Tuesday, July 26, 2016

Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016

Subject: Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016

 

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

 

Title: A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation

 

Authors

 

item Moore, S - item West Greenlee, M - item Smith, Jodi item Vrentas, Catherine item Nicholson, Eric item Greenlee, Justin

 

Submitted to: Frontiers in Veterinary Science Publication Type: Peer Reviewed Journal Publication Acceptance Date: April 15, 2016 Publication Date: N/A

 

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. Work by other research groups suggests that the stability of the distinguishing features of atypical BSE cases (phenotypical stability) can change to closely resemble classical BSE after experimental passage implicating atypical BSE as a possible origin of classical BSE. Interestingly, one case of H-type BSE in the US was associated with an inherited mutation in the prion protein gene referred to as E211K. The purpose of this work was to compare wild type and cattle with the E211K mutation after experimental inoculation with either classical BSE or H-BSE from the original E211K case. This study demonstrates that the disease features of E211K BSE-H remain stable when transmitted to cattle without the K211 polymorphism. In addition, passage of classical BSE to cattle with the K211 polymorphism results in disease with features consistent with classical BSE and not a switch to atypical BSE-H as a result of the K211 polymorphism. As the origin of classical, feedborne BSE remains unknown and low numbers of atypical BSE are diagnosed each year, 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: In 2006, a case of H-type bovine spongiform encephalopathy (BSE-H) was diagnosed in a cow that was associated with a heritable polymorphism in the bovine prion protein gene (PRNP) resulting in a lysine for glutamine amino acid substitution at codon 211 (called E211K) of the prion protein. Although the prevalence of this polymorphism is low, cattle carrying the K211 allele may be predisposed to rapid onset of BSE-H when exposed or to the potential development of a genetic BSE. This study was conducted to better understand the relationship between the K211 polymorphism and its effect on BSE phenotype. BSE-H from the US 2006 case was inoculated intracranially (IC) in one PRNP wild type (EE211) calf and one EK211 calf. In addition, one wild type calf and one EK211 calf were inoculated IC with brain homogenate from a US 2003 classical BSE case. All cattle developed clinical disease. The survival times of the E211K BSE-H inoculated EK211 calf (10 months) was shorter than the wild type calf (18 months). This genotype effect was not observed in classical BSE inoculated cattle (both 26 months). Significant changes in retinal function were observed in H-type BSE challenged cattle only. Cattle challenged with the same inoculum showed similar severity and neuroanatomical distribution of vacuolation and disease-associated prion protein deposition in the brain, though differences in neuropathology were observed between E211K BSE-H and classical BSE inoculated animals. Western blot results for brain tissue from challenged animals were consistent with the inoculum strains. This study demonstrates that the phenotype of E211K BSE-H remains stable when transmitted to cattle without the K211 polymorphism, and exhibits a number of features that differ from classical BSE in both wild type and heterozygous EK211 animals.

 


 

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

 

2015 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 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. Post-mortem examination of the animals inoculated with atypical scrapie has been initiated and laboratory analysis of the tissues is ongoing. 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 with a manuscript reporting these results was published (2012), and additional laboratory comparisons of genetic BSE to atypical and classical BSE are ongoing. 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, beyond those applied to the tissues at the time the tissues were archived, 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. Changes in retinal function in cattle can be used to identify different types of bovine spongiform encephalopathy (BSE). BSE belongs to a group of fatal, transmissible protein misfolding diseases known as transmissible spongiform encephalopathies (TSEs). Like other protein misfolding diseases including Parkinson's disease and Alzheimer's disease, TSEs are generally not diagnosed until the onset of disease after the appearance of unequivocal clinical signs. As such, identification of the earliest clinical signs of disease may facilitate diagnosis. The retina is the most accessible part of the central nervous system. ARS scientist in Ames IA described antemortem changes in retinal function and thickness that are detectable in BSE inoculated animals up to 11 months prior to the appearance of any other signs of clinical disease. Differences in the severity of these clinical signs reflect the amount of PrPSc accumulation in the retina and the resulting inflammatory response of the tissue. These results are the earliest reported clinical signs associated with TSE infection and provide a basis for understanding the pathology and evaluating therapeutic interventions. Further, this work shows that High-type BSE and classical BSE can be differentiated by eye examination alone, the first time BSE strains have been differentiable in a live animal.

 

2. Sheep genetics influences the susceptibility of sheep to scrapie. Sheep scrapie is a transmissible spongiform encephalopathy that can be transmitted between affected animals resulting in significant economic losses in affected flocks. The prion protein gene (PRNP) profoundly influences the susceptibility of sheep to the scrapie agent and the tissue levels and distribution of PrPSc in affected sheep. In this study, sheep of 3 different prion genetic types (denoted VRQ/VRQ, VRQ/ARR and ARQ/ARR) were inoculated and subsequently euthanized upon onset of disease. Disease aspects were uniform across genotypes and consistent with manifestations of classical scrapie. Mean survival time differences were associated with the genetic type such that VRQ/VRQ sheep survived 18 months, whereas VRQ/ARR and ARQ/ARR sheep survived 60 and 56 months, respectively. Microscopic evaluation revealed similar accumulations in central nervous system tissues regardless of host genetic type. PrPSc in lymphoid tissue was consistently abundant in VRQ/VRQ, present but confined to tonsil or retropharyngeal lymph node in 4/5 VRQ/ARR, and totally absent in ARQ/ARR sheep. The results of this study demonstrate the susceptibility of sheep with the ARQ/ARR genotype to scrapie by the intracranial inoculation route with PrPSc accumulation in CNS tissues, but prolonged incubation times and lack of PrPSc in lymphoid tissue. These results are important for science based policy with regard to testing of sheep for scrapie where some live animal testing is conducted using lymphoid tissues which would not detect scrapie in some specific genetic types which could limit the national scrapie eradication program.

 

Review Publications Greenlee J.J. 2014. The prion diseases of animals. In: McManus, L.M., Mitchell, R.N., editors. Pathobiology of Human Disease. San Diego: Elsevier. p. 1124-1133. Greenlee, J.J., Kunkle, R.A., Richt, J.A., Nicholson, E.M., Hamir, A.N. 2014. Lack of prion accumulation in lymphoid tissues of PRNP ARQ/ARR sheep intracranially inoculated with the agent of scrapie. PLoS One. 9(9):e108029. Greenlee, J.J., West Greenlee, M.,H. 2015. The transmissible spongiform encephalopathies of livestock. ILAR Journal. 56(1):7-25. Munoz-Gutierrez, J.F., Schneider, D.A., Baszler, T.V., Dinkel, K.D., Greenlee, J.J., Nicholson, E.M., Stanton, J.J. 2015. hTERT-immortalized ovine microglia propagate natural scrapie isolates. Virus Research. 198:35-43. Nicholson, E.M. 2015. Detection of the disease-associated form of the prion protein in biological samples. Bioanalysis. 7(2):253-261. West Greenlee, M.H., Smith, J.D., Platt, E.M., Juarez, J.R., Timms, L.L, Greenlee, J.J. 2015. Changes in retinal function and morphology are early clinical signs of disease in cattle with bovine spongiform encephalopathy. PLoS ONE. 10(3):e0119431. 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.

 


 

Emergence of a novel bovine spongiform encephalopathy (BSE) prion from an atypical H-type BSE

 

Kentaro Masujin , Hiroyuki Okada , Kohtaro Miyazawa , Yuichi Matsuura , Morikazu Imamura , Yoshifumi Iwamaru , Yuichi Murayama & Takashi Yokoyama

 

Scientific Reports 6, Article number: 22753 (2016) doi:10.1038/srep22753 Download Citation Infectious-disease diagnostics Microbiology

 

Received:23 November 2015Accepted:19 February 2016Published online:07 March 2016

 

Abstract

 

The H-type of atypical bovine spongiform encephalopathy (H-BSE) was serially passaged in bovinized transgenic (TgBoPrP) mice. At the fourth passage, most challenged mice showed a typical H-BSE phenotype with incubation periods of 223 ± 7.8 days. However, a different phenotype of BSE prion with shorter incubation periods of 109 ± 4 days emerged in a minor subset of the inoculated mice. The latter showed distinct clinical signs, brain pathology, and abnormal prion protein profiles as compared to H-BSE and other known BSE strains in mice. This novel prion was transmitted intracerebrally to cattle, with incubation periods of 14.8 ± 1.5 months, with phenotypes that differed from those of other bovine prion strains. These data suggest that intraspecies transmission of H-BSE in cattle allows the emergence of a novel BSE strain. Therefore, the continuation of feed ban programs may be necessary to exclude the recycling of H-BSE prions, which appear to arise spontaneously, in livestock. Such measures should help to reduce the risks from both novel and known strains of BSE.

 

Introduction

 

Prions cause transmissible spongiform encephalopathies (TSEs), which are characterized by a spongiform change in the central nervous system and the accumulation of an abnormal prion protein (PrPSc). PrPSc is a disease-associated isoform of the host-encoded prion protein1, and the conversion of the normal isoform (PrPC) to PrPSc is thought represent a central event in prion pathogenesis. PrPSc has been recognized as the major component of prions2, and variations in PrPSc are associated with different prion strains that, in turn, cause distinct disease phenotypes3.

 

Bovine spongiform encephalopathy (BSE) is a TSE of cattle. Most BSE cases show a unique phenotype that is thought to be caused by a single prion strain4. However, other atypical neuropathological and molecular phenotypes of BSEs (atypical BSEs) have been identified in aged animals5,6. Atypical BSEs have been classified into two groups, L-BSE and H-BSE, based on their biological and biochemical features5,6, which differ from those of classical BSE (C-BSE).

 

The worldwide occurrence of BSE is declining, primarily because of effective feed ban programs6. The emergence of atypical BSE cases has raised questions as to whether additional and/or modified control measures might be needed. Thus, characterization of atypical BSE prions is necessary for risk evaluation.

 

H-BSE was first reported in France7, and has been subsequently detected in several European countries and North America5,6. In one of two H-BSE cases detected in the U.S., a prion protein (PrP) amino-acid substitution that is associated with familial Creutzfeldt–Jakob disease in humans has been reported. This suggested the possibility that H-BSE might occur spontaneously or sporadically8. Regardless of its origin, previous studies have shown that H-BSE is transmissible to cattle9,10,11,12, as well as to wild type13,14, bovinized, and ovinized PrP transgenic mice that express murine, bovine, or ovine PrPC, respectively15,16,17. Those studies also revealed different characteristics of H-BSE relative to C-BSE and L-BSE.

 

Serial passages of H-BSE in wild type18,19 and bovinized PrP transgenic mice20 can lead to the emergence of a C-BSE-like phenotype. This suggests that H-BSE-affected cattle harbor heterogeneous prions and that structural variants of H-BSE might generate a C-BSE-like phenotype. This, in turn, raises the possibility that C-BSE originated from H-BSE. To attempt to clarify the origin of C-BSE, we serially passaged H-BSE in bovinized PrP transgenic (TgBoPrP) mice. In contrast to previous studies, we did not detect C-BSE-like prions during serial passages. However, a novel BSE prion—different from C-BSE, L-BSE, and H-BSE prions—was detected in a subset of inoculated mice. When this novel prion was inoculated intracerebrally into cattle, a novel BSE phenotype was confirmed. This study suggests that a novel BSE emerges during intraspecies transmission of H-BSE in cattle.

 

 Results

 

Serial transmission of H-BSE in TgBoPrP mice

 

The results of serial transmission of the H-BSE isolate in TgBoPrP mice are shown in Table 1. All the H-BSE challenged mice developed progressive neurological disease with the incubation periods of 320.1 ± 12.2 days at primary passage. H-BSE-affected animals showed a distinctive clinical sign, namely, constant chewing of the bedding, as reported previously16. The incubation periods of the second and third passages were 226.9 ± 4.2 and 215.6 ± 5.0 days, respectively (Table 1)16. No clear differences were observed in their clinical signs, the banding pattern of PrPSc, and histopathological features from the primary to third passage mice. At the fourth passage, mice from a single experimental group (#3), out of eight experiments, showed shorter incubation periods (108.8 ± 4.0 days) than the other groups. This group was challenged with brain homogenates of a mouse with 221-day incubation period. Group #3 animals showed weight loss, but no constant chewing of the bedding. This short incubation-type of BSE was designed BSE-SW (short incubation with weight loss) strain. BSE-SW was transmitted to TgBoPrP mice with 97.3 ± 3.7 day incubation periods, and their clinical signs were identical to those of mice in the experimental group #3. The other mice in the fourth passage groups showed the symptomatic chewing of the bedding, and their incubation periods were 223.3 ± 7.8 days (Table 1).

 

SNIP...

 

Molecular features of PrPcore of BSE-SW-affected cattle

 

Western blot analysis detected PrPSc from the obex tissue of the challenged cattle. The molecular features of PrPcore of BSE-SW-affected cattle were distinctly different from C-BSE, L-BSE, and H-BSE (Fig. 5). The molecular mass of PrPcore #1 of BSE-SW, as determined by mAb 6H4, was lower than H-BSE and similar to C-BSE (Fig. 5b). MAb P4 did not detect PrPcore of BSE-SW (Fig. 5a). PrPcore #2 was also observed in BSE-SW (Fig. 5c,d). These results revealed that the biochemical properties of BSE-SW have indeed been transmitted to cattle.

 

SNIP...

 

Discussion

 

Our previous reports have revealed the usefulness of TgBoPrP mice for characterizing BSE prions16,21,22. In this study, a novel BSE, BSE-SW, was detected using this mouse model. The incubation periods of H-BSE, L-BSE, and C-BSE prions in the TgBoPrP mice were approximately 215 days, 150 days, and 190 days, respectively16,21,22. The BSE-SW prion showed the shortest incubation period (approximately 90 days) among the known BSE prions. We have previously performed several transmission experiments of sheep scrapie to TgBoPrP mice, but their incubation periods were over 170 days23, and we have not observed any prions with ~90-day incubation periods in these mice. In addition, the biochemical and biological properties of PrPSc from BSE-SW were clearly different from C-BSE, L-BSE, H-BSE, and sheep scrapie (data not shown). PrPSc of BSE-SW has some similarity to H-BSE on the account of the presence of truncated 12-kDa fragments (PrPcore #2). Fig. 6 shows the putative PK digestion site of PrPSc from BSE-SW, as assessed by immunoreactivity with mAbs P4, 6H4, and SAF84. These results argue against the possibility that the BSE-SW prion resulted from a contamination of other laboratory prion strains.

 

SNIP...

 

It is known that sheep scrapie comprises different prion strains24,25, and some affected sheep harbor these mixed scrapie prion strains3. Numerous scrapie strains had emerged in the course of several passage histories26. We have also previously isolated distinct scrapie strains from the brain of a scrapie-affected sheep after primary passage in wild type mice27. The different scrapie prion strains appeared after primary passage in sheep scrapie cases, which was considered to be due to prion strain selection. For H-BSE prions, French and Polish cases were reported, which transformed into a C-BSE-like phenotype during mouse passages18,19,20, revealing their potential heterogeneity. However, the BSE-SW prions described herein appear to have emerged by a different manner than our previous scrapie case27. The average incubation period of H-BSE in TgBoPrP mice was 320 days at first passage, and then shortened to 227 days and 216 days at secondary and third passages, respectively. Based on this observation, H-BSE prions were adapted to TgBoPrP mice at second passage. By the third passage, no multiple prion strains in the H-BSE material were evident. BSE-SW prion with a shorter incubation period emerged after H-BSE has adapted to TgBoPrP mice. The results of this study suggest that BSE-SW emerged through a conformational rearrangement. Alternatively, the BSE-SW prion was only present in a very small titer in H-BSE and required several passages in sensitive animals to emerge after selection from a mixture of preexisting prion strains. The Canadian H-BSE sample that was used in this study was also used to inoculate wild type mice, but we did not observe the emergence of a C-BSE-like phenotype in those circumstances (unpublished data). The underlying mechanisms of the emergence of new prion strains are important to elucidate prion heterogeneity. This novel BSE strain has never been observed in field BSE cases, but our experiments reveal the potential risk associated with H-BSE.

 

It has been suggested that different conformations of PrPSc are involved in the prion strain diversity28, and that rearrangement of PrPSc from a uniform conformation causes the emergence of new host-adapted PrPSc 3. PrPSc of BSE-SW exhibited different conformational stability from H-BSE. It is also known that strain “mutation or transformation” may occur upon intraspecies transmission, where the PrP amino acid sequences of the host and the donor are identical3. These finding are consistent with the conclusion that PrPSc of BSE-SW has a different conformation than H-BSE.

 

Furthermore, our new strain was successfully transmitted to cattle. Standard diagnostic testing for BSE confirmed the presence of spongiform changes associated with PrPSc accumulation in the obex, and the challenged cattle fulfilled BSE criteria (Figs 4 and 5). The disease phenotype and features of PrPSc, different from the known types of BSE, indicated that this prion could cause a novel type of atypical BSE. The shorter incubation periods in cattle were consistent with the relative incubation periods in TgBoPrP mice, and indicate high virulence of this novel prion. Further analysis of diseased cattle is necessary to clarify its characteristics. Such studies could help to elucidate the mechanisms of conformational change in PrPSc, which lead to the propagation of new prion strains.

 

The ban on meat-and-bone meal in livestock feed has contributed to the decline in C-BSE occurrences6. Recently, easing of the BSE-related regulations and control measures has been discussed. The origin of atypical BSE remains unknown, but it has been proposed to be spontaneous or sporadic29. H-BSE has been reported to transform into a C-BSE-like phenotype during animal passages18,19,20. Furthermore, we have shown here that the sequential transmission of H-BSE in TgBoPrP mice, i.e., to a homologous bovine PrP context, generated a novel type of BSE. Considering these observations, a continuous feed ban program may be necessary even after C-BSE is eradicated. Prohibiting the recycling of spontaneously occurring H-BSE prions in cattle should help to prevent both re-emerging and emerging types of BSEs.

 


 

Monday, May 09, 2016

 

A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation

 


 

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?

 


 

***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

 


 

Tuesday, April 19, 2016

 

Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission

 


 


 


 

SCIENTIFIC REPORT OF EFSA

 

Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE1

 

European Food Safety Authority2,3

 

European Food Safety Authority (EFSA), Parma, Italy

 

ABSTRACT

 

Information on the pathogenesis and tissue distribution of Atypical Bovine Spongiform Encephalopathy (BSE) in cattle through the study of field cases and experimental transmission studies is lacking. The latter are limited to transmission of Atypical BSE through intracerebral (i.c.) inoculation of cattle. All data currently available relate to the presence or absence of PrPSc, but do not quantify relative amounts of PrPSc or levels of infectivity. A laboratory protocol for further studies is recommended, to allow the assessment of the relative infectious titre, PrPSc accumulation and prion seeding activity in the tissues of cattle that developed H-BSE or L-BSE (using posterior brainstem as a reference). Tissues to be covered by those studies are categorised in three priorities, based on their inclusion in the list of specific risk material in cattle, on the presence of infectivity, or PrPSc presence, demonstrated in Atypical BSEs or other Transmissible Spongiform Encephalopathies (TSEs) in ruminants, and on the importance in terms of input into the food chain in the EU. The protocol provides details in terms of the minimum number of animals to be tested, processing and preparation of tissues, and methods to be used to identify abnormal PrP and quantify infectivity, also depending on the expected level of infectivity and amount of tissue available for analysis. It is recommended that, through the implementation of the protocol, information should also be obtained on the performance of currently validated rapid tests for TSE active surveillance in cattle/bioassay for detecting H-BSE and L-BSE agents.

 

© European Food Safety Authority, 2014

 

KEY WORDS

 

Atypical BSE, cattle, H-BSE, L-BSE, laboratory protocol, prion

 

1 On request from the European Commission, Question No EFSA-Q-2013-01015, approved on 11 July 2014.

 

2 Correspondence: biohaz@efsa.europa.eu

 

3 Acknowledgement: EFSA wishes to thank the members of the Working Group on Atypical BSE study protocol: Olivier Andreoletti, Anne Balkema-Buschmann, Vincent Béringue, Marion Simmons and Juan-Maria Torres for the preparatory work on this scientific output, the members of the EFSA Panel on Biological Hazards (BIOHAZ) for their endorsement of the scientific output, and EFSA staff members: Winy Messens and Pietro Stella for the support provided to this scientific output.

 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 2

 

SUMMARY

 

Following a request from the European Commission, EFSA was asked to provide scientific and technical assistance on a protocol for further laboratory investigations into the distribution of infectivity of Atypical Bovine Spongiform Encephalopathy (BSE).

 

The European Union Reference Laboratory (EURL) for Transmissible Spongifom Encephalopathies (TSEs) conducted experiments (referred to as the EURL study) that resulted in the collection and storage of reference material originating from cattle experimentally infected with Atypical BSE (H-BSE and L-BSE). With the intention to generate relevant data that could inform further policy options regarding BSE, in particular as regards rules on specified risk material (SRM), DG SANCO wished to explore the possibility to submit these tissue samples to further investigations. EFSA was therefore asked to propose a laboratory protocol to perform new studies aimed at investigating the presence, distribution and relative level of infectivity of Atypical BSE (H-BSE and L-BSE). EFSA was also expected to reflect on whether the tissues available from the EURL study are sufficient for the purpose and/or suggest that investigations on other tissues might be possibly needed.

 

Data relating to the prevalence and geographical distribution of Atypical BSE in the European Union (EU) are incomplete and subject to variation owing to the ongoing retrospective typing of BSE cases. So far, 80 cases of Atypical BSE have been reported by EU Member States from 2001 to 2014. All Atypical BSE cases have been detected by active surveillance, typically in animals over eight years of age, with a similar number of cases detected each year.

 

This report provides an overview of the biological material collected from field cases of Atypical BSE and transmission studies, both in the framework of the EURL study and additional published scientific studies. It was concluded that information on the pathogenesis and tissue distribution of Atypical BSE in cattle through the study of field cases and experimental transmission studies is lacking. The latter are limited to transmission of Atypical BSE through intracerebral (i.c.) inoculation of cattle. Where data exist from both field cases and experimental animals (i.e. for L-BSE only), there is good agreement of the data with regard to abnormal PrP distribution. There are no data for field case H-BSE. All data currently available relate to the presence or absence of PrPSc, but do not quantify relative amounts of PrPSc or levels of infectivity.

 

Approaches to quantify Atypical BSE prions in cattle tissues are described and reviewed, including bioassay and in vitro methods.

 

A laboratory protocol for further studies is recommended. Its application would provide elements allowing the assessment of the relative infectious titre, PrPSc accumulation and prion seeding activity in the tissues of cattle that developed H-BSE or L-BSE (using posterior brainstem as a reference). Tissues to be covered by those studies were categorised in three priorities, based on their inclusion in the cattle SRM list, on the presence of infectivity, or PrPSc presence, demonstrated in Atypical BSEs or other TSEs in ruminants, and on the importance in terms of input into the food chain in the EU. The protocol provides details in terms of the minimum number of animals to be tested, processing and preparation of tissues, and methods to be used to identify abnormal PrP and quantify infectivity, also depending on the expected level of infectivity and amount of tissue available for analysis.

 

Applying the protocol only to the tissues obtained through the EURL study would provide information on some but not all the tissues from the cattle SRM list. It would also provide information on some additional tissues not included in the cattle SRM list, but relevant for the food chain. Material from other studies could be used to augment the range of SRM and non-SRM tissues available. It is acknowledged that there is no identified source able to provide all the samples necessary to assess infectivity in tissues belonging to the full cattle SRM list in H- and L-BSE-infected animals, and therefore, to complete this objective, new inoculation experiments with H- and L-BSE agents in cattle would have to be considered. Recommendations on general principles for such new experiments are provided.

 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 3

 

In accordance with former EFSA recommendations, it is recommended that, through the implementation of the protocol, information should also be obtained on the performance of currently validated rapid tests for TSE active surveillance in cattle/bioassay for detecting H-BSE and L-BSE agents.

 

snip...

 


 


 


 

Monday, June 20, 2016

 

Specified Risk Materials SRMs BSE TSE Prion Program

 


 

>>> Both of the atypical BSE subtypes are believed to occur spontaneously,<<<

 

LOL!

 

SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY

 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 

Atypical BSE...Spontaneous...LOL

 

BSE identified in France

 

​Posted May 2, 2016

 

A cow in northern France has been confirmed to have bovine spongiform encephalopathy, according to the World Organisation for Animal Health (OIE).

 

The cow had developed partial paralysis and was euthanized March 1, a March 25 OIE report states.

 

BSE is a fatal neurologic prion disease with a typical incubation period of four to five years. The cow in France was almost 5 years old.

 

The affected cow had the classic form of BSE, which is most often associated with feed containing neurologic tissue from infected animals. It is distinct from atypical BSE, which may develop spontaneously, according to information from the U.S. Centers for Disease Control and Prevention.

 

Investigators were trying to identify the source of infection and other animals at risk for BSE at the time the report was published.

 


 

The affected bovine, a Salers female born on April, 8th 2011, showed paresis and was euthanized on March, 1st 2016. Samples made on March, 4th 2016 during rendering were analyzed at the Department Laboratory of La Somme. The rapid test proved positive on March, 8th 2016 and the samples were then sent for further analysis to the National Reference Laboratory, ANSES, which confirmed a case of classical BSE on March, 21st 2016. The European Union Reference Laboratory confirmed those results on the basis of documentation on March, 23rd 2016.

 


 

>>> It is distinct from atypical BSE, which may develop spontaneously, according to information from the U.S. Centers for Disease Control and Prevention.

 

THIS IS A MYTH $$$

 

***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

 


 

Thursday, March 24, 2016

 

FRANCE CONFIRMS BOVINE SPONGIFORM ENCEPHALOPATHY BSE MAD COW (ESB) chez une vache dans les Ardennes

 


 

***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 $$$

 

If you Compare France to other Countries with atypical BSE, in my opinion, you cannot explain this with ‘spontaneous’.

 

Table 1: Number of Atypical BSE cases reported by EU Member States in the period 2001–2014 by country and by type (L- and H-BSE) (extracted from EU BSE databases on 1 July 2014). By 2015, these data might be more comprehensive following a request from the European Commission to Member States for re-testing and retrospective classification of all positive bovine isolates in the EU in the years 2003–2009

 

BSE type

 

Country 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013(a) 2014(a) Total

 

H-BSE Austria 1 1

 

France(b) 1 2 3 1 2 2 2 2 15

 

Germany 1 1 2

 

Ireland 1 1 2 1 5

 

The Netherlands 1 1

 

Poland 1 1 2

 

Portugal 1 1

 

Spain 1 1 2

 

Sweden 1 1

 

United Kingdom 1 1 1 1 1 5

 

Total 2 3 3 1 1 2 2 2 4 4 5 1 4 1 35

 

L-BSE Austria 1 1 2

 

Denmark 1 1

 

France(b) 1 1 1 1 2 1 3 2 1 1 14

 

Germany 1 1 2

 

Italy 1 1 1 1 1 5

 

The Netherlands 1 1 1 3

 

Poland 1 2 2 1 2 1 2 1 12

 

Spain 2 2

 

United Kingdom 1 1 1 1 4

 

Total 0 5 3 4 3 3 6 3 3 4 3 6 1 1 45

 

Total Atypical cases (H + L)

 

2 8 6 5 4 5 8 5 7 8 8 7 5 2 80

 

(a): Data for 2013-2014 are incomplete and may not include all cases/countries reported.

 

(b): France has performed extensive retrospective testing to classify BSE cases, which is probably the explanation for the higher number of Atypical BSE cases reported in this country.

 

The number of Atypical BSE cases detected in countries that have already identified them seems to be similar from year to year. In France, a retrospective study of all TSE-positive cattle identified through the compulsory EU surveillance between 2001 and 2007 indicated that the prevalence of H-BSE and L-BSE was 0.35 and 0.41 cases per million adult cattle tested, respectively, which increased to 1.9 and 1.7 cases per million, respectively, in tested animals over eight years old (Biacabe et al., 2008). No comprehensive study on the prevalence of Atypical BSE cases has yet been carried out in other EU Member States. All cases of Atypical BSE reported in the EU BSE databases have been identified by active surveillance testing (59 % in fallen stock, 38 % in healthy slaughtered cattle and 4 % in emergency slaughtered cattle). Cases were reported in animals over eight years of age, with the exception of two cases (one H-BSE and one L-BSE) detected in Spain in 2011/2012. One additional case of H-BSE was detected in Switzerland in 2012 in a cow born in Germany in 2005 (Guldimann et al., 2012).

 


 


 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 8

 

Table 1: Number of Atypical BSE cases reported by EU Member States in the period 2001–2014 by country and by type (L- and H-BSE) (extracted from EU BSE databases on 1 July 2014). By 2015, these data might be more comprehensive following a request from the European Commission to Member States for re-testing and retrospective classification of all positive bovine isolates in the EU in the years 2003–2009

 

BSE type Country 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013(a) 2014(a) Total

 

H-BSE

 

Austria 1 1

 

France(b) 1 2 3 1 2 2 2 2 15

 

Germany 1 1 2 Ireland 1 1 2 1 5

 

The Netherlands 1 1

 

Poland 1 1 2

 

Portugal 1 1

 

Spain 1 1 2

 

Sweden 1 1

 

United Kingdom 1 1 1 1 1 5

 

Total 2 3 3 1 1 2 2 2 4 4 5 1 4 1 35

 

L-BSE

 

Austria 1 1 2

 

Denmark 1 1

 

France(b) 1 1 1 1 2 1 3 2 1 1 14

 

Germany 1 1 2 Italy 1 1 1 1 1 5

 

The Netherlands 1 1 1 3

 

Poland 1 2 2 1 2 1 2 1 12

 

Spain 2 2

 

United Kingdom 1 1 1 1 4

 

Total 0 5 3 4 3 3 6 3 3 4 3 6 1 1 45

 

Total Atypical cases (H + L) 2 8 6 5 4 5 8 5 7 8 8 7 5 2 80

 

(a): Data for 2013-2014 are incomplete and may not include all cases/countries reported.

 

(b): France has performed extensive retrospective testing to classify BSE cases, which is probably the explanation for the higher number of Atypical BSE cases reported in this country.

 

SNIP...

 

The current lack of information on the distribution of infectivity in tissues from Atypical BSE-infected cattle does not allow judgement of whether the current list of bovine SRM, set by EU Atypical BSE study protocol legislation based on data relating to the pathogenesis and tissue distribution of C-BSE, is fit for the purpose of removing most of the Atypical BSE infectivity from bovine carcasses. As is the case for C-BSE, Atypical BSE (H-BSE and/or L-BSE) agents are able to propagate in experimentally challenged foreign species such as mice, sheep, voles, primates and hamsters, and in transgenic mice expressing heterologous, i.e. non-bovine, PrP sequences.

 

EFSA Journal 2014;12(7):3798 13

 

SNIP...

 

2.4. Concluding remarks

 

Where data exist from both field cases and experimental animals (i.e. for L-BSE only), there is good agreement of the data with regard to abnormal PrP distribution. There are no data for field case H-BSE.

 

All data currently available relate to the presence or absence of PrPSc, but do not quantify relative amounts of PrPSc or levels of infectivity.

 

Disease-related PrP has been reported consistently in CNS tissues, peripheral ganglia and nerves, muscles (predominantly muscle spindles), adrenal glands and retina for both H-BSE and L-BSE. All of these tissues are also positive in C-BSE.

 

By contrast with C-BSE, at this stage no lymphoid tissues or gastrointestinal tissues from H-BSE- and L-BSE-affected animals have tested positive for PrPSc presence (IHC, WB) or infectivity (bioassay).

 

There are insufficient data at present to be clear about whether these apparent differences in the distribution of disease-specific markers reflect absolute differences between C-BSE and the H-BSE and L-BSE variants, whether they are a consequence of detection threshold limitations, or whether they are a consequence of the different routes of challenge.

 

No studies have been explicitly designed to address the issue of Atypical BSE with respect to SRM regulations. Without further experimental challenges or tissue collection from ongoing studies it will not be possible to obtain any data on duodenum, the jejunum and ileum (without Peyer’s patches), the caecum, the colon and the mesenteric fat.

 

SNIP...

 

4.1. Selection of tissues

 

4.1.1. BSE infectivity in bovine tissues

 

The current SRM list in cattle (see Table 5) has been established and amended in accordance with current knowledge related to C-BSE agent distribution in the tissues of infected cattle.

 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 24

 

The SRM measure is aimed at preventing the entry into the food chain of tissues and anatomical structures that might contain significant amounts of infectivity. In the framework of C-BSE infection in cattle, these measures are extremely efficient. However, certain tissues that might contain low amounts of infectivity in certain BSE-infected cattle are not included in the cattle SRM list (Table 6).

 

Table 5: Bovine SRM list, as defined in Regulation (EC) No 999/2001

 

Bovine SRM list

 

The skull excluding the mandible and including the brain and eyes, and the spinal cord of animals aged over 12 months

 

The vertebral column excluding the vertebrae of the tail, the spinous and transverse processes of the cervical, thoracic and lumbar vertebrae and the median sacral crest and wings of the sacrum, but including the dorsal root ganglia, of animals aged over 30 months

 

The tonsils, the intestines from the duodenum to the rectum and the mesentery of animals of all ages

 

Table 6: Cattle tissues with known infectivity or PrPSc presence for C-BSE according to WHO (2010), and their inclusion or not in the current SRM list

 

Higher-infectivity tissues

 

SRM

 

Brain

 

Dura mater

 

Spinal cord

 

Optic nerve

 

Retina

 

Spinal ganglia

 

Trigeminal ganglia

 

Lower-infectivity tissues

 

Nictitating membrane

 

Autonomic ganglia

 

Tonsil

 

Ileum

 

Jejunum

 

Non-SRM

 

Peripheral nerves

 

Adrenal glands

 

Bone marrow

 

Skeletal muscle

 

All the TSE agents replicate and accumulate at a high level in the CNS and can disseminate (centrifugally and centripetally) along the peripheral (autonomic and motor) nervous system. However, in a given host the agent distribution and the relative level of infectivity in other tissues can vary substantially according to the TSE strain.

 

For instance, in humans, although sCJD infectivity is mostly confined to the CNS, numerous lymphoid organs have been shown to be infectious in patients affected with variant CJD (vCJD) (Gill et al., 2013).

 

Similarly, in sheep infected with Classical scrapie, a significant level of infectivity can be found in lymphoid organs (about 103 times less than in the same weight of brain tissue), whereas in animals affected with Atypical scrapie lymphoid organs contain either very low (about 107 times less than in the same weight of brain tissue) or no detectable infectivity (Andreoletti et al., 2011).

 

There are currently no quantitative data on the distribution of H-BSE and L-BSE in cattle tissues.

 

4.1.2. Prioritisation of tissues to be included in further studies

 

In order to assess the adequacy and the relative effectiveness of the current SRM measures for mitigating human dietary exposure to H-BSE and L-BSE, a large number of tissues/anatomical structures need to be tested for the presence of PrPSc and/or infectivity.

 

Considering the potential number of samples and the requirement for bioassay, the choice of tissues to be tested should be prioritised according to three criteria:

 

the level of infectivity they contain in C-BSE-infected cattle (SRM list);

 

the presence of infectivity, or PrPSc presence, demonstrated in Atypical BSEs or other TSEs in ruminants;

 

the importance in terms of input into the food chain in the EU.

 

SNIP...

 

CONCLUSIONS AND RECOMMENDATIONS

 

CONCLUSIONS

 

Data relating to the prevalence and geographical distribution of Atypical BSE are incomplete.

 

The recent cessation of the testing of healthy slaughtered cattle in some EU Member States will lead to a loss of capacity of the monitoring system to detect Atypical BSE cases.

 

For transmission studies, i.c. challenge would be an appropriate proxy for studying the distribution of the agent if the origin of the disease was spontaneous, and originating in the brain, while oral challenge would be more appropriate if the origin of the disease was through ingestion of infected material.

 

The current lack of information on the distribution of infectivity in tissues of Atypical BSE-infected cattle does not allow judgement of whether the current list of bovine SRM, set by EU legislation based on data relating to the pathogenesis and tissue distribution of C-BSE, is fit for the purpose of removing most of the Atypical BSE infectivity from bovine carcasses.

 

Where data exist from both field cases and experimental animals (i.e. for L-BSE only), there is good agreement of the data with regard to abnormal PrP distribution. There are no data for field case H-BSE.

 

Disease-related PrP has been reported consistently in CNS tissues, peripheral ganglia and nerves, muscles (predominantly muscle spindles), adrenal glands and retina for both H-BSE and L-BSE. All of these tissues are also positive in C-BSE.

 

By contrast with C-BSE, at this stage no lymphoid tissues or gastrointestinal tissues from H-BSE- and L-BSE-affected animals have tested positive for PrPSc presence (IHC, WB) or infectivity (bioassay).

 

The reference method for the estimation of prion infectious titre in tissues is endpoint dilution titration in animals. To achieve maximum sensitivity regarding Atypical H-BSE and L-BSE, this bioassay should ideally be done in mouse lines over-expressing bovine PrPC. Several mouse lines over-expressing bovine PrPC are available worldwide.

 

In vitro amplification techniques can be used to determine whether a tissue contains any prion seeding activity. A correlation must be made between the sensitivity achieved by the cell-free assays and bioassays using reference material such as brain tissue from animals at the terminal stage of disease.

 

The application of the proposed protocol would provide elements allowing the assessment of the relative infectious titre, PrPSc accumulation and prion seeding activity in the tissues of cattle that developed H-BSE or L-BSE (using posterior brainstem as a reference).

 

Tissues to be covered by further studies are categorised in three priorities, based on their inclusion in the cattle SRM list, on the presence of infectivity, or PrPSc presence, demonstrated in Atypical BSEs or other TSEs in ruminants, and on the importance in terms of input into the food chain in the EU.

 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 32

 

Applying the protocol only to the tissues obtained through the EURL study would provide information on some but not all the tissues from the cattle SRM list. It would also provide information on some additional tissues not included in the cattle SRM list, but relevant for the food chain.

 

Material from other studies could be used to augment the range of SRM and non-SRM tissues available.

 

There is no identified source able to provide all the samples necessary to assess infectivity in tissues belonging to the full cattle SRM list in H- and L-BSE-infected animals. Therefore, to complete this objective, new inoculations of cattle would have to be considered.

 

RECOMMENDATIONS

 

In accordance with former EFSA recommendations, through the implementation of the protocol information should also be obtained on the performance of currently validated rapid tests for TSE active surveillance in cattle/bioassay for detecting H-BSE and L-BSE agents.

 

If new inoculation experiments are carried out in cattle with H-BSE and L-BSE, the following should be considered:

 

- inoculation through both the i.c. and oral route (despite the potential length of the oral route experiment);

 

- inclusion of C-BSE controls in the i.c. route experiment;

 

- sequential time killing of animals;

 

- collection of all tissues listed in Table 7.

 

DOCUMENTATION PROVIDED TO EFSA

 

1. Summary of the samples available and the tests already carried out by the EURL-TSE. Submitted by the European Commission as Annex 1 to the mandate.

 

2. Information on protocols and tests results provided by the EURL-TSE. Submitted by the European Commission as Annex 2 to the mandate.

 

REFERENCES

 


 

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

 


 

>>>(b): France has performed extensive retrospective testing to classify BSE cases, which is probably the explanation for the higher number of Atypical BSE cases reported in this country.<<<

 

LMAO!!!

 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

we have seen the spontaneous BSE epidemic in France, what about the other HIGH INCIDENCE ATYPICAL BSE COUNTRY OF POLAND, another atypical spontaneous event of high incidence. how can this be blamed on a happenstance of nothing, i.e. old age? goes against all junk science to date on the spontaneous atypical BSE i.e.

 

> In 2015, the OIE determined that atypical BSE occurred spontaneously at a low rate in all cattle populations and would be excluded for BSE risk. ...

 

>Atypical BSE occurs in older cattle, usually 8 years of age or greater, and does not appear to be associated with contaminated feed. Like classic or sporadic CJD in humans, it seems to arise rarely and spontaneously.

 

and if you believe that lie, myth, junk science, then you will believe this i.e.

 

> Regulations from the Food and Drug Administration (FDA) have prohibited the inclusion of mammalian protein in feed for cattle and other ruminants since 1997 and have also prohibited high risk tissue materials in all animal feed since 2009.

 


 

LAUGH OUT LOUD ! LOL!

 

POLAND ATYPICAL BSE AND SPORADIC CJD

 

Issue 2 Journal for Veterinary Medicine, Biotechnology and Biosafety

 

Volume 1, Issue 2, June 2015, Pages 12–14

 

ISSN 2411-3174 (print version) ISSN 2411-0388 (online version)

 

EPIDEmIOLOGY Of BOVINE SPONGIfORm ENCEPHALOPATHY IN CATTLE IN POLAND

 

Polak M. P., Zmudzinski J. F.

 

National Veterinary Research Institute, Pulawy, Poland e-mail: ppolak@piwet.pulawy.pl

 

Download PDF (print version)

 

Citation for print version: Polak M. P. and Zmudzinski J. F. (2015) ‘Epidemiology of bovine spongiform encephalopathy in cattle in Poland’, Journal for Veterinary Medicine, Biotechnology and Biosafety, 1(2), pp. 12–14.

 

Download PDF (online version)

 

Citation for online version: Polak M. P. and Zmudzinski J. F. (2015) ‘Epidemiology of bovine spongiform encephalopathy in cattle in Poland’, Journal for Veterinary Medicine, Biotechnology and Biosafety. [Online] 1(2), pp. 12–14. Available at:

 


 

Summary. The aim of the paper was to present the epidemiological situation regarding BSE epidemic in Poland with respect to cattle population, active surveillance and the control measures. Epidemiological data from the archives of the national reference laboratory for animal TSEs at the National Veterinary Research Institute and from the archives of the General Veterinary Inspectorate in Warsaw were used in the study. Between 2001 and the end of April 2015 BSE was diagnosed in 75 animals. Sixty one cases were classical BSE and 14 were atypical BSE (12 of L-type and 2 of H-type). Almost 6 million animals were tested using rapid tests. Dynamics of C-type BSE shows constant rise until 2005 when the highest number of cases (20) was recorded with sharp drop in the following years. Prevalence of atypical BSE shows stable trend with slight fluctuations. Traditional feeding was used in 65 and 90% of classical and atypical BSE cases, respectively. On the other hand, traditional feed was supplemented with MBM and milk replacers in 46 and 10% of classical and atypical BSE cases, respectively. Despite the high infectious load introduced into Poland especially with MBM, the number of cases was relatively low. In Poland, relatively high number of atypical BSE cases was recorded, comprising 19% of all BSE-positive animals. Mean age of classical BSE cases diagnosed annually does not show a decreasing trend which may reflect the late introduction of feed ban in Poland.

 

Keywords: bovine spongiform encephalopathy, Poland, prevalence, prion protein, control measures

 

References:

 

Baron, T., Biacabe, A.‑G., Arsac, J.‑N., Benestad, S. and Groschup, M. H. (2007) ‘Atypical transmissible spongiform encephalopathies (TSEs) in ruminants’, Vaccine, 25(30), pp. 5625–5630. doi: http://dx.doi.org/10.1016/j.vaccine.2006.10.058

 

Baron, T. and Biacabe, A.‑G. (2006) ‘Origin of bovine spongiform encephalopathy’, The Lancet, 367(9507), pp. 297–298. doi: http://dx.doi.org/10.1016/s0140-6736(06)68060-4

 

Biacabe, A.‑G., Laplanche, J.‑L., Ryder, S. and Baron, T. (2004) ‘Distinct molecular phenotypes in bovine prion diseases’, EMBO reports, 5(1), pp. 110–115. doi: http://dx.doi.org/10.1038/sj.embor.7400054

 

Brown, P., McShane, L., Zanusso, G. and Detwiler, L. (2006) ‘On the question of sporadic or atypical bovine spongiform encephalopathy and Creutzfeldt-Jakob disease’, Emerging Infectious Diseases, 12(12), pp. 1816–1821. doi: http://dx.doi.org/10.3201/eid1212.060965

 

Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J. (1997) ‘Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent’. Nature, 389(6650), pp. 498–501. doi: http://dx.doi.org/10.1038/39057

 

Buschmann, A. and Groschup, M. H. (2005) ‘Highly bovine spongiform encephalopathy–sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle’, The Journal of Infectious Diseases, 192(5), pp. 934–942. doi: http://dx.doi.org/10.1086/431602

 

Casalone, C., Zanusso, G., Acutis, P., Ferrari, S., Capucci, L., Tagliavini, F., Monaco, S. and Caramelli, M. (2004) ‘Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease’, Proceedings of the National Academy of Sciences, 101(9), pp. 3065–3070. doi: http://dx.doi.org/10.1073/pnas.0305777101

 

Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996) ‘Molecular analysis of prion strain variation and the aetiology of ‘new variant’ CJD’, Nature, 383(6602), pp. 685–690. doi: http://dx.doi.org/10.1038/383685a0

 

Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C., Gowland, I., Collinge, J., Doey L. J. and Lantos, P. (1997) ‘The same prion strain causes vCJD and BSE’. Nature, 389(6650), pp. 448–450. doi: http://dx.doi.org/10.1038/38925

 

Jacobs, J. G., Langeveld, J. P. M., Biacabe, A.‑G., Acutis, P.‑L., Polak, M. P., Gavier-Widen, D., Buschmann, A., Caramelli, M., Casalone, C., Mazza, M., Groschup, M., Erkens, J. H. F., Davidse, A., van Zijderveld, F. G. and Baron, T. (2007) ‘Molecular discrimination of atypical bovine spongiform encephalopathy strains from a geographical region spanning a wide area in Europe’, Journal of Clinical Microbiology, 45(6), pp. 1821–1829. doi: http://dx.doi.org/10.1128/jcm.00160-07

 

Polak, M. P., Rożek, W., Rola, J., Żmudziński, J. F. (2004). ‘Prion protein glycoforms from BSE cases in Poland’. Bulletin of Veterinary Institute in Pulawy, 48(3), pp. 201–205. Available at: http://bulletin.piwet.pulawy.pl/images/stories/pdf/20043/20043201206.pdf

 

Simmons, M. M., Harris, P., Jeffrey, M., Meek, S. C., Blamire, I. W. H. and Wells, G. A. H. (1996) ‘BSE in Great Britain: consistency of the neurohistopathological findings in two random annual samples of clinically suspect cases’, Veterinary Record, 138(8), pp. 175–177. doi: http://dx.doi.org/10.1136/vr.138.8.175

 

2015-2016 © NSC IECVM All rights reserved.

 


 

Opinion of the

 

Scientific Steering Committee

 

on the

 

GEOGRAPHICAL RISK OF

 

BOVINE SPONGIFORM

 

ENCEPHALOPATHY (GBR) in

 

POLAND

 

Adopted on 30/03/2001

 

Opinion of the Scientific Steering Committee on the

 

GEOGRAPHICAL RISK OF BOVINE SPONGIFORM

 

ENCEPHALOPATHY (GBR)

 

in Poland

 

THE QUESTION

 

The Scientific Steering Committee (SSC) was asked by the Commission to express its scientific opinion on the Geographical BSE-Risk (GBR), i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, at a given point in time, in a number of Third Countries.

 

This opinion addresses the GBR of Poland.

 

THE BACKGROUND

 

In December 1997 the SSC expressed its first opinion on Specified Risk Materials where it stated, inter alia, that the list of SRM could probably be modulated in the light of the species, the age and the geographical origin of the animals in question.

 

In June 2000 the European Commission adopted a Decision on SRM (2000/418/EC), prohibiting the import of SRM from all Third Countries that have not been "satisfactorily" assessed with regard to their BSE-Risk.

 

In July 2000 the SSC adopted its final opinion on "the Geographical Risk of Bovine Spongiform Encephalopathy (GBR)". This opinion described a method and a process for the assessment of the GBR and summarised the outcome of its application to 23 countries. Detailed reports on the GBR-assessments were published on the Internet for each of these countries.

 

In September 2000 the Commission invited 46 Third Countries, which are authorised to export products to the EU that are listed in annex II to the above mentioned SRM-Decision, to provide a dossier for the assessment of their GBR.

 

Until today 36 dossiers have been received, 6 are already assessed, and 30 are in different state of assessment.

 

This opinion concerns only one country, Poland. The Commission requested this opinion as essential input into its Decision concerning the treatment of SRM that will be requested from Poland. It is recommended that this opinion on Poland is read in the light of the GBR of the SSC of July 2000.

 

The SSC is concerned that the available information was not confirmed by inspection missions as they are performed by the FVO in the Member States. It recommends that BSE-related aspects are included in the program of future inspection missions, as far as feasible.

 

THE ANALYSIS

 

Poland was exposed to a very low challenge between 1980-86, a very high external challenge between 1987-90 and an extremely high external challenge since 1991, mainly due to massive imports of MBM from BSE affected countries (in the range of 1,700,000 tonnes in total, mainly from DE: around 1,000,000 tonnes in total). High imports of cattle are also recorded for the period since 1988.

 

The BSE/cattle system of Poland was and is very unstable since 1980. Feeding MBM to cattle was legally possible until March 1997 and is likely to have occurred, even if it was uncommon practice. The efficiency of the feed-ban cannot be assessed, as feed controls were apparently not carried out. Rendering is and was common practice in Poland. Material includes ruminant material, including SRM, condemned material, and a limited proportion of fallen stock. The rendering processes used were adequate for reducing BSE-infectivity since a long time.

 

There is no SRM ban. Cross contamination is most probable (no specified feed lines, no controls described). BSE is notifiable since 1997 and surveillance was nearly non existent until 1997. Since 1977, passive surveillance does not fulfil OIE requirements. Active surveillance has started in 2001.

 

It is concluded that it is likely but not confirmed that one or several cattle that are (pre-clinically or clinically) infected with the BSE agent are currently present in the domestic herd of Poland (GBR III).

 

Given the very unstable system and the fact that the BSE-agent is likely to be already present in the country, it is assumed that the GBR is increasing.

 

A summary of the reasons for the current assessment is given in annex 1 to this opinion.

 

Likely present since 1987 and growing.

 


 

B. OIE LIST B DISEASES

 

International

 

Bovine Spongiform Encephalopathy

 

BSE in Poland, May 2002 -- A nine year old cow tested positive for BSE in the village of Mochnaczka near Poland’s southern border with Slovakia. Poland began routine testing for BSE in October 2001. Over 100,000 cattle have been tested under this program and this is the first case detected in Poland. Three other cows which had been kept together with the positive cow were tested and found negative.

 

Source: CEI Impact Worksheet, OIE, Agworldwide, AGAM

 


 

Bovine Spongiform Encephalopathy, Poland

 

Impact Worksheet, May 7, 2002

 

[ Impact Worksheets | CEI Home ]

 

Summary:

 

The first case of bovine spongiform encephalopathy (BSE) in Poland was confirmed on May 2, 2002. The affected nine-year old cow tested BSE positive at a slaughterhouse located in the village of Mochnaczka Wyzna, province of Little Poland (Malopolskie) near Poland’s southern border with Slovakia. Poland began routine testing for BSE of all slaughtered cattle over 24 months of age in October 2001. In January 2002, testing was changed to all slaughtered cattle over the age of 30 months.

 

In December 1997, APHIS prohibited the importation of live ruminants and most ruminant products from all of Europe including Poland. In December 2000, import restrictions regarding BSE were expanded to prohibit all imports of rendered animal protein products, regardless of species, from Europe. Between 1998 and 2001, the US imported non-species specific animal products used in animal feeds and non-species specific sausage and offal products. Given US restrictions on ruminant product imports, these US imports should not have contained ruminant material.

 

Poland’s stocks of cattle and sheep were less than 1 percent of world stocks in 2001. Poland is the world’s 5th largest exporter of live cattle exporting nearly 600,000 animals in 2000. Cattle exports go primarily to European countries although Israel imported significant numbers of Polish cattle in 2000 and 2001.

 

______________________________________________________________________________

 

How extensive is the outbreak of BSE in Poland?

 

The first case of bovine spongiform encephalopathy (BSE) in Poland was confirmed on May 2, 2002. The affected nine-year old cow tested BSE positive at a slaughterhouse located in the village of Mochnaczka Wyzna, province of Little Poland (Malopolskie), near Poland’s southern border with Slovakia. Poland began routine BSE testing of all slaughtered cattle over the age of 24 months in October 2001. In January 2002, testing was changed to all slaughtered cattle over the age of 30 months. The affected cow was the first positive test result in over 100,000 cattle tested. Police and veterinary services are investigating the source of the disease.

 

Sources: OIE; Promed (ABC news); USDA, Foreign Agricultural Service GAIN Reports #PL1037 (October 11, 2001) and #PL2004 (February 1, 2002)

 

What actions has Poland taken to protect its livestock from BSE?

 

The Polish Veterinary Service banned imports of cattle from BSE countries in December 2000. A ban on imports of meat and bone meal was enacted in January 2001.

 

Source: USDA, Foreign Agricultural Service GAIN Report #PL1037, October 11, 2001

 

What is Poland’s production and trade in affected animals and animal products?

 

Poland's stocks of cattle and sheep were less than 1 percent of world stocks in 2001 (Table 1). Cattle imports totaled nearly 7,000 animals in 2000 while sheep imports were less than 200 head. Cattle imports were from European countries. Poland is the 5th largest exporter of live cattle in the world, exporting nearly 600,000 animals in 2000 (6 percent of world trade). Polish farmers produce young fattening cattle for export as a side enterprise of their dairy herds. Cattle exports were sent primarily to Italy (over 50 percent of the total), the Netherlands, Germany, Spain, Greece, Croatia, Bosnia-Herzegovina, and Slovenia. Israel received over 50,000 cattle from Poland in 2000. In addition to cattle, Poland exported over 200,000 sheep in 2000. The destination of these sheep exports was not available.

 

Table 1. Poland’s live animal stocks and exports and imports of live animals.

 

Live Animal 2001 Stocks Trade

 

2000 Exports 2000 Imports

 

Head % World Head % World Head % World

 

Cattle 5,723,000 <1 1.3="" 161="" 212="" 337="" 593="" 6.2="" 6="" div="" sheep1="">
 

Poland’s production of beef/veal and mutton/lamb in 2001 was small on a worldwide scale representing less than 1 percent of total world production (Table 2). Beef production within Poland has been decreasing since 1998. Polish consumers have been reducing their beef consumption due to BSE fears and switching to poultry. Poland’s imports and exports of beef/veal and mutton/lamb were also small representing less than 1 percent of world imports and exports.

 

Table 2. Production and trade in relevant products by Poland.

 

Products 2001 Production Trade

 

2000 Exports 2000 Imports

 

Metric Ton % World Metric Ton % World Metric Ton % World

 

Beef and Veal 300,000 <1 162="" 1="" 24="" 96="" 9="" and="" div="" lamb1="" mutton="">
 

1 Sheep were included in Table 1 and Table 2 as ‘affected’ because USDA/APHIS includes all ruminants and ruminant products in its restrictions pertaining to BSE. Goat production and trade information was unavailable.

 

Source: United Nations FAO; USDA, Foreign Agricultural Service GAIN Reports #PL1022 (July 30, 2001) and #PL2004 (February 1, 2002)

 

What are the U.S. imports of affected animals or animal products from Poland?

 

The US imported no live ruminant animals or ruminant meat from Poland during 1998 to 2001. During the past four years (1998 - 2001), US imports from Poland included non-species specific animal products used in animal feeds and non-species specific sausage and offal products (Table 3). Given US restrictions on ruminant product imports, these US imports should not have contained ruminant material.

 

Mexico imported non-species specific preparations used in animal feed (HS code 23099099) from Poland during 1998 to 2001. Canada did not import any items of risk from Poland during 1998 to 2001.

 

Table 3. Relevant US imports from Poland in 1998, 1999, 2000, and 2001

 

HS Code Description Unit 1998 1999 2000 2001

 

Feed - non species specific Total 6,684 0 0 0

 

0511993000 Products Used as Food, For Animals KG 6,684 0 0 0

 

Meat & offal- non species specific Total 92,945 27,274 44,102 78,332

 

0504000040 Gut/Bladder/Stomach of Animals For Sausage Casing, Not Hog or Fish KG 0 0 420 280

 

1601006060 Sausage/Similar Prdct Meat Etc NESOI Food Prep Cnd KG 81,413 25,872 0 0

 

1602204000 Animal Livers Except Goose, Prepared or Preserved KG 11,532 1,402 43,682 78,052

 

Source: World Trade Atlas

 

Did the US have restrictions on ruminant imports from Poland prior to this case?

 

In December 1997, APHIS prohibited the importation of live ruminants and most ruminant products from all of Europe including Poland until a thorough assessment of the risks of introduction of BSE into the US could be made. Prior to December 1997, import restrictions were applied only to those countries which had reported cases of BSE in native animals. Also, importation of ruminant meat from BSE-affected countries was permitted if the meat was deboned and free of visually identifiable lymphatic and nervous tissue and if it met other restrictions. Import regulations enacted December 1997 extended the import restrictions to countries which had not had a declared BSE case, yet had risk factors for BSE occurrence.

 

These regulatory changes also removed provisions that allowed importation of ruminant meat from the restricted countries, and thereby prohibited importation of ruminant meat from all Europe. These import restrictions also applied to bone meal, blood meal, meat meal, offal, fat, glands, and serum from ruminants. In December 2000, APHIS expanded its import restrictions regarding BSE to prohibit all imports from Europe of rendered animal protein products, regardless of species.

 

Source: USDA, APHIS, VS

 

What is the level of passenger traffic arriving in the United States from Poland?

 

A total of 188,946 passengers arrived at US airports on direct flights from Poland in fiscal year 2000. An undetermined number of passengers arrived in the US from Poland via indirect flights.

 

Under APHIS-PPQ’s agricultural quarantine inspection monitoring, 451 air passengers from Poland were sampled for items of agricultural interest in fiscal year 2000. Thirteen (13) of these passengers, or 2.9 percent, carried a total of 26.2 kg of meat items that could potentially harbor the pathogen(s) that cause BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the US.

 

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

 

CEI’s plans for follow up:

 

CEI has no plans to provide additional information on this situation.

 

If you need more information or wish to comment, you may contact Judy Akkina at (970) 490-7852 or Carol Tuszynski at (970) 490-7893.

 


 

What measures has USDA-APHIS taken to prevent the introduction of BSE? To prevent BSE from entering the United States, APHIS has restricted the importation of live ruminants and certain ruminant products from countries where BSE is known to exist.

 

In 1989, APHIS banned the importation of all ruminants and restricted the importation of certain cattle products from the United Kingdom and other countries where BSE was diagnosed.

 

On December 6, 1991, APHIS restricted the importation of ruminant meat and edible products and banned most byproducts of ruminant origin from countries known to have BSE (56 Federal Register [FR] 63868 and 63869). Prior to this, the products were prohibited by not issuing permits.

 

Certain products cannot be imported into the United States, except under special permit for scientific, educational or research purposes, or under special conditions to be used in cosmetics. These products include serum, glands, collagen, etc.

 

As of December 12, 1997, APHIS has prohibited the importation of live ruminants and most ruminant products from all of Europe. The restrictions applied to Albania, Austria, Bosnia-Herzegovina, Bulgaria, Croatia, Czech Republic, Denmark, Federal Republic of Yugoslavia, Finland, Germany, Greece, Hungary, Italy, the former Yugoslavian republic of Macedonia, Norway, Poland, Romania, Slovak Republic, Slovenia, Spain, and Sweden. These actions were in addition to those already in place regarding countries that had reported BSE in native cattle.

 

This action was taken in 1997 because the Netherlands, Belgium, and Luxembourg have reported their first cases of BSE in native-born cattle. There is evidence that European countries may have had high BSE risk factors for several years and less-than-adequate surveillance.

 

An interim rule was published and the comment period closed on March 9, 1998. Criteria to assess the risk factors were developed in accordance with the standards adopted by the Office of International Epizootics (OIE).

 


 

TECHNICAL REPORT

 

Annual report of the Scientific Network on BSE-TSE 20131 European Food Safety Authority2, 3 European Food Safety Authority (EFSA), Parma, Italy

 

snip...

 

Case study on the typing of a potential BSE-like isolate from a goat in Poland

 

The representative from Poland described the scientific, technical and procedural aspects for the typing of TSE isolates from small ruminants. Firstly, the description of the bases for BSE and Scrapie strain-differentiation where presented with detail. This included not only the laboratory methods used but also an indication of the criteria that is applied for the characterisation of TSE isolates in animals. Secondly, available results of the typing of a potential BSE-like isolate from a goat in Poland were shown with detail. The EURL-TSE Strain Typing Expert Group (STEG) has preliminary classified the strain as not BSE, but BSE could not be fully excluded. Inoculation studies employing bioassay are ongoing in order to gain further information on the characteristics of this strain.

 


 

*** The EURL-TSE Strain Typing Expert Group (STEG) has preliminary classified the strain as not BSE, but BSE could not be fully excluded.

 

I am not sure exactly what the hell that means...TSS

 

Subject: A Surprisingly High Number of the Plaque-Like VV sCJD Subtype Among the Polish sCJD-is There a Connection with BASE?

 

PPo4-15: A Surprisingly High Number of the Plaque-Like VV sCJD Subtype Among the Polish sCJD—is There a Connection with BASE?

 

Beata Sikorska and Pawel P. Liberski Department of Molecular Pathology and Neuropathology; Medical University of Lodz; Lodz,

 

Poland Recently described bovine amyloidotic spongiform encephalopathy (BASE) or L type BSE—was is overrepresented in Poland (15% of all cases of BSE). Moreover, the number of BASE cases in Poland per million bovines is the highest in Europe. A potential human risk from BASE is evident from experimental transmission to “humanized” transgenic animals and primates. Taking into consideration that non-human primate inoculated with BASE had a shorter incubation period than monkeys infected with classical BSE, and that humanized Tg mice have been found to be highly susceptible to infection with atypical form of BSE, it seems probable that BASE may be more pathogenic for humans than BSE, but the transmitted disease may differ from BSE-derived vCJD. Among 47 cases which have been diagnosed as definite in our laboratory, in 19 cases complete histopathological examination and codon 129 status were available. On the basis of the histological pattern and codon 129 status the cases of sCJD were divided into subtypes according to the Parchi&Gambetti classification. The results are as follows: type 1 (MMorMV)- 42%, type 2 (VV)-32%, type 3 (MV)-10.5%, type 4c (MM)- 10.5% and type 5 (VV)-5 %. Although the number of cases is too low to conclude a significantly different distribution of sCJD subtypes in Polish population those data show surprisingly high number of the plaque-like VV sCJD subtype. Interestingly, it was shown before that Tg mice inoculated with BASE showed granular and plaque-like aggregates or PrPSc in brains resembling those observed in VV2 subtype of sCJD.

 

PPo2-26: Transmission of Classical and Atypical (L-type) Bovine Spongiform Encephalopathy (BSE) Prions to Cynomolgus macaques

 

Fumiko Ono,1 Yoshio Yamakawa,2 Minoru Tobiume,3 Yuko Sato,3 Harutaka Katano,3 Kenichi Hagiwara,2 Iori Itagaki,1 Akio Hiyaoka,1 Katuhiko Komatuzaki,1 Yasunori Emoto,1 Hiroaki Shibata,4 Yuichi Murayama,5 Keiji Terao,4 Yasuhiro Yasutomi4 and Tetsutaro Sata3 1The Corporation for Production and Research of Laboratory Primates; Tsukuba City, Japan; 2Departments of Cell Biology and Biochemistry; and 3Pathology; National Institute of Infectious Diseases; Tokyo, Japan; 4Tsukuba Primate Research Center; National Institute of Biomedical Innovation; Tsukuba City, Japan; 5Prion Disease Research Team; National Institute of Animal Health; Tsukuba City, Japan

 

Key words: L-type BSE, cBSE, cynomolgus macaques, transmission

 

BSE prion derived from classical BSE (cBSE) or L-type BSE was characterized by inoculation into the brain of cynomolgus macaques. The neurologic manifestation was developed in all cynomolgus macaques at 27–43 months after intracerebral inoculation of brain homogenate from cBSE-affected cattle (BSE JP/6). Second transmission of cBSE from macaque to macaque shortened incubation period to 13–18 months. cBSE-affected macaques showed the similar clinical signs including hyperekplexia, tremor and paralysis in both primary and second transmission. Two macaques were intracerebrally inoculated brain homogenate from the L-type BSE-affected cattle (BSE JP/24). The incubation periods were 19–20 months in primary transmission. The clinical course of the L-type BSE-affected macaques differed from that in cBSE-affected macaques in the points of severe myoclonus without hyperekplexia. The glycoform profile of PrPSc detected in macaque CNS was consistent with original pattern of either cBSE or L-typeBSE PrPSc, respectively. Although severe spongiform change in the brain was remarkable in all BSE-affected macaques, severe spongiform spread widely in cerebral cortex in L-type BSE-affected macaques. Heavy accumulation of PrPSc surrounded by vacuola formed florid plaques in cerebral cortex of cBSE-affected macaques. Deposit of PrPSc in L-type BSE-affected macaque was weak and diffuse synaptic pattern in cerebrum, but large PrPSc plaques were evident at cerebellum. MRI analysis, T2, T1, DW and flair sequences, at the time of autopsy revealed that brain atrophy and dilatation of cerebral ventricles were significantly severe in L-type BSE-affected macaques. These results suggest that L-type BSE is more virulent strain to primates comparing to cBSE.

 

SP1-4: Evidence from Molecular Strain Typing

 

Gianluigi Zanusso Department of Neurological and Visual Sciences; Section of Clinical Neurology; University of Verona; Verona, Italy

 

Key words: molecular analysis, strain typing, atypical BSE, CJD

 

In 2001, active surveillance for bovine spongiform encephalopathy (BSE) led to the discovery of atypical BSE phenotypes in aged cattle distinct from classical BSE (C-type). These atypical BSE cases had been classified as low L-type (BASE) or high H-type BSE based on the molecular mass and the degree of glycosylation of of the pathological prion protein (PrPSc). Transmission studies in TgBov mice showed that H-type BSE, C-type BSE and BASE behave as distinct prion strains with different incubation periods, PrPSc molecular patterns and pathological phenotypes. A still unclear issue concerns the potential transmissibility and phenotypes of atypical BSEs in humans. We previously indicated that BASE was similar to a distinct subgroup of sporadic form of Creutzfeldt-Jakob disease (sCJD) MV2, based on molecular similarities and on neuropathological pattern of PrP deposition. To investigate a possible link between BASE and sCJD, Kong et al. and Comoy et al. experimentally inoculated TgHu mice (129MM) and a non-human primate respectively, showing in both models that BASE was more virulent compare to BSE. Further, non-human primate reproduced a clinical phenotype resembling to that of sCJD subtype MM2. Here, we presented a comparative analysis of the biochemical fingerprints of PrPSc between the different sCJD subtypes and animal TSEs and after experimental transmission to animals.

 


 

Opinion of the Scientific Steering Committee on the GEOGRAPHICAL RISK OF BOVINE SPONGIFORM ENCEPHALOPATHY (GBR) in POLAND Adopted on 30/03/2001 It is concluded that it is likely but not confirmed that one or several cattle that are (pre-clinically or clinically) infected with the BSE agent are currently present in the domestic herd of Poland (GBR III).

 


 

Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide*(excluding the United Kingdom) Country/Year

 

89 90 91 92 93 94 95 96 97 98 99 00 01 02 03 04 05 06 07 08 09 10

 

Poland

 

0 0 0 0 0 0 0 0 0 0 0 0 0 4f 5 11 19 10 9 5 4

 


 

Annual incidence rate* of bovine spongiform encephalopathy (BSE) in OIE Member Countries that have reported cases, excluding the United Kingdom

 


 

Bovine Spongiform Encephalopathy, Poland Impact Worksheet, May 7, 2002 What is the level of passenger traffic arriving in the United States from Poland? A total of 188,946 passengers arrived at US airports on direct flights from Poland in fiscal year 2000. An undetermined number of passengers arrived in the US from Poland via indirect flights. Under APHIS-PPQ’s agricultural quarantine inspection monitoring, 451 air passengers from Poland were sampled for items of agricultural interest in fiscal year 2000. Thirteen (13) of these passengers, or 2.9 percent, carried a total of 26.2 kg of meat items that could potentially harbor the pathogen(s) that cause BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the US. Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

 


 

Diagnosis of the first cases of scrapie in Poland

 

Miroslaw P. Polaka, , , Magdalena Larskaa, Jan P.M. Langeveldb, Anne Buschmannc, Martin H. Groschupc, Jan F. Zmudzinskia

 

.doi:10.1016/j.tvjl.2009.07.032Get rights and content

 

Abstract

 

This is the first report of cases of scrapie in Poland. The disease was an atypical phenotype, diagnosed in two aged sheep which were found dead. Brainstem samples from both animals were positive on the applied ELISA rapid test, while the confirmatory immunoblot indicated abnormal banding patterns of protease resistant prion protein (PrPres). The genotypes of these sheep were ALRQ/ALHQ and ALRQ/ALRR. The absence of premonitory clinical signs, the advanced age of the affected sheep, the higher concentration of PrPres in the cerebellum relative to the obex, the unusual banding profile of the prion protein and its relatively low resistance to proteolytic degradation confirmed the diagnosis of atypical scrapie (Nor98-like) in both cases.

 

Keywords Sheep; Atypical scrapie; Nor98; Western blot; Molecular typing

 

Corresponding author. Tel.: +48 81889 3316; fax: +48 81886 2595. Copyright © 2009 Elsevier Ltd. All rights reserved.

 


 


 


 


 

Wednesday, November 13, 2013

 

Atypical Scrapie Prions from Sheep and Lack of Disease in Transgenic Mice Overexpressing Human Prion Protein

 


 


 

Thursday, July 31, 2014

 

EFSA Scrapie reduction unlikely without effective breeding programme

 


 

Sunday, July 27, 2008

 

Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Toxin List Docket Type Rulemaking APHIS-2007-0033-0001

 

Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Docket Type Rulemaking Document APHIS-2007-0033-0001 Document Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Public Submission APHIS-2007-0033-0002.1 Public Submission Title Attachment to Singeltary comment

 

Comment DOCKET APHIS-2007-0033 Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List

 

August, 29, 2007

 

Greetings APHIS,

 

I would kindly like to submit the following to ;

 

DEPARTMENT OF AGRICULTURE Animal and Plant Health Inspection Service

 

7 CFR Part 331 9 CFR Part 121

 

Docket No. APHIS-2007-0033 RIN 0579-AC53

 

This is my second submission to APHIS about Bioterrorism and the Transmissible Spongiform Encephalopathy TSE agent. My first submission was Mon, 27 Jan 2003 15:54:57 -0600 Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002 (see my old submission at bottom dated Subject: Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; Date: Mon, 27 Jan 2003 15:54:57 -0600 From: "Terry S. Singeltary Sr." To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000328/!x-usc:mailto:regulations@aphis.usda.gov ).

 

WHAT I am most concerned about is that ONLY BSE is listed as a dangerous toxin in the family of TSE. With the ever growing list of atypical TSE like atypical BSE BASE, and the atypical Scrapie Nor-98, and also the typical scrapie strains, and Chronic Wasting Disease CWD, why is it only BSE is listed ?

 

I think that all of these TSE's should be listed with the BSE agent as a potential Biological weapon. With these atypical TSE, even more so, due to the fact the possibility of vertical and lateral transmission, unlike BSE (not documented to date to transmit that way). With the atypical BSE BASE being more virulent to humans than the typical BSE, why is it not listed ?

 

WHY is the atypical Scrapie Nor-98, with this being a potential threat to not only animals, but humans as well, why is this not listed ?

 

WHY is Chronic Wasting Disease CWD of deer and elk not listed, especially since CWD has transmitted to the bovine by inoculation to date, with oral studies still ongoing, and the fact the oral route would take much longer, would CWD wreck havoc on a countries economy too, let alone the very real potential for CWD to transmit to humans, why is CWD not listed as a Bio-toxin ?

 

IF these terrorist are willing to walk into a mall and blow themselves up as a walking bomb, what is to keep them from exposing themselves to one of these deadly TSEs, and then going to a hospital and exposing many with CJD somehow. This may seem far fetched, but very possible. Why is CJD not listed ?

 

IN short, and very simple, all you would have to do is change the BSE, to human and animal TSE, thus all bases would be covered. but in only including the BSE strain of TSE agent, I think you are only fooling yourselves, again. ...

 

SOURCES

 

snip....

 

more on non-species coding system and TSEs and potential 'suitcase bombs';

 

To: Bovine Spongiform Encephalopathy Subject: Re: POLAND FINDS 4TH MAD COW CASE/USA IMPORTS FROM POLAND/non-species coding system strikes again References: <[log in to unmask]> Content-Type: text/plain; charset=ISO-8859-1; format=flowed Content-Transfer-Encoding: 8bit X-Virus-Scanner: Found to be clean

 

Greetings again List Members,

 

let me kick a madcow around here a bit.

 

on the imports from Poland and the infamous USA 'non-species' coding system.

 

the USDA/APHIS states;

 

During the past four years (1998 - 2001), US imports from Poland included non-species specific animal products used in animal feeds and non-species specific sausage and offal products (Table 3). Given US restrictions on ruminant product imports, these US imports should not have contained ruminant material.

 

NOW, if you read Polands GBR risk assessment and opinion on BSE, especially _cross-contamination_, it states;

 

ANNEX 1

 

Poland - Summary of the GBR-Assessment, February 2001

 

EXTERNAL CHALLENGE STABILITY INTERACTION OF EXTERNAL CHALLENGE AND STABILITY

 

The very high to extremely high external challenge met a very unstable system and could have led to contamination of domestic cattle in Poland from 1987 onwards.

 

This internal challenge again met the still very unstable system and increased over time.

 

The continuing very high external challenge supported this development.

 

Not OK MBM-ban since 1997, but no feed controls. Reasonably OK Heat treatment equivalent to 133°C / 20min / 3 bar standards, but no evidence provided on compliance.

 

Not OK. No SRM-ban, SRM are rendered and included in cattle feed.

 

BSE surveillance:

 

Not sufficient before 2001.

 

Cross-contamination:

 

Lines for ruminant and non-ruminant feed in feed-mills only separated in time and no analytical controls carried out. Likely present since 1987 and growing.

 

see full text and ANNEX 1 at;

 


 

so in my humble opinion, the statement by the USDA/APHIS that ''these US imports _should_ not have contained ruminant materials, is a joke. a sad joke indeed.

 

* POLAND BSE GBR RISK ASSESSMENT

 


 

snip...

 


 


 


 

PLEASE NOTICE THAT SPORADIC CJD IN POLAND TRIPLED FROM THE YEAR 2008 TO 2009, FROM 10 TO 30 CASES. AS with sporadic CJD in the USA drastically increasing over the years. ...TSS

 


 


 


 


 

BSE Cases Identified in the United States

 

There have been 4 cases of BSE identified in the United States. The following information provides descriptions of these four cases:

 

2012 - California collapsed On April 24, 2012, the USDA confirmed a BSE case in a dairy cow in California. This cow was tested as part of the USDA targeted BSE surveillance at rendering facilities in the United States. The cow was 10 years and 7 months old and was classified as having the L-type BSE strain.

 

For more information, see the USDA/APHIS notice, the SDA/APHIS Final Report[PDF – 179 KB] and the FDA Final Feed Investigation Summary.

 

2006 - Alabama collapsed On March 15, 2006, the USDA announced the confirmation of BSE in a cow in Alabama. The case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. The age of the cow was estimated by examination of the dentition as 10 years old.

 

It had no ear tags or distinctive marks; the herd of origin could not be identified despite an intense investigation (see Alabama BSE Investigation, Final Epidemiology Report, May 2006[PDF - 105KB]).

 

In August 2008, several ARS investigators reported that a rare, genetic abnormality that may persist within the cattle population "is considered to have caused" BSE in this atypical (H-type) BSE animal from Alabama. (See Identification of a Heritable Polymorphism in Bovine PRNP Associated with Genetic Transmissible Spongiform Encephalopathy: Evidence of Heritable BSE. Also see BSE Case Associated with Prion Protein Gene Mutation.)

 

2005 - Texas collapsed On June 24, 2005, the USDA announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming BSE in a cow that had conflicting test results in 2004. This cow was from Texas, died at approximately 12 years of age, and represented the first endemic case of BSE in the United States. (see Texas BSE Investigation, Final Epidemiology Report, August 2005[PDF - 82KB]) 2003 - Washington State collapsed On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a presumptive diagnosis of the first known case of BSE in the United States. It was in an adult Holstein cow from Washington State. This diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Trace-back based on an ear-tag identification number and subsequent genetic testing confirmed that the BSE-infected cow was imported into the United States from Canada in August 2001.

 

Because the animal was non-ambulatory (a "downer cow") at slaughter, brain tissue samples were taken by USDA’s Animal and Plant Health Inspection Service as part of its targeted surveillance for BSE. However the animal’s condition was attributed to complications from calving. After the animal was examined by a USDA Food Safety and Inspection Service (FSIS) veterinary medical officer both before and after slaughter, the carcass was released for use as food for human consumption. During slaughter, the tissues considered to be at high risk for the transmission of the BSE agent were removed.

 

On December 24, 2003, FSIS recalled beef from cattle slaughtered in the same plant on the same day as the BSE positive cow. (see Bovine Spongiform Encephalopathy in a Dairy Cow—Washington State, 2003(http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5253a2.htm).)

 

Preliminary Investigation Suggests BSE-Infected Cow in Washington State Was Likely Imported from Canada

 

On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a presumptive diagnosis of bovine spongiform encephalopathy (BSE, or "mad cow" disease) in an adult Holstein cow from Washington State. Samples were taken from the cow on December 9 as part of USDA's BSE surveillance program. The BSE diagnosis was made on December 22 and 23 by histopathology and immunohistochemical testing at the National Veterinary Services Laboratory, Ames, Iowa. The diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Preliminary trace-back based on an ear-tag identification number suggests that the BSE-infected cow was imported into the United States from Canada in August 2001.

 

USDA, in close cooperation with Canadian agricultural authorities, has launched an epidemiologic investigation to determine the source of the disease. Beef from the slaughtered cow had been processed for human consumption. On December 23, 2003, the Food Safety and Inspection Service (FSIS), USDA announced the recall of all beef from cattle slaughtered on December 9 at the involved slaughter plant.

 

Strong evidence indicates that BSE has been transmitted to humans primarily in the United Kingdom, causing a variant form of Creutzfeldt-Jakob disease (vCJD)(http://www.cdc.gov/prions/vcjd/about.html). In the United Kingdom, where over 1 million cattle may have been infected with BSE, a substantial species barrier appears to protect humans from widespread illness. As of December 1, 2003, a total of 153 vCJD cases had been reported worldwide; of these, 143 cases had occurred in the United Kingdom. The risk to human health from BSE in the United States is extremely low.

 

CDC monitors the trends and current incidence of CJD in the United States by analyzing death certificate information from U.S. multiple cause-of-death data compiled by the National Center for Health Statistics. With the support of the Council of State and Territorial Epidemiologists, CDC conducts follow-up review of clinical and neuropathology records of CJD decedents younger than 55 years of age. In addition, during 1996-1997, in collaboration with the American Association of Neuropathologists (AANP), CDC established the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, Ohio. This pathology center provides free, state-of-the-art diagnostic services to U.S. physicians. It also helps to monitor the possible occurrence of emerging forms of prion diseases, such as vCJD, in the United States. For more information about the center visit its website at:

 

USDA About BSE FDA Bovine Spongiform Encephalopathy CDC Prion Diseases(http://www.cdc.gov/prions/index.html) NIH NINDS Creutzfeldt-Jakob Disease Information Page For more information about BSE in the United States, see the Animal and Plant Health Inspection Service, USDA BSE site.

 

Related Links Prion Diseases(http://www.cdc.gov/prions/index.html) Chronic Wasting Disease (CWD)(http://www.cdc.gov/prions/cwd/index.html) Creutzfeldt-Jakob Disease (CJD)(http://www.cdc.gov/prions/cjd/index.html) Variant Creutzfeldt-Jakob Disease (vCJD)(http://www.cdc.gov/prions/vcjd/index.html) File Formats Help: How do I view different file formats (PDF, DOC, PPT, MPEG) on this site? Adobe PDF file Microsoft PowerPoint file Microsoft Word file Microsoft Excel file Audio/Video file Apple Quicktime file RealPlayer file Text file Zip Archive file SAS file ePub file RIS file Page last reviewed: February 10, 2015 Page last updated: February 10, 2015 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)

 


 

Saturday, July 23, 2016

 

*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016 ***

 


 

SPONTANEOUS TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW TYPE DISEASE ???

 

*** We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes.

 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 

>>> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <<<

 


 

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.

 


 

Maximizing profits is all that is going on now, thanks to the OIE BSE MRR policy, the legal trading of all strains of TSE prion disease globally. ...Terry S. Singeltary Sr.

 

atypical BSE spontaneous sporadic ???

 

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...

 


 

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. ...

 


 

”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” ...page 26.

 


 

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

 


 

Saturday, July 23, 2016

 

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016

 


 

O.08: H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: Clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation

 

S Jo Moore, M Heather West Greenlee, Jodi Smith, Eric Nicholson, Cathy Vrentas, and Justin Greenlee

 

United States Department of Agriculture; Ames, IA USA

 

In 2006 an H-type bovine spongiform encephalopathy (BSE) case was reported in an animal with an unusual polymorphism (E211K) in the prion protein gene. Although the prevalence of this polymorphism is low, cattle carrying the K211 allele are predisposed to rapid onset of H-type BSE when exposed. The purpose of this study was to investigate the phenotype of this BSE strain in wild-type (E211E) and E211K heterozygous cattle.

 

One calf carrying the wild-type allele and one E211K calf were inoculated intracranially with H-type BSE brain homogenate from the US 2006 case that also carried one K211 allelle. In addition, one wild-type calf and one E211K calf were inoculated intracranially with brain homogenate from a US 2003 classical BSE case. All animals succumbed to clinical disease. Survival times for E211K H-type BSE inoculated catttle (10 and 18 months) were shorter than the classical BSE inoculated cattle (both 26 months). Significant changes in retinal function were observed in H-type BSE challenged cattle only. Animals challenged with the same inoculum showed similar severity and neuroanatomical distribution of vacuolation and disease-associated prion protein deposition in the brain, though differences in neuropathology were observed between E211K H-type BSE and classical BSE inoculated animals. Western blot results for brain tissue from challenged animals were consistent with the inoculum strains.

 

This study demonstrates that the phenotype of E211K H-type BSE remains stable when transmitted to cattle without the E211K polymorphism, and exhibits a number of features that differ from classical BSE in both wild-type and E211K cattle.

 

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

 

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.

 

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

 

Monday, May 09, 2016

 

A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation

 


 

I ask Professor Kong ;

 

Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

 

''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''

 

Professor Kong reply ;

 

.....snip

 

''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''

 

Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA

 

END...TSS

 

Thursday, December 04, 2008 2:37 PM

 

"we have found that H-BSE can infect humans."

 

personal communication with Professor Kong. ...TSS

 

BSE-H is also transmissible in our humanized Tg mice.

 

The possibility of more than two atypical BSE strains will be discussed.

 

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

 


 


 

Monday, March 19, 2012

 

Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy PLoS One. 2012; 7(2): e31449.

 


 

Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain

 

▿ Qingzhong Kong1,*, Mengjie Zheng1, Cristina Casalone2, Liuting Qing1, Shenghai Huang1,†, Bikram Chakraborty1, Ping Wang1, Fusong Chen1, Ignazio Cali1, Cristiano Corona2, Francesca Martucci2, Barbara Iulini2, Pierluigi Acutis2, Lan Wang1, Jingjing Liang1, Meiling Wang1, Xinyi Li1, Salvatore Monaco3, Gianluigi Zanusso3, Wen-Quan Zou1, Maria Caramelli2 and Pierluigi Gambetti1,* + Author Affiliations

 

1Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106 2CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy 3Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy Next Section ABSTRACT Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to be caused by only one strain, BSE-C. BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE strains by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE strain-infected cattle. Sixty percent of the inoculated Tg mice became infected after 20 to 22 months of incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE strain-infected Tg mice, but none of the Tg mice infected with prions causing a sporadic human prion disease, showed the presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE strain-infected humanized Tg mouse brains are different from those from the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation times are observed for the BASE strain-infected Tg mice. These results suggest that in humans, the BASE strain is a more virulent BSE strain and likely lymphotropic.

 

Overwhelming evidence indicates that bovine spongiform encephalopathy (BSE), a prion disease that has been detected in several hundred thousand cattle in the United Kingdom and many other countries since the 1980s, has been transmitted to humans through the consumption of prion-contaminated beef, causing a prion disease named variant Creutzfeldt-Jakob disease (vCJD) (5, 19, 24). Over 200 cases of vCJD have been reported around the world (19). In 2004, two types of bovine prion disease that differ from the original BSE, now named classical BSE (BSE-C), were reported (3, 8). The two atypical BSE types were associated with prion protein (PrP) scrapie isoforms (PrPSc) that after protease digestion, displayed distinct electrophoretic mobility or ratios of the PrPSc glycoforms different from those of BSE-C (3, 8). Currently, a total of at least 36 cases of these two atypical BSE types have been reported for cattle older than 8 years (5; M. Caramelli, unpublished data). The two atypical BSE types are identified as BSE-H and bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L); the “L” and “H” identify the higher and lower electrophoretic positions, respectively, of their protease-resistant PrPSc isoforms (7). The bovine phenotype and the PrPSc molecular features of BASE have previously been described in detail (8). The histopathology of BASE and the PrP immunostaining pattern of BASE strains are characterized by the presence of prion amyloid plaques and a more rostral distribution of the PrPSc, which at variance with BSE-C is present in the cerebral cortex, including the hippocampus, but is underrepresented in the brain stem (8). These phenotypic features and PrPSc characteristics resemble a subtype of sporadic Creutzfeldt-Jakob disease (sCJD) named sCJDMV2, which affects subjects who are methionine (M)/valine (V) heterozygous at codon 129 of the PrP gene, and it is associated with PrPSc identified as type 2 (15). This similarity has raised the question of whether sCJDMV2 is not sporadic but acquired from the consumption of BASE strain-contaminated meat (5, 8). To begin to investigate the transmissibility to humans and the “human” disease phenotype of BASE, including the involvement of the lymphoreticular system, we have inoculated brain homogenates from BASE-affected cattle to transgenic (Tg) mice expressing normal human PrP with Met at codon 129 (HuPrP-129M) in a mouse PrP-ablated background [Tg(HuPrP)] (13). The inoculated Tg mice were examined for attack rates and the disease phenotype, including the presence and characteristics of protease-resistant PrPSc in the brain and spleen and the histopathology, along with the PrPSc topography and pattern of deposition in the brain.

 

snip...

 

Two distinct histopathological and PrP immunohistochemical phenotypes have been reported following BSE-C inoculation: one reproduced the distinctive features of vCJD with the “florid” plaques that intensely immunostained for PrP, and the other was reminiscent of sCJDMM1, with prominent spongiform degeneration and no plaque PrP immunostaining (1, 23). The brain histopathology, the PrPSc distribution, and the PrP immunostaining pattern of BASE strain-inoculated Tg40 mice were definitely distinct from such features described above (1, 23), further supporting the notion that BASE and classical BSE are associated with two distinct prion strains (8).

 

The relatively easy transmission of BASE to humanized Tg mice indicates that effective cattle prion surveillance should be maintained until the extent and origin of this and other atypical forms of BSE are fully understood.

 


 

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

 

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

 

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

 

"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.

 

Analysis: What that mad cow means

 

By STEVE MITCHELL, UPI Senior Medical Correspondent | March 15, 2006 at 6:27 PM

 

WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.

 

The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.

 

 These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

 

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

 

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

 

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

 

"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.

 

Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.

 

"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.

 

However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.

 

"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.

 

Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.

 

"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."

 

The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.

 

The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."

 

USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.

 

Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.

 

"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.

 

"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.

 

UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.

 

Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.

 

Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.

 

Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.

 

"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.

 


 

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

 

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

 

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

 

"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.

 

Emerg Infect Dis. 2006 Dec; 12(12): 1816–1821. doi: 10.3201/eid1212.060965 PMCID: PMC3291375

 

On the Question of Sporadic or Atypical Bovine Spongiform Encephalopathy and Creutzfeldt-Jakob Disease

 

Paul Brown,corresponding author* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§

 


 

PAUL BROWN COMMENT TO ME ON THIS ISSUE

 

Tuesday, September 12, 2006 11:10 AM

 

"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS

 


 


 

48 hr BSE confirmation turnaround took 7+ months to confirm this case, so the BSE MRR policy could be put into place. ...TSS

 

 -------- 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 OR, what the Honorable Phyllis Fong of the OIG found ;

 

Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program ­ Phase II and Food Safety and Inspection Service

 

Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III

 

Report No. 50601-10-KC January 2006

 

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain

 


 

FDA STATEMENT FOR IMMEDIATE RELEASE May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

 

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).

 

FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, 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.

 

To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.

 

Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.

 

FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.

 

#

 


 

SEE FULL TEXT OF ALL THIS HERE ;

 

2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

 


 

ALABAMA MAD COW CASE

 


 


 

Saturday, August 14, 2010

 

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

 

(see COPIOUS AMOUNTS OF mad cow feed in COMMERCE IN ALABAMA...TSS)

 


 

Texas BSE Investigation Final Epidemiology Report August 2005

 


 

State-Federal Team Responds to Texas BSE Case

 

JUNE 30, 2005

 

(please note 7+ month delay in final confirmation so the BSE MRR policy could be set in stone first. $$$...tss)

 


 


 

SEE ATTEMPTED COVER-UP BEFORE THE END AROUND BY FONG ET AL OF THE O.I.G

 

The U.S. Department of Agriculture confirmed June 29 that genetic testing had verified bovine spongiform encephalopathy (mad cow disease) in a 12-year-old cow that was born and raised in a Texas beef cattle herd.

 

Subsequent epidemiological investigations resulted in the culling and testing of 67 adult animals from the index herd. Bio-Rad tests for BSE were conducted on all 67 animals by the National Veterinary Services Laboratory (NVSL) in Ames, Iowa. All tests were negative.

 

On July 12, Texas officials lifted the quarantine on the source herd. At press time, USDA's Animal and Plant Health Inspection Service was tracing animals of the same age that had left the ranch.

 

Timeline

 

The BSE-positive animal was a Brahman-cross cow born and raised in a single Texas herd. The location of the ranch was not disclosed.

 

On Nov. 11, 2004, the 12-year-old cow was taken to a Texas auction market. Because of its condition, the cow was sent to Champion Pet Foods in Waco, Texas. The company produces several blends of dog food, primarily for the greyhound industry.

 

On Nov. 15, the animal arrived dead at Champion. Under procedures established by USDA's intensive surveillance program, a sample was sent to the USDA-approved Texas Veterinary Medical Diagnostic Testing Laboratory (TVMDL) at Texas A&M University.

 

Between June 1, 2004, and June 1, 2005, TVMDL tested nearly 34,000 samples from Texas, New Mexico, Arkansas and Louisiana. They tested the sample from Champion on Nov. 19 using a Bio-Rad ELISA rapid test for BSE. Initial results were inconclusive.

 

Because of the inconclusive results, a representative from USDA took the entire carcass to TVMDL where it was incinerated. USDA's Animal and Plant Health Inspection Service (APHIS) began tracing the animal and herd.

 

The sample was then sent to the National Veterinary Services Laboratory for further testing. Two Immunohistochemistry (IHC) tests were conducted and both were negative for BSE. At that point APHIS stopped their trace.

 

USDA scientists also ran an additional, experimental IHC "rapid" tissue fixation test for academic purposes. This test has not been approved internationally.

 

Some abnormalities were noted in the experimental test, but because the two approved tests came back negative, the results were not reported beyond the laboratory.

 

Monitoring by OIG

 

USDA's Office of Inspector General (OIG) has been monitoring implementation of the BSE expanded surveillance program and evaluating the following:

 

* Effectiveness of the surveillance program;

 

* Performance of BSE laboratories in complying with policies and procedures for conducting tests and reporting results;

 

* Enforcement of the ban on specified risk materials in meat products;

 

* Controls to prevent central nervous system tissue in advanced meat recovery products;

 

* Ante mortem condemnation procedures; and

 

* Procedures for obtaining brain tissue samples from condemned cattle.

 

While reviewing voluminous records, OIG auditors noticed conflicting test results on one sample-rapid inconclusive, IHC negative, experimental reactive.

 

Sample retested

 

At the recommendation of the Inspector General, the sample was retested during the week of June 5 with a second confirmatory test, the Western Blot. The results were reactive.

 

USDA scientists then conducted an additional IHC confirmatory test, using different antibodies from the November 2004 test. On Friday, June 10, Secretary of Agriculture Mike Johanns publicly announced the results as a "weak positive."

 

On June 16 an official with USDA's National Veterinary Services Laboratory hand-carried samples for further testing to the Veterinary Laboratory Agency (VLA) in Weybridge, England. Since 1991, the VLA has been a BSE reference laboratory for the World Organization for Animal Health (OIE).

 

Experts from the Weybridge lab confirmed the accuracy of the results of USDA's November confirmatory IHC test, concurring that the case could not have been confirmed on the basis of this sample. They also examined the November experimental IHC test and interpreted the results to be positive.

 

Weybridge also conducted additional tests, including IHC, OIE-prescribed Western Blot, NaTTA Western Blot and Prionics Western Blot tests.

 

To better understand the conflicting results, USDA also conducted Bio-Rad and IDEXX rapid screening tests, IHC and OIE-prescribed Western Blot. USDA also used DNA sequencing to determine the prion protein gene sequence of the animal.

 


 

Texas even had a 'secret' test that showed that mad cow positive; experimental IHC test results, because the test was not a validated procedure, and because the two approved IHC tests came back negative, the results were not considered to be of regulatory significance and therefore were not reported beyond the laboratory. . A Western blot test conducted the week of June 5, 2005, returned positive for BSE.

 


 

48 hr BSE confirmation turnaround took 7+ months to confirm this case, so the BSE MRR policy could be put into place. ...TSS

 

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

 

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

 

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

 

From: "Terry S. Singeltary Sr."

 

To: Carla EverettReferences: [log in to unmask]; [log in to unmask] ;

 

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: <[log in to unmask]><[log in to unmask] us><[log in to unmask]> <[log in to unmask]us> <[log in to unmask]>

 

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. ;

 

FROM HERE, IT TOOK 7 MONTHS TO CONFIRM THIS MAD COW, while the BSE MRR policy was being bought and sold...(in my opinion...tss)

 


 

Texas has been covering up mad cow disease for decades. on the second attempt at covering up a second mad cow in Texas, myself and others wrote to the Honorable Phyllis Fong of the OIG and asked for a second test be done in Weybridge, this after I wrote ever scientist around the globe. finally, this 2nd attempt at covering up mad cow disease in Texas failed, the Texas BSE madcow was finally confirmed, 7 months after a supposedly 48 hour turnaround on testing per their own BSE RED BOOK. this is why I have absolutely no faith in what’s going on now in Texas. it’s just another dog pony show imo...

 


 

BSE RED BOOK

 

Saturday, August 16, 2008

 

Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)

 


 

Statement of Gov. Rick Perry on BSE Announcement

 

Thursday, June 30, 2005 • Press Release

 

AUSTIN – Gov. Rick Perry issued the following statement today on the announcement by the U.S. Department of Agriculture that a cow recently tested for Bovine Spongiform Encephalopathy – commonly known as mad cow disease – is from a Texas herd.

 

“I want to urge calm and reassure the public that they can have the highest confidence in our beef supply, and the safeguards we have in place to protect the public from the spread of BSE. There is not, nor has there ever been, a known instance of BSE contaminating the food supply in Texas or anywhere else in the United States.

 

The animal in question was not processed into food or any other product. Texans can be sure that the beef they buy at their local supermarkets or restaurants is as safe today as it was yesterday, and I encourage Texans to continue to enjoy Texas beef products.”

 


 

Section 2. Testing Protocols and Quality Assurance Controls

 

In November 2004, USDA announced that its rapid screening test, Bio-Rad Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test result as part of its enhanced BSE surveillance program. The ELISA rapid screening test performed at a BSE contract laboratory produced three high positive reactive results.40 As required,41 the contract laboratory forwarded the inconclusive sample to the APHIS National Veterinary Services Laboratories (NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again produced three high positive reactive results.42 In accordance with its established protocol, NVSL ran its confirmatory test, an immunohistochemistry (IHC) test, which was interpreted as negative for BSE. In addition, NVSL performed a histological43 examination of the tissue and did not detect lesions44 consistent with BSE.

 

Faced with conflicting results, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded no further testing was necessary because testing protocols were followed. In our discussions with APHIS officials, they justified their decision not to do additional testing because the IHC is internationally recognized as the "gold standard." Also, they believed that conducting additional tests would undermine confidence in USDA’s established testing protocols.

 


 

USDA orders silence on mad cow in Texas

 

Susan Combs by no means has public and consumer health at heart while she is protecting the cattle industry. She is oblivious to mad cow disease. Her soul purpose is to protect the cattle industry at all cost, including my mothers life (DOD 12/14/97), or maybe one of your family members from any strain of mad cow disease in TEXAS. SHE helped cover-up mad cow disease in TEXAS both on that inconclusive that was positive so many times it will make your head spin. PLUS, the other mad cow in TEXAS they rendered without testing at all, that came from the top out of Austin. THEY should be tried for murder. corporate homicide is what i call it. they knew for years, but kept on keeping on.

 


 

Faced with conflicting results between the rapid screening and IHC tests, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded that no further testing was necessary since testing protocols were followed and the confirmatory test was negative. In our discussions with APHIS officials, they justified their decision to not do additional testing because the IHC test is internationally recognized as the “gold standard” of testing. Also, they believed that

 

USDA/OIG-A/50601-10-KC/ Page iv

 

conducting additional tests would undermine confidence in USDA’s testing protocols.

 

OIG obtained evidence that indicated additional testing was prudent. We came to this conclusion because the rapid screening tests produced six high positive reactive results, the IHC tests conflicted, and various standard operating procedures were not followed. Also, our review of the relevant scientific literature, other countries’ protocols, and discussions with experts led us to conclude that additional confirmatory testing should be considered in the event of conflicting test results.

 

To maintain objectivity and independence, we requested that USDA’s Agricultural Research Service (ARS) perform the Office International des Epizooties (OIE) Scrapie-Associated Fibrils (SAF) immunoblot test. The additional testing produced positive results. To confirm, the Secretary of Agriculture requested that an internationally recognized BSE laboratory in Weybridge, England (Weybridge) perform additional testing. Weybridge conducted various tests, including their own IHC tests and three Western blot tests. The tests confirmed that the cow was infected with BSE. The Secretary immediately directed USDA scientists to work with international experts to develop new protocols that include performing dual confirmatory tests in the event of an inconclusive BSE screening test.

 

We attribute the failure to identify the BSE positive sample to rigid protocols, as well as the lack of adequate quality assurance controls over its testing program. Details of our concerns are discussed in Findings 3 and 4.

 


 


 

Texas BSE Investigation Final Epidemiology Report August 2005

 

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.

 

Background of the Investigation

 

On June 10, 2005, USDA announced that the November 2004 inconclusive BSE sample tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s National Animal Disease Center (NADC) upon the recommendation of USDA’s Office of the Inspector General. Samples were sent to a World Organization for Animal Health (OIE) reference laboratory for BSE in Weybridge, England, for confirmatory tests. Farm A, located in Texas, was the suspected farm of origin for the index cow and was placed under hold order on June 20, 2005 pending confirmation of the positive results and DNA analysis of the herd. Weybridge confirmed the BSE positive on June 24, 2005. The carcass of the index cow had been disposed of by incineration in November 2004.

 


 

News Release

 

Texas Animal Health Commission

 

Box l2966 * Austin, Texas 78711 * (800) 550-8242 * FAX (512) 719-0719

 

Bob Hillman, DVM * Executive Director

 

For info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710, or mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:mailto:ceverett@tahc.state.tx.us

 

For immediate release---

 

State-Federal Team Responds to Texas BSE Case

 

The US Department of Agriculture announced June 29 that genetic testing has verified that an aged cow that tested positive for Bovine Spongiform Encephalopathy or BSE originated from a Texas beef cattle herd. Tissues for laboratory testing were initially collected from the animal in November 2004, and the carcass was incinerated and did not enter the human food, animal feed or fertilizer supply system. While tests in November indicated the animal did not have BSE, retesting in England in June confirmed the animal had the disease. The Texas Animal Health Commission (TAHC), the state’s livestock and poultry health regulatory agency, and USDA have jointly assigned a state-federal team to conduct the epidemiological investigation and response.

 

“The TAHC and US Department of Agriculture’s Veterinary Services are working with a complement of experts from federal and state animal health, food safety, public health and feed regulatory agencies to ensure the continued safety and wholesomeness of our meat supply,” said Dr. Bob Hillman, Texas state veterinarian and executive director of the TAHC, the state’s livestock and poultry health regulatory agency. “Epidemiological investigations are thorough and focus on verifying the herd of origin, and when, where and how the animal and potentially, any herd mates, were exposed to the abnormal prion, or disease agent, that causes BSE. Additionally, epidemiology investigations trace the infected animal’s movement and herd mates. Animals potentially exposed to the disease will be depopulated, with proper disposal. The animals will not be introduced into the human or animal food chain.”

 

The USDA’s BSE testing protocol requires testing of emaciated or injured cattle, cattle that exhibit central nervous system disorder, cattle unable to rise or to walk normally, and cattle that die of unknown causes. Since June 1, 2004, brain tissue samples from more than 394,000 cattle have been tested in the U.S. and were negative for BSE. Of those, 38,320 were tested in Texas, Dr. Hillman noted. BSE surveillance has been conducted in the U.S. since l990.

 

The U.S. has taken preventive measures against the introduction of BSE since l989, when prohibitions were placed on cattle and other ruminants from BSE-affected countries, noted Dr. Hillman. In 1997, the importation ban was extended to all of Europe.

 

Dr. Hillman said the U.S. Food and Drug Administration (FDA) in 1997 banned the use of ruminant-derived protein (from animals such as cattle and sheep) in feed for cattle and other ruminants. There is no evidence that BSE spreads from live animal to animal in the herd, but cattle can be exposed by eating feed that contains rendered protein from infected animals. “These measures taken by the USDA and the FDA are safeguards that work to protect livestock, and ultimately, our meat supply,” he said.

 

--30--

 


 

Second BSE case occurred in Texas, USDA says Jun 30, 2005 (CIDRAP News) – The United States' second case of bovine spongiform encephalopathy (BSE) was in a 12-year-old cow that came from a Texas herd and would have been made into pet food if it hadn't been flagged for BSE testing, federal officials announced yesterday evening.

 

US Department of Agriculture (USDA) officials said the cow was to be processed at a pet food plant in Waco, Tex., when it was diverted for testing because it couldn't walk. Officials didn't name the plant or say exactly where the cow came from. But an Associated Press (AP) report today identified the plant as Champion Pet Food in Waco and said the cow was already dead when brought there last November.

 

"The source herd is now under a hold order as we identify animals of interest within the herd," USDA Chief Veterinarian John Clifford said in a prepared statement. Investigators will look for cattle born within a year before or after the BSE-infected cow and any of the cow's offspring born within the past 2 years, he explained.

 

"If the age of the animal cannot be pinpointed, then we may expand our inquiry to include all animals in this herd before the feed ban went into place in 1997," Clifford said. To prevent BSE, the government banned putting cattle protein into cattle feed in August 1997.

 

The infected cow was incinerated, and no parts were used in human food or animal feed, according to the USDA. "The safety of our food supply is not in question," Clifford stated.

 

Because of the cow's age, the USDA suspects it became infected by eating contaminated feed before the government ban began in 1997. The USDA and the Food and Drug Administration (FDA) will try to trace the source herd's feed history, officials said.

 

The FDA will also check whether firms that may have processed meat-and-bone meal from animals from that herd have complied with the 1997 feed ban, Dr. Steve Sundlof, director of the FDA's Center for Veterinary Medicine, said at a news conference last night.

 

The Texas case is the first US BSE case in a native-born animal; Clifford said the cow lived on one farm all its life. The previous US case, found in December 2003, involved a Canadian-born dairy cow in Washington state.

 

An initial screening test on the Texas cow last November was inconclusive, and two confirmatory immunohistochemistry tests were negative. But early this month the USDA's inspector general ordered a Western blot test, which came back positive. Further confirmatory tests at an international reference lab in Britain were also positive, prompting the USDA to announce the findings last week.

 

The USDA waited for the results of DNA tests before announcing that the infected cow came from Texas. The step was necessary because parts of the infected cow were stored with those of four other cattle, causing some uncertainty, officials said.

 

"We felt that we had the correct herd; we wanted to identify that appropriately with DNA," Clifford said at the news conference. Investigators analyzed DNA from the infected animal and then looked for relatives in the presumed source herd by analyzing DNA from members of the herd, he said. The investigation turned up two cattle that are related to the infected cow, he added.

 

The AP report said Champion Pet Food is under contract to take samples from animals in poor health. The company's owner, Benjy Bauer, told the AP that his workers took samples from the cow and sent them to the Texas Veterinary Diagnostic Laboratory at Texas A&M University. The lab is one of several the USDA uses to screen cattle for BSE, the story said.

 

See also:

 

USDA news release

 


 

USDA fact sheet on BSE epidemiologic investiation

 


 

USDA press conference transcript

 


 

TEXAS OFFICIALS DEAD WRONG ON AMOUNT OF INFECTIVITY TO CAUSE A TSE PRION DISEASE ;

 

"FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds."

 

5.5 GRAMS OF INFECTIOUS PROHIBITED MAD COW FEED FOR EACH OF THE 1,222 ANIMALS (5.5 GRAMS X 1,222 ANIMALS) IS ENOUGH INFECTIOUS MAD COW FEED TO KILL A SMALL HERD OF COWS...TSS

 

U.S. Food and Drug Administration FDA News | Today the Food and Drug Administ…U.S. Food and Drug Administration FDA News

 

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle — a violation of FDA’s 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

 

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds.

 

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

 

According to Dr. Bernard Schwetz, FDA’s Acting Principal Deputy Commissioner, “The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture’s (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE.”

 

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

 

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

 

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

 

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

 


 

FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

 

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT

 

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

 

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

 

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

 

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

 

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

 

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

 

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

 

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

 


 


 

Friday, April 15, 2016

 

Whole Blood Gene Expression Profiling in Preclinical and Clinical Cattle Infected with Atypical Bovine Spongiform Encephalopathy

 


 

Saturday, April 16, 2016

 

*** APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission ***

 


 

Thursday, January 29, 2015

 

Atypical H-TYPE BSE Case Confirmed in Norway

 


 

Tuesday, April 12, 2016

 

The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging reindeer from the Nordfjella population in South-Norway.

 


 

Tuesday, June 14, 2016

 

*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag Norway ***

 


 

Thursday, July 07, 2016

 

Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd Norwegian moose

 

14/06/2016 - Norway reports a third case

 


 

Sunday, July 17, 2016

 

CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016

 


 

Saturday, May 28, 2016

 

*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***

 


 

Monday, May 02, 2016

 

*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***

 


 

*** NIH awards $11 million to UTHealth researchers to study deadly CWD prion diseases Claudio Soto, Ph.D. ***

 

Public Release: 29-Jun-2016

 


 

Tuesday, July 12, 2016

 

Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE, TSE, Prion Zoonosis Science History

 

see history of NIH may destroy human brain collection

 


 

I urge everyone to watch this video closely...terry

 

*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***

 


 

Sunday, July 24, 2016

 

Chronic Wasting Disease Prions in Elk Antler Velvet and Marketing of this Product in Nutritional Supplements for Humans?

 

Research Project: TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: THE ROLE OF GENETICS, STRAIN VARIATION, AND ENVIRONMENTAL CONTAMINATION IN DISEASE CONTROL

 


 

Saturday, April 23, 2016

 

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X

 


 

Saturday, July 16, 2016

 

Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10

 

WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.

 

THIS is absolutely insane. it’s USDA INC.

 


 

Tuesday, June 07, 2016

 

Comparison of two US sheep scrapie isolates supports identification as separate strains

 

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

 


 

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

 

see Singeltary comment ;

 


 

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

 


 

P.9.21

 

Molecular characterization of BSE in Canada

 

Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada

 

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.

 

Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.

 

Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

 

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

 

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. *This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. ***It also suggests a similar cause or source for atypical BSE in these countries.

 

*** 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

 


 

SEE THE DRASTIC REDUCTION OF CONFIRMED BSE CASES IN THE UK ONCE THE FEED BAN TOOK HOLD FROM THE TOP YEAR DOWN TO THE FIRST ZERO YEAR ;

 

1992 36680 SLAUGHTERED SUSPECTS IN WHICH BSE CONFIRMED

 

2013 0 0 0 0 0 0 0 0

 


 


 


 


 


 

Saturday, January 31, 2015

 

RAPID ADVICE 17-2014 : Evaluation of the risk for public health of casings in countries with a “negligible risk status for BSE” and on the risk of modification of the list of specified risk materials (SRM) with regard to BSE

 


 

In the USA, USDA et al sometimes serves SRM’s up as appetizers or horderves.

 

Thursday, November 28, 2013

 

Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows

 


 

seems USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ???

 

Saturday, September 21, 2013

 

Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT

 


 

DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???

 

this recall was not for the welfare of the animals. ...tss you can check and see here ; (link now dead, does not work...tss)

 


 

try this link ;

 


 

Sunday, November 13, 2011

 

*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock

 


 

Wednesday, March 2, 2016

 

RANCHO He did not know that they were placing healthy cow heads next to suspect carcasses 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

 


 

Thursday, June 12, 2014

 

Missouri Firm Recalls Ribeye and Carcass Products That May Contain Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal root ganglia may not have been completely removed

 


 

Saturday, November 10, 2012

 

Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials Nov 9, 2012 WI Firm Recalls Beef Tongues

 


 

Saturday, July 23, 2011

 

CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

 


 

Sunday, October 18, 2009

 

Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009

 


 

Thursday, October 15, 2009

 

Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009

 


 

Thursday, June 26, 2008

 

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

 


 

Tuesday, July 1, 2008

 

Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs

 


 

Friday, August 8, 2008

 

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed

 


 

Saturday, April 5, 2008

 

SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

 


 

Wednesday, April 30, 2008

 

Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings

 


 

Wednesday, April 30, 2008

 

Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings

 


 

Friday, October 15, 2010

 

BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle

 


 

SPECIFIED RISK MATERIALS SRMs

 


 

USDA BSE TSE PRION SURVEILLANCE, FEED, TESTING, SRM FIREWALLS...LMAO!

 

THE USDA FDA TRIPLE MAD COW DISEASE FIREWALL, WERE NOTHING MORE THAN INK ON PAPER !

 

infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et al TRIPLE MAD COW FIREWALL, 10 YEARS AFTER ;

 

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

 


 

Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV

 

Date: September 6, 2006 at 7:58 am PST

 

PRODUCT

 

a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick Starter, Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d) Performance Pheasant Finisher, Recall # V-133-6.

 

CODE None

 

RECALLING FIRM/MANUFACTURER

 

Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.

 

REASON

 

Dairy and poultry feeds were possibly contaminated with ruminant based protein.

 

VOLUME OF PRODUCT IN COMMERCE

 

477.72 tons

 

DISTRIBUTION

 

AL

 

______________________________

 

PRODUCT

 

a) Dairy feed, custom, Recall # V-134-6; b) Custom Dairy Feed with Monensin, Recall # V-135-6. CODE None. Bulk product

 

RECALLING FIRM/MANUFACTURER

 

Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006.

 

Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete.

 

REASON

 

Possible contamination of dairy feeds with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

1,484 tons

 

DISTRIBUTION

 

TN and WV

 


 

Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS

 

Date: August 16, 2006 at 9:19 am PST

 

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-115-6

 

CODE None

 

RECALLING FIRM/MANUFACTURER

 

Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing.

 

REASON

 

Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

Approximately 2,223 tons

 

DISTRIBUTION

 

KY

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-116-6

 

CODE None

 

RECALLING FIRM/MANUFACTURER

 

Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing.

 

REASON

 

Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

1,220 tons

 

DISTRIBUTION

 

KY

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-117-6

 

CODE None

 

RECALLING FIRM/MANUFACTURER

 

Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed.

 

REASON

 

Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

40 tons

 

DISTRIBUTION

 

LA and MS

 

______________________________

 

PRODUCT

 

Bulk Dairy Feed, Recall V-118-6

 

CODE None

 

RECALLING FIRM/MANUFACTURER

 

Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete.

 

REASON

 

Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

7,150 tons

 

DISTRIBUTION

 

MS

 

______________________________

 

PRODUCT

 

Bulk custom dairy pre-mixes, Recall # V-119-6

 

CODE None

 

RECALLING FIRM/MANUFACTURER

 

Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm initiated recall is complete.

 

REASON

 

Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

87 tons

 

DISTRIBUTION

 

MS

 

______________________________

 

PRODUCT

 

Bulk custom dairy pre-mixes, Recall # V-120-6

 

CODE None

 

RECALLING FIRM/MANUFACTURER

 

Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.

 

REASON

 

Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

350 tons

 

DISTRIBUTION

 

AL and MS

 

______________________________

 

PRODUCT

 

a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6; b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6; c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6; d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6; e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6; f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6; g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6

 

CODE

 

All products manufactured from 02/01/2005 until 06/20/2006

 

RECALLING FIRM/MANUFACTURER

 

Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.

 

REASON

 

Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".

 

VOLUME OF PRODUCT IN COMMERCE

 

7,541-50 lb bags

 

DISTRIBUTION

 

AL, GA, MS, and TN

 

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

 

###

 


 

Subject: MAD COW FEED RECALL MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs

 

Date: August 6, 2006 at 6:14 pm PST

 

PRODUCT

 

Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6

 

CODE

 

All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.

 

RECALLING FIRM/MANUFACTURER

 

Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.

 

REASON

 

The feed was manufactured from materials that may have been contaminated with mammalian protein.

 

VOLUME OF PRODUCT IN COMMERCE

 

27,694,240 lbs

 

DISTRIBUTION

 

MI

 

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

 

###

 


 

Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

 

Date: August 6, 2006 at 6:16 pm PST

 

PRODUCT

 

a) CO-OP 32% Sinking Catfish, Recall # V-100-6; b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6; e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6; f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; j) CO-OP LAYING CRUMBLES, Recall # V-109-6; k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6; l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6; m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6

 

CODE

 

Product manufactured from 02/01/2005 until 06/06/2006

 

RECALLING FIRM/MANUFACTURER

 

Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.

 

REASON

 

Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".

 

VOLUME OF PRODUCT IN COMMERCE

 

125 tons

 

DISTRIBUTION

 

AL and FL

 

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

 

###

 


 

Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? Date: August 6, 2006 at 6:19 pm PST

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-114-6

 

CODE None

 

RECALLING FIRM/MANUFACTURER

 

Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.

 

REASON

 

Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

?????

 

DISTRIBUTION

 

KY

 

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

 

###

 


 

CJD WATCH MESSAGE BOARD TSS

 

MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE

 

Sun Jul 16, 2006 09:22

 

71.248.128.67

 

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II

 

______________________________

 

PRODUCT

 

a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6; b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6; c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6; d) Feather Meal, Recall # V-082-6 CODE a) Bulk b) None c) Bulk d) Bulk

 

RECALLING FIRM/MANUFACTURER

 

H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.

 

REASON

 

Possible contamination of animal feeds with ruminent derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

10,878.06 tons

 

DISTRIBUTION

 

Nationwide

 

END OF ENFORCEMENT REPORT FOR July 12, 2006

 

###

 


 

Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006

 

Date: June 27, 2006 at 7:42 am PST

 

Public Health Service

 

Food and Drug Administration

 

New Orleans District 297 Plus Park Blvd. Nashville, TN 37217

 

Telephone: 615-781-5380 Fax: 615-781-5391

 

May 17, 2006

 

WARNING LETTER NO. 2006-NOL-06

 

FEDERAL EXPRESS OVERNIGHT DELIVERY

 

Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204

 

Dear Mr. Shirley:

 

On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).

 

Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:

 

You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.

 

You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.

 

As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.

 

This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.

 

You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.

 

Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.

 

Sincerely,

 

/S

 

Carol S. Sanchez Acting District Director New Orleans District

 


 

SINCE THE LAST TIME I REPORTED :

 

Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through September 30, 2005

 

Date: March 20, 2006 at 12:58 pm PST

 

YOU can see that report at the bottom of this update.

 

UPDATEs AS FOLLOWS ;

 

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT July 1, 2006 through September 30, 2006

 

snip...

 

Table 5. Administrative Actions: Large HACCP Plants (7/01/06 to 9/30/06)

 

Administrative Actions Pending or Taken at Large HACCP Plants [includes actions initiated in prior quarters]

 

CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS

 

On 6/15/06, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

snip...

 

EXCEL CORP 00086R M FORT MORGAN, CO

 

On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.

 

snip...

 

TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

TYSON FRESH MEATS INC. 00245L M LEXINGTON, NE X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

snip...

 

Table 6. Administrative Actions: Small HACCP Plants (7/01/06 to 9/30/06)

 

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

 

SSOP HACCP SPS INH INT Other LOI LOW

 

BOOKER PACKING COMPANY 07162 M BOOKER, TX 6/2/06 6/5/06 X 9/19/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

SSOP HACCP SPS INH INT Other LOI LOW

 

GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X 8/31/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

HI COUNTRY BEEF JERKY 01248 M01248 P LINCOLN, MT 3/24/06 4/14/06 X 8/31/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X 8/15/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

 

GIBSON PACKING COMPANY 05843 M05843 P SEYMOUR, MO 9/21/06 X Plant failed to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli). The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

SSOP HACCP SPS INH INT Other LOI LOW

 

HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X 9/26/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06 4/14/06 6/30/06 7/5/06 X 8/11/06 On 3/16/06, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E.coli) was issued. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X 7/25/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 


 

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT April 1, 2006 through June 30, 2006

 

Table 5. Administrative Actions: Large HACCP Plants (4/01/06 to 6/30/06)

 

CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X On 6/15/06, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

snip...

 

EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On

 

12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.

 

snip...

 

TYSON FRESH MEATS INC 00245L M LEXINGTON, NE X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

snip...

 

SSOP HACCP SPS INH INT Other LOI LOW

 

TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

snip...

 

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

 

BOOKER PACKING COMPANY 07162 M BOOKER, TX 4/13/06 4/19/06 X Plant failed to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli).

 

6/2/06 6/5/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

???

 

3/24/06 4/14/06

 

X

 

The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

C & C MEAT SALES, INC., 18494 M18494 P, DURHAM, NC ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.

 

snip...

 

FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X 4/13/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

FRONTIER FOODS & COLD STORAGE, INC 20741 M20741 P EL PASO, TX 5/31/06 X On 6/8/06, DM closed case by firm’s requested voluntary withdrawal. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X 5/19/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06 4/14/06 6/30/06 X On 3/16/06, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E.coli) was issued. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

SAVORY CONNECTION, INC., 31764 M31764 P, SELINGSGROVE, PA. ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.

 

snip...

 

STEAK MASTER, 21159 M21159 P, ELWOOD, NE. ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.

 

snip...

 

THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X 4/4/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X 5/4/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 


 

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT January 1, 2006 through March 31, 2006

 

Table 5. Administrative Actions: Large HACCP Plants (1/01/06 to 3/31/06)

 

CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X 3/13/06 On 10/11/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

snip...

 

EXCEL CORP. 00086R M FORT MORGAN, CO 8/11/04 2/22/05 X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.

 

snip...

 

TYSON FRESH MEATS INC. 00245L M 3/12/04 3/18/04 X

 

LEXINGTON, NE

 

X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

snip...

 

TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

snip...

 

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

 

GULF PACKING COMPANY, 00696 M00696 P, SAN BENITO, TX, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

HI COUNTRY BEEF JERKY, 01248 M01248 P, LINCOLN, MT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

HITCHIN POST STEAK COMPANY, 20773 M20773 P, KANSAS CITY, KS, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

ROCK CREEK SLAUGHTER CO., 09150 M09150 P, FAIRBURY, NE, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

Table 7. Administrative Actions: Very Small HACCP Plants (1/01/06 to 3/31/06)

 

A.J. CEKAK'S MEAT MARKET 21562 M ORD. NE, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

ALTA VISTA LOCKER 31931 M ALTA VISTA, KS, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

C&C MEAT SALES, INC. 18494 M18494 P UPPER MARLBORO, MD 2/27/06 3/16/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X 3/6/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X 1/13/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

PARAGON SPRAY DRYING, L.L.C. 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X 2/9/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

SAVORY CONNECTION, INC. 31764 M31764 P SELINGSGROVE, PA 3/14/06 3/31/06 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

STEAK MASTER, 21159 M21159 P, ELWOOD, NW, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

TEARS MARKET, 04535 M04535 P, PENN YAN, NY, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

THE MEAT SHOP, 31561 M BENSON, VT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

THEURER'S QUALITY MEATS, INC. 31647 M31647 P, LEWISTON, UT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

TOOELE VALLEY MEATS 20594 M20594 P, GRANTSVILLE, UT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

 

snip...

 

WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 

WILLIAM. G. MEST PACKING CO. 04431 M STRYKERSVILLE, NY 2/2/06 2/23/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. On 3/21/06, NOIE was modified and reissued. On 6/29/06, NOIE was rescinded.

 

YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X 2/23/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

snip...

 


 

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005

 

SRM REMOVAL USA

 

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005

 

snip....

 

CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X X On 10/11/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.

 

00245L M LEXINGTON, NE 3/12/04 3/18/04 X 5/4/05 X X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

9/16/05 9/29/05 X X TYSON FRESH MEATS INC. 09268 M PASCO, WA X X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

TYSON FRESH MEATS INC. X X 00245D M EMPORIA, KS On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

 

DESERET MEAT 04852 M SPANISH FORK, UT 7/20/05 8/1/05 X X 12/29/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

A.J. CEKAK'S MEAT MARKET 9/1/05 9/20/05 X X X On 9/1/05, an enforcement action 21562 M concerning failure to meet regulatory ORD, NE requirements for Escherichia coli Biotype 1 (E. coli) was taken. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

ALTA VISTA LOCKER 10/5/05 10/26/05 X X The enforcement action included, as a 31931 M basis, failure of the establishment toALTA VISTA, KS comply with Agency requirements concerning specified risk material.

 

BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 8/8/05 8/16/05 X X X 11/16/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

CHAMPLAIN BEEF INC 2/28/05 3/4/05 3/8/05 X X X 08547 M WHITEHALL, NY 10/17/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

FIVE STAR PACK INC. 9/1/05 9/9/05 X X 12/29/05 On 9/1/05, an enforcement action 08725 M08725 P concerning failure to meet regulatory GOLDEN CITY, MO requirements for Escherichia coli Biotype 1 (E. coli) was taken. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. FRESH FARMS BEEF 12/16/05 12/28/05 X X X The enforcement action included, as a 18579 M basis, failure of the establishment toRUTLAND, VT comply with Agency requirements concerning specified risk material.

 

GOETZ AND SONS WESTERN 11/15/05 11/23/05 12/1/05 X X MEATS INC 06245 M06245 P EVERETT, WA 12/17/05 12/28/05 X X X On 12/17/05, firm violated a regulatory control action by selling U.S.D.A retained product.

 

H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 7/28/05 8/1/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 7/26/05 7/29/05 X X 11/15/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. PARAGON SPRAY DRYING, LLC 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

S & S MEAT COMPANY 01046 M01046 P KANSAS CITY, MO 8/4/05 8/19/05 X X 11/16/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

STEAK MASTER 21159 M21159 P ELWOOD, NE 11/4/05 11/17/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X X X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

THEURER'S QUALITY MEATS, INC 31647 M31647 P LEWISTON, UT 7/27/05 7/29/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

TOOELE VALLEY MEATS 20594 M20594 P GRANTSVILLE, UT 7/25/05 8/1/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

WALNUT VALLEY PACKING LLC 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

 

full text 54 pages ;

 


 

Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through September 30, 2005 Date: March 20, 2006 at 12:58 pm PST

 

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT July 1, 2005 through September 30, 2005

 

snip...

 

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

DESERET MEAT 04852 M SPANISH FORK, UT 07/27/05 08/01/05 X On 7/27/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

 

snip...

 

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

MONTEBELLO MEAT PROCESSING, INC 19075 M19075 P MANATI, PR 08/01/05 08/18/05 X 09/26/05 On 8/1/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

 

snip...

 

Table 7. Administrative Actions: Very Small HACCP Plants (7/01/05 to 9/30/05)

 

snip...

 

A.J. CEKAK'S MEAT MARKET 09/01/05 09/20/05 On 9/1/05, an enforcement action

 

21562 M

 

concerning failure to meet regulatory ORD, NE requirements for Escherichia coli X X X Biotype 1 (E. coli) and Bovine Spongiform Encephalopathy/Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

 

snip...

 

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 08/08/05 08/16/05 X On 8/8/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

 

snip...

 

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

FIVE STAR PACK INC. 08725 M08725 P GOLDEN CITY, MO 09/01/05 09/09/05 X X On 9/1/05, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli) and Bovine Spongiform Encephalopathy/Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

 

snip...

 

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

H AND P MEATS 21352 M SOUTH PITTSBURG, TN 07/28/05 08/08/05 08/17/05 08/19/05 X X On 8/17/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

 

snip...

 

HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 07/28/05 08/01/05 X On 7/28/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

 

snip...

 

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 07/26/05 07/29/05 X X On 7/26/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

 

snip...

 

PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 09/21/05 X On 9/21/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

 

PARAGON SPRAY DRYING, LLC 31792 M31792 P WAUKON, IA 09/06/05 09/12/05 X On 9/6/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

 

snip...

 

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 07/01/05 07/28/05 X On 7/1/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

 

snip...

 

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

08/04/05

 

08/19/05

 

On 8/4/05,

 

an enforcement action 01046 M01046 P concerning Bovine SpongiformKANSAS CITY, MO X X Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

 

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

 

snip...

 

THE MEAT SHOP 08/18/05 09/06/05

 

09/09/05

 

On 9/6/05, a suspension action 31561 M concerning Bovine SpongiformBENSON, VT Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3. XX X X X

 

THEURER'S QUALITY MEATS, 07/27/05 07/29/05

 

On 7/27/05, a suspension action INC concerning Bovine Spongiform31647 M31647 P Encephalopathy and Specified Risk X X

 

LEWISTON, UT Material was taken in accordance with 9 CFR Part 500.3.

 

TOOELE VALLEY MEATS 07/25/05 08/01/05

 

On 7/25/05, a suspension action 20594 M20594 Pconcerning Bovine Spongiform

 

GRANTSVILLE, UT X X Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

 

snip...

 

52 pages

 


 

PREVIOUS

 


 


 


 

Monday, June 23, 2014

 

PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES

 

***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion

 

Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada

 

Keywords: Atypical BSE, oral transmission, RT-QuIC

 

The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.

 

The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.

 

Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.

 

P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)

 

Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA

 

Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein

 

Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.

 

Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.

 

Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.

 

Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

 

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

 

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.

 


 

Wednesday, May 30, 2012

 

PO-028: Oral transmission of L-type bovine spongiform encephalopathy (L-BSE) in primate model Microcebus murinus

 

Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel Verdier1

 

1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux Civils de Lyon; Lyon, France

 

Here, we demonstrate that the L-BSE agent can be transmitted by oral route from cattle to young and adult mouse lemurs. In comparison to IC inoculated animals, orally challenged lemurs were characterized by longer survival periods as expected with this route of infection.

 


 

 P04.27

 

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

 

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

 

Background:

 

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

 

Aims:

 

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

 

Methods:

 

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

 

Results:

 

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

 

Conclusions:

 

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.

 

The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

 


 

What Do We Feed to Food-Production Animals? A Review of Animal FeedIngredients and Their Potential Impacts on Human Health

 

Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker11Johns Hopkins Center for a Livable Future, Bloomberg School of PublicHealth, Baltimore, Maryland, USA; 2Maryland Institute forApplied Environmental Health, College of Health and Human Performance,University of Maryland, College Park, Maryland, USA;3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA

 

snip...

 

Table 1. Animal feed ingredients that are legally used in U.S. animal feeds

 

Animal

 

Rendered animal protein from Meat meal, meat meal tankage, meat and bonemeal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals andother meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, andanimal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products

 

snip...

 

Conclusions

 

Food-animal production in the United States has changed markedly in the past century, and these changes have paralleled major changes in animal feed formulations. While this industrialized system of food-animal production may result in increased production efficiencies, some of the changes in animal feeding practices may result in unintended adverse health consequences for consumers of animal-based food products. Currently, the use of animal feed ingredients, including rendered animal products, animal waste, antibiotics, metals, and fats, could result in higher levels of bacteria, antibiotic resistant bacteria, prions, arsenic, and dioxin like compounds in animals and resulting animal-based food products intended for human consumption. Subsequent human health effects among consumers could include increases in bacterial infections (antibiotic resistant and nonresistant) and increases in the risk of developing chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide range of potential human health impacts that could result from animal feeding practices, there are little data collected at the federal or state level concerning the amounts of specific ingredients that are intentionally included in U.S. animal feed. In addition, almost no biological or chemical testing is conducted on complete U.S. animal feeds; insufficient testing is performed on retail meat products; and human health effects data are not appropriately linked to this information. These surveillance inadequacies make it difficult to conduct rigorous epidemiologic studies and risk assessments that could identify the extent to which specific human health risks are ultimately associated with animal feeding practices. For example, as noted above, there are insufficient data to determine whether other human foodborne bacterial illnesses besides those caused by S. enterica serotype Agona are associated with animal feeding practices. Likewise, there are insufficient data to determine the percentage of antibiotic-resistant human bacterial infections that are attributed to the nontherapeutic use of antibiotics in animal feed. Moreover, little research has been conducted to determine whether the use of organoarsenicals in animal feed, which can lead to elevated levels of arsenic in meat products (Lasky et al. 2004), contributes to increases in cancer risk. In order to address these research gaps, the following principal actions are necessary within the United States: a) implementation of a nationwide reporting system of the specific amounts and types of feed ingredients of concern to public health that are incorporated into animal feed, including antibiotics, arsenicals, rendered animal products, fats, and animal waste; b) funding and development of robust surveillance systems that monitor biological, chemical, and other etiologic agents throughout the animal-based food-production chain “from farm to fork” to human health outcomes; and c) increased communication and collaboration among feed professionals, food-animal producers, and veterinary and public health officials.

 

REFERENCES...snip...end

 

Sapkota et al.668 VOLUME 115 NUMBER 5 May 2007 • Environmental Health Perspectives

 


 

Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. ......... http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose

 

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused7% (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, NathalieLescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-PhilippeDeslysSummary The uncertain extent of human exposure to bovine spongiformencephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease(vCJD)--is compounded by incomplete knowledge about the efficiency of oralinfection and the magnitude of any bovine-to-human biological barrier totransmission. We therefore investigated oral transmission of BSE tonon-human primates. We gave two macaques a 5 g oral dose of brain homogenatefrom a BSE-infected cow. One macaque developed vCJD-like neurologicaldisease 60 months after exposure, whereas the other remained free of diseaseat 76 months. On the basis of these findings and data from other studies, wemade a preliminary estimate of the food exposure risk for man, whichprovides additional assurance that existing public health measures canprevent 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 inoculumused in our study with primates against a bovine brain inoculum with asimilar 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. icip=intracerebral and intraperitoneal.

 

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

 

Published online January 27, 2005

 


 

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.

 


 

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. ...

 


 


 

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...

 


 


 


 

”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” ...page 26.

 


 

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

 


 

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 ***

 


 

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

 


 

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

 


 

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

 

see Singeltary comment ;

 


 

Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission

 


 


 


 

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

 

Monday, November 16, 2015

 

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

 


 

Draft Guidance for Industry on Ensuring Safety of Animal Feed Maintained and Fed On-Farm; Availability

 

# 203 entitled “Ensuring Safety of Animal Feed Maintained and Fed On-Farm.”

 


 

Terry S. Singeltary Sr. submission ;

 


 

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

 

Posted: 12/30/2014ID: APHIS-2014-0107-0001

 


 

Notice: Environmental Impact Statements; Availability, etc.: Animal Carcass Management

 

Document ID: APHIS-2013-0044-0001 Docket ID: APHIS-2013-0044 Comment ID: APHIS-2013-0044-0002

 


 

(APHIS) Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001)

 


 

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

 


 

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

 

Sent:Thursday, September 08, 2005 6:17 PM

 

To:fsis.regulationscomments@fsis.usda.gov

 

Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle

 


 

APHIS-2006-0118-0096 CWD

 


 

DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 0500 EMC 1 Terry S. Singeltary Sr. Vol #: 1

 


 


 

PLEASE SEE FULL TEXT SUBMISSION ;

 


 

2001 Terry S. Singeltary Sr. comment submission

 


 

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 long 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***

 

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

 


 

PRION 2016 TOKYO

 

Zoonotic Potential of CWD Prions: An Update

 

Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6

 

1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.

 

4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,

 

2Encore Health Resources, 1331 Lamar St, Houston, TX 77010

 

Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.

 

PRION 2016 TOKYO

 

In Conjunction with Asia Pacific Prion Symposium 2016

 

PRION 2016 Tokyo

 

Prion 2016

 


 

PRION 2016 TOKYO CONFERENCE

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

 

Taylor & Francis

 

Prion 2016 Animal Prion Disease Workshop Abstracts

 

WS-01: Prion diseases in animals and zoonotic potential

 

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

 

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

 

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

 

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

 

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

 

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

 

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 


 

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

 

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

 

Authors

 

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

 

Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573.

 

Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health.

 

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.

 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.

 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

Saturday, April 23, 2016

 

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

 


 

Saturday, July 23, 2016

 

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016

 


 

Wednesday, May 2, 2012

 

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

 


 

Saturday, June 12, 2010

 

PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse

 


 

Wednesday, July 28, 2010

 

re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010

 


 

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.***

 

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

 


 

*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

 

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

 

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

 

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.

 


 


 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

 


 

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

 


 

Sunday, July 17, 2016

 

CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016

 


 

Saturday, May 28, 2016

 

*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***

 


 

Monday, May 02, 2016

 

*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***

 


 

*** NIH awards $11 million to UTHealth researchers to study deadly CWD prion diseases Claudio Soto, Ph.D. ***

 

Public Release: 29-Jun-2016

 


 

I urge everyone to watch this video closely...terry

 

*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***

 


 

Sunday, July 24, 2016

 

Chronic Wasting Disease Prions in Elk Antler Velvet and Marketing of this Product in Nutritional Supplements for Humans?

 

Research Project: TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: THE ROLE OF GENETICS, STRAIN VARIATION, AND ENVIRONMENTAL CONTAMINATION IN DISEASE CONTROL

 


 

Saturday, April 23, 2016

 

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X

 


 

Saturday, December 12, 2015

 

CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015

 


 

Thursday, April 14, 2016

 

Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD

 


 

Tuesday, July 12, 2016

 

Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE, TSE, Prion Zoonosis Science History

 

see history of NIH may destroy human brain collection

 


 

Terry S. Singeltary Sr. Bacliff, Texas USA

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