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From: TSS ()
Subject: Class II firm-initiated BSE FEED recall is ongoing USA
Date: October 12, 2007 at 10:20 am PST


A Class II firm-initiated recall is ongoing by the Springer Magrath Co. of McCook, NE, for approximately 13,255 bottles of “O-NO-MORE” Calf Claimer Powder, packaged in 11-oz. bottles. The recall was undertaken because the finished product was manufactured with bovine blood meal that contained an excess of hair and bone and did not bear the cautionary BSE statement that the product should not be fed to ruminants. Distribution of the recalled product was nationwide.

Subject: Calf Claimer Powder with prohibited bovine blood meal which did not bear the cautionary BSE statement DISTRIBUTION NATIONWIDE
Date: June 13, 2007 at 10:59 am PST

O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 11-oz. bottles, For Animal Use Only. Recall # V-043-2007
Springer Magrath Co., Mc Cook, NE, by telephone on January 2, 2007, fax dated January 9, 2007, by letters on February 22, 2007, March 12, March 14 and March 21, 2007. Firm initiated recall is ongoing.

REASON The finished product was manufactured with prohibited bovine blood meal and did not bear the cautionary BSE statement that the product should not be fed to ruminants.

Approximately 13,255 bottles




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

Date: May 24, 2007 at 6:59 am PST

HAVE THEY EVEN DONE transmission studies of the new atypical BSE or what they call BASE.

HERE IN THE USA, where BASE was discovered, they find that BASE is more virulent to humans ;


18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***

6:30 Close of Day One

1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.

Research Project: Study of Atypical Bse

Location: Virus and Prion Diseases of Livestock

Project Number: 3625-32000-073-07
Project Type: Specific C/A

Start Date: Sep 15, 2004
End Date: Sep 14, 2007

The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.

This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.


Case Report of Variant Creutzfeldt-Jakob Disease in a Macaque after Blood

Lescoutra-Etchegaray, N1; Ruchoux, MM1; Correia, E1; Jolit, A1; Freire, S1;
CI2; Deslys, JP1; Comoy, E1 1CEA/DSV/IMETI/SEPIA, France; 2Scripps Florida,

A fourth human case of probable transmission of vCJD through transfusion has now
been reported but a number of features affecting transfusion-related infection remain
imprecise, including infectious dose, length of incubation period and critical infectious
window of blood donors.

We report here the first case of experimental transmission of vCJD in primates by
blood transfusion. Experimental infection of Cynomolgus macaque has been
demonstrated to be a sensitive model for the investigation of human prion
diseases, inducing similar distribution of infectivity in peripheral lymphoid tissues
and equivalent brain pathology. In our study, transfusion was performed with 40 ml of
whole blood drawn from a vCJD-infected macaque at the terminal stage of the disease.
Clinical symptoms of vCJD appeared in the recipient animal after five years of
incubation. The total amount of infectivity in the transfused blood was approximately 106
fold lower than in the brain (titration still in progress). In several animals infected
intravenously with brain homogenate, the presence of PrPres in serial lymph nodes biopsies
and in other organs at autopsy was examined and results will be presented.


Atypical Presentation of Variant Creutzfeldt-Jakob Disease in a 73 Year Old
Blood Transfusion Recipient

Wroe, S1; Pal, S1; Webb, T1; Alner, K2; Hewitt, P3; Brander, S4; Wadsworth,
JD5; Collinge, J1 1National Hospital for Neurology and Neurosurgery, National Prion Clinic,
UK; 2National Hospital for Neurology and Neurosurgery, Department of Neuropsychology, UK;
3Health Protection Agency, UK; 4National Hospital for Neurology and Neurosurgery,
Department of Neuropathology, UK; 5Institute of Neurology, UCL, UK

We report atypical presentation of variant Creutzfeldt-Jakob Disease (vCJD) identified
ante-mortem in a 73 year-old recipient of blood products. This patient was transfused
following orthopaedic surgery in December 1997. Tracing of blood products identified
a single unit of non-leucodepleted red cells from an individual who developed
neuropathologically confirmed vCJD eleven months after donation. Nine years post
transfusion, this individual was referred to the National Prion Clinic for specialist
investigation. Six years post transfusion the recipient complained of fluctuating fatigue
and impaired concentration. At this time neurological examination and MRI brain
(T1/T2 weighted/DWI) were normal. Progressive symptoms emerged six months later
with imbalance and deteriorating cognition. Examination two months after onset of
neurological symptoms demonstrated cognitive deficits, dyspraxia or visuospatial
dysfunction and normal motor, sensory and gait examination. Six weeks later cognitive
impairment was identified alongside tremulousness, impaired manual dexterity and
limb ataxia. Serological investigations were normal. MRI (T1/T2 weighted/FLAIR/DWI)
demonstrated prominent signal change throughout the dorsal thalamus, consistent
with vCJD. PRNP genotyping revealed no mutations and homozygosity for methionine
at codon 129. The prolonged incubation period of vCJD and possibility of
asymptomatic carrier states pose major public health concerns. This case highlights
the significant risk encountered by recipients of contaminated blood products and the
necessity for their specialist monitoring.


Enhanced Surveillance of Persons Identified as at Increased Risk of CJD Due
to Blood Transfusion or Healthcare Procedures

Brookes, D1; Chow, Y1; Ward, HJT2; Will, RG2; Hewitt, P3; Gill, ON1
1HPA, CJD, UK; 2National CJD Surveillance Unit, UK; 3Colindale, NHS Blood
and Tissue, UK


Reports of four iatrogenic transmissions of variant-CJD (vCJD) infection
in the UK (all due to transfusion of blood from donors who later developed vCJD),
evidence from iatrogenic transmissions of sporadic CJD and experimental work on
CJD infectivity in tissues and on healthcare instruments have given rise to concern
about the risks of iatrogenic transmission of CJD. This risk warrants a) certain public
health precautions, and b) follow-up of individuals with identified risks in order to gain
evidence about their risks and ensure appropriate management of these risks.
Evidence of transmission via iatrogenic routes is important to inform public health
measures and so prevent ongoing transmission of CJD.


The Health Protection Agency and Health Protection Scotland holds details
of persons identified as ‘at-risk’ of vCJD due to blood transfusion and of
persons identified as ‘at-risk’ of CJD (of any type) from other healthcare
procedures. The GPs/clinicians of all persons identified as ‘at-risk’ for public health
purposes are provided with: information; risk assessment updates; advice on
public health precautions and advice on referral to specialist care. Procedures are being
established to obtain enhanced surveillance data on these individuals, including:
clinical status updates, date and cause of death, surplus tissue and blood
specimens, and postmortem investigations.


Persons ‘at-risk’ of CJD have experienced a range of exposures. Estimated
risks are uncertain and overlapping. Some individuals - recipients of vCJD
implicated blood components - are considered to be at a clearly higher risk
of infection: active follow-up is currently conducted for these individuals. In
time, the enhanced surveillance of persons at increased risk of CJD will provide
estimates of transmission risks and of the impact of iatrogenic exposures on mortality.
Conclusion: Knowledge about iatrogenic transmission of CJD is being gained
by the follow-up of individuals who have been identified as ‘at-risk’ of CJD
in the UK. This enhanced surveillance may need to be sustained for many years.

Prions in Plasma of Patients with Sporadic Creutzfeldt-Jakob Disease
Safar, J.G1,3, Geschwindm M.D2,3, Letessier, F1,
Kuo, A1, Pomeroy, K1, Deering, C1, Serban, A1,
Groth, D1, Miller, B.L2,3, DeArmond, S.J1,4,
Prusiner, S.B1,3,5
1Institute for Neurodegenerative Diseases,
2Memory and Aging Center, Departments of
3Neurology, 4Pathology, and 5Biochemistry
and Biophysics, University of California,
San Francisco, California 94143

Date: September 24, 2007 at 6:52 pm PST

Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2;
Baron, TGM1
1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have
demonstrated 3 different molecular phenotypes regarding to the apparent molecular
masses and glycoform ratios of PrPres bands. We initially described isolates
(H-type BSE) essentially characterized by higher PrPres molecular mass and decreased
levels of the diglycosylated PrPres band, in contrast to the classical type of BSE.
This type is also distinct from another BSE phenotype named L-type BSE, or also BASE
(for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low
representation of the diglycosylated PrPres band as well as a lower PrPres
molecular mass. Retrospective molecular studies in France of all available BSE cases
older than 8 years old and of part of the other cases identified since the beginning of the
exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases,
among 594 BSE cases that could be classified as classical, L- or H-type BSE.
By Western blot analysis of H-type PrPres, we described a remarkable
specific feature with antibodies raised against the C-terminal region of PrP that
demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in
addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2
migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the
PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another
PK–resistant fragment at about 7 kDa was detected by some more N-terminal
antibodies and presumed to be the result of cleavages of both N- and C-terminal parts
of PrP. These singular features were maintained after transmission of the disease to
C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and
7kDa band) *** reminds features reported respectively in sporadic Creutzfeldt-Jakob disease
and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.

BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc
C-terminal Truncated Fragments

Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux,
MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4;
Monaco, S3 1University of Verona, of Neurological and Visual Sciences,
Italy; 2CEA,
IMETI/SEPIA, France; 3University of Verona, Neurological and Visual
Sciences, Italy;
4IMETI/SEPIA, France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA

The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent human
prion disease, remains still unknown. The marked disease phenotype heterogeneity
observed in sCJD is thought to be influenced by the type of proteinase K-resistant
prion protein, or PrPSc (type 1 or type 2 according to the electrophoretic
mobility of the unglycosylated backbone), and by the host polymorphic Methionine/Valine
(M/V) codon 129 of the PRNP. By using a two-dimensional gel electrophoresis
(2D-PAGE) and imunoblotting we previously showed that in sCJD, in addition to the
PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with
different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished
three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1 of all

(ii) the second was found in M/M-2 (cortical form); (iii) the third in amyloidogenic M/V-
2 and V/V-2 subtypes (Zanusso et al., JBC 2004) . Recently, we showed that sCJD
subtype M/V-2 shared molecular and pathological features with an atypical
form of BSE, named BASE, thus suggesting a potential link between the two
conditions. This connection was further confirmed after 2D-PAGE analysis, which showed an
identical PrPSc signature, including the biochemical pattern of CTFs. To pursue this
issue, we obtained brain homogenates from Cynomolgus macaques intracerebrally
inoculated with brain homogenates from BASE. Samples were separated by using
a twodimensional electrophoresis (2D-PAGE) followed by immunoblotting. We here
show that the PrPSc pattern obtained in infected primates is identical to BASE
and sCJD MV-2 subtype. *** These data strongly support the link, or at least a common
ancestry, between a sCJD subtype and BASE. This work was supported by Neuroprion




USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it
today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were
''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007
11:52 PM. ...TSS


FC5.5.2 Transmission of Italian BSE and BASE Isolates in Cattle Results into
a Typical BSE Phenotype and a Muscle Wasting Disease

Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2;
Torcoli, G2;
Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati,
M1; Iulini, B3;
Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L2
1University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER,
Italy; 3IZSPLVA,
Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta,

The clinical phenotype of bovine spongiform encephalopathy has been extensively
reported in early accounts of the disorder. Following the introduction of statutory active
surveillance, almost all BSE cases have been diagnosed on a pathological/molecular
basis, in a pre-symptomatic clinical stage. In recent years, the active surveillance
system has uncovered atypical BSE cases, which are characterized by distinct
conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose
clinicopathological phenotypes remain unknown. We recently reported two
Italian atypical cases with a PrPSc type similar to BSE-L, pathologically
characterized by PrP amyloid plaques. Experimental transmission to TgBov
mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely
virulent. A major limitation of transmission studies to mice is the lack of reliable information on
clinical phenotype of BASE in its natural host. In the present study, we experimentally
infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE
isolates by i.c. route. BASE infected cattle showed survival times significantly
shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with
previous observations in TgBov mice. Clinically, BSE-infected cattle developed a
disease phenotype highly comparable with that described in field BSE cases and in
experimentally challenged cattle. On the contrary, BASE-inoculated cattle
developed an amyotrophic disorder accompanied by mental dullness.
The molecular and neuropathological profiles, including PrP deposition
pattern, closely matched those observed in the original cases. This study further confirms
that BASE is caused by a distinct prion isolate and discloses a novel disease
phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle
*** and in some subtypes of inherited and sporadic Creutzfeldt-Jakob disease.
Oral Abstracts

PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase

1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17 inconclusive and 9 pending (1 from 2006, 8
from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3
from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, *** 26 from 2007)


The finished product was manufactured with prohibited bovine blood meal and

did not bear the cautionary BSE statement that the product should not be fed

to ruminants

i went and looked at warning letters a few months ago that read ;


Blood meal used to make cattle feed was recalled because it was
cross-contaminated with

prohibited bovine meat and bone meal that had been manufactured on common
equipment and

labeling did not bear cautionary BSE statement.

WE do know that it is perfectly legal to feed blood to livestock for

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


Rendered animal protein from Meat meal, meat meal tankage, meat and bone

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


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

wouldn't it be wonderful to finally be able to give an



'great move'

'it's about time'

to the fda for finally taking a step in the right direction about blood in
livestock feed,
but i don't think that's the case, hell, they cannot even stop the ruminant
protein in feed for livestock,
so this was probably an error that will be corrected. we will just have to
wait and see next enforcement report. ...

October 2007 Update on Feed Enforcement Activities to Limit the Spread of

kind regards,

Terry S. Singeltary Sr., in Sunny Baycliff, Texas 77518

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