know.

 

 Sincerely,

 

 XXXXX X. XXXXXX

 

 Henry A. Waxman

 

 Ranking Minority Member

 

 Congressman Henry Waxmans's Letter to the Honorable Ann Veneman

 


 

 TSS

 


 

 *** Qualitative Analysis of BSE Risk Factors in the United States

 

 February 13, 2000 at 3:37 pm PST (BSE red book)

 


 

 Tuesday, July 14, 2009 U.S.

 

 *** Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book

 

 Date: February 14, 2000 at 8:56 am PST

 

 WHERE did we go wrong $$$

 


 

 *********-------- Original Message --------**********

 

 Subject: re-USDA's surveillance plan for BSE aka mad cow disease

 

 Date: Mon, 02 May 2005 16:59:07 -0500

 

 From: "Terry S. Singeltary Sr."

 

 To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us

 

 Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............

 

 snip...

 

 There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...

 

 Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx

 

 Date: June 14, 2005 at 1:46 pm PST In

 

 Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:

 

 Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS

 

 MAD COW IN TEXAS NOVEMBER 2004. ...TSS

 

 -------- Original Message --------

 

 Director, Public Information Carla Everett ceverett@tahc.state.tx.us

 

 Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

 Date: Mon, 22 Nov 2004 17:12:15 –0600

 

 From: "Terry S. Singeltary Sr."

 

 To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>

 

 Greetings Carla,still hear a rumor;

 

 Texas single beef cow not born in Canada no beef entered the food chain?

 

 and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???

 

 terry

 

 -------- Original Message --------

 

 Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

 Date: Fri, 19 Nov 2004 11:38:21 –0600

 

 From: Carla Everett

 

 To: "Terry S. Singeltary Sr." References: <[log in to unmask]>

 

 The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas. Carla At 09:44 AM 11/19/2004, you wrote:>Greetings Carla,>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from>TEXAS. can you comment on this either way please?>>thank you,>Terry S. Singeltary Sr.>>

 

 -------- Original Message --------

 

 Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

 Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett

 

 To: "Terry S. Singeltary Sr."

 

 References: ...sniptss

 

 our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something. At 06:05 PM 11/22/2004,

 

 you wrote:

 

 >why was the announcement on your TAHC site removed?

 

 >>Bovine Spongiform Encephalopathy:

 

 >November 22: Press Release title here

 

 >>star image More BSE information

 

 >>>>terry

 

 >>Carla Everett wrote:

 

 >>>no confirmation on the U.S.' inconclusive test...

 

 >>no confirmation on location of animal.>>>>>>

 

 ==========================

 

 -------- Original Message --------

 

 Director, Public Information Carla Everett ceverett@tahc.state.tx.us

 

 Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

 Date: Mon, 22 Nov 2004 17:12:15 –0600

 

 From: "Terry S. Singeltary Sr."

 

 To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>

 

 Greetings Carla,still hear a rumor;

 

 Texas single beef cow not born in Canada no beef entered the food chain?

 

 and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???

 

 terry

 

 ==============================

 


 


 

 2004, highly suspect stumbling and staggering mad cow reported, however, NO TESTING DONE, ON ORDERS FROM AUSTIN $

 

 May 4, 2004

 

 Statement on Texas Cow With Central Nervous System Symptoms

 

 On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

 

 FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.

 

 FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.

 

Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison)...

 


 

USDA regulations, any cow that exhibits signs of central nervous system (CNS)

 

According to a 1997 Animal and Plant Health Inspection Service (NHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "it is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."

 

The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5

 

May 13,2004

 

Page 2

 

snip...

 

The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5

 

This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:

 


 

USDA did not test possible mad cows

 

By Steve Mitchell

 

United Press International

 

Published 6/8/2004 9:30 PM

 

WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims ittested 500 cows with signs of a brain disorder for mad cow disease last year, but agency documents obtained by United Press International show the agency tested only half that number.

 


 


 

"These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."

 

THIS WAS DONE FOR A REASON!

 

THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS

 

TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND CALLS FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS CONFIRMED

 

THE USDA MAD COW FOLLIES POSITIVE TEST COVER UP

 

JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED

 

OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7 MONTHS LATER

 

TEXAS MAD COW

 

THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i confirmed this case 7 months earlier to the TAHC, and then, only after i contacted the Honorable Phyllis Fong and after an act of Congress, this animal was finally confirmed ;

 

During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 200 adult animals of interest were determined to have left the index farm. Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. In addition to the adult animals, APHIS was looking for two calves born to the index animal. Due to record keeping and identification issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.

 


 

Executive Summary In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.

 

 snip...

 

 Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having received an animal of interest. The herd was placed under hold order on 7/27/05. The herd inventory was conducted on 7/28/05. The animal of interest was not present within the herd, and the hold order was released on 7/28/05. The person who thought he sold the animal to the owner of Trace Herd 3 had no records and could not remember who else he might have sold the cow to. Additionally, a search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.

 

 Trace Herd 4 The owner of Trace Herd 4 was identified as having received one of the COI through an order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were examined individually by both State and Federal personnel for all man-made identification and brands. The animal of interest was not present within the herd. Several animals were reported to have died in the herd sometime after they arrived on the premises in April 2005. A final search of GDB records yielded no further results on the eartag of interest at either subsequent market sale or slaughter. With all leads having been exhausted, this animal of interest has been classified as untraceable. The hold order on Trace Herd 4 was released on 8/23/05.

 

 Trace Herd 5 The owner of Trace Herd 5 was identified as having received two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple pastures. During the course of the herd inventory, the owner located records that indicated that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was subsequently found alive. Upon completion of the herd inventory, the other animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.

 

 Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having received an animal of interest and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on two pastures. A herd inventory was conducted and the animal of interest was not present within the herd. The owner of Trace Herd 6 had very limited records and was unable to provide further information on where the cow might have gone after he purchased her from the livestock market. A search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. Additionally, many of the animals presented for sale by the owner of the herd had been re-tagged at the market effectually losing the traceability of the history of that animal prior to re-tagging. The animal of interest traced to this herd was classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.

 

 Trace Herd 7 The owner of Trace Herd 7 was identified as having received an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple pastures in multiple parts of the State, including a unit kept on an island. The island location is a particularly rough place to keep cattle and the owner claimed to have lost 22 head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the animal of interest was not found present within Trace Herd 7. A GDB search of all recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to locate the identification tag of the animal of interest. The cow was subsequently classified as untraceable. It is quite possible though that she may have died within the herd, especially if she belonged to the island unit. The hold order on Trace Herd 7 was released on 8/8/05.

 


 

 *** 2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006 ***

 


 

 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. ...

 


 

snip...see full text ;

 

 Thursday, October 22, 2015

 

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

 


 

Comments on technical aspects of the risk assessment were then submitted to FSIS.

 

Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.

 

This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:

 


 

Owens, Julie

 

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

 

Sent: Monday, July 24, 2006 1:09 PM

 

To: FSIS RegulationsComments

 

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

 

Page 1 of 98

 


 

FSIS, USDA, REPLY TO SINGELTARY

 


 

Singeltary to APHIS FDA USDA et al ;

 


 


 

CJDIBSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)

 

PDF]Freas, William TSS SUBMISSION

 

File Format: PDF/Adobe Acrobat -

 

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

 

Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...

 


 

IN A NUT SHELL ;

 

(Adopted by the International Committee of the OIE on 23 May 2006)

 

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

 


 

CANADA BSE TSE PRION

 

Confirmed Cases of Bovine Spongiform Encephalopathy (BSE) in 2015

 

BSE is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

 

Current as of: 2015-11-30

 

The following table lists individual animals confirmed to be infected with BSE in Canada in 2015.

 

Date confirmed

 

Location

 

Animal type infected

 

Age of Animal

 

February 11 Alberta Beef cow 70 months

 


 

Monday, November 30, 2015

 

*** Report on the Investigation of the Nineteenth Case of Bovine Spongiform Encephalopathy (BSE) in Canada November 2015 ***

 


 

Herds infected with Chronic Wasting Disease in Canada in 2015

 

The CFIA works with provincial governments and industry to conduct regular Chronic Wasting Disease (CWD) surveillance. Ongoing provincial surveillance for CWD varies with each particular province's perceived threat and infection status. Testing is mandatory in Manitoba, Saskatchewan, Alberta and the Yukon; it is voluntary, completed by random submission, or organized through policy in other provinces and territories.

 

In addition, CWD is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

 

Current as of: 2015-11-30

 

Domestic cervid herds confirmed to be infected with CWD in Canada in 2015

 

Date confirmed

 

Location

 

Animal type infected

 

November 25 Saskatchewan Deer

 

July 16 Alberta Elk

 

June 11 Saskatchewan Elk

 

April 9 Saskatchewan Deer

 

March 19 Saskatchewan Elk

 

January 16 Alberta Elk

 


 

Flocks infected with Scrapie in Canada in 2015

 

The CFIA, in co-operation with provincial governments and industry, launched a national scrapie surveillance program in 2005. Under the program, producers are encouraged to report animals that die on the farm or exhibit symptoms of the disease.

 

In addition, scrapie is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

 

Current as of: 2015-11-30

 

Sheep flocks and/or goat herds confirmed to be infected with classical scrapie in Canada in 2015

 

Date confirmed

 

Location

 

Animal type infected

 

January 5 Ontario Goat

 

May 22 Quebec Sheep

 

June 16 Ontario Sheep

 


 

Friday, July 10, 2015

 

CANADA TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION UPDATE

 


 

Monday, February 23, 2015

 

20th BSE Case Raises New Concerns about Canada's Feeding Practices and Voluntary Testing Program; Highlights Importance of COOL

 


 

Friday, February 20, 2015

 

A BSE CANADIAN COW MAD COW UPDATE Transcript - Briefing (February 18, 2015)

 


 

Saturday, February 14, 2015

 

Canadian Food Inspection Agency Confirms Bovine Spongiform Encephalopathy (BSE) in Alberta

 


 

SNIP...see more TSE prion stats from Canada with CJD update as well...

 

Friday, July 10, 2015

 

CANADA TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION UPDATE

 


 

EDMONTON - Some of former Alberta premier Ralph Klein's most colourful quotes — and the reactions they elicited:

 

SNIP...

 

"This all came about through the discovery of a single, isolated case of mad cow disease in one Alberta cow on May 20th. The farmer — I think he was a Louisiana fish farmer who knew nothing about cattle ranching. I guess any self-respecting rancher would have shot, shovelled and shut up, but he didn't do that." — Klein recalls how the mad cow crisis started and rancher Marwyn Peaster's role. The premier was speaking at the Western Governors Association meeting in Big Sky, Mont. September 2004.

 

"The premier meant that in an ironic or almost a sarcastic way." — Klein spokesman Gordon Turtle.

 

---

 

"You would have to eat 10 billion meals of brains, spinal cords, ganglia, eyeballs and tonsils." — Klein speaking in Montreal in January 2005 on the risk of humans contracting mad cow disease.

 

---

 

"I would offer $5 billion to have a Japanese person to come over here and eat nothing but Alberta beef for a year. And if he gets mad cow disease, I would be glad to give him $5 billion — make it $10 billion — Canadian." — Klein speaking after Japan closed its borders to Canadian beef.

 

---

 


 


 

Thursday, February 10, 2011

 

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

 


 

Wednesday, August 11, 2010

 

REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

 


 

Thursday, August 19, 2010

 

REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

 


 

Friday, March 4, 2011

 

Alberta dairy cow found with mad cow disease

 


 

Tuesday, May 21, 2013

 

Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$

 


 

2015

 

***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.

 

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

 

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

 

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.

 


 

Evidence for zoonotic potential of ovine scrapie prions

 

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

 

Abstract

 

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 

Subject terms: Biological sciences• Medical research At a glance

 


 

please see file attachment for full submission and recent science and my deep concerns on the TSE Prion disease... No documents available. AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:

 


 

Thursday, March 29, 2012

 

atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

 


 

Increased Atypical Scrapie Detections

 

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

 


 

Current as of: 2015-01-31

 

Sheep flocks and/or goat herds confirmed to be infected with classical scrapie in Canada in 2015 Date confirmed Location Animal type infected January 5 Ontario Goat

 


 


 

Tuesday, February 10, 2015

 

Alberta Canada First case of chronic wasting disease found in farm elk since 2002

 


 

Atypical Scrapie Canada

 


 


 

Thursday, March 29, 2012

 

atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

 


 

P03.141

 

Aspects of the Cerebellar Neuropathology in Nor98

 

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

 

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 


 

PR-26

 

NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS

 

R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway

 

Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.

 

*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.

 

119

 


 

A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

 

Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations

 

*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

 

***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)

 

Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three 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.

 


 

Monday, December 1, 2008

 

When Atypical Scrapie cross species barriers

 

Authors

 

Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.

 

Content

 

Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.

 

The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.

 

Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.

 

Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

 

(i) the unsuspected potential abilities of atypical scrapie to cross species barriers

 

(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

 

These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.

 


 

Tuesday, April 28, 2009

 

Nor98-like Scrapie in the United States of America

 


 

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. <<<

 


 

Sunday, October 18, 2015

 

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

 

From: Terry S. Singeltary Sr.

 

Sent: Friday, October 16, 2015 5:23 PM

 

To: kebanks@bmj.com

 

Cc: gill.harris@bmj.com ; lhoney@bmj.com ; gmills@bmj.com ; joflaherty@bmj.com ; sjarvis@bmj.com Subject: THE World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research

 

 Veterinary Record 2015;177:381 doi:10.1136/vr.h5454 News and Reports One health THE World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research

 

THE World Organisation for Animal Health (OIE) and the Institut Pasteur have agreed to strengthen their cooperation in the fields of animal disease and zoonosis research, education, surveillance and control, in line with the One Health concept, through a new collaborative agreement.

 

The Institut Pasteur is

 


 

Veterinary Record 2015;177:379 doi:10.1136/vr.h5446

 

News and Reports

 

Defra seeks a dialogue on animal import controls Defra is seeking ‘ideas and discussion’ as part of a review in England of the Trade in Animals and Related Products Regulations 2011. The Regulations govern veterinary border controls for live animals and products of animal origin.

 


 

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

 

please forgive me if I don’t believe you $$$

 

I remember...

 

>>>PARIS -- The World Organization for Animal Health said on Wednesday it had lowered to the safest level the official risk of six countries for mad cow disease, a move expected to open international market access for their beef exports. These countries are France, Ireland, Switzerland, the Czech Republic, Cyprus and the Lichtenstein.<<<

 

THIS move is _not_ based on science, but on corporate profits and big ag. to say now that France is a "negligible risk", would be like saying North America is a "negligible risk", which is preposterous. not based on sound science, but on greed and special interest. the only _move_ this ‘’BSE mad cow negligible risk’’ assessment makes, is a move to increase global Transmissible Spongiform Encephalopathy prion mad cow type disease, via the legal trading of the TSE prion aka mad cow type disease via the BSE MRR i.e. Minimal Risk Region policy, a policy set up to fail from the start. please, for whatever God you pray to sake, please be warned.

 

‘’AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.’’

 

IN A NUT SHELL ;

 

(Adopted by the International Committee of the OIE on 23 May 2006)

 

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

 


 

Wednesday, March 11, 2015

 

OIE and Centers for Disease Control and Prevention Reinforce Collaboration

 


 

Friday, April 4, 2014

 

China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa and Saudi Arabia still retain BSE-related closures

 


 

Thursday, May 30, 2013

 

World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease

 

U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease

 


 


 

The OIE is nothing more than a trading brokerage for the Transmissible Spongiform Encephalopathy TSE prion disease aka mad cow type disease. Frances is still in the midst of a mad cow disease outbreak with atypical BSE cases still growing. mad cow disease is so bad in France, as with the USA, they stopped testing for mad cow disease (France altogether and the USA to figures so low, you would only detect a case of mad cow disease, only by chance).

 

from the inside looking out ;

 

Quote: Maybe familirise yourself with the OIE. The primary concern is animal health of the world they are the animal version of the WHO. It is a long way down from that ivory tower but here we go, until pressured by the USA representatives a country could not export animals for 6 years after finding a BSE/BASE positive animal so under the old rules the US would not be able to export anywhere in the world for another 4 1/2 years. Who got the risk levels system put in to allow some trade - your US representatives. You guys want to change rules - OK , but you do not get special rules that only apply to the US. As i have told you before Sand h I market all my own slaughter animals and you know that, so don't do the whole holier than thow act.

 

With all due respect, it is obvious that you know little about the OIE and how it actually works. Having been to their offices in Paris and talked personally with the Head of the Animal Test Section, you would choke if you knew how many lobby groups attend that office daily. There is a steady stream of paid lobby groups that have one goal in life and that is to sway the Section Heads of each department within the OIE to suit the needs of different jurisdictions around the world, which curiously enough, also includes the USA and Canada. Anyone can go there and chat with them - providing they can provide valid cause to be let in. To say that the only goal of the OIE is animal health is actually only part of their function. They are more than that and my discussions with Dr. Diaz there has showed me that. But to blindly make a statement regarding what they do when you have no idea what they actually do is like eating the skin of the orange and not knowing what is actually under.

 

Interestingly you state that the US Government applied pressure (to the OIE) I assume and that is a great example of the lobby groups doing their job. So, at the end of the day, one can safely assume that it is the pressure applied by certain influential lobby groups that will determine a likely outcome to an apparent OIE directive. Man alive, isn't it great to live in a democracy wherein the people get to make the choices and not just some "other" interested party or group - say like........Cargill or Tyson for example?

 

So, one last question, question?

 

Who wags the tail of that dog?? And for what reason other than one that is purely associated with trade and international agreements and greed?

 

And you think it is so simply explainable.

 

end...tss

 

Subject: UPDATED WHO Guidelines include tissues from Cervidae affected with Chronic Wasting Disease (CWD)

 

snip...see full text ;

 

 Sunday, October 18, 2015

 

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

 


 

IRELAND

 

Saturday, October 3, 2015

 

Wales Welsh Government Written Statement - Isolated case of Classical Bovine spongiform encephalopathy detected in deceased bovine

 


 

Thursday, June 11, 2015

 

Ireland Department of Agriculture, Food and the Marine Identifies Suspected BSE Case

 


 

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 ***

 


 

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

 

Singeltary et al

 

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

 


 

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

 


 

Sunday, October 25, 2015

 

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

 


 

Thursday, July 30, 2015

 

Professor Lacey believes sporadic CJD itself originates from a cattle infection number of cattle farmers falling victim to Creutzfeld-Jakob Disease is much too high to be mere chance

 


 

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

 

Master Obi-Wan Kenobi, Kemosabe...THIS IS NOT GOOD GOOSE!...grasshopper...tonto...tss

 


 

BRAZIL

 

Friday, October 30, 2015

 

Brazil Agriculture minister to visit Saudi Arabia over BSE mad cow trade

 


 

WALES WELSH

 

Saturday, October 3, 2015

 

Wales Welsh Government Written Statement - Isolated case of Classical Bovine spongiform encephalopathy detected in deceased bovine

 


 

SLOVENIA

 

Wednesday, September 16, 2015

 

Ljubljana Slovenia First Mad Cow Disease Case in Eight Years Confirmed

 


 

ITALY BSE

 

Italye BSE 1994-2b 2001-48 2002-38 2003-29 2004-7 2005-8 2006-7 2007-2 2008-1 2009-2

 

e Italy: Year 2002 - Includes 2 imported cases.

 


 


 

Monday, September 07, 2015

 

ITALY REPORTING INCREASE IN CASES OF MAD COW TYPE TSE PRION DISEASE IN HUMANS CJD

 


 

Tuesday, October 20, 2015

 

FBI: Agroterrorism not likely, but very possible, Dr. Stephen Gold­smith FBI Laboratory Division, here's your sign

 

CC-Dr. Steve Goldsmith, FBI Laboratory Division

 

please note, I tried to forward this to the FBI, spoke with several folks at FBI headquarters, and they were not interested...just saying...terry

 


 

Friday, May 29, 2015

 

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

 


 

Saturday, December 12, 2015

 

NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE Prion REPORT December 14, 2015

 


 

Saturday, December 12, 2015

 

CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015

 


 

Saturday, December 12, 2015

*** CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
 
RIP MOM December 14, 1997


 
USDA Announces Preliminary Concurrence with OIE Risk Designations for BSE in 16 Countries USDA Animal and Plant Health Inspection Service sent this bulletin at 12/04/2015 11:15 AM EST

 

 Bookmark and Share

 

 USDA Announces Preliminary Concurrence with World Animal Health Organization Risk Designations for Bovine Spongiform Encephalopathy in 16 Countries

 

 December 4, 2015—The United States Department of Agriculture’s Animal and Plant Health Inspection Service (APHIS) is preliminarily concurring with the World Organization for Animal Health’s (OIE) bovine spongiform encephalopathy (BSE) risk designations for 16 countries. The OIE recognizes these regions as being of negligible risk for BSE. APHIS reviewed the information supporting the OIE’s risk designations for these regions and agrees with the OIE designations.

 

 The 16 countries are: Bulgaria, Cyprus, Czech Republic, Estonia, France, India, Korea (Republic of), Hungary, Latvia, Liechtenstein, Luxembourg, Malta, Portugal, Romania, Slovakia, and Switzerland.

 

The OIE recommendations regarding each of the above countries can be viewed online.

 

 APHIS considers all countries of the world to fall into in one of three BSE risk categories: negligible risk, controlled risk, or undetermined risk. Any region that is not classified by APHIS as presenting either negligible risk or controlled risk for BSE is considered to present an undetermined risk.

 

 Under the regulations, APHIS may classify a region for BSE in one of two ways. One way is for countries that have not received a risk classification from the World Organization for Animal Health (OIE) to request classification by APHIS. The other way is for APHIS to concur with the classification given to a country by the OIE.

 

 This notice is available for 60 days for review and comment. APHIS will consider all comments received on or before February 2, 2016. After reviewing any comments we receive, we will announce our final determination regarding the BSE classification of these countries in the Federal Register.

 


 

LMAO !!! pot calling kettle black...BSE MRR policy equals the legal trading of all strains of TSE Prion aka mad cow disease...any consumers death there from are now acceptable $$$...TSS

 

these blogs are for educational use. I do not advertise or make money from them.

 

MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget, and never let them forget...

 

Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net

Monday, December 7, 2015

STRICTLY IN CONFIDENCE WHY WE DON'T TEST ANIMAL FEED FOR ANIMAL PROTEIN BSE TSE PRION

STRICTLY IN CONFIDENCE

 

EXTRACT FROM MINUTES OF SCIENTIFIC COMMITTEE MEETING HELD ON 29 SEPTEMBER 1994

 

BSE: S33/94

 

a) Sampling of Ruminant Feeding stuffs for Ruminant Protein:

 

The voluntary sampling‘ on farms with suspected cases of BSE had commenced on 1 July 1994. The ELISA technique detected the presence of ruminant meat and bone meal to a level of 0.25% in finished feeding stuffs. MAFF had released a pre-publication copy of a paper discussing this technique which had been developed at the VI Centre Luddington. It provided detail of the use of the technique in meat and bone meal. It did not, however, discuss the extension of the assay for use in compound feeding stuffs. At the request of UKASTA, MAFF was looking at making the service commercially available in order for individual compounders to do their own testing. MAFF estimated that the charge for such testing would be £35 per sample (plus VAT).

 

It was reported that Luddington was carrying out further work in identifying potential sources of interference, from individual raw materials, which might produce a false positive result It was understood that glutens were considered to present a particular problem. During a discussion the Committee suggested that the conditioning temperatures, in different mills, might have varying effects on the breakdown of proteins in animal feeding stuffs.

 

A number of sites where cross contamination between animal proteins and other types of raw materials might occur were identified. These included not only on-farm but in-store, in the country of origin, in boats, in transport as well as different points within the feed mill. It was noted, however, that it might be counter productive to stress these varying numbers and sites.

 

Concern was expressed that the MAFF had commenced on-farm testing without necessarily thinking through the consequences for the whole of the agricultural industry. Officials were aware that one course of action open to feed compounders was to stop using meat and bone meal in the manufacture of any feeding stuff. An alternative for the industry was the establishment of ruminant feed only Such a step would only be open to those companies with more than one manufacturing site.

 

Cont'd/...2

 

94/9.29/3.1

 

b)

 

-2-

 

A decision by the industry as a whole to stop using meat and bone meal would have cost implications for the whole livestock industry. Not only would there be poorer returns to beef producers but also higher raw material costs for compounders when producing pig and poultry feeding stuffs. There would also be the problem of disposing of the unwanted animal by-products. Thus, it was agreed that whatever the actual consequences the effect o:n the livestock industry as a whole would be very damaging.

 

Proposed Survey of Past a.nd Present Practices in Members Feed Mills:

 

A copy of the draft questionnaire was circulated to Committee members “Strictly in Confidence". This was designed to investigate the likelihood that feed produced after the introduction of the ruminant feed ban could have become contaminated with ruminant derived protein and whether the likelihood of contamination had changed over time. In discussing the contents, UKASTA had not given any indication, on behalf of members, that they wanted them to complete the questionnaire when finalised. MAFF had also been made fully aware of UKASTA's concern that information submitted in response to the questionnaire by individual companies might, at some future time, be subpoenaed by a Court. This would be in any case taken against the company by a farmer seeking compensation for BSE in his herd.

 

The Committee was advised that a member company was still in debate over a case concerning the Fowl Pest outbreak in 1984. Lawyers acting for poultry producers had. submitted subpoenas for relevant Ministry documents. MAFF Legal Department was looking at the papers and aimed to resist the subpoena. However, the outcome of this action would not be known until March 1995. At the very least, it was considered that compounders should not: complete the questionnaire until the outcome of the Fowl Pest discussions were known. It was also reported that another company had been recommended, by its legal advisors, not to complete the questionnaire.

 

At a scientific level, it was noted that the aim of the CVL was to explain why BABs had occurred. Unfortunately, in the investigations it was necessary to identify the name and address of individual mills on the questionnaire in order to reconcile information on BABs regarding feeding practices on farm. It would not be possible for questionnaires to be sent to the CVL via UKASTA on an anonymous basis. UKASTA was seeking guidance from the Association's solicitors on what powers MAFF might have to require completion of the questionnaire.

 

It was suggested that whilst the CVL was finalising details of the questionnaire UKASTA should co-operate. Thus members were asked to send to the Secretariat their comments on the contents of the questionnaire by mid-November. Views were particularly required on which questions were difficult and/ or impossible to answer both because they were

 

Cont'd/...3 94/9.29/3.2

 

-3-

 

impractical as well as being able to put individual companies in a vulnerable position. These were to be passed on to the CVL with a request for amendments and/ or detailed responses in time for the Committee to discuss at the December meeting. Members were asked to discuss the questionnaire with as few people as possible because of the sensitive nature of this subject.

 

Members were also asked to keep the Secretariat informed of the nature of any enquiries which MAFF officials might address to them. It was also noted, by one member company who no longer used meat and bone meal, that since taking such action they had not received any queries from MAFF.

 

C) Recent Legislation:

 

The MAFF was implementing the two EU Decisions agreed in May. The ban on the use of mammalian meat and bone meal in ruminant feedingstuffs was to be incorporated into the BSE Order. At the same time the SBO ban was to be extended to cover the thymus and intestines of calves less than six months of age.

 

The European legislation on the rendering industry introduced a processing time/ temperature combination based on the results of rendering trials which had achieved an 80-fold diminution of the BSE agent. The legislation was not due to be brought into operation until the end of 1994. It was, however, hoped that UK rendering plants could have their processes validated and thus be in compliance with the new legislation by the end of October. Although it was not possible to prove zero infectivity, MAFF considered that adherence to the new standards would be a huge step forward in the control of BSE.

 

The Ministry was also reviewing the SBO legislation in order to make it more straightforward an.d simple to operate. The Committee also noted that, because of the nature of the material concerned, it would be extremely difficult to enforce the legislation. Concern was expressed, therefore, that the Ministry might just be introducing controls on paper. Effective auditing of the legislation should be introduced; for example by weighing the amount of SBO's collected and comparing this against the number of animals slaughtered.

 

In the light of all these concerns, the Committee considered that an easy reaction would be for the feed industry to stop using meat and bone meal in the manufacture of any animal feeding stuff. However, whereas this would be relatively painless, if somewhat expensive, for the feed industry, it would have serious repercussions throughout the whole of the livestock industry. It would also beg the question as to why it was safe for humans to eat meat whilst the by-products of the butchery trade that we use to produce meat and bone meal were unsatisfactory for animals.

 

Cont'd/...4

 

94/9.29/3.3

 

-4-

 

d) Origins of BSE:

 

A transcript of the Radio 4 interview with Mr. Keith Meldrum, Chief Veterinary Officer, held on 22 September was circulated. This raised the possibility of BSE being of bovine as opposed to ovine origin. Clarification had, therefore, been sought from the CVL. The response was that it was not possible to dismiss the possibility that BSE was bovine in origin. However, it was more difficult to support such a theory given current knowledge whereby the BSE epidemic had seen a sudden increase in numbers in the mid 1980's. It was thus still considered that the epidemic was explained by :-

 

- High level of sheep numbers in the UK;

 

- A change in the rendering practices in the late 1970's which permitted infected ovine material to survive the production process;

 

- The recycling of bovine material in the cattle population.

 

For BSE to be solely of bovine origin there would have had to have been a high prevalence of infected animals prior to the mid—1980‘s and this was not seen. It was thus possible that there was an element of politics in the comments made by Mr. Meldrum and it was probably no coincidence that a report of possible BSE cases in northern Germany had emerged at about the same time.

 

Meeting with Minister:

 

The Committee was advised that if necessary the Association would request

 

a meeting with the Minister to outline members‘ concerns regarding BSE and associated matters.

 

94/9.29/3.4

 


 

TEXAS One sorghum DDGS sample out of 168 DG samples was contaminated with bovine spongiform encephalopathy, but the transmission route of the bovine spongiform encephalopathy agent could not be clearly defined.

 

J Food Prot. 2015 Oct;78(10):1861-9. doi: 10.4315/0362-028X.JFP-15-157.

 

Evaluation of Selected Nutrients and Contaminants in Distillers Grains from Ethanol Production in Texas.

 

Lee KM1, Herrman TJ2. Author information 1Office of the Texas State Chemist, Texas A&M AgriLife Research, Texas A&M University System, College Station, Texas 77841, USA. kml@otsc.tamu.edu. 2Office of the Texas State Chemist, Texas A&M AgriLife Research, Texas A&M University System, College Station, Texas 77841, USA.

 

Abstract

 

This study evaluated distillers grain (DG) by-products produced in different ethanol plants and supplemented in animal diets in Texas, based on samples analyzed from 2008 to 2014. The samples were assessed for concentration, occurrence, and prevalence of selected nutrients and contaminants. Protein and sulfur contents of DG were largely different between corn and sorghum by-products as well as wet distillers grain with solubles and dry distillers grain with solubles (DDGS), indicating a significant effect of grain feedstock and dry-grind process stream on DG composition and quality. Salmonella was isolated in 4 DDGS samples out of a total of 157 DG samples, a percentage (2.5%) that is much lower than the percentage of Salmonella-positive samples found in other feed samples analyzed during the same period. A small amount of virginiamycin residue was found in 24 corn DDGS, 1 corn wet distillers grain with solubles, and 2 sorghum DDGS samples out of 242 samples in total. One sorghum DDGS sample out of 168 DG samples was contaminated with bovine spongiform encephalopathy, but the transmission route of the bovine spongiform encephalopathy agent could not be clearly defined. The concentrations of aflatoxin and fumonisin DG by-products averaged 3.4 μg/kg and 0.7 mg/kg, respectively. Among contaminated corn DG samples, five DDGS samples for aflatoxin contained a higher concentration than the U.S. Food and Drug Administration action level for use in animal feed, whereas no sample for fumonisin was found above the action level. The study results raised some important issues associated with the quality and use of DG by-products, suggesting several approaches and strategies for their effective and safe use as a feed ingredient to promote animal and human health and welfare.

 

PMID: 26408135 [PubMed - in process]

 


 

Sunday, September 27, 2015

 

TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES

 

 please note, the author of this study contacted me ;

 

 corrected to

 

 "One sorghum DDGS out of 168 DG samples was contaminated with animal protein prohibited for use in ruminant feed and was channeled to poultry feed."

 

 We requested the journal editor to correct some errors and the relevant statements, or to withdraw the article from the journal.

 


 

 Monday, October 26, 2015

 

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

 


 

Saturday, January 31, 2015

 

European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

 


 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations 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.

 

======

 

31 Jan 2015 at 20:14 GMT

 

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

 

31 Jan 2015 at 20:14 GMT

 


 

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...

 


 

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

 

Posted by flounder on 03 Jul 2015 at 16:53 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

 


 

P.97: 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

 

Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State University; Ames, IA USA

 

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 D 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 2 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, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.

 


 

From: Terry S. Singeltary Sr.

 

Sent: Tuesday, December 01, 2015 5:05 PM

 

To: Terry Singeltary Sr.

 

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

 

*** 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 from Terry Singeltary This is a Comment on the Animal and Plant Health Inspection Service (APHIS) Proposed Rule: Scrapie in Sheep and Goats

 

For related information, Open Docket Folder Docket folder icon

 

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

 

Show agency attachment(s) AttachmentsView All (0)

 

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

 

Comment View document: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.

 


 

please see file attachment for full submission and recent science and my deep concerns on the TSE Prion disease... No documents available. AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:

 


 

***********OCTOBER 2015*************

 

*** 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.

 

P.108: Successful oral challenge of adult cattle with classical BSE

 

Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada

 

Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, 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. Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.

 


 

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...

 

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

 


 

***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.

 

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

 


 


 

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

 

***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.

 

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

 

It also appears to Mr MacLean that Mr Bradley’s answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight: particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the “attack rate” experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective

 

2

 

dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.

 

It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

it is clear that the designing scientists must have also shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

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. <<<

 


 

small amount of leftover contaminated feed’ ...LOL...maybe large amount in USA. see ;

 

Monday, November 30, 2015

 

*** Report on the Investigation of the Nineteenth Case of Bovine Spongiform Encephalopathy (BSE) in Canada November 2015 ***

 


 

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

 


 

10 years post mad cow feed ban August 1997

 

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

 

Date: March 21, 2007 at 2:27 pm PST

 

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

 

PRODUCT

 

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

 

CODE

 

Cattle feed delivered between 01/12/2007 and 01/26/2007

 

RECALLING FIRM/MANUFACTURER

 

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

 

Firm initiated recall is ongoing.

 

REASON

 

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

 

VOLUME OF PRODUCT IN COMMERCE

 

42,090 lbs.

 

DISTRIBUTION

 

WI

 

___________________________________

 

PRODUCT

 

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

 

CODE

 

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

 

RECALLING FIRM/MANUFACTURER

 

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

 

REASON

 

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

 

VOLUME OF PRODUCT IN COMMERCE

 

9,997,976 lbs.

 

DISTRIBUTION

 

ID and NV

 

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

 


 

16 years post mad cow feed ban August 1997

 

2013

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

17 years post mad cow feed ban August 1997

 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

Monday, October 26, 2015

 

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

 


 

Sunday, June 14, 2015

 

Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion

 


 

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. ...

 


 

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.

 


 

***atypical spontaneous BSE in France LOL***

 

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

 


 

Sunday, October 18, 2015

 

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

 


 

 

Terry S. Singeltary Sr.