**From:** [Terry S. Singeltary Sr.](mailto:flounder9@verizon.net)

**To:** <FREAS@CBER.FDA.GOV>

**Cc:**
[**william.freas@fda.hhs.gov**](mailto:william.freas@fda.hhs.gov) ;
<rosanna.harvey@fda.hhs.gov>

**Sent:** Friday, December 01, 2006 2:59 PM

**Subject:** Re: **TSE advisory committee for the meeting December 15,
2006** \[TSS SUBMISSION PART III\]

Lancet Neurology DOI:10.1016/S1474-4422(06)70413-6

**Predicting susceptibility and incubation time of human-to-human
transmission of vCJD**

MT Bishop a, P Hart b, L Aitchison b, HN Baybutt b, C Plinston b, V
Thomson b, NL Tuzi b, MW Head a, JW Ironside a, RG Will a and JC Manson
b

Summary\
Background\
Identification of possible transmission of variant Creutzfeldt-Jakob
disease (vCJD) via blood transfusion has caused concern over spread of
the disease within the human population. We aimed to model iatrogenic
spread to enable a comparison of transmission efficiencies of vCJD and
bovine spongiform encephalopathy (BSE) and an assessment of the effect
of the codon-129 polymorphism on human susceptibility.

Methods\
Mice were produced to express human or bovine prion protein (PrP) by
direct replacement of the mouse PrP gene. Since the human PrP gene has
variation at codon 129, with MM, VV, and MV genotypes, three inbred
lines with an identical genetic background were produced to express
human PrP with the codon-129 MM, MV, and VV genotypes. Mice were
inoculated with BSE or vCJD and assessed for clinical and pathological
signs of disease.

Findings\
BSE was transmitted to the bovine line but did not transmit to the human
lines. By contrast, vCJD was transmitted to all three human lines with
different pathological characteristics for each genotype and a gradation
of transmission efficiency from MM to MV to VV.

Interpretation\
Transmission of BSE to human beings is probably restricted by the
presence of a significant species barrier. However, there seems to be a
substantially reduced barrier for human-to-human transmission of vCJD.
Moreover, all individuals, irrespective of codon-129 genotype, could be
susceptible to secondary transmission of vCJD through routes such as
blood transfusion. A lengthy preclinical disease is predicted by these
models, which may represent a risk for further disease transmission and
thus a significant public-health issue.

Affiliations

a\. National CJD Surveillance Unit, Bryan Matthews Building, Western
General Hospital, Edinburgh, UK\
b. Institute for Animal Health, Neuropathogenesis Unit, King\'s
Buildings, Edinburgh, UK

Correspondence to: Prof J C Manson, Institute for Animal Health,
Neuropathogenesis Unit, Ogston Building, King\'s Buildings, West Mains
Road, Edinburgh EH9 3JF, UK

snip\...

 Discussion

Although the cattle BSE epidemic in the UK has amounted to more than 180
000 cases since the 1980s,\
the extent of the human vCJD epidemic has so far remained limited with
the total number of cases\
worldwide currently at 190. One explanation for this apparent
discrepancy is that there exists a significant\
species barrier between cattle and human beings, which limits the
susceptibility of the human population to BSE. The data shown here
suggest that this could indeed be the case since BSE was readily
transmissible to the bovine transgenic mice but not to the human
transgenic mice. However, once BSE has passed through human beings in
the form of vCJD, the transmissibility of this TSE strain is altered for
the human population.

All the human transgenic lines inoculated with BSE were negative for TSE
transmission, which suggests that either the human transgenic lines are
relatively resistant to transmission of BSE or the incubation time is
longer than the length of the experiment (approximately 700 days). BSE
transmission previously observed by others, in human transgenic lines
overexpressing the human prion protein, could be due to overexpression
of the PrP gene and may not therefore give a true reflection of the
species barrier between BSE and human beings.15,25,26 This apparent
resistance of human transgenic mice to BSE could be explained by a large
species barrier and this in turn could explain the low number of vCJD
cases in the human population.

vCJD was transmitted to all three human lines with different
pathological characteristics for each genotype, and a gradation of
transmission efficiency from MM to MV to VV. The greater transmission
efficiency in HuMM mice suggests that homozygosity for methionine at
codon 129 leads to earlier onset of TSE-related pathological features
and clinical disease than for the other two genotypes. The differences
in PrPSc deposition in the HuMM and HuMV lines suggest that the
codon-129 polymorphism in human beings is likely to affect the
distribution of PrPSc deposition in the brain. Moreover, the similar
numbers that scored positive for PrP deposition in each of the MM and MV
groups (11/15 and 11/13 respectively) suggest that the two genotypes
might be equally susceptible to vCJD, but with different incubation
periods. Titration experiments are needed to fully compare the
susceptibility of each line. The single HuVV mouse positive for PrPSc
shows that VV individuals may be susceptible to vCJD with very long
incubation times, including a lengthy subclinical phase. Transmission
studies from all three genotype mice are now underway to examine the
infectious nature of the disease and determine any alterations in the
strain characteristics on passage through human transgenic mice. By
contrast with published data suggesting that VV individuals cannot
propagate the vCJD biochemical phenotype,15 the data presented here
suggest that the PrPSc type will remain a useful diagnostic feature of
secondary vCJD infection irrespective of codon-129 genotype, as has been
observed for the two extant cases of transfusion-associated vCJD
infection. 5,27

Transmission of vCJD to the three lines of human transgenic mice
indicates that the human population\
could be at significantly heightened risk of developing disease after
iatrogenic exposure to vCJD. Secondary transmission of vCJD has partly
removed the cattle-to- human species barrier and has resulted in an
agent that can be transmitted from human to human with relative
efficiency. Transmission studies in cynomolgus macaques provide further
evidence for this agent adaptation as they show reduction in incubation
times after serial passage of BSE.28 Our BSE inoculation at 10-1
dilution was\
compared with vCJD inoculation at 10-2 because the latter inoculum was
found to be toxic to the mice at 10-1. Use of a higher dose ofvCJD
inoculum would have maintained or increased the transmission efficiency
of vCJD and enhanced the current findings.

**Our findings raise concerns relevant to the possibility of secondary
transmission** **of vCJD through** blood transfusion, **fractionated
blood products**, or contaminated surgical instruments. For this study
mice were injected intracerebrally, whereas the probable human exposure
to these agents is by peripheral routes (eg, oral or intravenous), and
thus human-to-human exposures might be significantly less efficient.
However, it is difficult to know for sure what the practical
implications might be in human beings. Peripheral route challenge is in
progress; however, BSE transmission studies in primates have shown the
intravenous route to be as efficient as the intracerebral route, with an
extension of the incubation time.28

Although all cases of vC\]D up to now have been observed in the MM
genotype, this model of human-to-\
human vCJD transmission suggests that other genotypes are also
susceptible. In our experimental setting, all PRNP codon-129 genotypes
are susceptible to vCJD infection; however, progressive development of
pathological TSE features (vacuolation and PrP deposition) is more rapid
in the MM-genotype mice. An explanation for this finding might be
provided by in-vitro conversion of recombinant human PrP by BSE and vCJD
agents, which has shown that PrP with methionine at position 129 is more
efficiently converted than PrP with valine, and that conversion by vCJD
is significantly more efficient than by BSE.29 Long incubation periods
during which PrPSc is deposited predicts that, in human beings,
infection could be present in all genotypes for a significant period
before clinical onset. Incubation periods of more than 30 years have
been reported in the human TSE disease kuru.30

The possibility that an MV or VV genotype could result in a phenotype
distinct from that recognised in vCJD draws attention to the importance
of systematic assessment of the clinical, genetic, pathological, and
biochemical features of all human prion diseases. Our findings indicate
that for human-to-human vCJD infection

it should be assumed that all codon-129 genotype individuals (not just
MM) can be infected, that\
long incubation times can occur, and that a significant level of
subclinical disease might be present in the population.

Contributors

MTB, PH, and CP did immunocytochemical and western blot analysis;

JCM, NT, HNB, and LA produced the transgenic mouse lines; JWI supplied
vCJD case material and reviewed the neuropathology; VT did the mouse
inoculations; and MTB, PH, MWH, RGW, JWI, and JCM\
prepared the manuscript.

Conflicts of interest

We have no conflicts of interest.

Acknowledgments

snip\... end

\-\-\-\-- Original Message \-\-\-\--

**From:** [Terry S. Singeltary Sr.](mailto:flounder9@verizon.net)

**To:** [Terry S. Singeltary Sr.](mailto:flounder9@verizon.net) ;
<FREAS@CBER.FDA.GOV>

**Cc:** <william.freas@fda.hhs.gov> ; <rosanna.harvey@fda.hhs.gov>

**Sent:** Thursday, November 30, 2006 1:47 PM

**Subject:** Re: TSE advisory committee for the meeting December 15,
2006 \[TSS SUBMISSION PART II\]

** **

**EUROPEAN UNION**

**SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE**

**Draft minutes of the 94th meeting held on 21st September 2006**

Approval of draft open minutes from SEAC 94

**ITEM 5 -- CJD UPDATE**

16\. Dr Richard Knight (NCJDSU) provided an update on the epidemiology
of cases of sporadic CJD (sCJD) and vCJD in the UK and elsewhere.
Between May 1990 and June 2006, 845 cases of sCJD had been identified in
the UK with a mean age at onset of 66 (range 15-94) years and mean age
of death of 67 (range 20-95) years. There is no significant gender
difference in sCJD incidence. There had been a trend towards an
increasing number of cases over time to almost 80 cases per year in
2003. This phenomenon had also been observed in other countries and was
considered to be a result of better ascertainment. Fewer cases were
identified in the UK in 2004 compared to 2003 and 2005 but this finding
may not be significant. The genotype distribution of sCJD cases was 64%
methionine (M) M, 18% M valine (V) and 18% VV at codon 129 of the prion
protein gene.

 

17\. The total number of definite and probable vCJD cases in the UK up
to September 2006 was 162, with six cases still alive. Two of these are
considered to have been infected by blood transfusion rather than a
dietary route. No statistically significant gender difference had been
observed in vCJD cases. The age distribution of vCJD had not altered
over the course of the UK epidemic, with the median age of death of 28
(range 12-72) years. The median duration of clinical vCJD was 14 (range
6-40) months. Statistical analysis of the UK incidence of deaths from
vCJD suggested the epidemic had peaked in 2000 with 28 deaths. All 141
vCJD cases tested to date are of the MM genotype. Elsewhere in the world
up to September 2006, 34 vCJD cases have been reported with 20 in
France, four in the Republic of Ireland (RoI), two in the USA, two in
the Netherlands and single cases in Italy, Canada, Japan, Saudi Arabia,
Spain and Portugal. The clinical, pathological and prion protein gene
PrP codon 129 genotype of all these cases is similar to that of UK
cases. Infection was likely to have occurred in the UK in two RoI cases,
both USA cases, one French case and the Japanese and Canadian cases.

 18. Dr Knight explained that evidence from experiments to compare BSE
transmission to bovinised and humanised mice suggested a significant
barrier to transmission of BSE between cattle and humans. There appears
to much less of a barrier between humans, suggesting that secondary
transfer from human to human may be relatively efficient. This is borne
out by the three recent blood transfusion associated cases of vCJD.
However, although all clinical cases of vCJD that have been genotyped
are of the MM genotype, there is evidence that cases of non-MM genotypes
should be expected. Infected individuals of non-MM genotypes may have
longer incubation periods, subclinical infections and, or a different
clinico-pathological phenotype. Experiments on the transmission of vCJD
to humanised mice of the MM, MV or VV genotype suggested that
susceptibility to vCJD was highest in MM, lower in MV and lowest in
VV18. Mice of MM and MV genotypes showed similar rates of brain
involvement, however differences in neuropathology were observed between
the three genotypes. The incubation period was shortest in MM mice and a
higher rate of subclinical disease was found in MV and VV mice.

19\. Dr Knight explained that data from the UK appendix and tonsil
study19 provided further evidence for the existence of subclinical vCJD
infections. In this survey, three out of 12 674 samples had tested
positive for abnormal prion protein (PrPSc), indicating a prevalence of
237 (95% confidence interval 49-692) cases per million. An extrapolation
of these data suggest 3 808 (95% confidence interval 785-1128) people
could be infected out of approximately 16 million in the 10 to 30 year
old age group. However, the actual number of clinical cases of vCJD
observed in the 10 to 30 age group was 102, and in decline. The
discrepancy in observed and predicted cases in the 10 to 30 year age
group could be due to subclinical infections. Whether these individuals
will eventually develop vCJD clinical disease, with a longer incubation
period, is unknown. Importantly, two out of the three positive appendix
samples were VV, a much higher proportion than the 11% of VV individuals
in the UK population. If it is assumed that the third positive appendix
is non-VV, statistical analysis indicates a prevalence ratio of VV to
non-VV of 18:1. If the third positive appendix is MM, then the VV:MM
prevalence ratio is 8:1. This suggests that, although VV may have the
longest incubation period, it may be most susceptible genotype.
**[However, this]{.underline}**

18 Bishop *et al*. (2006) Predicting susceptibility and incubation time
of human-to-human transmission of vCJD. *Lancet Neurol.* 5, 374-375

19 Hilton *et al.* (2004) Prevalence of lymphoreticular prion protein
accumulation in UK tissue samples. *J. Pathol.* 203, 733-739.  

**[seemed counterintuitive and]{.underline}** not consistent with data
from humanised mice, thus there may be an important unidentified factor
involved. Although the downward trend in vCJD clinical cases is
reassuring, it is possible that subclinical infections may be more
widespread. Further peaks in vCJD cases could occur, however the
timescale in which these peaks could occur is uncertain. It is therefore
very important to ascertain the prevalence of subclinical infection in
the UK population.

20\. Dr Knight explained that three blood transfusion associated vCJD
cases had been identified through the Transfusion Medicine and
Epidemiological review (TMER)20. The first case (MM), developed vCJD 6.5
years after receiving non-leucodepleted red blood cells (RBC) from a
donor, who themselves developed vCJD 3.3 years after donation21. The
second case (MM), developed vCJD 7.8 years after receiving
non-leucodepleted RBC from a donor, who themselves developed vCJD 1.8
years after donation. The third case22(MV) died of a non-neurological
illness five years after receiving non-leucodepleted RBC from a donor,
who themselves developed vCJD 1.5 years after donation. PrPSc was
detected in the spleen of this recipient, with no other clinical or
neuropathological evidence of vCJD infection. Statistical analysis
indicated that the chances of the three recipients having developed vCJD
through consuming BSE infected meat was one in a thousand million,
therefore it could be concluded that transmission had occurred via blood
transfusion.

21\. The TMER also identified 66 individuals who received blood from
donors who later developed vCJD. Out of these individuals, 42 recipients
have died and of those still alive, seven have survived over 10 years
after receiving the donation, without developing vCJD. There were 25
blood donations from 11 individuals that subsequently developed vCJD
that were used for plasma fractionation, however no cases of vCJD have
occurred in recipients of plasma.

22\. In the reverse TMER study, seven vCJD cases were identified as
having received blood from 121 identified donors, two of which were
known vCJD cases. If these two cases are excluded, together with a third
case, because of the small amount of time between the onset of disease
**[and the timing of the transfusion,]{.underline}**

20 Hewitt *et al.* (2006) Creutzfeld-Jakob disease and blood
transfusion: results of the UK Transfusion Medicine Epidemiological
Review Study. *Vox Sang.* 91, 221-230.

21 Llewelyn *et al*. (2004) Possible transmission of variant Creutzfeld
Jakob disease by blood transfusion. *Lancet* 363, 417-421.

22 Peden *et al*. (2004) Preclinical vCJD after blood transfusion in a
PRNP codon 129 heterozygous patient*. Lancet* 364, 527-529.

**[four cases remain. One]{.underline}** of these recipients received
two transfusions in the same year and developed clinical vCJD four or
five years post transfusion. In a second recipient of two blood
transfusions, the onset of vCJD was 17 years after the first transfusion
and between six and seven years after the second transfusion. The two
other recipients each received one transfusion with the onset of vCJD at
around six and 14 years following transfusion.

23\. The Chair noted that although the incidence of clinical vCJD was
reducing, recent evidence suggested that there may be a substantial
number of subclinical carriers that could potentially give rise to
secondary transmissions. Therefore it was very important to know the
prevalence of subclinical vCJD.

24\. A member asked how the incidence of vCJD and BSE compare in other
countries, relative to that of the UK. Dr Knight indicated that the
numbers of BSE and vCJD cases in some countries correlate poorly. In
addition, in some countries the historic incidence of BSE is not well
known or uncertain and numbers of vCJD cases are too small to make
meaningful comparisons.

25\. A member noted that the genotype of the PrPSc positive samples from
the appendix and tonsil survey raised many questions. These include
whether individuals of the VV genotype were protected from clinical
disease, whether PrPSc resided in the appendix rather than in the brain
in these individuals and whether these individuals were themselves
infectious. Further studies were needed to answer these questions. A
member noted that the susceptibility to vCJD could not be equated with
incubation time and asked whether transmission studies using the PrPSc
positive appendix material were underway. Dr Knight was not aware if
transmission studies had begun on this material.

26\. A member asked if the genotype of the transfused patients surviving
for 10 years after receiving vCJD infected blood was known. Dr Knight
indicated this was not known and agreed these are important data.

27\. Regarding the possible barrier to transmission of BSE from cattle
to humans, a member noted that this could be due to inefficient entry or
inefficient replication of the BSE agent in humans and these
possibilities are under investigation.

28\. Members agreed it was important to continue surveillance to be able
to detect the onset of secondary epidemics of vCJD. It was noted that
there may be periods of a number of years with few or no cases of vCJD,
before an increase in cases may be observed.

 snip\...

 

39\. Dr Gleadle explained that FSA will continue to develop the
contingency policy, should BSE be found in sheep. The current policy
involves a graduated response, with increasing levels of control
proposed depending on the number of unrelated cases of BSE in sheep that
might be identified. FSA would be asking for advice from SEAC on the
criteria for determining whether cases of BSE are related, should more
than one case of BSE be identified in the national sheep flock, and on
the appropriate level of surveillance should BSE be found in sheep. SEAC
would also be consulted on the emerging science and contingency plans
under development in relation to atypical scrapie. FSA would continue to
maintain a watching brief on chronic wasting disease in deer and may
wish SEAC to comment on its project examining the transmissibility of
BSE to deer.

 snip\...

 NCJDSU

42\. Dr Knight explained that NCJDSU is considering how it may identify
new cases of human illness should they arise from exposure to atypical
scrapie or TSE cases in cattle that appear different from BSE and to
examine whether, as has been suggested by some, there are links between
sCJD and atypical scrapie. He noted that the possibility of vCJD
infection in individuals of non-MM genotypes and that these individuals
may present with a different clinical phenotype, were particular areas
of uncertainty in relation to the vCJD epidemic. As the incubation
period of human TSEs was long, continued surveillance was very important
to identify new types of TSE and to identify potential routes of
secondary transmission. Evaluation of the sensitivity and specificity of
ante mortem blood tests for subclinical vCJD and the appropriate use of
blood samples from vCJD cases was also of importance. It is likely that
very large numbers of false positive results would arise from blood
tests and it would be very important to consider the implications and
handling of the results, prior to the introduction of blood testing.

Discussion

43\. The Chair explained that Professor **John Collinge** (National
Prion Unit \[NPU\]) had been invited to contribute to the horizon
scanning session, however he was unable to attend. However, Professor
Collinge had personally informed the Chair that the NPU had partially
characterised a number of mouse and human genes that appear to modify
the incubation period and susceptibility to TSEs. hus, it was possible
that the clinical cases of vCJD identified to date were in individuals
from a group that are genetically the most susceptible to this disease
and further, possibly larger, numbers of cases might appear in the
future in other genetic groups. A member noted that the prion protein
gene is the major gene influencing susceptibility to TSEs. Although
other genes may modify susceptibility to infection, they may have
relatively small, but possibly, additive effects. Professor Collinge had
suggested that some of the genes identified had substantial effects on
the susceptibility to infection. Members considered it important to
review these data when published. Dr Knight noted that EU funded
projects were examining the existence of such modifier genes, using
large numbers of subjects.

 

snip\...

 

**ITEM 9 -- EVALUATION CRITERIA FOR ANTE MORTEM DIAGNOSTIC TESTS FOR
SUBCLINICAL vCJD**

**(SEAC 94/3)**

56\. The Chair explained that the UK blood services and DH requested
SEAC's advice on the scientific criteria by which ante mortem diagnostic
tests for subclinical vCJD could be validated. A position statement
would be produced based on the committee's consideration.

57\. Dr John Stephenson (DH) presented an overview of DH research
related to the development and evaluation of ante mortem tests for vCJD,
prototype tests developed by commercial companies and the work of DH
advisory committees that had considered issues related to diagnostic
tests for vCJD. The available information on prototype tests was limited
for reasons of commercial sensitivity, however most, if not all, appear
to be based on the detection of PrPSc. DH had set up a CJD Tissue
Management Group to oversee the collection and allocation of human
tissues with which to evaluate tests. However a new group was being
convened with a wider remit that included the allocation of blood
samples and oversight of the vCJD tissue resource centre at the National
Institute of Biological Standards and Controls (NIBSC). A Subgroup of
the Committee of Microbiological Safety of Blood Tissues and Organs had
provided advice on the preparative work required, should a screening
test for subclinical vCJD become available. The Subgroup concluded that,
unless a test was developed with very high specificity, large numbers of
false positive results would be obtained leading to an unnecessary
shortage of blood, therefore a reliable confirmatory test was required.

Establishment of a panel of blood samples from cohorts of UK and USA
blood donors to evaluate diagnostic tests was also recommended. The HPA
Expert Advisory Group on a Testing Strategy for NATA was considering the
criteria for screening tests for tonsil samples. The UK blood services
have also convened the Prion Assay Working Group to provide guidance on
the suitability of diagnostic tests for use within the blood services.
The ethical implications of screening tests for subclinical vCJD had
been considered by the HPA, together with the Nuffield Council for
Bioethics and a report was due for release.

58\. Dr Roger Eglin (National Blood Service) presented an overview of
the performance requirements for screening tests for subclinical vCJD
for use in the blood services. It was considered that a screening test
must be CE marked23 and meet an, as yet undefined, Common Technical
Specification (CTS) for an Annex IIA assay, as specified in the In Vitro
Diagnostic Medical Devices (IVD) Directive 98/79/EC. Initially a test
should have a sensitivity of at least one infectious dose (ID)/mL and a
specificity that gave an initial reactive result rate of below 0.3% and
for a repeat reactive result rate of below 0.15%. A panel of blood
samples is being prepared from 5 000 UK and 5 000 USA blood donors
separated into plasma, red cells and white cells to assess the
specificity of blood tests. It was envisaged that one or two other tests
would be performed on reactive samples from a screening test to confirm
the presence of PrPSc, with repeat positive results resulting in
deferral of the blood donor. Reactive samples from the screening test
could be confirmed by the secondary or tertiary test, as the tests would
all use a different mechanism(s) to capture the analyte.

59\. Dr Philip Minor (NIBSC) presented an overview of the samples
available for use in evaluation of tests for subclinical vCJD. These
include dilution series of brain and spleen from vCJD cases and
classical scrapie infected sheep, blood spiked with brain or spleen from
vCJD cases or healthy individuals and blood samples from classical
scrapie infected and healthy sheep. It was proposed that large numbers
of blood samples from classical scrapie endemic and classical scrapie
free flocks, UK and non UK blood donors and importantly blood from vCJD
cases be collected to assess and compare the performance of diagnostic
tests. In addition, panels of blood collected from mice and sheep
through the TSE incubation period, from individuals classified as 'at
risk of vCJD for public health purposes' and from haemophiliacs would
also be useful to assess the time in the incubation period when blood
become infectious and detectable by tests.

60\. Dr Minor noted that, at present, the performance of tests was not
specified and they could be freely marketed. However, should diagnostic
tests for subclinical vCJD be included in Annex IIA of the IVD Directive
98/79/EC, all such tests would have to comply with a CTS.

23 CE (Conformité Européene) mark is a declaration by the manufacturer
that a product meets all the necessary requirements of the relevant EU
legislation.  

61\. Dr John Parry (HPA) provided an overview of the issues arising from
the evaluation, validation and implementation of blood tests in relation
to the human immunodeficiency virus.

62\. Members agreed that it was very important that diagnostic tests for
subclinical vCJD be included in Annex IIA of the IVD Directive 98/79/EC,
to ensure proper evaluation against a CTS.

63\. A member noted that all the diagnostic tests were based on the
major assumption that PrPSc is a good marker of the infectious agent,
however PrPSc does not always correlate with TSE infectivity. As a
better marker has not been identified, PrPSc is currently the most
appropriate marker, although this assumption should be reviewed in light
of any data that may become available. It must be recognised that PrPSc
levels are a non quantitative measure of infectivity. As the
relationship between PrPSc and the infectious agent is unclear, tests
that recognise different parts of the PrPSc molecule may produce
conflicting results, possibly making it difficult to identify suitable
confirmatory tests. Therefore, it would be very important in the
evaluation of screening and confirmatory blood tests that blood from
vCJD cases be tested, as blood from animal models or blood spiked with
vCJD brain or spleen may not reflect the response from tests when
applied to the detection of the vCJD agent in blood. Preliminary
evaluation of the specificity and sensitivity of tests could be achieved
by using spiked blood or blood from animal models, however final
evaluation of tests must include blood from vCJD cases.

64\. A member queried whether there was any evidence that PrPSc is in a
different form in blood than in spleen or brain. Dr Minor responded that
there were no such data, however some tests were able to detect both
PrPSc in the brain and spleen, providing some assurance that the test
may detect the form of PrPSc in blood. A member suggested that PrPSc may
be in a more soluble form in blood compared with the form in spleen or
brain, thus it was important to collect blood from preclinical and
clinical vCJD patients for use in the assessment of the efficacy of
blood tests and to assess the point in the incubation period when blood
becomes infectious. Blood collected from individuals "at risk of vCJD
for public health purposes" would provide a valuable source of blood
from potentially preclinical vCJD cases. This issue was being considered
by CGAG.

65\. Members agreed that independent evaluation of tests using the same
panels of blood was very important. Dr Eglin noted that the blood
services have a Kit Evaluation Group which independently evaluates test
kits, using staff trained by the companies in the use of their products.

66\. A member noted that two key considerations for the applicability of
a blood test were the volume of material required and the
reproducibility of a concentration step, should it be required. Dr Minor
responded that tests vary in the volume of sample required and the
requirement for sample concentration. However manufacturers recognise
the difficulty a concentration step poses to the blood services.

67\. It was noted that work with the vCJD agent requires a category 3
containment facility. Dr Eglin responded that, as for the blood born
viruses, the screening is conducted on a largely negative population and
can be derogated to category 2 laboratory conditions. However, further
testing on reactive samples would be undertaken in a category 3
laboratory.

68\. A member asked whether any of the prototype diagnostic tests had
been assessed using blood from classical scrapie infected and healthy
sheep. Dr Minor explained that some companies had obtained these samples
and had been able to correctly identify blood from infected animals. It
was important that the same panels of blood samples be sent to
manufacturers to ensure a consistent approach. However, stocks of these
samples may be insufficient to evaluate the number of diagnostic tests
that may become available.

69\. A member asked about the collection of blood from vCJD patients and
whether there were sufficient samples available to evaluate tests. Dr
Knight explained that relatively small amounts of blood had been
collected and this had been fractionated into plasma, red cells and
white cells. Dr Minor suggested there was insufficient blood from vCJD
patients to conduct proper evaluations with the required number of
replicate tests. A member suggested collection of larger volumes of ante
mortem blood from vCJD cases. It was also suggested that blood collected
at post mortem from vCJD cases would be a source of large quantities of
blood. Dr Knight explained that not all vCJD cases underwent autopsy and
many were performed up to two days after death when significant
autolysis may have occurred. Furthermore, it is difficult to obtain
large volumes of blood post mortem. It was suggested that blood from
familial cases of CJD be collected. Members noted that the form of PrPSc
may be different between familial CJD and vCJD and that, unlike vCJD,
familial cases of CJD did not express PrPSc systemically. Members
suggested that a non-human primate model of vCJD could provide large
volumes of blood.

70\. The Chair considered it important that the volume of blood required
to evaluate diagnostic tests be calculated and that a mechanism to
acquire sufficient blood from vCJD patients was developed. Replicate
tests to evaluate the efficacy of tests could be conducted using spiked
blood samples and, or, blood from animal models. However it is very
important that the final evaluation is conducted using blood from vCJD
cases. Dr Stephenson noted that the CJD Tissue Management Group was
established to ensure that tissue samples from vCJD cases were used
appropriately. The Chair noted that a number of research organisations
had collected blood from vCJD patients and these samples should be made
available. A Group was required to calculate the quantities of blood
required to evaluate tests, oversee the collection of samples, develop
clear performance criteria that must be fulfilled by manufacturers
before they receive these very valuable samples and to make decisions
about the supply of these samples to manu-facturers. Dr Stephenson
responded that such a group was being convened at NIBSC. Members
considered it important there is coordination of collection and supply
of animal as well as human tissues.

71\. The Chair suggested that risk assessments be conducted to examine
the required sensitivity and specificity for blood tests and to examine
scenarios of the effect of such tests on the blood supply and
transmission of vCJD.

72\. Members noted that use of screening tests was not restricted to the
blood services and tests could be used for other purposes with less
stringent performance criteria. Use of tests for other purposes may
create a market that encourages commercial companies to develop improved
tests.

73\. A member asked when an evaluated test might be available. Dr Minor
responded that a preliminary evaluation of tests could be started
relatively soon, however it was difficult to predict when a fully
evaluated and validated test may be implemented. Members recommended
that the ethical issues must be resolved prior to the introduction of a
blood test.

74\. The **Chair summarised the discussion**, noting that:

• Until diagnostic tests for subclinical vCJD are included in Annex IIA
of the IVD Directive 98/79/EC and validated against a defined CTS, the
CE mark cannot be relied upon to indicate  a test had been properly
evaluated and validated. In the meantime, tests should be independently
validated using blinded samples.

• Preliminary evaluation of the specificity and sensitivity of tests
could be achieved using blood spiked with brain or spleen from vCJD
cases or blood from animal models. However, it is very important that
the final evaluation include testing of blood from vCJD cases.

• It is critical to collect sufficient quantities of appropriate
tissues, to prepare panels of samples with which to evaluate and
validate tests and to manage this material appropriately. Mechanisms
need to be put in place to ensure these are readily available for
testing potential products, but that guard against inappropriate use of
a valuable resource.

• Risk assessments are required to establish the performance
requirements of blood tests and to examine scenarios of the effect of
introduction of such tests on the blood supply and transmission of vCJD.

• The ethical issues around ante mortem testing for subclinical vCJD
need to be resolved prior to implementation of such tests.

**ITEM 10 -- ANY OTHER BUSINESS**

75\. There was no other business.

 

snip\...

 

<http://www.seac.gov.uk/papers/95-1.pdf>

 13European Commission Scientific Committee on Emerging and Newly
Identified Health Risks

\(2006\) Safety of Human-derived Products with regard to vCJD

<http://ec.europa.eu/health/ph_risk/committees/04_scenihr/scenihr_cons_02_en.htm>

 14
<http://www.food.gov.uk/aboutus/ourboard/boardmeetings/boardmeetings2006/boardmeeting130706/agenda13jul06>

 15 <http://www.food.gov.uk/news/newsarchive/2006/aug/srmupdate0708>

 16  <http://www.seac.gov.uk/statements/state260106.htm>

  

**Report from the SEAC Sheep Subgroup**

 *Are the numbers of cases of vCJD in line with model predictions if the
only source of infection was cattle or is there evidence of an ovine
origin? Have vCJD cases from food borne sources stabilised or declined?*

20\. There have, up to September 2006, been 162 definite and probable
cases of vCJD in the UK16. The Sheep Subgroup accepted the data and
conclusions on the human vCJD epidemic, presented at SEAC 9417, that the
number of vCJD cases is entirely consistent with infection originating
from BSE-infected cattle. Specifically, the peak of the current wave of
human cases mirrors the peak of infected cattle entering the human food
chain with a delay of approximately eight years. However it was not
possible to exclude the possibility that another source of dietary
infection was the cause of a small proportion of the clinical vCJD
cases. It would only become apparent that there were non-bovine sources
of primary infection in the circumstance that a significant number of
vCJD cases arise in individuals who could only have been infected after
the introduction of the feed and SRM controls for cattle.

21\. It was not possible to answer the question of whether vCJD cases
from food borne sources had stabilised or declined. The current profile
of clinical cases shows a peak in 2000, and a subsequent decline.
However, all these individuals are of the MM genotype and further peaks
of vCJD cases may well occur, with longer incubation periods, in non-MM
individuals still attributable to the original BSE epidemic in cattle.
It was noted that there were a number of cases of vCJD worldwide, with
no history of UK residence, whose source of infection was not yet
elucidated.

*If BSE is present in the national sheep flock, what is the amount of
BSE infectivity that might be entering the food chain and from how many
sheep? How does this compare with the amount of infectivity that is
estimated to have entered the food chain historically due to bovine
and/or ovine BSE?*

 

**SEAC 95/2 Annex 1**

**DRAFT**

Page 8

©SEAC 2006

22\. The Sheep Subgroup noted that modelling12 showed that one BSE
infected sheep, close to the end of its incubation period, may
contribute 10 to 1000 times more infectious material to the food chain
than an infected cow. This is because thirty per cent of the risk from a
BSE infected sheep is likely to come from infectivity in lymphatic and
peripheral tissue that cannot be completely removed from a carcass by
removal of SRM under normal abattoir conditions. This modelling
indicated that although a maximum of four flocks might currently harbour
an ongoing BSE epidemic, the annual human exposure from four flocks
could be as much as 0.5% of the total exposure from cattle over the
whole BSE epidemic. This is, of course, a worst case scenario. Given
that, to date 162 definite and probable vCJD cases have arisen in the UK
ascribed to the bovine epidemic, extrapolation suggests that, in the
worst case, if BSE were in the UK sheep flock it might add a further 1
to 2 deaths per annum, assuming that these 162 cases represented the
total number of people infected through exposure to cattle BSE. The most
likely number is, however, zero.

23\. From the modelling study12, small reductions in the risk of food
chain exposure from sheep could be achieved by strategies based on
tissue testing, a 12 month age restriction or expanded definitions of
high risk tissues. However, the most effective risk reduction strategies
would remain genotype based.

24\. It was also noted that recent unpublished studies suggested that
the BSE agent, once passaged through ovine transgenic mice, might become
more virulent, transmitting more quickly with faster incubation times
and infecting a greater number of species.18 If this result can be
confirmed, extrapolation suggests that **ovine BSE may be more
infectious to humans than bovine BSE**. However, the Subgroup has not
seen the primary, unpublished, data and therefore cannot comment on
their reliability.

*What reduction in risk to public health is delivered by (i) an aim to
produce small year on year increases in the percentage of resistant and
semi-resistant animals being eaten? (ii) reduce the incidence of
classical scrapie and BSE if present?*

*What studies are needed to inform on whether there is a risk to public
health from atypical scrapie? What data would lead the subgroup to
consider that atypical scrapie is a greater potential risk to public
health than BSE in sheep? How long are such studies likely to take? Can
the risks to consumers, if any, from BSE or atypical scrapie in sheep be
compared and if so, how?*

33\. No studies examining the human health risks of atypical scrapie
have been completed. Therefore, such a risk cannot yet be excluded.
Current risk reduction measures such as SRM and MBM feeding bans reduce
any risk, should it exist. The Subgroup referred to its position
statement which contained recommendations for further studies6. The
Subgroup noted that experiments were under way to assess the
transmissibility of atypical scrapie in mice expressing human PrP
genotypes. They were encouraged by a recent report25, although the
unpublished data was not presented to the Subgroup, that atypical
scrapie was present in sheep samples from 1989, making it less likely
that it is a new and rapidly spreading infection or a risk to human
health. The Subgroup agreed that studies to assess the risk of atypical
scrapie relative to BSE and classical scrapie in mice would take many
years, and it needs to be recognised that results from the mouse model
alone may not necessarily inform whether or not atypical scrapie is a
human health risk.

34\. On the transmissibility of atypical scrapie, which may have
implications for human health, it was suggested that relevant 25
Unpublished information from the Institute for Animal Health departments
should consider in advance their responses to results which may emerge.

*If the RGS continues, what are the risks associated with potentially
creating a sheep population that is susceptible to atypical scrapie?
What are the implications for a) human health and b) animal health?*

35\. The Subgroup agreed that the current RGS would likely be less
effective in reducing susceptibility to atypical scrapie in the national
flock than it is in reducing susceptibility to classical scrapie. It was
not yet clear how the RGS would alter susceptibility to atypical scrapie
in the national flock, and the present data are so scarce that it is not
possible to be certain whether the RGS would increase or decrease
prevalence 26. It was agreed that further work was needed to establish
the prevalence of atypical scrapie within the different genotypes and
breeds, and modelling of these data could inform on the expected impact
of the RGS over the next 5 to 10 years on atypical scrapie prevalence.

36\. The Subgroup was informed of preliminary and limited
epidemiological data27 indicating, on the basis of trading associations,
that atypical scrapie is unlikely to be spreading quickly. Given a slow
spread of disease, the Subgroup considered that, since atypical scrapie
cases were present in many European countries, this is consistent with
the hypothesis that it is not a new disease but has been present for
some considerable time. If atypical scrapie has been present for 200
years, as has classical scrapie, it was considered that the risks to
human health would be small. Data collected long term were needed to
inform on this aspect. To date, the earliest case of atypical scrapie in
GB dates back to 1989 25.

37\. The RGS operates on a 3 codon screening system for codons 136, 154
and 171. The Subgroup recommended consideration of the inclusion of
codon 141 in any genotyping programme for sheep, to take account of the
importance of this allele regarding susceptibility to atypical
scrapie28.

38\. There have been six clinical cases of atypical scrapie to October
2006 in the GB flock, but others may **[have gone undetected.
The]{.underline}** 26 Baylis M., Bishop S., Hope J. and Kao R., (2006)
Analysis for the SEAC sheep subgroup

27 Data provided by Rowland Kao

28 Saunders G.C., Cawthraw S., Mountjoy S.J., Hope J. and Windl O.
(2006) PrP genotypes of atypical scrapie cases in Great Britain. *J.Gen.
Virol*. **87**, 3141-9

**SEAC 95/2 Annex 1**

**DRAFT**

Page 13

©SEAC 2006

**[full clinical phenotype is still undefined. It was]{.underline}**
noted that clinical signs tend to appear in older animals than for
classical scrapie. The Subgroup considered the data insufficient to
assess the potential impact of atypical scrapie on animal health.
Additional research is needed here.

snip\...full text ;

<http://www.seac.gov.uk/papers/95-2.pdf>

SRM controls at abattoirs and cutting plants

<http://www.seac.gov.uk/papers/95-3.pdf>

 

\-\-\-\-- Original Message \-\-\-\--

**From:** [Terry S. Singeltary Sr.](mailto:flounder9@verizon.net)

**To:** <FREAS@CBER.FDA.GOV>

**Cc:** <william.freas@fda.hhs.gov> ; <rosanna.harvey@fda.hhs.gov>

**Sent:** Wednesday, November 29, 2006 1:24 PM

**Subject:** TSE advisory committee for the meeting December 15, 2006
\[TSS SUBMISSION\]

November 29, 2006

 

 

Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,

 

 

 

a kind and warm Holiday Greetings to you all.

 

 

i kindly wish to submit the following to the TSE advisory committee for
the meeting December 15, 2006,  

about the assessment for potential exposure to vCJD in human
plasma-derived antihemophilic factor  (FVIII) products

manufactured from U.S. plasma donors and related communication material
;

 

 

<http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm>

 

i see the media picked up on this as a \'low risk\', from what the gov.
agency\
perceived to be to them;\
\
<http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines>

however, i seem to disagree. from my primitive ciphering, i see it
another way. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call
that 2% which is 1 in 50 or twenty per thousand or 20,000 per million.
also, what about the mixed genotypes/mixed susceptibility? what about
the silent carriers that donated tainted blood? what about the sporadic
CJDs of UNKNOWN strain or phenotype? this risk assessment is just more
BSe to me. Just another in a long line of industry fed crap. i pray that
my assessment is the one that is wrong. but it is THEY who roll the dice
with your life. It is THEY who refuse to regulate an industry that has
run amok. just from a recall aspect of potentially tainted blood, and
these are just recent recalls ;

PRODUCT\
Source Plasma, Recall \# B-0054-7\
CODE\
Units: 03MMNC5465, 03MMNC6361, 03MMNC6801, 03MMNC7510, 03MMNC7891,\
03MMNC8252, 03MMNC8801, 03MMNC9144, 03MMND1122, 03MMND1478, 03MMND1969,\
03MMND2350, 03MMND2825, 03MMND3211, 03MMND3708, 03MMND4072, 03MMND4588,\
03MMND4831, 03MMND5320, 03MMND5719, 03MMND6268, 03MMND6683, 03MMND7228,\
03MMND7656, 03MMND8211, 03MMND8652, 03MMND9195, 03MMND9618, 03MMNE0628,\
03MMNE0884, 03MMNE1597, 03MMNE1979, 03MMNE2644, 03MMNE3064, 03MMNE3707,\
03MMNE4122, 03MMNE4750, 03MMNE5080, 03MMNE5876, 03MMNE6218, 03MMNE7189,\
03MMNE7587, 03MMNE8027, 03MMNE8645, 03MMNE9029, 03MMNE9641, 03MMNE9979,\
03MMNF0491, 03MMNF0685, 03MMNF0937, 03MMNF1260, 04MMNA0351, 04MMNA0707,\
04MMNA1241, 04MMNA1650, 04MMNA2291, 04MMNA2646, 04MMNA3340, 04MMNA3719,\
04MMNA4312, 04MMNA4683, 04MMNA5298, 04MMNA5750, 04MMNA6407, 04MMNA6816,\
04MMNA7482, 04MMNA7915, 04MMNA8632, 04MMNA9076, 04MMNA9723, 04MMNB0063,\
04MMNB0696, 04MMNB1100, 04MMNB1845, 04MMNB2285, 04MMNB3035, 04MMNB3485,\
04MMNB4213, 04MMNB4672, 04MMNB5841, 04MMNB6652, 04MMNB7162, 04MMNB7930,\
04MMNB8453, 04MMNB9239, 04MMNB9747, 04MMNC0456, 04MMNC0931, 04MMNC1578\
RECALLING FIRM/MANUFACTURER\
BioLife Plasma Services, L.P., Mankato, MN, by facsimile on June 4,
2004.\
Firm initiated recall is complete.\
REASON\
**Blood products, collected from a donor who was at increased risk for
new\
variant Creutzfeldt-Jakob Disease (nvCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
89 units\
DISTRIBUTION\
CA and Austria\
\
\
END OF ENFORCEMENT REPORT FOR October 25, 2006\
\
\###\
\
\
<http://www.fda.gov/bbs/topics/enforce/2006/ENF00975.html>

USA FDA MAD COW BLOOD HUMANS RECALL (these are dime a dozen)\
\
\
RECALLS AND FIELD CORRECTIONS: BIOLOGICS \-- CLASS II\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
Source Plasma, Recall \# B-1708-6\
CODE\
Units: MI180733, MI180927, MI181625, MI181780, MI182337, MI182519,
MI183140,\
MI183311, MI183955, MI185006, MI185278, MI185822, MI186081, MI186855,\
MI187183, MI187903, MI188273, MI188695, MI189257, MI189553, MI190136,\
MI190473, MI191073, MI191395, MI191972, MI192303, MI193473, MI194343,\
04MINA0377, 04MINA0801, 05MINA7147, 05MINA7451, 05MINA8094, 05MINA8504,\
05MINA9548, 05MINA9883, 05MINB0489, 05MINB0875, 05MINB1469, 05MINB1874,\
05MINB3116, 05MINB7192, 05MINB7529, 05MINB8246, 05MINB8612, 05MINB9236,\
05MINB9366, 05MINB9475, 05MINB9641, 05MINC0031, 05MINC0237, 05MINC0336,\
05MINC0894, 05MINC0964, 05MINC1138, 05MINC1619, 05MINC1750, 05MINC1907,\
05MINC1977, 05MINC2375, 05MINC2774, 05MINC3113, 05MINC3484, 05MINC4277,\
05MINC4623, 05MINC5623, 05MINC5914, 05MINC7545, 05MINC7870, 05MINC8355,\
05MINC8689, 05MINC9437, 05MINC9775, 05MIND0067, 05MIND0393, 05MIND0892,\
05MIND0951, 05MIND1836, 05MIND2183 and 05MIND2962\
RECALLING FIRM/MANUFACTURER\
BioLife Plasma Services L.P., Muncie, IN, by facsimile on November 22,
2005.\
Firm initiated recall is complete.\
REASON\
**Blood products, collected from unsuitable donors based on risk factors
for\
Creutzfeldt-Jakob Disease (CJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
80 units\
DISTRIBUTION\
CA, NC, and MD\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
\
PRODUCT\
a) Red Blood Cells, Leukocytes Reduced, Recall \# B-1714-6;\
b) Fresh Frozen Plasma, Recall \# B-1715-6;\
c) Platelets, Recall \# B-1716-6\
CODE\
a), b), and c) Unit: 2443732\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by letters dated\
November 11, 2003 and December 18, 2003. Firm initiated recall is
complete.\
REASON\
**Blood products, collected from a donor who was at increased risk for
new\
variant Creutzfeldt-Jakob Disease (nvCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
3 units\
DISTRIBUTION\
TX and WI\
\
END OF ENFORCEMENT REPORT FOR SEPTEMBER 13, 2006\
\
\###\
\
<http://www.fda.gov/bbs/topics/enforce/2006/ENF00969.html>

PRODUCT\
Fresh Frozen Plasma, Recall \# B-1751-6\
CODE\
Unit: 4936623\
RECALLING FIRM/MANUFACTURER\
Gulf Coast Regional Blood Center, Houston, TX, by facsimile dated
September\
16, 2005. Firm initiated recall is complete.\
REASON\
**Blood product, which was collected from an unsuitable donor based on
risk\
factors for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
1 unit\
DISTRIBUTION\
TX\
\
END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006\
\
\###\
\
<http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html>\
\
\
\
Mon Aug 7, 2006 10:24\
71.248.132.189\
\
PRODUCT\
a) Red Blood Cells, Recall \# B-1587-6;\
b) Cryoprecipitated AHF, Recall \# B-1588-6;\
c) Recovered Plasma, Recal \# B-1589-6\
CODE\
a), b) and c) Unit: 2016719\
RECALLING FIRM/MANUFACTURER\
Walter Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile
on\
March 13, 2003. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
3 units\
DISTRIBUTION\
GA and Germany\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1590-6;\
b) Fresh Frozen Plasma, Recall \# B-1591-6\
CODE\
a) and b) Unit: 2443595\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
June\
30, 2004. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
TX\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1592-6;\
b) Fresh Frozen Plasma, Recall \# B-1593-6\
CODE\
a) and b) Unit: 2545596\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on\
December 14, 2004 and January 3, 2005. Firm initiated recall is
complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
TX\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
\
<http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html>\
\
\
\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1550-6;\
b) Fresh Frozen Plasma, Recall \# B-1551-6\
CODE\
a) and b) Unit 2395371\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by fax on August
20,\
2003. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
TX\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1552-6;\
b) Platelets, Recall \# B-1553-6;\
c) Fresh Frozen Plasma, Recall \# B-1554-6\
CODE\
a), b) and c) Unit 2438702\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by fax on May 29,\
2003. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
3 units\
DISTRIBUTION\
TX\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1555-6;\
b) Fresh Frozen Plasma, Recall \# B-1556-6\
CODE\
a) and b) Unit 2454970\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by fax on July 23
and\
December 11. 2003. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
TX\
\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
a) Red Blood Cells, Recall \# B-1494-6\
b) Cryoprecipitated AHF, Recall \# B-1495-6\
CODE\
a) and b) Unit 5013100\
RECALLING FIRM/MANUFACTURER\
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on
May\
17, 2005. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
GA\
\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
Source Plasma, Recall \# B-1450-6\
CODE\
Unit numbers ST0824313 and ST0824764\
RECALLING FIRM/MANUFACTURER\
Stillwater Plasma Center LLC, Stillwater, OK, by fax on November 21,
2003.\
Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor whose suitability\
pertaining to risk factors for Creutzfeldt-Jakob Disease (vCJD) was not\
adequately determined, were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
UK\
\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
Plasma Frozen, Recall \# B-1422-6;\
Recovered Plasma, Recall \# B-1423-6\
CODE\
a) Unit 03E42218;\
b) Unit 03E38153\
RECALLING FIRM/MANUFACTURER\
American Red Cross Blood Services, Atlanta, GA, by telephone, e-mail or\
letter on February 20 or 21, 2004. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
GA and Switzerland\
\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1374-6;\
b) Recovered Plasma, Recall \# B-1375-6\
CODE\
a) and b) unit 2453906\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by fax on October
31\
and November 5, 2003. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
TX and Austria\
\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
Source Plasma. Recall \# B-1295-6\
CODE\
Units: NG0046551, NG0045950\
RECALLING FIRM/MANUFACTURER\
DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax
on\
December 20, 2002, Firm initiated recall is complete.\
REASON\
**Blood products, collected from a donor who did not answer the
questions on\
the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire\
appropriately, were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
KY\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
Source Plasma. Recall \# B-1296-6\
CODE\
Unit: NG 0044520\
RECALLING FIRM/MANUFACTURER\
DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax
on\
December 12, 2002. Firm initiated recall is complete.\
REASON\
**Blood product, collected from a donor who did not answer the questions
on\
the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire, was\
distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
1 unit\
DISTRIBUTION\
KY\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
Source Plasma. Recall \# B-1297-6\
CODE\
Units: NG0042874, NG0043139, NG0043312, NG0043618, NG0043797,
NG0044020,\
NG0044209, NG0044507, NG0044718, NG0044977, NG0045161, NG0045412,
NG0045555\
RECALLING FIRM/MANUFACTURER\
DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax
on\
December 20, 2002. Firm initiated recall is complete.\
REASON\
**Blood products, collected from a donor considered to be at increased
risk\
for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
13 units\
DISTRIBUTION\
KY\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
Source Plasma, Recall \# B-1298-6\
CODE\
Units: NG 0046823, NG 0046671, NG 0045205, NG 0044635, NG 0043095, NG\
0042525, NG 0042341\
RECALLING FIRM/MANUFACTURER\
DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax
on\
December 20, 2002. Firm initiated recall is complete.\
REASON\
**Blood products, collected from a donor who answered questions on the
variant\
Creutzfeldt-Jacob disease (vCJD) questionnaire inappropriately, were\
distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
7 units\
DISTRIBUTION\
KY\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
Recovered Plasma, Recall \# B-1299-6\
CODE\
Unit: 4357117\
RECALLING FIRM/MANUFACTURER\
Department of the Navy, Naval Medical Center, San Diego, CA, by fax and\
letter on September 25, 2003. Firm initiated recall is complete.\
REASON\
**Blood product, collected from a donor considered to be at risk of
exposure\
to Creutzfeldt-Jacob Disease (CJD), was distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
1 unit\
DISTRIBUTION\
Germany\
\
\
END OF ENFORCEMENT REPORT FOR July 12, 2006\
\
\###\
\
\
<http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html>\
\
\
\
CJD WATCH MESSAGE BOARD\
TSS\
FDA mad cow nvCJD \'only\' blood recalls 1ST WEEK JULY\
Fri Jul 7, 2006 09:37\
70.110.83.160\
\
\
FDA mad cow nvCJD \'only\' blood recalls 1ST WEEK JULY\
\
\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1379-6;\
b) Platelets, Recall \# B-1380-6;\
c) Fresh Frozen Plasma, Recall \# 1381-6;\
d) Recovered Plasma, Recall \# B-1382-6\
CODE\
a) Unit numbers: 2343106, 2377779, and 2403533;\
b) and c) Unit numbers: 2377779;\
d) Unit numbers: 2343106 and 2403533\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
June\
12, 2003. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
7 units\
DISTRIBUTION\
TX and Austria\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
\
\
\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1467-6;\
b) Recovered Plasma, Recall \# B-1468-6\
CODE\
a) and b) Unit numbers: 2329380\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
May 8,\
2003. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
TX and Switzerland\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
\
\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1479-6;\
b) Cryoprecipitated AHF, Recall \# B-1480-6;\
c) Recovered Plasma, Recall \# B-1481-6\
CODE\
a), b), and c) Unit numbers: 2383280\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
July\
23 and 29, 2004. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
3 units\
DISTRIBUTION\
TX and Switzerland\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1482-6;\
b) Fresh Frozen Plasma, Recall \# B-1483-6\
CODE\
a) and b) Unit number: 2501452\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on\
October 5, 2004. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
2 units\
DISTRIBUTION\
TX and NY\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
PRODUCT\
a) Red Blood Cells Leukocytes Reduced, Recall \# B-1484-6;\
b) Plasma Cryoprecipitated Reduced, Recall \# B-1485-6;\
c) Recovered Plasma, Recall \# B-1486-6\
CODE\
a) and c) Unit number: 2554077;\
b) Unit number: 2415708\
RECALLING FIRM/MANUFACTURER\
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
August\
13, 2004. Firm initiated recall is complete.\
REASON\
**Blood products, which were collected from a donor who may be at
increased\
risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.\
**VOLUME OF PRODUCT IN COMMERCE\
3 units\
DISTRIBUTION\
TX and Austria\
\
\
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\
\
\
END OF ENFORCEMENT REPORT FOR July 5, 2006\
\
\###\
\
\
<http://www.fda.gov/bbs/topics/enforce/2006/ENF00959.html>

 

 

Greetings again Dr. Freas et al at FDA,

 

WITH new atypical TSE in the bovine, in the sheep, goat, and humans, and
the fact that the new BASE TSE in cattle being very very similar to
sporadic CJD, rather than the nvCJD, the fact that now science showing
the TSE agent of the atypical cattle in Japan showing infectivity other
than CNS tissue, the fact that the latest Texas mad cow and the recent
Alabama mad cow both being of the atypical strain, it would seem prudent
to include all human TSE in the blood ban, in my opinion. with sporadic
CJD, you have many strains and or phenotypes, some of which are
\'UNKNOWN\', so we do not know how this will transmit, what tissues are
infectious and or if blood transmits. that\'s the bottom line, however
it has been reported that the BASE is more virulent to humans. With
this, and the fact that sporadic CJD has tripled in the past few years
or so, i see it as being prudent to take serious and immediate action ;

 

 

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

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

Strategies to investigate the possible existence of sporadic bovine
spongiform encephalopathy (BSE) require\
systematic testing programs to identify cases in countries considered to
have little or no risk for orally acquired disease, or to detect a
stable occurrence of atypical cases in countries in which orally
acquired disease is disappearing. To achieve 95% statistical confidence
that the prevalence of sporadic BSE is no greater than 1 per million
(i.e., the annual incidence of sporadic Creutzfeldt-Jakob disease
\[CJD\] in humans) would require negative tests in 3 million randomly
selected older cattle. A link between BSE and sporadic CJD has been
suggested on the basis of laboratory studies but is unsupported by
epidemiologic observation. Such a link might yet be established by the
discovery of a specific molecular marker or of particular combinations
of trends over time of typical and atypical BSE and various subtypes of
sporadic CJD, as their numbers are influenced by a continuation of
current public health measures that exclude high-risk bovine tissues
from the animal and human food chains. \...\...\
\
\
PLEASE READ FULL TEXT ;\
\
\
<http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e>

 

CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006\
\
\
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 USDA did before
2005 suspect,\" Brown said. \...snip\...end\
\
\
<http://www.upi.com/>

 

\*\*\* Inherent Challenges in Identifying and Testing

High-Risk Cattle Still Remain\
\
\
<http://www.usda.gov/oig/webdocs/50601-10-KC.pdf>

 

 

 

**Prion infections, blood and transfusions\
**\
**Adriano Aguzzi\* and Markus Glatzel**\
\
\
Prion infections lead to invariably fatal diseases of the CNS, including
Creutzfeldt-Jakob disease (CJD) in humans, bovine spongiform
encephalopathy (BSE), and scrapie in sheep. There have been hundreds of
instances in which prions have been transmitted iatrogenically among\
humans, usually through neurosurgical procedures or administration of
pituitary tissue extracts. Prions have not generally been regarded as
bloodborne infectious agents, and case-control studies have failed to
identify CJD in transfusion recipients. Previous understanding was,
however, questioned by reports of prion infections in three recipients
of blood donated by individuals who subsequently developed variant CJD.
On reflection, hematogenic prion transmission does not come as a
surprise, as involvement of extracerebral compartments such as lymphoid
organs and skeletal muscle is common in most prion infections, and
prions have been\
recovered from the blood of rodents and sheep. Novel diagnostic
strategies, which might include the use of surrogate markers of prion
infection, along with prion removal strategies, might help to control
the risk of iatrogenic prion spread through blood transfusions. \...\
\
\
snip\...\
\
\
Last, despite all epidemiological evidence to the contrary, patients who
are methionine/valine\
heterozygous at codon 129 of the PRNP gene are susceptible to infection
with vCJD prions, which raises several important questions. Is the
virulence of BSE prions enhanced when passaged from human to human, as
opposed to the original bovine to human situation? Passaging\
experiments of scrapie infectivity between mice and hamsters indicate
that this scenario is highly\
plausible.6 Even more importantly, can vCJD infection of heterozygous
individuals establish a permanent subclinical carrier state? Although
this situation might constitute a best-case scenario for the infected
individuals, it could be disastrous from an epidemiological viewpoint,
as it might lead to an unrecognized and possibly self-sustaining
epidemic. \...\
\
\
snip\... full text ;\
\
\
JUNE 2006 VOL 2 NO 6 AGUZZI AND GLATZEL NATURE CLINICAL PRACTICE
NEUROLOGY\
329\
\
[www.nature.com/clinicalpractice/neuro](http://www.nature.com/clinicalpractice/neuro)\
\
\
\
\
FDA Fines American Red Cross \$4.2 Million (BLOOD CJD)\
Fri Sep 8, 2006 20:01\
71.248.154.242\
\
\
\
FDA Statement\
FOR IMMEDIATE RELEASE\
Statement\
September 8, 2006\
Media Inquiries:\
301-827-6242\
Consumer Inquiries:\
888-INFO-FDA\
\
\
\
FDA Fines American Red Cross \$4.2 Million for Failure to Meet
Established Blood Safety Laws\
\
\
<http://www.fda.gov/cber/talkpapers.htm#arc>\
\
\
snip\...

One way the Red Cross erred was by **failing to ask donors about travel
history that could increase the chances of having malaria or the human
version of mad cow disease**, FDA officials said.\
\
snip\...

<http://today.reuters.co.uk/news/articlenews.aspx?type=healthNews&storyID=2006-09-08T224834Z_01_N08403053_RTRIDST_0_HEALTH-REDCROSS-DC.XML>\
\
\
<http://today.reuters.co.uk/news/articlenews.aspx?type=healthNews&storyID=2006-09-08T224834Z_01_N08403053_RTRIDST_0_HEALTH-REDCROSS-DC.XML&pageNumber=1&imageid=&cap=&sz=13&WTModLoc=NewsArt-C1-ArticlePage1>

 

Greetings again Dr. Freas et al at FDA,\
\
\
THIS was like closing the barn door after the mad cows got loose. not
only the red cross, but the FDA has failed the public in protecting them
from the TSE aka mad cow agent. TSE agent i.e. bse, base, cwd, scrapie,
tme, and any sub strains thereof. we do not know if these strains will
or have transmitted to humans as subclinical TSE or clinical disease,
and we do not know if they have or will transmit second, third, forth
passage via friendly fire i.e. multiple potential routes via medical,
surgical, pharmaceutical etc.

 

IF you remember correctly Dr. Freas et al, i called this long ago,
almost 6 years ago ;

 

PDF\]Freas, William TSS SUBMISSION\
File Format: PDF/Adobe Acrobat - Page 1. J Freas, William From: Sent:
To: Subject: Terry S. Singeltary\
Sr. \[<flounder@wt.net>\] Monday, January 08,200l 3:03 PM freas \...

 

  

Freas, William

From: Terry S. Singeltary Sr. \[flounder@wt.net\]

**Sent: Monday, January 08,200l** 3:03 PM

To: freas@CBS5055530.CBER.FDA.GOV

Subject: CJDIBSE (aka madcow) Human/Animal TSE's\--U.S.\--Submission To
Scientific Advisors and

Consultants Staff January 2001 Meeting (short version)

 

Greetings again Dr. Freas and Committee Members,

 

I wish to submit the following information to the Scientific Advisors
and Consultants Staff 2001 Advisory Committee (short version). I
understand the reason of having to shorten my submission, but only hope
that you add it to a copy of the long version, for members to take and
read at their pleasure, (if cost is problem, bill me, address below).

So when they realize some time in the near future of the \'real\' risks
i speak of from human/animal TSEs and blood/surgical products. I cannot
explain the \'real\' risk of this in 5 or 10 minutes at some meeting,
but will attempt here: remember AIDS/HIV, \'no problem to heterosexuals
in the U.S.? no need to go into that, you know of this blunder: DO NOT
make these same stupid mistakes again with human/animal TSE\'s aka
MADCOW DISEASE. I lost my Mom to hvCJD, and my neighbor lost his Mother
to sCJD as well (both cases confirmed). I have seen many deaths, from
many diseases. I have never seen anything as CJD, I still see my Mom
laying helpless, jerking tremendously, and screaming \"God, what\'s
wrong with me, why can\'t I stop this\". I still see this, and will
never forget. Approximately 10 weeks from 1st of symptoms to death. This
is what drives me. I have learned more in 3 years about not only
human/animal TSE\'s but the cattle/rendering/feeding industry/government
than i ever wished to. I think you are all aware of CJD vs vCJD, but i
don\'t think you all know the facts of human/animal TSE\'s as a whole,
they are all very very similar, and are all tied to the same thing,
GREED and MAN.

I am beginning to think that the endless attempt to track down and ban,
potential victims from known BSE Countries from giving blood will be
futile. You would have to ban everyone on the Globe eventually? AS well,
I think we MUST ACT SWIFTLY to find blood test for TSE\'s, whether it be
blood test, urine test, eyelid test, anything at whatever cost, we need
a test FAST.  DO NOT let the incubation time period of these TSEs fool
you. To think of Scrapie as the prime agent to compare CJD, but yet
overlook the Louping-ill vaccine event in 1930\'s of which 1000\'s of
sheep where infected by scrapie from a vaccine made of scrapie infected
sheep brains, would be foolish. I acquired this full text version of the
event which was recorded in the Annual Congress of 1946 National Vet.
Med. Ass. of Great Britain and Ireland. From the BVA and the URL is
posted in my (long version). U.S.A. should make all human/animal TSE\'s
notifiable at all ages, with requirements for a thorough surveillance
and post-mortem examinations free of charge, if you are serious about
eradicating this horrible disease in man and animal.

There is histopathology reports describing  \"florid plaques\" in CJD
victims in the USA and some of these victims are getting younger. I have
copies of such autopsies, there has to be more. PLUS, sub-clinical human
TSE\'s will most definitely be a problem.

THEN think of vaccineCJD in children and the bovine tissues used in the
manufacturing process, think of the FACT that this agent surviving
6OO\*C.

PNAS \-- Brown et al. 97 (7): 3418 scrapie agent live at 600\*C

Then think of the CONFIDENTIAL documents of what was known of
human/animal TSE and vaccines in the mid to late 8Os, it was all about
depletion of stock, to hell with the kids, BUT yet they knew. To think
of the recall and worry of TSE\'s from the polio vaccine, (one taken
orally i think?), but yet neglect to act on the other potential TSE
vaccines (inoculations, the most effective mode to transmit TSEs) of
which thousands of doses were kept and used, to deplete stockpile, again
would be foolish.

\--Oral polio; up to 1988, foetal calf serum was used from UK and New
Zealand (pooled); since 1988 foetal calf serum only from New Zealand.
Large stocks are held.

\--Rubella; bulk was made before 1979 from foetal calf serum from UK and
New Zealand. None has been made as there are some 15 years stock.

\--Diphtheria; UK bovine beef muscle and ox heart is used but since the
end of 1988 this has been sourced from Eire. There are 1,250 litres of
stock.

\--Tetanus; this involves bovine material from the UK mainly Scottish.
There are 21,000 litres of stock.

\--Pertussis; uses bovine material from the UK. There are 63,000 litres
of stock.

\--They consider that to switch to a non-UK source will take a minimum
of 6-18 months and to switch to a non-bovine source will take a minimum
of five years.

3\. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These are
sourced from the USA and the company believes that US material only is
used. 89/2.14/2.1

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

BSE3/1 0251

4\. XXXXXXXXXXX have a  measles vaccine using bovine serum from the UK.
there are 440,000 units of stock. They have also got MMR using bovine
serum from the UK.

5\. XXXXXXXXXXX have influenza, rubella, measles,\' MMR vaccines likely
to be used in children. Of those they think that only MMR contains
bovine material which is probably a French origin.

6\. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial.
These use veal material, some of which has come from the UK and has been
ade by XXXXXXXXXXX (see above).

I have documents of imports from known BSE Countries, of ferments, whole
blood, antiallergenic preparations, human blood plasma, normal human
blood sera, human immune blood sera, fetal bovine serum, and other blood
fractions not elsewhere specified or included, imported glands, catgut,
vaccines for both human/animal, as late as 1998.

Let us not forget about PITUITARY EXTRACT. This was used to help COWS
super ovulate. This tissue was considered to be of greatest risk of
containing BSE and consequently transmitting the disease.

**ANNEX 6: MEETING HELD ON 8 JUNE 1988 TO DISCUSS THE IMPLICATIONS OF
BSE TO BIOLOGICAL PRODUCTS CONTAINING BOVINE - EXTRACTED MATERIAL**

 How much of this was used in the U.S.? Please do not keep making the
same mistakes. \'Absence of evidence is not evidence of absence\'. What
are the U.S. rules for importing and manufacturing vaccines, medicines
and medical devices? Does the U.S.A. allow sourcing of raw material of
ruminants from the U.S.A.?

U.S. cattle, what kind of guarantee can you give for serum or tissue
donor herds.? The U.S. rendering system would easily amplify T.S.E.\'s:
Have we increased the stability of the system (improved heat treatments)
since the EU SSC report on the U.S.A. was published in july 2000?

What is done to avoid cross-contaminations in the U.S.A.? How can the
U.S. control absence of cross-contaminations of animal TSE\'s when pig
and horse MBM and even deer and elk are allowed in ruminant feed, as
well as bovine blood? I sadly think of the rendering and feeding policy
before the Aug. 4, 1997 \'partial\' feed ban, where anything went, from
the city police horse, to the circus elephant, i will not mention all
the scrapie infected sheep.

I am surprised that we have not included man \'aka soyent green\'. It is
a disgusting industry and nothing more than greed fuels it. When will
the U.S.. start real surveillance of the U.S. bovine population (not
passive, this will not work)?

When will U.S. start removing SRMs? Have they stopped the use of
pneumatic stunners in the U.S.? If so, will we stop it in all U.S.
abattoirs or only in those abattoirs exporting to Europe? If not, WHY
NOT? same questions for removal of SRM in the U.S.A., or just for
export? If not, WHY NOT?

How do we now sterilize surgical/dental instruments in the U.S.A.? Where
have we been sourcing surgical catgut? (i have copies of imports to
U.S., and it would floor you) When will re-usable surgical instruments
be banned? \'Unregulated \"foods\" such as \'nutritional supplements\'
containing various extracts from ruminants, whether imported or derived
from US cattle/sheep/cervids (\"antler velvet\" extracts!) should be
forbidden or at least very seriously regulated. (neighbors Mom, whom
also died from CJD, had been taking bovine based supplement, which
contained brain, eye, and many other bovine/ovine tissues for years,
\'IPLEX\').

What is the use of banning blood or tissue donors from Germany, France,
etc\... when the U.S.A. continues exposing cattle, sheep and people to
SRM, refuses to have a serious feed ban, refuses to do systematic
BSE-surveillance? The FDA should feel responsible for the safety of what
people eat.

prohibit the most dangerous foods, not only prohibit a few more donors,
the FDA should be responsible for the safe sourcing of medical devices,
not only rely on banning donors \"from Europe\", The \'real\' risks are
here in the U.S. as well, and have been for some time.

We must not forget the studies that have proven infectivity in blood
from TSE\'s.

 

The Lancet, November 9, 1985

\" Sir, \--Professor Manuelidis and his colleagues (Ott 19, p896) report
transmission to animals of Creutzfeldt-Jakob disease (CJD) from the
buffy coat from two patients. **We also transmitted the disease from ,
whole blood samples** **of a patient** (and of mice) **infected with
CJD**.l Brain, Cornea, and urine from this patient were also infectious,
and the clinicopathological findings2 are summarised as follows.

snip\...

full text ;\
\
\
<http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf>

 

 

Greetings again Dr. Freas et al at FDA,

 

NOW, here we are in 2006, worried and still fumbling around with what
should have been

done long, long ago ;

 

Subject: **91ST MEETING OF THE SEAC MEETING LONDON 24TH FEB 2006\
**Date: **March 10, 2006 at 7:36 am PST**

1

© SEAC 2006

NINETY FIRST MEETING OF THE SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE

The Spongiform Encephalopathy Advisory Committee held its 91st meeting
in London on 24th February 2006.

 

snip\...

 

MEDICAL IMPLANTS CONTAINING BOVINE MATERIAL

SEAC considered the risk to human health from medical implants that
include bovine material sourced from the USA. This material was used for
a wide range of medical devices, some of which are life saving and for
which there are no alternative products.

SEAC considered that the source of the animal was crucial to manage the
risk. The committee suggested that other precautionary steps be taken
where practicable, such as using material from young animals, sourcing
material from countries with good surveillance procedures and a low
prevalence of disease. \...\...

 

snip\...

 

<http://www.seac.gov.uk/minutes/final90.pdf>

 

A BIT OF HISTORY ON THIS TOPIC

 

TWA LITTLE minute

<http://www.bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf>

COMMERCIAL IN CONFIDENCE

<http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf>

NOT FOR PUBLICATION

<http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf>

<http://www.bseinquiry.gov.uk/yb/1988/11/04003001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf>

NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE

snip\...

I was quite prepared to believe in unofficial pituitary hormones, also
in the 1970\'s, whether as described by Dr. Little, or in other
circumstances, for animal use.

snip\...

The fact that there were jars of pituitaries (or extract) around on
shelves is attested by the still potent 1943 pituitaries, described in
Stockell Hartree et al. (J/RF/17/291) which had come from the lab. at
Mill Hill. Having taken the trouble to collect them, they were not
lightly thrown out\...

<http://www.bseinquiry.gov.uk/files/ws/s467bx.pdf>

more on the 1968 medicine act, they forgot to follow

<http://www.bseinquiry.gov.uk/files/yb/1989/01/30008001.pdf>

8\. The Secretary of State has a number of licences. We understand that
the inactivated polio vaccine is no longer being used. There is a stock
of smallpox vaccine. We have not been able to determine the source
material. (Made in sheep very unlikely to contain bovine ingredients).\
\
<http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf>\
\
\
<http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf>

although 176 products do \_not\_ conform to the CSM/VPC\
guidelines.

<http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf>

Draft cover letter to product licence holders (considered by Human and
Vet Medicines including deer)

<http://www.bseinquiry.gov.uk/files/yb/1989/02/22008001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1989/02/22011001.pdf>

(It was noted with concern that hormone extracts could be manufactured
by a veterinary surgeon for administration to animals under his care
without any Medicines Act Control.)

<http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf>

<http://www.bseinquiry.gov.uk/files/yb/1988/06/07010001.pdf>

TWA LITTLE STATEMENT 331

<http://www.bseinquiry.gov.uk/files/ws/s331.pdf>

  

WE know about USA serum and tissue donor herds from the now infamous
Jan. 9, 2001 FDA emergency 50 state BSE conference call, that in
fact, USA serum and tissue donor herds were eating banned ruminant feed
as well ;

 

 

Date:         Sun, 7 Jan 2001 09:45:19 -0800\
Reply-To:     Sustainable Agriculture Network Discussion Group\
Sender:       Sustainable Agriculture Network Discussion Group\
From:         Beth von Gunten\
Subject:      \[BSE\] FDA/IMPORTANT NOTICE: 50 STATE CONFERENCE CALL

IMPORTANT NOTICE:  50 STATE CONFERENCE CALL - BSE

TUESDAY, JANUARY 9, 2001\
1:00-2:00 PM EST   CALL: 1-888-273-9887

A special \"50 STATE CONFERENCE CALL\" to discuss BSE (Bovine Spongiform
Encephalopathy) issues for Food and Drug Administration (FDA) regulated
animal feed products in the United States and imported animal feeds. The
conference call will discuss the FDA proposed response to the current
BSE issue and the assistance needed from state feed and agriculture
programs. THIS ISSUE MAY IMPACT ALL STATES AND ALL ANIMAL FEED AND
PRODUCTION INDUSTRIES.\
\
The 50 State call is scheduled for Tuesday, January 9, 2001 from
1:00-2:00 pm EST. Any state agency responsible for animal feed issues
wishing to participate should call 1-888-273-9887 and ask to be\
connected to the \"50 State BSE Call\".  The conference host operator
will explain how to participate, including asking questions during the
call. If possible, please coordinate within your state to utilize only
one phone line per state agency.\
\
We request that you forward this message to your agency management and
feed coordinators or other agencies or departments who may be
responsible for any animal feed issues related to FDA regulated\
products.

The agenda will be as follows:\
\
1.  Center For Veterinary Medicine (FDA) - Discussion of the problem
related to BSE events in Europe and the impact on US feed ingredients
for animals and feed operations. Discussion of the proposed
actions/inspections/compliance of licensed and unlicensed feed mills,
commercial feed manufacturers, animal feed imports, renderer\'s, protein
blenders, on-farm mixers, and ruminant feeders.\
\
2.   Office of Regional Operations (FDA) - Discussion of
contracting/working with states to inspect the universe of feed
mills/industry for \"Animal Proteins Prohibited from Use in Animal
Feed\". Discussion of working with FDA field offices.

3.   Questions and answers.\
\
Richard H. Barnes, Director\
Division of Federal-State Relations (HFC-150)\
5600 Fishers Lane Room 1207\
Rockville, Md.  20857\
ph: (301) 827-6906  FAX: (301) 443-2143

<http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0101&L=sanet-mg&P=13410>

 

Subject: BSE\--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001\
Date: Tue, 9 Jan 2001 16:49:00 -0800\
From: \"Terry S. Singeltary Sr.\"\
Reply-To: Bovine Spongiform Encephalopathy\
To: <BSE-L@uni-karlsruhe.de>

 

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

 Greetings List Members,

 I was lucky enough to sit in on this BSE conference call today and even
managed to ask a question.\
that is when the trouble started. I submitted a version of my notes to
Sandra Blakeslee of the New York Times, whom seemed very upset, and
rightly so.

 \"They tell me it is a closed meeting and they will release whatever
information they deem fit. Rather infuriating.\"

 

and i would have been doing just fine, until i asked my question. i was
surprised my time to ask a question so quick.  

(understand, these are taken from my notes for now. the spelling of
names and such could be off.)

\[host Richard Barns\] and now a question from Terry S. Singeltary of
CJD Watch. \[TSS\]

yes, thank you, U.S. cattle, what kind of guarantee can you give for
serum or tissue donor herds?

 \[no answer, you could hear in the back ground, mumbling and \'we
can\'t. have him ask the question\
again.\]

 \[host Richard\] could you repeat the question?

\[TSS\] U.S. cattle, what kind of guarantee can you give for serum or
tissue donor herds?

 \[not sure whom ask this\] what group are you with?

\[TSS\] CJD Watch, my Mom died from hvCJD and we are tracking CJD
world-wide.

 \[not sure who is speaking\] **could you please disconnect Mr.
Singeltary**

\[TSS\] you are not going to answer my question?

\[not sure whom speaking\] NO

 from this point, i was still connected, got to listen and tape the
whole conference. at one point someone\
came on, a woman, and ask again;

\[unknown woman\] what group are you with?

\[TSS\] CJD Watch and my Mom died from hvCJD we are trying to tract down
CJD and other\
human TSE\'s world wide. i was invited to sit in on this from someone
inside the USDA/APHIS\
and that is why i am here. do you intend on banning me from this
conference now?

 at this point the conference was turned back up, and i got to finish
listening. They never answered\
or even addressed my one question, or even addressed the issue. BUT, i
will try and give you a run-down\
for now, of the conference.

 IF i were another Country, I would take heed to my notes, BUT PLEASE do
not depend on them. ask for\
transcript from;

 RBARNS@ORA.FDA.GOV\
301-827-6906

he would be glad to give you one ;-)

 

Rockville Maryland,\
Richard Barns Host

**BSE issues in the U.S., How they were labelling ruminant feed?\
**Revising issues.

The conference opened up with the explaining of the U.K. BSE epidemic
winding down with about 30\
cases a week. although new cases in other countries were now appearing.
Look at Germany whom said NO BSE and now have BSE.

BSE increasing across Europe.

Because of Temporary Ban on certain rendered product, heightened
interest in U.S.

A recent statement in Washington Post, said the New Administration (old
GW) has a list of issues.\
BSE is one of the issues. BSE Risk is still low, minimal in U.S. with a
greater interest in MBM not to enter U.S. HOWEVER, if BSE were to enter
the U.S. it would be economically disastrous to the render, feed,
cattle, industries, and for human health.

(human health-they just threw that in cause i was listening. I will now
jot down some figures in\
which they told you, \'no need to write them down\'. just hope i have
them correct. hmmm, maybe i hope\
i don\'t ???)

80% inspection of rendering

\*Problem-Complete coverage of rendering HAS NOT occurred. sizeable
number of 1st time FAILED INITIAL INSPECTION, have not been reinspected
(70% to 80%).

Compliance critical, Compliance poor in U.K. and other European Firms.

Gloria Dunason\
Major Assignment 1998 goal TOTAL compliance. This \_did not\_ occur.
Mixed level of compliance,\
depending on firm.

Rendering FDA license and NON FDA license

system in place for home rendering & feed\
76% in compliance\
79% cross contamination\
21% DID NOT have system\
92% record keeping\
less than 60% total compliance

279 inspectors\
185 handling prohibited materials

Renderer at top of pyramid, significant part of compliance.\
84% compliance

failed to have caution statement render

72% compliance & cross contamination\
caution statement on feed, \'DO NOT FEED TO CATTLE\'

56 FIRMS NEVER INSPECTED

1240 FDA license feed mills\
846 inspected

\"close to 400 feed mills have not been inspected\"

80% compliance for feed.

10% don\'t have system.

NON-FDA licensed mills\
There is NO inventory on non licensed mills.\
approximately 6000 to 8000 Firms ???\
4,344 ever inspected.\
\"FDA does not have a lot of experience with\"

40% do NOT have caution statement \'DO NOT FEED\'.

74% Commingling compliance

\"This industry needs a lot of work and only half gotten to\"

\"700 Firms that were falitive, and need to be re-inspected, in addition
to the 8,000 Firms.\"

Quote to do BSE inspection in 19 states by end of January or 30 days,
and other states 60 days.\
to change feed status??? Contract check and ask questions and pass info.

At this time, we will take questions.

\[I was about the third or fourth to ask question. then all B.S.eee
broke loose, and i lost my train\
of thought for a few minutes. picked back up here\]

someone asking about nutritional supplements and sourcing, did not get
name. something about inspectors not knowing of BSE risk??? the
conference person assuring that Steve Follum? and the TSE advisory
Committee were handling that.

Some other Dr. Vet, whom were asking questions that did not know what to
do???

\[Dennis Wilson\] California Food Agr. Imports, are they looking at
imports?

\[Conference person\] they are looking at imports, FDA issued imports
Bulletin.

\[Linda Singeltary ??? this was a another phone in question, not related
i don\'t think\]\
Why do we have non-licensed facilities?

(conference person) other feed mills do not handle as potent drugs???

Dennis Blank, Ken Jackson\
licensed 400\
non FDA 4400 inspected of a total of 6000 to 8000,

(they really don\'t know how many non licensed Firms in U.S. they guess
6000 to 8000??? TSS)

Linda Detwiler\
asking everyone (me) not to use emergency BSE number, unless last
resort.\
(i thought of calling them today, and reporting the whole damn U.S.
cattle herd ;-) \'not\'

Warren-Maryland Dept. Agr.\
Prudent to re-inspect after 3 years. concerned of Firms that have
changed owners.

THE END

TSS

\############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html\
\############

 

FROM New York TIMES

Subject: Re: **BSE 50 STATE CONFERENCE CALL thread** from BSE List and
FDA\
Posting of cut version\...

Date: Thu, 11 Jan 2001 22:02:47 -0700\
From: \"Sandy Blakeslee\"\
To: \"Terry S. Singeltary Sr.\"

References: 1

 Hi terry \-- thanks for all your help. I know it made a difference with
the FDA getting out that release.

 

\-\-\-\-- Original Message \-\-\-\--\
From: \"Terry S. Singeltary Sr.\"\
To:\
Sent: Thursday, January 11, 2001 2:06 PM\
Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA

 

\-\-\-\-- Original Message \-\-\-\--

From: \"Terry S. Singeltary Sr.\"

To:

Sent: Thursday, January 11, 2001 2:06 PM

Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA

 

\> hi sandy,

 

\>From the New York Times NYTimes.com,

 

 

 

January 11, 2001

 

Many Makers of Feed Fail to Heed Rules on Mad Cow Disease

By SANDRA BLAKESLEE

 

Large numbers of companies involved in manufacturing animal feed are
not\
complying with regulations meant to prevent the emergence and spread of
mad cow disease in the United States, the Food and Drug Administration
said yesterday.

The widespread failure of companies to follow the regulations, adopted\
in August 1997, does not mean that the American food supply is unsafe,\
Dr. Stephen Sundlof, director of the Center for Veterinary Medicine at\
the F.D.A., said in an interview.

But much more needs to be done to ensure that mad cow disease does not\
arise in this country, Dr. Sundlof said.

The regulations state that feed manufacturers and companies that render\
slaughtered animals into useful products generally may not feed mammals\
to cud-chewing animals, or ruminants, which can carry mad cow disease.

All products that contain rendered cattle or sheep must have a label\
that says, \"Do not feed to ruminants,\" Dr. Sundlof said.
Manufacturers\
must also have a system to prevent ruminant products from being\
commingled with other rendered material like that from chicken, fish or\
pork. Finally, all companies must keep records of where their products\
originated and where they were sold.

Under the regulations, F.D.A. district offices and state veterinary\
offices were required to inspect all rendering plants and feed mills to\
make sure companies complied. But results issued yesterday demonstrate\
that more than three years later, different segments of the feed\
industry show varying levels of compliance.

Among 180 large companies that render cattle and another ruminant,\
sheep, nearly a quarter were not properly labeling their products and\
did not have a system to prevent commingling, the F.D.A. said. And
among\
347 F.D.A.-licensed feed mills that handle ruminant materials - these\
tend to be large operators that mix drugs into their products - 20\
percent were not using labels with the required caution statement, and\
25 percent did not have a system to prevent commingling.

Then there are some 6,000 to 8,000 feed mills so small they do not\
require F.D.A. licenses. They are nonetheless subject\
to the regulations, and of 1,593 small feed producers that handle\
ruminant material and have been inspected, 40 percent\
were not using approved labels and 25 percent had no system in place to\
prevent commingling.

On the other hand, fewer than 10 percent of companies, big and small,\
were failing to comply with the record-keeping regulations.

The American Feed Industry Association in Arlington, Va., did not
return\
phone calls seeking comment.

 

<http://www.nytimes.com/2001/01/11/science/11COW.html>

 

 

Subject: USDA/APHIS response to BSE-L\--U.S. 50 STATE CONFERENCE CALL\
Jan. 9, 2001\
Date: Wed, 10 Jan 2001 14:04:21 -0500\
From: \"Gomez, Thomas M.\"  

Reply-To: Bovine Spongiform Encephalopathy

 

To: <BSE-L@uni-karlsruhe.de>

 

 

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

 

USDA/APHIS would like to provide clarification on the following point
from\
Mr. Singeltary\'s 9 Jan posting regarding the 50 state conference call.

\[Linda Detwiler asking everyone (me) not to use emergency BSE number,\
unless last resort. (i thought of calling them today, and reporting the
whole\
damn U.S. cattle herd ;-) \'not\'\] Dr. Detwiler was responding to an
announcement made during the call to use the FDA emergency number if
anyone wanted to report a cow with signs suspect for BSE. Mr. Singeltary
is correct that Dr. Detwiler asked participants to use the FDA emergency
number as a last resort to report cattle suspect for BSE. What Mr.
Singeltary failed to do was provide the List with Dr. Detwiler\'s entire
statement. Surveillance for BSE in the United States is a cooperative
effort between states, producers, private veterinarians, veterinary
hospitals and the USDA. The system has been in place for over 10 years.
Each state has a system in place wherein cases are reported to either
the State Veterinarian, the federal Veterinarian in Charge or through
the veterinary diagnostic laboratory system. The states also have
provisions with emergency numbers. Dr. Detwiler asked participants to
use the systems currently in place to avoid the possibility of a
BSE-suspect report falling through the cracks. Use of the FDA emergency
number has not been established as a means to report diseased cattle of
any nature.

 

\############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
\############

 

 

Subject: Re: USDA/APHIS response to BSE-L\--U.S. 50 STATE CONFERENCE\
CALL Jan.9, 2001

Date: Wed, 10 Jan 2001 13:44:49 -0800

From: \"Terry S. Singeltary Sr.\"

Reply-To: Bovine Spongiform Encephalopathy

To: <BSE-L@uni-karlsruhe.de>

References: 1

 

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

 

 

Hello Mr. Thomas,

 

 

\> What Mr. Singeltary failed to do was provide the List with Dr.
Detwiler\'s entire statement.

  

Would you and the USDA/APHIS be so kind as to supply this list with a
full text version of the conference call and or post on your web-site?
If so when, and thank you. if not, why not?

 

  

\> The system has been in place for over 10 years.

 

 

That seems to be a very long time for a system to be in place, and only
test 10,700 cattle from some 1.5 BILLION head (including calf crop).
Especially since French are testing some 20,000 weekly and the E.U. as a
whole, are testing many many more than the U.S., with less cattle, same
risk of BSE/TSEs.

 

 

Why does the U.S. insist on not doing massive testing with the tests
which the E.U. are using?

 \
Why is this, please explain?

  

Please tell me why my question was not answered?

  

\> U.S. cattle, what kind of guarantee can you give for serum or tissue
donor herds?

 

  

It was a very simple question, a very important question, one that
pertained to the topic of BSE/feed, and asked in a very diplomatic way.
Why was it not answered?

 

 

If all these years, we have been hearing that pharmaceutical grade
bovines were raised for pharmaceuticals vaccines etc. But yet the USA
cannot comply with feed regulations of the ruminant feed ban, PLUS
cannot even comply with the proper labelling of the feed, cross
contamination etc.

Then how in the world can you Guarantee the feed fed to pharmaceutical
grade bovine, were actually non ruminant feed?

 

Before i was ask to be \'disconnected\', i did hear someone in the
background\
say \'we can\'t\'\-- have him ask the question again. could you please
be so kind, as to answer these questions?

 

thank you,\
Terry S. Singeltary Sr. Bacliff, Texas USA

 

P.S. if you will also notice, i did not post that emergency phone number
and do not intend on passing it on to anyone. I was joking when i said i
should call and report the whole damn U.S. Herd. So please pass that on
to Dr. Detwiler, so she can rest easily. BUT, they should be reported,
some are infected with TSE. The U.S. is just acting as stupid as Germany
and other\
Countries that insist they are free of BSE.

 

TSS

 

Subject: Report on the assessment of the Georgraphical BSE-risk of the\
USA July 2000 (not good)\
Date: Wed, 17 Jan 2001 21:23:51 -0800\
From: \"Terry S. Singeltary Sr.\"\
Reply-To: Bovine Spongiform Encephalopathy\
To: <BSE-L@uni-karlsruhe.de>

 

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

Greetings List Members and ALL EU Countries,

 

Because of this report, and the recent findings of the 50-state BSE
Conference call, I respectfully seriously suggest that these Countries
and the SSC re-evaluate the U.S.A. G.B.R. to a risk factor of #3.

 

 

snip\...

 

 

Terry S. Singeltary Sr.,\
P.O. Box 42, Bacliff, Texas USA 77518

 

 

<http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html>

 

  

 

 

# CVM Update

[\<\<Back](http://www.fda.gov/cvm/bse_updates.htm)

January 10, 2001

**UPDATE ON RUMINANT FEED (BSE) ENFORCEMENT ACTIVITIES**

Bovine spongiform encephalopathy (BSE) is a type of "transmissible
spongiform encephalopathy" disease that infects cattle. After the first
case in 1986 in the United Kingdom, BSE quickly became an epidemic in
cattle herds there. No cases of BSE have been found in U.S. cattle,
despite active monitoring.

Rendered feed ingredients contaminated with an infectious agent are
believed to be the source of BSE infection in cattle. Some of the feed
given to cattle includes remnants of the slaughtering process, such as
the brain and spinal cord, which may harbor the agent that causes BSE.
Although the material is cooked during the rendering process, the BSE
agent can survive.

To prevent the establishment and amplification of BSE through feed in
the United States, FDA implemented a final rule that prohibits the
feeding of mammalian protein to ruminant animals in most cases. This
rule, Title 21 Part 589.2000 of the Code of Federal Regulations, became
effective on August 4, 1997.

FDA developed an enforcement plan with the goal of 100% compliance with
this rule. For the first two years it was in effect, the enforcement
plan included education as well as inspections with FDA taking
compliance actions for egregious actions or repeated non-compliance. As
part of the enforcement plan, an assignment was issued to all FDA
District Offices in 1998 to conduct inspections of 100% of all renderers
and feed mills and some ruminant feeders to determine compliance.

FDA\'s Center for Veterinary Medicine (CVM) has assembled data from the
inspections conducted thus far, and presented the following data in a
conference call FDA held with Federal and State feed control officials
on January 9, 2001.

To date, there have been a total of 9,947 inspections. The majority of
these inspections (around 80%) were conducted by State officials and the
remainder by FDA. Various segments of the feed industry had different
levels of compliance.

**For Renderers**, who are at the \"top of the pyramid\" since they are
the first to handle rendered protein, and who send materials to feed
mills and other ruminant feeders:

Total number of inspections \-- 239. Firms handling prohibited material
\-- 180

-   Firms whose products were labeled with the required caution
    statement \-- 84%

-   Had a system to prevent commingling \-- 72%

-   Followed recordkeeping regulations \-- 96-98%

**For FDA Licensed Feed Mills** \-- 1,240 total \-- Inspected \-- 846.
Of those feed mills inspected, 347 were handling prohibited material:

-   Firms whose products were labeled with the required caution
    statement \-- 80%

-   Had a system to prevent commingling \-- 91%

-   Followed recordkeeping regulations \-- 98

**For Non-FDA Licensed Feed Mills** \-- 4,344 inspected (FDA does not
know the total number since they are not required to be licensed by the
Agency, but it could be 6,000 - 8,000.) Of those feed mills inspected,
1,593 were handling prohibited material:

-   Firms whose products were labeled with the required caution
    statement \-- 59%

-   Had a system to prevent commingling \-- 74%

-   Followed recordkeeping regulations \-- 91%

FDA is continuing its enforcement efforts to achieve the goals of 100%
inspection of all renderers and feed mills and some ruminant feeders and
100% compliance with the ruminant feed regulations. FDA Field offices
have an assignment to re-inspect 700 firms that were not in full
compliance with the rule but have committed to implementing the
regulation. In addition, FDA is seeking assistance from State feed
control officials to identify non-FDA licensed feed mills and to conduct
additional inspections in all categories.

FDA anticipates higher levels of compliance after completion of
follow-up inspections.

**Issued by:\
FDA, Center for Veterinary Medicine,\
Office of Management and Communications, HFV-12\
7519 Standish Place, Rockville, MD 20855\
Telephone: (301) 827-3800 FAX: (301) 827-4065\
Internet Web Site: <http://www.fda.gov/cvm>**

 

[**http://www.fda.gov/cvm/bseup.htm**](http://www.fda.gov/cvm/bseup.htm)

 

 

From:

Subject: confidential

To: <flounder@wt.net>

Sorry did not get back to you. (Ran out of time!!)\
\
Of interest\...don\'t repeat.  On Jan 9, was somewhere and not able to
tie into conference call.  Was around an official who should have been
on conference\
call..another person with me also remembered it and we both inquired as
to how the call went.  Was told (to both of us) that the call had been
cancelled!!  (Told us several times that the call was cancelled and they
did not know why!!!) I will try to find out why this person said
that\...maybe they got off the call or they were told to tell everyone
that the call was cancelled. You need to POST your interaction with the
conference call on a web site\....let me know when you do\...

snip\...

There must be a reason for the lying\....??? Surely people who are
really interested will found out what went on?  There are quite a few
people who listened in and declined to identify or acknowledge that they
listened in\...why the big secrecy or this person may have been told to
do this.  Need to know!!!  Something dirty is going on\...some sort of
treachery seems to be in the works\... Not a good situation for me right
now\...wish I could tell you more as to what is going on\...but too
dangerous right now\...got to sort it out.

\*\*\*

 

Date: Sun, 21 Jan 2001 23:50:31 +0000 (GMT)\
From:

Subject: stuff

To: \"Terry S. Singeltary Sr.\"
[\<flounder@wt.net\>](mailto:flounder@wt.net)\
\
Confidential:

Budget:  let me know what you find out and the breakdown.  There may be
some stuff stuffed into it which is not legit\... They may figure some
salaries and such\...the real gist of the matter is the shocking amount
of \$ that is actually used to \"ferret\" out the disease and the \$
that are used to P.R. the whole affair and give appearance of being
concerned and involved\...again it was said years ago and it should be
taken seriously\....BSE will NEVER be found in the US!

As for the BSE conference call\...I think you did a great service to
freedom of information and making some people feign integrity\...I find
it scary to see that most of the \"experts\" are employed by the federal
government or are supported on the \"teat\" of federal funds.  A scary
picture! 

 

snip\...

 

 

The most frightening thing I have read all day is the report of
Gambetti\'s finding of a new strain of sporadic cjd in young
people\...\...\...Dear God, what in the name of all that is holy is
that!!!

If the US has different strains of scrapie\.....why????than the
UK\...then would the same mechanisms that make different strains of
scrapie here make different strains of BSE\...if the patterns are
different in sheep and mice for scrapie\.....could not the BSE be
different in the cattle, in the mink, in the humans\...\....I really
think the slides or tissues and everything from these young people with
the new strain of sporadic cjd should be put up to be analyzed by many,
many experts in cjd\...\.....bse\.....scrapie

Scrape the damn slide and put it into mice\.....wait\.....chop up the
mouse brain and and spinal cord\...\.....put into some more
mice\.....dammit amplify the thing and start the damned
research\.....This is NOT rocket science\...we need to use what we know
and get off our butts and move\....the whining about how long everything
takes\.....well it takes a whole lot longer if you whine for a year and
then start the research!!!

Not sure where I read this but it was a recent press release or
something like that: I thought I would fall out of my chair when I read
about how there was no worry about infectivity from a histopath slide or
tissues because they are preserved in formic acid, or formalin or
formaldehyde\.....for God\'s sake\...\..... Ask any pathologist in the
UK what the brain tissues in the formalin looks like after a
year\...\....it is a big fat sponge\...the agent continues to eat the
brain \...\...you can\'t make slides anymore because the agent has never
stopped\...\.....and the old slides that are stained with Hemolysin and
Eosin\...\...they get holier and holier and degenerate and
continue\...what you looked at 6 months ago is not
there\...\.....Gambetti better be photographing every damned thing he is
looking at\.....

Okay, you need to know. You don\'t need to pass it on as nothing will
come of it and there is not a damned\
thing anyone can do about it. Don\'t even hint at it as it will be
denied and laughed at\...\...\....

USDA is gonna do as little as possible until there is actually a human
case in the USA of the nvcjd\...\.....if you want to move this thing
along and shake the earth\....then we gotta get the victims families to
make sure whoever is doing the autopsy is credible, trustworthy, and a
saint with the courage of Joan of Arc\...\.....I am not kidding!!!!

so, unless we get a human death from EXACTLY the same form with EXACTLY
the same histopath lesions as seen in the UK nvcjd\...\.....forget any
action\...\.....it is ALL gonna be sporadic!!!

And, if there is a case\...\....there is gonna be every effort to link
it to international travel, international food, etc. etc. etc. etc. etc.
They will go so far as to find out if a sex partner had ever traveled to
the UK/europe, etc. etc. \....

It is gonna be a long, lonely, dangerous twisted journey to the truth.
They have all the cards, all the money, and are willing to threaten and
carry out those threats\....and this may be their biggest downfall\...

Thanks as always for your help.

(Recently had a very startling revelation from a rather senior person in
government here\...\...\....knocked me out of my chair\...\.....you must
keep pushing. If I was a power person\....I would be demanding that
there be a least a million bovine tested as soon as possible and
aggressively seeking this disease. The big players are coming out of the
woodwork as there is money to be made!!!

In short: \"FIRE AT WILL\"!!! for the very dumb\....who\'s \"will\"!
\"Will be the burden to bare if there is any coverup!\"

 

snip\...end

 

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

 

 

\[Docket No. 03-025IFA\] **FSIS Prohibition of the Use of Specified
Risk\
Materials for Human Food and Requirement for the Disposition of\
Non-Ambulatory Disabled Cattle\
\
**<http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf>

 

\[Docket No. FSIS-2006-0011\] FSIS Harvard Risk Assessment of Bovine\
Spongiform Encephalopathy (BSE)\
\
<http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf>

 

**THE SEVEN SCIENTIST REPORT \*\*\*\
**\
<http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf>

 

PAUL BROWN M.D.\
\
<http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf>

 

9 December 2005\
Division of Dockets Management (RFA-305)\
\
SEROLOGICALS CORPORATION\
James J. Kramer, Ph.D.\
Vice President, Corporate Operations\
\
\
\
<http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf>

 

Full Text\
\
**Diagnosis and Reporting of Creutzfeldt-Jakob Disease\
\
Singeltary, Sr et al. JAMA.2001; 285: 733-734.**\
\
\
\
<http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama>

<http://www.neurology.org/cgi/eletters/60/2/176#535>

BRITISH MEDICAL JOURNAL\
\
BMJ

<http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2>

BMJ

<http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1>

 

You're only fooling yourselves with this stupid uk / bse / nvcjd only
theory, and the BSE methology of the OIE. most any country that went by
those OIE BSE guidelines all went down with BSE.

 

THE OIE has now shown they are nothing more than a National Trading
Brokerage for all strains of animal TSE.

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

Page 95 of 98

8/3/2006

 

<http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf>

 

O.K., let me get this straight. after the first documented case of BSE
in the USA, the rest i.e (the next two documented TSE cows) became
atypical, of which USDA now wants us to believe are of a spontaneous
nature, that feed did not cause this?

r i g h t \...\...\...\...

IF typical BSE spread via feed, why can\'t atypical BSE or BASE spread
the same way ???\
\
STUDIES in Mission Texas of USA sheep scrapie to USA produced a TSE
unlike BSE.\
\
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8133096&dopt=Citation>

 

<http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf>

Visit to USA \... info on BSE and Scrapie

<http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf>

snip\...

<http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf>

<http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf>

<http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf>

**Title: Experimental Transmission of Transmissible Mink Encephalopathy
(Tme) to Cattle by Intracerebral Inoculation**

<http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=191825>

Subject: **USA MINK FARMS AND TSE TESTING** ???\
Date: July 15, 2006 at 5:52 am PST\
\
Pelt Production Up 3 Percent\
\
Mink pelt production in the United States in 2005 totaled 2.63 million
pelts, up 3 percent from 2004. Wisconsin, the largest mink producing
State, produced 778,000 pelts. Utah the second largest producing State,
produced 600,000 pelts.\
\
The number of pelts by color class as a percent of the total U.S.
production in 2005 is as follows: Black at 47.6 percent, Mahogany at
20.9 percent, Blue Iris at 11.3 percent, Demi/Wild at 6.3 percent,
Sapphire at 4.0 percent, and White at 3.8 percent. The remaining color
classes accounted for 6.1 percent.\
\
Value of Pelt Production Up 33 Percent\
\
Mink pelts produced during the 2005 crop year were valued at \$160
million, up 33 percent from \$120 million a year ago. The average price
per pelt for the 2005 crop year was \$60.90, up from \$47.10 in 2004.
\.....snip\...\....end

<http://usda.mannlib.cornell.edu/reports/nassr/other/zmi-bb/mink0706.pdf>

TME

<http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahtme.html>

3.9.11 Mink Producers\
\
Mink offal is now rendered with other species and will decline in value
under the first four regulatory options.

<http://www.fda.gov/cvm/Documents/bse3.pdf>

2.8 PROFILE OF MINK PRODUCERS\
\
Mink are raised for their pelts and oil. Most mink farmers kill and pelt
their own animals once a year near the end of November or in early
December. Once the pelts are removed, the fat is then scrapped from the
hide. This fat is used to manufacture mink oil that is sought for
cosmetic uses because of its hypoallergenic qualities and in leather
treatments. The total value of mink production in 1995 was \$143
million, an increase of 72 percent from 1994.\
\
In 1995, 446 mink farms produced a total of 2.69 million pelts (NASS,
1996b). Mink producers vary in size but most are small operations. Mink
farming is concentrated in Utah (130 2-11 farms), Wisconsin (77 farms),
and Minnesota (52 farms). There has been recent consolidation within the
industry, with the number of farms decreasing by 8 percent from 1993 to
1994 and 3 percent from 1994 to 1995. The market price for mink pelts is
subject to wide demand fluctuations\
\
based on fashion and weather.\
\
Once the pelt and fat are removed, the entire carcass is then rendered.
Mink carcasses sent to rendering (minus the pelt and fat) weigh an
average of 2.5 pounds, so the total estimated offal produced per year is
6.7 million pounds. Mink farmers are reported to have difficulty with
getting renderers to pick-up their material because of its low volume
and the infrequency of offal\
generation.

<http://www.fda.gov/cvm/Documents/bse2.pdf>

WHAT sort of TME surveillance program is in place now, if any???\
\
DO they test for TSE in Mink and what are these figures if so ???

 

ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear
with me)

 

THE USA is in a most unique situation, one of unknown circumstances with
human and animal TSE.

THE USA has the most documented TSE in different species to date, with
substrains growing in those

species (BSE/BASE in cattle and CWD in deer and elk, there is evidence
here with different strains),

and we know that sheep scrapie has over 20 strains of the typical
scrapie with atypical scrapie documented and also BSE is very likely to
have passed to sheep. all of which have been rendered and fed back to
animals for human and animal consumption, a frightening scenario. WE do
not know the outcome, and to play with human life around the globe with
the very likely TSE tainted blood from the USA, in my opinion is like
playing Russian roulette, of long duration, with potential long and
enduring consequences, of which once done, cannot be undone.

These are the facts as i have come to know through daily and extensive
research of TSE over 9 years, since 12/14/97. I do not pretend to have
all the answers, but i do know to continue to believe in the ukbsenvcjd
only theory of transmission to humans of only this one strain from only
this one TSE from only this one part of the globe, will only lead to
further failures, and needless exposure to humans from all strains of
TSE, and possibly many more needless deaths from TSE via a multitude of
proven routes and sources via many studies with primates and rodents and
other species. \...

 

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518