Sunday, June 14, 2015

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

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

 

Class II Recall 090-2015

 

Health Risk: Low Jun 12, 2015

 

Congressional and Public Affairs Megan Buckles (202) 720-9113

 

WASHINGTON, June 12, 2015 – Larry’s Custom Meats Inc., a Hartwick, N.Y. establishment, is recalling approximately 529 pounds of beef tongue products that may have been shipped with lingual tonsils still attached, the U.S. Department of Agriculture’s Food Safety and Inspection Service (FSIS) announced today.

 

The beef tongue items were produced on various dates between October 23, 2014 and June 12, 2015. The following products are subject to recall:

 

[View Label (PDF Only)] • 1 ½ lb. packages of “Larry’s Custom Meats Inc. Beef Tongue.”

 

The products subject to recall bear the establishment number “EST. 40359” inside the USDA mark of inspection. These items produced were shipped to retail locations in New York and Pennsylvania.

 

The problem was discovered during in-plant verification activities. Lingual tonsil, located at the back of the base of the tongue, is a small mound of lymphatic tissue which is considered specified risk materials (SRMs) and must be removed from cattle in accordance with FSIS regulations. SRMs are tissues that may contain the infective agent in cattle infected with Bovine Spongiform Encephalopathy (BSE), as well as materials that are closely associated with these potentially infective tissues. Therefore, FSIS prohibits SRMs from use as human food to minimize potential human exposure to the BSE agent.

 

FSIS and the company have received no reports of adverse reactions due to consumption of these products. Anyone concerned about an injury or illness should contact a healthcare provider.

 

FSIS routinely conducts recall effectiveness checks to verify recalling firms notify their customers of the recall and that steps are taken to make certain that the product is no longer available to consumers.

 

Consumers and media with questions about the recall can contact Lawrence Althis, at (607) 293-7927.

 

Consumers with food safety questions can "Ask Karen," the FSIS virtual representative available 24 hours a day at AskKaren.gov or via smartphone at m.askkaren.gov. The toll-free USDA Meat and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through Friday. Recorded food safety messages are available 24 hours a day. The online Electronic Consumer Complaint Monitoring System can be accessed 24 hours a day at: http://www.fsis.usda.gov/reportproblem.

 

USDA Recall Classifications Class I This is a health hazard situation where there is a reasonable probability that the use of the product will cause serious, adverse health consequences or death. Class II This is a health hazard situation where there is a remote probability of adverse health consequences from the use of the product. Class III This is a situation where the use of the product will not cause adverse health consequences.

 

Last Modified Jun 12, 2015

 


 

BSE, beef tongue, tonsil, lymphoid tissue

 

lingual This scientific article describes the distribution of lymphoid tissue in bovine tongue and the location of bovine lingual tonsil. In addition, it concludes that the method currently prescribed for harvesting bovine tongues in slaughterhouses is not appropriate for removing all specified risk material (SRM) and proposes an alternative harvesting method.

 

EFSA was requested (i) to evaluate the design of the study and its scientific validity in relation to the distribution of lymphoid tissue in bovine tongue and (ii) to evaluate the conclusions and recommendations of the study in relation to BSE risk from bovine tonsil following the harvesting method currently prescribed by EU legislation compared to the alternative one proposed in the study.

 

The BIOHAZ Panel reviewed the scientific article and concluded that the study further confirms and extends observations that the lingual tonsil at the base of the tongue may not be entirely eliminated when harvesting tongues by means of the method currently prescribed.

 


 

In conclusion:

 

• The available evidence indicates that the infectivity of bovine tonsil is low, but it is not possible to determine precisely the extent to which the proposed method would reduce the amount of infectivity remaining in the part of the tongue intended for human consumption compared with the harvesting method currently applied.

 

• However, in view of the overall low level of infectivity, it is likely that the proposed method would only provide a marginal reduction in the risk from bovine tonsil compared with the one currently applied. For example, if 10% of all bovine lingual tonsil material would remain with the current method and 1% would remain with the proposed method, the infective load would decrease from 10-4.8 to 10-5.8 bovine oral ID50.

 

CONCLUSIONS AND RECOMMENDATIONS

 

CONCLUSIONS

 

ToR 1 on “the design of the study and its scientific validity, in particular with reference to the distribution of lymphoid tissue in the tongue of bovine animals”.

 

• In general, the study by Casteleyn et al. (2007) provides valuable insights into the anatomomorphological aspects of lymphoid tissue distribution in bovine tongue. However, the significance of the study from Casteleyn and colleagues with such a low number of samples analysed may be questionable, in view of the intrinsic variability of the distribution of lymphoid formations in the bovine tongue.

 

• The study has further confirmed and extended observations that the lingual tonsil at the base of the tongue may not be entirely eliminated by severing and removal at slaughter according to the implementation of measures as currently set out by Regulation (EC) No 999/2001.

 

• No quantitative elements are provided by the study, in particular in relation to the relative amounts of lymphoid tissue in the different areas of tongue examined and in relation to the comparison of the amount of lymphoid tissue that would be removed from bovine tongue by implementing the proposed alternative harvesting method with the amount removed by the harvesting method currently applied.

 

• As a limitation to this assessment, the study did not take into account the rostral part of the tongue which may also harbor part of the lingual tonsil. Therefore, both qualitative and quantitative estimation of the importance of these lymphoid formations by comparison with the area of the tongue caudal to vallate papillae is not feasible at present.

 

ToR 2 on “the conclusions and recommendations of the study in respect to current and future BSE risk from bovine tonsil following the harvesting method of bovine tongues at the level of the slaughterhouse as currently set out by Regulation (EC) No 999/2001 compared to the harvesting method proposed in the study”.

 

• Overall, the level of infectivity in bovine tonsil is low. This, together with the declining and overall low BSE prevalence and the current policy on SRM removal, suggests a very low, if not negligible, human BSE exposure risk associated with exposure to lymphoid tissue in bovine tongue harvested as currently prescribed by EU legislation.

 

Consumption of beef tongue

 

The EFSA Journal (2008) 700, 17-24

 

• Currently there are not sufficient quantitative data available allowing a comparison of the human BSE exposure risk reduction achieved by the alternative tongue harvesting method proposed by the study in comparison to the harvesting method currently prescribed by Regulation (EC) No 999/2001. However, it is likely that the proposed method would only provide a marginal reduction in the risk from bovine tonsil compared to the one currently prescribed.

 

RECOMMENDATIONS

 

• To quantitatively assess the efficacy of the procedure currently prescribed in Regulation (EC) 999/2001 for the harvesting of bovine tongue in achieving the removal of bovine lingual tonsil.

 

• Should a quantification of the distribution of lymphoid tissue in the bovine tongue be necessary, additional morphological and immunohistochemical investigations should be performed.

 

• Should future studies of BSE infectivity in bovine tonsils be performed, bioassay of both palatine and lingual tonsils should be considered.

 

• This opinion only considers the risk associated with lymphoid formations in bovine tongue handled according to the measures currently set out by EU legislation. Infectivity in other tissues or structures of the tongue, as described in TSE animal models other than cattle, may contribute to infectivity in this organ. If new data become available with respect to involvement of such other tissues or structures in cattle BSE, further risk assessment should be performed.

 

• An estimation of the number of undetected BSE infected bovines entering into the food chain would assist in quantifying the residual BSE infectivity after SRM removal.

 


 

 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 specified risk material (SRM), set by EU legislation based on data relating to the pathogenesis and tissues distribution of C-BSE, is fit for the purpose of removing most of the Atypical BSE infectivity from bovine carcasses.

 

1.3. Transmission studies in animal models other than cattle

 

Both L-BSE and H-BSE agents are able to propagate in experimentally challenged foreign species. There is a wider host susceptibility for L-BSE, with transmissions demonstrated in mice, sheep, voles, primates and hamsters, as well as in transgenic mice expressing heterologous, i.e. non-bovine, PrP sequences, whereas H-BSE has not yet proven transmissible to sheep, hamsters or humanised transgenic mice. Proof of principle of the ability of L-BSE to propagate in sheep was provided by the i.c. propagation of an L-BSE isolate in ARQ/ARQ sheep and also in transgenic mice expressing the ovine PrPC variants. The propagation of L-BSE in sheep seemed to result in a TSE with a different profile to that of C-BSE (Nonno et al., 2008; Nicot et al., 2014). L-BSE isolates transmitted to transgenic mice expressing ovine PrPC (Beringue et al., 2007), or inbred wild-type mouse lines (Capobianco et al.,

 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 11

 

2007), acquired a phenotype indistinguishable from the BSE agent. However, the inoculation of tissues collected from mice over-expressing ovine PrPC, inoculated with C-BSE and L-BSE, to bovine PrPC transgenic mice resulted into two different phenotypes specific to each agent, suggesting that the agents passaged in ovine PrP transgenic mice, although producing a similar signature in the brain, were actually different (Beringue et al., 2010). Transmission of H-BSE isolates originating from France and Poland to bovine PrP transgenic mice has been reported. While in the majority of the cases the propagated TSE was different from C-BSE, C-BSE has emerged in a proportion of the mice inoculated with two distinct isolates (one from France and one from Poland) (Torres et al., 2011). Baron et al. (2011) also observed strain features similar to C-BSE after inoculation of conventional mice with H-BSE. Together these data indicate that there may be an aetiological relationship between Atypical and Classical BSE.

 

Intracerebral inoculation of brain tissue from L-BSE-infected cattle to cynomolgus macaques induced a spongiform encephalopathy distinct in all its aspects (clinical, pathological and biochemical) from macaque BSE (Comoy et al., 2008). Incubation periods were shorter for L-BSE (23–25 months) than for C-BSE (38–40 months), suggesting that L-BSE may be more virulent than C-BSE for infecting primates. L-BSE was also transmissible to microcebus, with shorter incubations than C-BSE (Baron et al., 2008). Moreover, experiments demonstrated the transmissibility of L-BSE to macaques by the oral route (Comoy, 2010). L-BSE was transmitted with success also to mouse lemurs, another primate model, after both i.c. and oral inoculation, with a longer incubation period and less severe clinical symptoms following oral challenge (Mestre-Franc├ęs et al., 2012).

 

Histology and biochemistry studies showed similarities between L-BSE-inoculated macaques and MM2 sporadic Creutzfeldt–Jakob disease (sCJD) patients: infected primates and those rare patients exhibited similar lesional profiles, and the disease-specific PrP from both groups showed the same N-terminal protease sensitivity. Moreover, a macaque inoculated with brain tissue from a MM2 sCJD patient showed a similar lesion profile to L-BSE-infected macaques (Comoy et al., 2009). Similarly, transmission of L-BSE into bank voles resulted in a TSE with phenotypic characteristics (incubation period, PrPSc biochemical properties and vacuolar lesion profiles) indistinguishable from those observed after transmission of a VV2 sCJD case in this rodent model (Nonno et al., 2009).

 

The i.c. inoculation of L-BSE field isolates produced TSE disease in two lines of mice over-expressing human PrP (Met129), exhibiting a molecular phenotype distinct from that of C-BSE (Beringue et al., 2008a; Kong et al., 2008). In one of them, the L-BSE agent appeared to propagate with no obvious transmission barrier: a 100 % attack rate was observed on first passage, the incubation time was not reduced on subsequent passaging (Beringue et al., 2008a) and the L-BSE PrPSc biochemical signature was essentially conserved (Beringue et al., 2008a; Kong et al., 2008), appearing to be indistinguishable from that seen after experimental inoculation of MM2 sCJD in these mice (Beringue et al., 2007). These transmission features markedly differed from the low transmission efficiency of cattle C-BSE isolates to this (Beringue et al., 2008a; Beringue et al., 2008b) and other (Asante et al., 2002; Wilson et al., 2012) human PrP transgenic mouse lines, based on the presence of clinical signs and/or protease-resistant prion protein (PrPres) in the brain (Beringue et al., 2012).

 

H-BSE isolates failed to infect one line of “humanised” mice (Met129 PrP) (Beringue et al., 2008a). These mice over-express human PrP and were inoculated i.c. with a low dilution inoculum, supporting the view that the transmission barrier of H-BSE from cattle to humans (expressing this allele) might be quite robust.

 

The permissiveness to Atypical BSEs of “humanised” transgenic mice expressing the valine allele at codon 129 is currently unknown. Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 12

 

1.4. Detection of infection

 

Limited data are available on the performance of the validated rapid tests used for cattle TSE testing for the detection of Atypical BSE cases, in terms of either their analytical sensitivity or their ability to detect infected asymptomatic animals. This results in uncertainty about the true prevalence of these conditions. However, Meloni et al. (2012) compared the analytical sensitivity of EU-approved commercial TSE rapid tests for C-BSE, H-BSE and L-BSE, and, although some differences in the analytical sensitivity were reported, all tests succeeded in detecting the three BSE forms at a 1:16 dilution prepared following the manufacturers’ instructions.

 

In C-BSE cases, pathogenesis studies have established that abnormal PrP deposition in the brainstem first occurs at the obex level, where substantial amounts of this disease-specific protein accumulate during the late incubation phase (Arnold et al., 2007; Wells et al., 2007; Simmons et al., 2010). As a consequence, targeting of the brainstem at the level of the obex for C-BSE rapid testing is considered to be the most sensitive approach for detecting cases within the framework of the active surveillance system.

 

In Atypical BSE (both H- and L-BSE), the suitability of the obex as the target tissue for testing that would allow an early and sensitive detection of these conditions remains questionable, although all the Atypical BSE cases detected so far have been identified through the active surveillance system, indicating that obex testing with currently validated tests allows the detection of at least a proportion of these cases. When discriminating the different forms of BSE, immunohistochemistry (IHC) in brain has been reported to allow discrimination of distinguishable immunolabelling patterns for C-BSE, L-BSE and H-BSE, especially when focusing on rostral areas of the brain, and cerebellum (Konold et al., 2012). Western blotting (WB) allows prompt identification of H-BSE cases according to the molecular mass of the unglycosylated PrP fraction and the detection of the protein by antibodies binding to N-terminal epitopes (e.g. SAF32, P4); L-BSE can be identified by the lower molecular mass of the unglycosylated PrP fraction and the altered glycoprofile (similar quantities of di- and monoglycosylated PrP). This WB classification is the method currently stipulated in the EU TSE Regulation.

 

1.5. Concluding remarks Data relating to the prevalence and geographical distribution of Atypical BSE are incomplete and subject to variation owing to the ongoing retrospective typing of BSE cases. 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 from 2001 to 2013. 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. Sampling and rapid testing procedures, as currently performed, have not been formally evaluated for the detection of Atypical BSE and might have an impact on the capacity to monitor the epidemiological situation of the disease. 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 i.c. inoculation of cattle. 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 from Atypical BSE-infected cattle does not allow judgement of whether the current list of bovine SRM, set by EU

 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 13

 

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.

 

2. Biological material collected from field cases and transmission studies in cattle

 

2.1. Information available from published literature

 

Intracerebral transmission studies in cattle with both Atypical BSE forms have been performed at different institutes. Lombardi et al. (2008) described the i.c. challenge of six cattle with L-BSE and, as a control, six cattle with C-BSE. The clinical signs were described and the PrPSc distribution in different brain regions and the spinal cord were analysed. A follow-up study by Suardi et al. (2012) reported on the presence of BSE infectivity and PrPSc deposition in peripheral muscle samples taken from these L-BSE challenged cattle.

 

A similar study was performed in Japan, in which the first Japanese L-BSE isolate was used for an i.c. challenge experiment in five cattle (Fukuda et al., 2009). It could be shown by WB analysis that numerous peripheral nervous tissues contained PrPSc (Iwamaru et al., 2010). In contrast, all samples from the lymphoreticular system turned out to be negative. A similar study was performed by the same group using a Canadian H-BSE isolate for the i.c. challenge of three cattle. As already shown for L-BSE, the presence of PrPSc in various peripheral nervous tissues could be determined (Okada et al., 2011b).

 

In a different i.c. challenge study, five cattle were inoculated with L-BSE and six cattle with H-BSE (Balkema-Buschmann et al., 2011). The general restriction to the central nervous system (CNS) that had already been described for C-BSE was confirmed in these cattle.

 

Intracerebral challenge studies with both Atypical BSE forms were also performed by Konold et al. (2012), in which PrPSc deposition was identified in muscle spindles and in the trigeminal ganglion following a limited study of potential peripheral distribution. This study is described in more detail in Section 2.2.

 

There have also been a few field cases of L-BSE in which more extensive examination and collection of peripheral tissues was possible (Mazza et al., 2007; Suardi et al., 2012).

 

2.2. The European Union Reference Laboratory (EURL) study

 

snip...

 

of tissues from both the central and peripheral nervous systems, the lymphoreticular system, the musculoskeletal system and the gastrointestinal tract, together with other principal edible organs. However, none of these studies was explicitly designed to address the issue of potential infectivity in the context of the current legislation on SRM, and so there are some SRM tissues that have not been collected within any of these studies, namely the duodenum, the jejunum and ileum (without Peyer’s patches), the caecum, the colon and the mesenteric fat. For these tissues there are therefore no data, and no possibility to create data without undertaking further experimental challenges. All of the experimental material is derived from animals that have been challenged intracerebrally.

 

In total, data are available for 15 experimental H-BSE and 23 L-BSE cases, representing challenges with 4 donors respectively, while data on PrP distribution in naturally-occurring field cases have been published for only three L-BSE-affected cattle.

 

There are no data for field case H-BSE. Where data exist from both field cases and experimental animals (i.e. for L-BSE only), there is good agreement between the data with and abnormal PrP distribution, with the CNS and muscles both consistently affected. However, these data relate to the presence or absence of PrPSc, and do not attempt to quantify relative amounts of PrPSc or levels of infectivity.

 

Overall, disease-related PrP has been reported in CNS tissues, peripheral ganglia and nerves, muscles (predominantly muscle spindles), adrenal glands and retina for both H-BSE and L-BSE. By contrast, no lymphoid tissues or gastrointestinal tissues have tested positive by IHC, WB or bioassay. Some tissues have been collected, but with no testing outcome explicitly reported.

 

Comparative data relating to C-BSE (see Appendix A, Table 12) are to a large extent fragmented, and have evolved over a long period as different analytical methods have been developed and applied. Many of the original infectivity data are based on conventional mouse bioassay rather than transgenic models so, although positive results are robust, negative results do not necessarily have the same sensitivity thresholds (see also EFSA BIOHAZ Panel (2014)). It must also be noted that data available for C-BSE are derived predominantly from field cases or oral challenge models. There are few data from i.c. challenge studies that can be directly compared with existing data for Atypical BSE.

 

However, collective data indicate that C-BSE shares the same tissue distribution as the Atypical BSE cases, with PrPSc and/or infectivity detected in the central and peripheral nervous systems, including ganglia and nerves, and the muscle spindles in skeletal muscle. As in Atypical BSE, the adrenal glands and the retina are also affected.

 

Additionally, in C-BSE there is also evidence of involvement of the lymphoreticular system, particularly, but not exclusively, in those tissues associated with the gastrointestinal tract. The PrPSc distribution and relative levels of infectivity in the gastrointestinal tissues were presented in detail in a previous EFSA Opinion (EFSA BIOHAZ Panel, 2014). Nasal mucosa and bone marrow have also been shown to contain infectivity.

 

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.

 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 17

 

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...

 


 


 

Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010

 


 

Subject: 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

 

SCIENTIFIC COMMITTEE OF THE BELGIAN FEDERAL AGENCY FOR THE SAFETY OF THE FOOD CHAIN

 

RAPID ADVICE 17-2014

 

Subject: 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 (Dossier SciCom 2014/22) Rapid advice approved by the Scientific Committee on 22nd October 2014.

 

Summary

 

The Scientific Committee was asked to answer two questions in regard to a proposal from the European Commission to no longer obligate Member States with a negligible BSE risk status to remove and dispose the specified risk materials as specified in Annex V to Regulation (EC) No 999/2001 of the European Parliament and of the Council of 22 May 2001 laying down rules for the prevention, control and eradication of certain transmissible spongiform encephalopathies. The aim of this modification of the Regulation is to ensure that conditions for imports of commodities from third countries are not more favorable than the conditions applying to Member States with the same OIE BSE negligible risk status. More specifically it was asked to the Scientific Committee:

 

- If there is a difference in public health risk between the casings imported from third countries with a “negligible risk status for BSE” and casings that come from the 18 EU Member States with a “negligible risk status for BSE”?

 

- If there is a significantly increased public health risk if, in the EU Member States with a “negligible risk status for BSE”, the intestines are no longer removed as SRM and if the other risk materials for BSE (the skull including the brains and eyes, the spinal cord, the tonsils and the spine) are indeed considered as SRM?

 

Due to lack of availability of data on true prevalence and tissue infectivity of BSE (classical as well as atypical BSE) the Scientific Committee was not able to thoroughly investigate the questions.

 

Removal of specified risk materials from cattle at slaughter prevents BSE infected materials from entering the human food chain.

 

The Scientific Committee is of the opinion that, taking into consideration the uncertainties in regard to the true prevalence of BSE (classical as well as atypical BSE) in countries with a “negligible risk status for BSE” and given the problems related with the early detection of asymptomatic BSE and given the zoonotic significance of atypical BSE, that stopping with the routine removal of specified risk materials during bovine slaughter will increase the risk for public health.

 

2/14

 

The Scientific Committee is not able to compare the public health risk of casings from third countries and from the 18 EU Member States, both with a negligible risk status for BSE, because of lack of data on true BSE prevalence and BSE tissue infectivity (classical BSE and atypical BSE) in the considered countries.

 

The Scientific Committee is also not able to properly answer the second question if there is a significantly increased public health risk if, in the EU Member States with a “negligible risk status for BSE”, the intestines are no longer removed as SRM due to lack of quantitative data on tissue infectivity of different specified risk materials in slaughtered bovines in these countries. There is also no information on tissue infectivity of atypical BSE cases. It is known however that intestines are the portal of entry of prions and that they are already infective before the prions reach the central nervous system.

 

The final decision pertaining the need of removal of all or part of the specified risk materials is a risk management decision and goes beyond the competencies of the Scientific Committee.

 

Samenvatting Sneladvies over de risico’s voor de volksgezondheid van worstenvellen in landen met een “verwaarloosbaar risicostatuut voor BSE” en over de risico’s van wijziging van een lijst van gespecifieerde risicomaterialen (GRM) voor BSE

 

snip...

 

In conclusion the Scientific Committee is not able to answer this question with an acceptable degree of uncertainty because of lack of data on true prevalence of BSE (classical as well as atypical forms of BSE) in the considered countries. It reiterates its concern regarding the import of certain animal products from third countries with a ‘negligible BSE risk status’ as stated in rapid advice SciCom 16-2013.

 

snip...

 

2. Is there a significantly increased public health risk if, in the EU Member States with a “negligible risk status for BSE”, the intestines are no longer removed as SRM while the other risk materials for BSE (the skull including the brains and eyes, the spinal cord, the tonsils and the spine) are indeed considered as SRM?

 

Once again the Scientific Committee is not able to properly answer this question because of lack of quantitative data on tissue infectivity of different specified risk materials in slaughtered bovines in EU Member States with a “negligible risk status for BSE”.

 

BSE infected animals may enter undetected the food chain due to the low sensitivity of the diagnostic tests. Further on the classical BSE agent accumulates from the first months post exposure in particular segments of the bovine intestines and persists till clinical onset. In addition no information is available about the infectivity of tissues by the atypical BSE agent, especially in the intestines.

 

If intestines from cattle in EU Member States with a “negligible risk status for BSE” are no longer removed as SRM and are allowed to enter the food chain the public health risk will be increased. The degree of rise in risk level cannot be determined. According to EFSA Journal 2014;12(2):3554, the TSEi model indicated that the removal of the last four meters of the small intestine and of the caecum from the food and feed chain would result in a major reduction of the Classical BSE exposure risk associated with intestine and mesentery in cattle.

 

Referring to its previous advice 16-2013 the Scientific Committee repeats that stopping with the routine removal of all specified risk materials during bovine slaughter will increase the risks of exposure of the population to BSE because of the uncertainty related to the detection of BSE. This uncertainty is the consequence of the long incubation period (especially in cases of atypical BSE), the low sensitivity of the available diagnostic methods, the apparent spontaneous nature of atypical BSE, the lack of a clear clinical picture of atypical BSE cases and the reduction in number of tests in healthy slaughtered animals.

 

The final decision pertaining the need of removal of all or part of the specified risk materials is a decision to be taken by the risk manager and goes beyond the competencies of the Scientific Committee.

 

5. Conclusion

 

Removal of specified risk materials from cattle at slaughter prevents BSE infected materials from entering the human food chain.

 

The Scientific Committee is of the opinion that, taking into consideration the uncertainties in regard to the true prevalence of BSE (including classical as well asaAtypical BSE) in countries with a “negligible risk status for BSE” and given the problems related with the early detection of asymptomatic BSE and given the zoonotic character of atypical BSE, stopping with the routine removal of all specified risk materials during bovine slaughter will increase the risk for public health.

 

12/14

 

The Scientific Committee is not able to compare the public health risk of casings from third countries and from the 18 EU Member States both with a negligible risk status for BSE because of lack of data on true BSE prevalence (classical BSE and atypical BSE) in the considered countries.

 

The Scientific Committee is not able to properly answer the question if there is a significantly increased public health risk if, in the EU Member States with a “negligible risk status for BSE”, the intestines are no longer removed as SRM due to lack of quantitative data on tissue infectivity of different specified risk materials in slaughtered bovines in these countries. There is also no information on tissue infectivity by the agent of atypical BSE.

 

On behalf of the Scientific Committee, The President Prof. Dr. E. Thiry (Sgd.) Brussels, 06/11/2014

 

References

 

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Thursday, July 24, 2014

 

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

 


 

SPECIFIED RISK MATERIAL SRM

 


 

*** 2015 ***

 

*** PRION 2015 CONFERENCE ***

 

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

 

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

 

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

 

 ===============

 

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

 

 ===============

 

 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. ***

 

 ================

 

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

 

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

 

 Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults.

 

 Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease.

 

 At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

 

 ***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.

 

 ==============

 

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

 

 ==============

 

 Saturday, May 30, 2015

 

 PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 


 


 

Wednesday, June 10, 2015

 

 Zoonotic Potential of CWD Prions

 

 LATE-BREAKING ABSTRACTS

 


 

 From: Terry S. Singeltary Sr.

 

Sent: Thursday, April 09, 2015 9:17 AM

 

To: BSE-L@LISTS.AEGEE.ORG

 

Subject: [BSE-L] Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180 Singeltary Comment

 

Comment from Terry Singeltary

 

This is a Comment on the Food and Drug Administration (FDA) Notice: Draft Guidance for Industry on Ensuring Safety of Animal Feed Maintained and Fed On-Farm; Availability

 

For related information, Open Docket Folder Docket folder icon

 

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Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180 Singeltary Comment

 

Greetings FDA et al,

 

I wish to comment on Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180.

 

Once again, I wish to kindly bring up the failed attempt of the FDA and the ruminant to ruminant mad cow feed ban of August 4, 1997. This feed ban is still failing today, as we speak. Even more worrisome, is the fact it is still legal to feed cervids to cervids in the USA, in fact, the FDA only _recommends_ that deer and elk considered to be of _high_ risk for CWD do not enter the animal food chain, but there is NO law, its only voluntary, a recipe for a TSE prion disaster, as we have seen with the ruminant to ruminant feed ban for cattle, where in 2007, one decade post August 1997 mad cow feed ban, where in 2007 10,000,000 POUNDS OF BANNED BLOOD LACED MEAT AND BONE MEAL WHEN OUT INTO COMMERCE, TO BE FED OUT. Since 2007, these BSE feed ban rules have been breached time and time again. tons and tons of mad cow feed went out in Alabama as well, where one of the mad cows were documented, just the year before in 2006, and in 2013 and 2014, breaches so bad (OAI) Official Action Indicated were issued. those are like the one issued where 10 million pounds of banned blood laced meat and bone meal were fed out.

 

What is the use of having a Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180, if it cannot be enforced, as we have seen with a mandatory ruminant to ruminant feed ban?

 

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

 


 

19 May 2010 at 21:21 GMT

 

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

 


 

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

 


 

2013

 

Sunday, December 15, 2013

 

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

 


 

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 ;

 


 

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

 

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

 

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

 


 

Terry S. Singeltary Sr.

 

*** See attached file(s) No documents available. Attachments View All (1) Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Terry Singeltary Comment View Attachment:

 


 

 Sunday, April 5, 2015

 

*** Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180 ***

 


 

 Comment from Terry Singeltary Sr.

 

This is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products

 

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

 

I believe that there is more risk to the world from Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from the United States and all of North America, than there is risk coming to the USA and North America, from other Countries. I am NOT saying I dont think there is any risk for the BSE type TSE prion coming from other Countries, I am just saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present mad cow risk factors in North America like they are not here?

 

North America has more strains of TSE prion disease, in more species (excluding zoo animals in the early BSE days, and excluding the Feline TSE and or Canine TSE, because they dont look, and yes, there has been documented evidence and scientific studies, and DEFRA Hound study, that shows the canine spongiform encephalopathy is very possible, if it has not already happened, just not documented), then any other Country in the world. Mink TME, Deer Elk cervid CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type BSE cattle, atyical HG type BSE cow (the only cow documented in the world to date with this strain), typical sheep goat Scrapie (multiple strains), and the atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical Scrapie has spread from coast to coast. sporadic CJD on the rise, with different strains mounting, victims becoming younger, with the latest nvCJD human mad cow case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL CDC.

 

typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al), and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. its all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$

 

the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing but ink on paper.

 

for this very reason I believe the BSE MRR policy is a total failure, and that this policy should be immediately withdrawn, and set back in place the BSE GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all TSE PRION disease in all species of animals, and that the BSE GBR risk assessments be made stronger than before.

 

lets start with the recent notice that beef from Ireland will be coming to America.

 

Ireland confirmed around 1655 cases of mad cow disease. with the highest year confirming about 333 cases in 2002, with numbers of BSE confirmed cases dropping from that point on, to a documentation of 1 confirmed case in 2013, to date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad cow feed ban, and the enforcement of that ban, has drastically reduced the number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in 2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow disease in the USA, we still have no clue as to the true number of cases of BSE mad cow disease in the USA or North America as a whole. ...just saying.

 

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

 

Country/Year

 

snip...please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS No documents available. Attachments View All (1) Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission View Attachment:

 


 

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

 


 

Thursday, November 18, 2010

 

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS

 

Dustin Douglass was indicted and charged with making a fraudulent application to the VA, in an effort to obtain benefits from injuries Douglas represented he suffered while deployed in Iraq. Based on his application, the VA provided benefits totaling $22,148.53. Douglass claimed he suffered various injuries and illnesses as a result of his service in combat. The investigation revealed Douglass had, in fact, been deployed to Iraq, but had served as a computer specialist, had never been in combat, and did not suffer the service-related injuries and illnesses he claimed to have suffered. Douglass was placed on supervised release for 3 years, and required to pay $22,148.53 in restitution. Galen Niehues, an inspector for the Nebraska Department of Agriculture, (NDA), was convicted of mail fraud for submitting falsified reports to his employer concerning inspections he was supposed to perform at Nebraska cattle operations. Niehues was tasked with performing inspections of Nebraska ranches, cattle and feed for the presence of neurological diseases in cattle including Bovine Spongiform Encephalopathy (BSE), also known as “Mad Cow Disease”. Niehues was to identify cattle producers, perform on-site inspections of the farm sites and cattle operations, ask producers specific questions about feed, and take samples of the feed. Niehues was to then submit feed samples for laboratory analysis, and complete reports of his inspections and submit them to the NDA and to the Federal Food and Drug Administration (FDA). An investigation by the FDA and NDA revealed Niehues had fabricated approximately 100 BSE inspections and inspection reports. When confronted, Niehues admitted his reports were fraudulent, and that had fabricated the reports and feed samples he submitted to the NDA. Niehues received a sentence of 5 years probation, a 3-year term of supervised release, and was required to pay $42,812.10 in restitution.

 


 


 

Date: June 21, 2007 at 2:49 pm PST

 

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

 

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

 

snip...

 

Topics that will be covered in ongoing or planned reviews under Goal 1 include:

 

soundness of BSE maintenance sampling (APHIS),

 

implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),

 

snip...

 

The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.

 

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half

 


 

-MORE Office of the United States Attorney District of Arizona

 

FOR IMMEDIATE RELEASE For Information Contact Public Affairs

 

February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681

 

CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD COW DISEASE SURVEILLANCE PROGRAM

 

PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, “The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA’s Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law.” Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the “USDA Agreement”) to collect obex samples from cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.

 

Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.

 

Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA’s ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:

 

(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;

 

(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;

 

(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s testing laboratory that were false and misleading;

 

(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;

 

(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and

 

(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.

 

Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #

 


 

WE can only hope that this is a single incident. BUT i have my doubts. I remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5 grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and the FDA was bragging at the time that the amount of potentially BANNED product was so little and the cattle were so big ;

 

"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."

 


 

On Friday, April 30 th , 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'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.

 


 

WE now know all that was a lie. WE know that literally Thousands of TONS of BANNED and most likely tainted product is still going out to commerce. WE know now and we knew then that .005 to a gram was lethal. WE know that CWD infected deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been rendered and fed back to livestock (including cattle) for human and animal consumption.

 

Paul Brown, known and respected TSE scientist, former TSE expert for the CDC said he had ''absolutely no confidence in USDA tests before one year ago'', and this was on March 15, 2006 ;

 

"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 USDA did before 2005 suspect," Brown said. ...snip...end

 


 

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...

 


 

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."

 

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

 

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

 


 

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 bone meal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals and other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal 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, antibioticresistant bacteria, prions, arsenic, and dioxinlike 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 (antibioticresistant 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

 


 

Wednesday, December 4, 2013

 

Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December 4, 2013

 

TO ALL IMPORTING COUNTRIES THAT IMPORTS FROM THE USA, BE WARNED, NEW MAD COW BSE REGULATIONS USDA, AND OIE, not worth the paper the regulations were wrote on, kind of like the mad cow feed ban of August 1997, nothing but ink on paper $$$

 

full text ;

 


 

Friday, January 23, 2015

 

Replacement of soybean meal in compound feed by European protein sources and relaxing the mad cow ban $

 


 

ah yes, big ag at it's finest $$$

 

COOL H.R. 2393 Agriculture Chairman K. Michael Conaway (R-TX) Fears of US imports infected with mad cow disease is emerging as an issue in trans-Pacific trade talks

 

Posted by Terry S. Singeltary Sr. on May 20, 2015 at 9:00am

 


 

Thursday, June 11, 2015

 

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

 


 

spontaneous atypical BSE ???

 

if that's the case, then France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$

 

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

 


 

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, 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

 


 

 Thursday, August 12, 2010

 

Seven main threats for the future linked to prions

 

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

 

Second threat

 

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Monday, October 10, 2011

 

EFSA Journal 2011 The European Response to BSE: A Success Story

 

snip...

 

*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

 

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***In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

 


 

Thursday, June 04, 2015

 

Catholic Medical Center v. Civil No. 14-cv-180-JL Opinion No. 2015 DNH 110 Fireman’s Fund Insurance Company Creutzfeldt Jakob Disease TSE Prion tainted medical instruments

 

UNITED STATES DISTRICT COURT DISTRICT OF NEW HAMPSHIRE

 


 

 Tuesday, May 26, 2015

 

Minimise transmission risk of CJD and vCJD in healthcare settings Last updated 15 May 2015

 


 

 Terry S. Singeltary Sr.