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From: Terry S. Singeltary Sr. (216-119-144-33.ipset24.wt.net)
Subject: Re: Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. [FULL TEXT]
Date: December 14, 2004 at 7:51 am PST

In Reply to: Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. [FULL TEXT] posted by TSS on March 28, 2003 at 9:32 am:

-------- Original Message --------
Subject: re-Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734
Date: Sun, 14 Nov 2004 12:16:07 -0600
From: "Terry S. Singeltary Sr."
To: Lisa_Hardin@jama-archives.org


Greetings again JAMA,

I would please like to address the issue of sporadic CJD (all human TSEs)
in the USA once again, and the attempt to accurately report this agent.
Since my previous attempt ;

Full Text
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001 285: 733-734.


Full Text

Tue, 13 Feb 2001 JAMA Vol. 285 No. 6, February 14, 2001 Letters

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

To the Editor:

In their Research Letter in JAMA. 2000;284:2322-2323, Dr Gibbons and
colleagues1 reported that the annual US death rate due to
Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These
estimates, however, are based only on reported cases, and do not include
misdiagnosed or preclinical cases. It seems to me that misdiagnosis
alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD,
although only a small number of these patients receive the postmortem
examination necessary to make this diagnosis. Furthermore, only a few
states have made CJD reportable. Human and animal transmissible
spongiform encephalopathies should be reportable nationwide and
internationally.

Terry S. Singeltary, Sr Bacliff, Texas

I would kindly like to readdress the reply below by Schonberger, Belay
et al.
There have been a great deal of disturbing findings with human/animal
TSEs since
there answer to me below was published that needs to be readdressed asap.

Schonberger, Belay et al reply to Singeltary 2001;

In Reply:

Mr Singeltary and Ms Kraemer express an underlying concern that our
recently reported mortality surveillance estimate of about 1 CJD case
per million population per year in the United States since 1985 may
greatly underestimate the true incidence of this disease. Based on
evidence from epidemiologic investigations both within and outside the
United States, we believe that these national estimates are reasonably
accurate.

Even during the 1990s in the United Kingdom, where much attention and
public health resources have been devoted to prion disease surveillance,
the reported incidence of classic CJD is similar to that reported in the
United States.

In addition, in 1996, active US surveillance for CJD and new variant
(nv) CJD in 5 sites detected no evidence of the occurrence of nvCJD and
showed that 86% of the CJD cases in these sites were identifiable
through routinely collected mortality data.

Our report provides additional evidence against the occurrence of nvCJD
in the United States based on national mortality data analyses and
enhanced surveillance. It specifically mentions a new center for
improved pathology surveillance. We hope that the described enhancements
along with the observations of Singeltary and Kraemer will encourage
medical care providers to suggest brain autopsies for more suspected CJD
cases to facilitate the identification of potentially misdiagnosed CJD
cases and to help monitor the possible occurrence of nvCJD.

Creutzfeldt-Jakob disease is not on the list of nationally notifiable
diseases. In those states where surveillance personnel indicate that
making this disease officially notifiable would meaningfully facilitate
collection of data that are needed to monitor the incidence of CJD and
nvCJD, including the obtaining of brain autopsy results, we encourage
such a change. However, adding CJD to the notifiable diseases
surveillance system may lead to potentially wasteful, duplicative
reporting because the vast majority of the diagnosed cases would also be
reported through the mortality surveillance system.

Furthermore, making CJD a notifiable disease may not necessarily help
identify undiagnosed CJD cases. The unique characteristics of CJD make
mortality data a useful surrogate for ongoing surveillance. Unlike many
other neurologic diseases, CJD is invariably fatal and in most cases
rapidly progressive and distinguishable clinically from other neurologic
diseases.

Because CJD is least accurately diagnosed early in the course of the
illness, notifiable disease surveillance of CJD could be less accurate
than mortality surveillance of CJD. In addition, because death as a
condition is more completely and consistently reported, mortality
surveillance has the advantage of being ongoing and readily available.

The absence of CJD and nvCJD from the list of nationally notifiable
diseases should not be interpreted to mean that they are not important
to public health; this list does not include all such diseases. We
encourage medical caregivers to report to or consult with appropriate
public health authorities about any diagnosed case of a transmissible
disease for which a special public health response may be needed,
including nvCJD, and any patient in whom iatrogenic transmission of CJD
may be suspected.

Robert V. Gibbons, MD, MPH Robert C. Holman, MS Ermias D. Belay, MD
Lawrence B. Schonberger, MD, MPH Division of Viral and Rickettsial
Diseases National Center for Infectious Diseases Centers for Disease
Control and Prevention Atlanta, Ga


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

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

JAMA, I kindly wish to submit the following 11/14/2004;

Singeltary reply to Schonberger, Belay et al 2004 ;


Schonberger, Belay et al state ;

> Even during the 1990s in the United Kingdom, where much attention and
> public health resources have been devoted to prion disease
> surveillance, the reported incidence of classic CJD is similar to that
> reported in the United States.
>

> identifiable through routinely collected mortality data.


INDEED, very similar, it is rising, but the USA would not know under
present circumstances due
to the fact CJD (all human TSEs) are not reportable in every state, and
it is biased by age
discrimination, which will make reportable, fundamentally inaccurate.
nvCJD has been reported
in a 74 year old. ALSO, very young (20's) are dying from sporadic CJD in
the USA, some with
MM genotype. WE have new atypical TSEs showing up in cattle and sheep
that are very similar
to sporadic CJD. By simply relying on mortality data and only looking
for nv/v CJD, you are
missing the bigger picture, thus the agent continues to spread.


I kindly wish to submit the following to dispute Schonberger, Belay et al;


Draft Proposal For The Monitoring of Creutzfeldt-Kakob Disease 1989
Dr. R. Will

snip...

IDENTIFICATION OF CASES

Cases of CJD may be identified from death certificates, but this alone
is unlikely to provide adequate monitoring. ERRORS are made in
certification and diagnosis; in the Oxford study death certificates were
obtained on a series of known confirmed cases and CJD was mentioned
in only 66% of certificates. In another series of 175 certified cases,
42 patients were judged not to have suffered from CJD after examination
of case notes (7)...

full text;

http://www.bseinquiry.gov.uk/files/yb/1989/05/00005001.pdf


THE EPIDEMIOLOGY OF CJD RG WILL 1984 (182 PAGES)

snip...

One reason for this was the _inaccuracy_ in coding of cases correctly
certified as CJD Coding is carried out by staff who are not medically
qualified and it is not surprising that coding errors occur in the
processing of large numbers of certificates. In 1982, 12,000
certificates per week were processed at the office of population
censuses and surveys bu 15 coders and 6 checkers (Alderson et al.,
1983). The occurrence of both inter- and intra-observer coding errors
has been described (Curb et al., 1983) and the _inaccuracies_ of BOTH
certification and coding discovered in this study _support_ the
introduction of a more accurate system of death certificates and a more
detailed and specific coding system...

snip...

http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf


ALSO, there seems to be some false information about sporadic CJD being on
the decline in the UK. This is simply not so.


I kindly wish to submit the following to dispute this;


Mouse model sheds new light on human prion disease

snip...

Professor John Collinge said We are not saying that all or even most
cases of sporadic CJD are as a result of BSE exposure, but some more
recent cases may be the incidence of sporadic CJD has shown an upward
trend in the UK over the last decade. While most of this apparent
increase may be because doctors are now more aware of CJD and better at
diagnosing it, serious consideration should be given to a proportion of
this rise being BSE-related. Switzerland, which has had a substantial
BSE epidemic, has noted a sharp recent increase in sporadic CJD.

snip...

http://www.mrc.ac.uk/index/public-interest/public-bse_and_sporadic_cjd.htm

http://www.mrc.ac.uk/txt/index/public-interest/public-news-4/public-news_archive/public-news-archive_nov_dec_02/public-bse_and_sporadic_cjd.htm


A simple look at sporadic CJD statistics in EU countries with BSE will
reveal this;

CANADA 2 IN 94 COMPARED TO 30 IN 2002

FRANCE 35 IN 93 COMPARED TO 102 IN 2003

GERMANY 21 IN 93 COMPARED TO 112 IN 2003

ITALY 27 IN 93 TO COMPARED TO 75 IN 2003

UK 37 IN 93 COMPARED TO 74 IN 2003

USA (UNKNOWN...TSS)

http://www.eurocjd.ed.ac.uk/sporadic.htm


EVEN SEAC admits a rise in sporadic CJD in UK;

SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE
Draft minutes of the open session of the 84th meeting held on 28th
September 2004

snip...

>> In contrast, the number of deaths in the UK from sCJD
>> per annum had increased but this may reflect improved case
>> ascertainment. A similar increase in sCJD had been observed in
>> other countries...
>
>

snip...


http://www.seac.gov.uk/minutes/draft84.pdf


HOWEVER, I do not agree with this _assumption_!

I believe there are multiple routes and sources for this agent
and they are going ignored, while being called 'sporadic' and
or 'spontaneous' or 'classic' CJD. To continue to believe
in this BSE/nv/v CJD only theory will simply continue to
spread this agent from border to border, continent to
continent and around the globe through the already proven routes
and sources. TO flounder any longer will have grave consequences
on the medical and surgical community, especially with the
findings recently of nv/v CJD being transmitted by blood in
two people.

I kindly wish to submit the following to dispute the BSE nv/vCJD only theory.
THESE new studies should warrant immediate action in the medical and surgical
communties;


11 November 2004

Genetic make-up may determine what type of CJD occurs when humans are
infected with BSE

New research published by a team from the Medical Research Council (MRC)
Prion Unit offers an explanation about why only people with a particular
genetic make-up have so far developed vCJD. It also provides evidence
that other types of BSE-derived prion infection with a different pattern
of symptoms might occur in humans. The findings are published in the
journal Science.

Variant CJD (vCJD) is the human disease thought to be caused by eating
food contaminated with the infectious agent, known as a prion,
responsible for the epidemic of BSE or mad cow disease in cattle. So
far, everyone known to have developed vCJD has been of a particular
genetic type known as MM. Until now it has been a mystery why everyone
that has developed vCJD is of the MM type and one possibility is that
they are simply the first to develop the disease when infected with BSE,
and that people with the other genetic types1 (known as VV and MV*)
infected with BSE prions will also develop vCJD, but some years later.

In a series of experiments spanning more than ten years, the MRC team
has been studying mice genetically modified so that they make human
prion proteins which are used to model human susceptibility to BSE.
The team has now shown that mice with the human VV genetic type do
become infected when given BSE or vCJD prions, but manifest a different
form of the disease which looks quite different to vCJD and has a novel
prion strain type.

Remarkably, when these novel prions were used to infect mice of the MM
genetic type, the mice either developed a disease very like vCJD, or
else a pattern of disease that looks like so-called sporadic CJD the
classical form of CJD. This form has been known about for many years,
is seen all over the world and has not hitherto been associated with
BSE. However, the new strain identified in the mice, being called type
5, has not been seen yet in people and we do not know what pattern of
disease it would cause. It could look like one of the forms of classical
or sporadic CJD or perhaps be yet another different variant form.

The work from the MRC team suggests that type 4 prions, the type
associated with vCJD, can only propagate themselves in people that make
the M form of the protein. It seems the V form of the protein just
cannot adopt the particular molecular shape that characterises type 4.

The studies in mice also suggest that if these prions were to pass from
person to person (for example by blood transfusion) then, depending on
the genetic type of the person becoming infected, at least three
different patterns of disease might result: type 2 (which is seen in
sporadic CJD); type 4 (which causes vCJD) or type 5 (which may cause a
new pattern of disease).

Professor John Collinge, Director of the MRC Prion Unit, which is based
at University College London, said: These mouse studies give us vital
clues about the behaviour of prions and how they appear to modify and
adapt depending on the genetic makeup of the individual they are infecting.

We always have to be cautious about making direct comparison to the
human condition, but our work strongly suggests that we can not assume
only those with one genetic profile are vulnerable to BSE infection.

At this stage it is not possible to say how this should alter estimates
of those likely to become ill, but our findings do suggest we should be
taking steps to draw up a more sophisticated system of categorizing the
disease so that we dont mistake BSE related infection for a version of
sporadic CJD.

For more information call the MRC press office on 020 7 637 6011

Notes to Editors

*The human prion protein comes in two common forms, known as M and V.
Because everyone has two copies of this gene, there are three possible
genetic types: MM, MV and VV.

Paper - Human Prion protein v129 prevent expression of vCJD phenotype
Science On line 11.11.04

Prions are rogue forms of one of the bodys own proteins known as the
prion protein which are misshapen. There are several different rogue
or misshapen forms that can infect humans, and these different types of
prions are known as strains. This is analogous to different strains of
other germs such flu virus causing influenza or strains of salmonella
causing different forms of food poisoning for example.

The strain of prion causing vCJD is known as type 4, types 1-3 cause the
different forms of sporadic or classical CJD. Each strain causes a
different pattern or type of disease. It is known that prion strains can
change or mutate when they pass between different animals.

The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRCs expenditure of £430 million is invested in its 40
Institutes, Units and Centres. The remaining half goes in the form of
grant support and training awards to individuals and teams in
universities and medical schools.


©2004 Medical Research Council

http://www.mrc.ac.uk/public-11_november_2004

BSE prions propagate as either variant CJD-like or sporadic CJD-like
prion strains in transgenic mice expressing human prion protein

Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan
Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah
E. Lloyd, Jonathan D.F. Wadsworth and John Collinge1

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of
Neurology, University College, Queen Square, London WC1N 3BG, UK 1
Corresponding author e-mail: j.collinge@prion.ucl.ac.uk


Received August 1, 2002; revised September 24, 2002; accepted October
17, 2002

Abstract


Variant CreutzfeldtJakob disease (vCJD) has been recognized to date
only in individuals homozygous for methionine at PRNP codon 129. Here we
show that transgenic mice expressing human PrP methionine 129,
inoculated with either bovine spongiform encephalopathy (BSE) or variant
CJD prions, may develop the neuropathological and molecular phenotype of
vCJD, consistent with these diseases being caused by the same prion
strain. Surprisingly, however, BSE transmission to these transgenic
mice, in addition to producing a vCJD-like phenotype, can also result in
a distinct molecular phenotype that is indistinguishable from that of
sporadic CJD with PrPSc type 2. These data suggest that more than one
BSE-derived prion strain might infect humans; it is therefore possible
that some patients with a phenotype consistent with sporadic CJD may
have a disease arising from BSE exposure...

http://embojournal.npgjournals.com/cgi/content/full/21/23/6358


THE new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic Creutzfeldt-Jakob disease


http://www.pnas.org/cgi/content/abstract/0305777101v1


Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1


Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

Sarah E. Lloyd, Jacqueline M. Linehan, Melanie Desbruslais,
Susan Joiner, Jennifer Buckell, Sebastian Brandner,
Jonathan D. F. Wadsworth and John Collinge

Correspondence
John Collinge
j.collinge@prion.ucl.ac.uk

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of
Neurology,
University College, London WC1N 3BG, UK
Received 9 December 2003
Accepted 27 April 2004

Distinct prion strains can be distinguished by differences in incubation
period, neuropathology and biochemical properties of disease-associated
prion protein (PrPSc) in inoculated mice. Reliable comparisons of mouse
prion strain properties can only be achieved after passage in
genetically identical mice, as host prion protein sequence and genetic
background are known to modulate prion disease phenotypes. While multiple
prion strains have been identified in sheep scrapie and Creutzfeldt Jakob
disease, bovine spongiform encephalopathy (BSE) is thought to be caused by
a single prion strain. Primary passage of BSE prions to different lines
of inbred mice resulted in the propagation of two distinct PrPSc types,
suggesting that two prion strains may have been isolated. To investigate
this further, these isolates were subpassaged in a single line of inbred
mice (SJL) and it was confirmed that two distinct prion strains had been
identified. MRC1 was characterized by a short incubation time (110±3 days),
a mono-glycosylated-dominant PrPSc type and a generalized diffuse
pattern of PrP-immunoreactive deposits, while MRC2 displayed a much longer
incubation time (155±1 days), a di-glycosylated-dominant PrPSc type and a
distinct pattern of PrP-immunoreactive deposits and neuronal loss. These
data indicate a crucial involvement of the host genome in modulating
prion strain selection and propagation in mice. It is possible that
multiple disease phenotypes may also be possible in BSE prion infection in
humans and other animals.

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


THE recent discoveries of previously unidentified strains of
Scrapie such as 221C44 and the Nor9845;

FULL TEXT APPRX. 91 PAGES

UK Strategy for Research and
Development on Human and Animal
Health Aspects of Transmissible
Spongiform Encephalopathies

2004-2007

http://www.mrc.ac.uk/pdf-uk_strategy_v5.2.pdf


IP/04/1324

Brussels, 28 October 2004


Commission submits French Research Findings on TSE in a goat to Expert
Panel

Following the findings by a research group in France that they suspect
the presence of a TSE infection in a goats brain which tests cannot
distinguish from BSE, the European Commission has submitted data
received from the French authorities to the Community Reference
Laboratory (CRL) for TSEs based in Weybridge, England, for an evaluation
by an expert panel. TSEs are transmissible spongiform encephalopathies,
namely BSE affecting cattle, and scrapie affecting goats and sheep. The
expert panel will evaluate, over the next two weeks or so, the
scientific evidence to see if it indicates the presence of BSE in the
goat. This isolated incident does not present a risk to public health as
the goat and its herd did not enter the food and feed chain.

snip...

http://europa.eu.int/rapid/pressReleasesAction.do?reference=IP/04/1324&format=HTML&aged=0&language=EN&guiLanguage=en


According to Nov. 2 Yomiuri Newspaper, researchers of the Prion
Disease Research Center, the National Institute of Animal Health
of Japan reported in the International Symposium of Prion Diseases
held in Sendai from October 31 to November 2., 2004, that they
detected prion in the adrenal gland and peripheral (sciatic and
peroneal) nerves of the 11th BSE case of Japan (a 94-months old
cow found dead on the farm on March 4 this year).

http://www.maff.go.jp/www/press/cont2/20041101press_7.htm
(only in Japanese)

Sendai and the International
Symposium of
Prion Diseases held here from October 31 to November 2.,2004

Abstract

ORAL 8

Bovine spongiform encephalopathy (BSE) in Japan

Takashi Yokoyama, Kumiko M. Kimura, Morikazu Shinagawa
Prion Disease Research Center, National Institute of Animal Health, Japan

Bovine spongiform encephalopathy (BSE) has become an important problem
not only for animal industry, but also for public health. In Japan, BSE
was first recognized in September 2001 by fallen stock surveillance. Since
October 2001, BSE examination for all cattle slaughtered at abattoirs has
started. In April 2004, all dead cattle examination (over 24 months) has
been conducted at livestock hygiene service center. Samples positive in
enzyme linked immunosorbent assay (ELISA) are further subjected to western
blot (WB) and immunohistochemistry (IHC). Thirteen BSE cases have been
reported by September 2004. Twelve cases were classified as typical BSE,
and the remained one was an atypical BSE. Variant forms of BSE with
atypical histopathological and/or biochemical phenotype were reported in
Italy and France. Further study is required for BSE prion characteristics.
To characterize BSE prion properties, brain homogenates of Japanese BSE
cases were intracerebrally inoculated into wild-type mice. The first
case (BSE/Chiba) was successfully transmitted to rodents. The mean
incubation periods (409.0 days) in this experiment was preferably longer
than that of previously reported. PrPSc distribution, prion titer, mice
susceptibility and/or storage condition of sample might be influenced the
result. Recently, we introduced transgenic mice that overexpress a
bovine PrP gene to overcome the species barrier problem. These mice are
expected to accelerate the transmission experiment of BSE prion. Transmission
of atypical BSE case is undergoing by using these transgenic mice.

http://www.knt.co.jp/ec/2004/prion/E2.htm


Comparative PRNP genotyping of U.S. cattle sires for potential
association with BSE


Christopher M. Seabury1, James E. Womack1, Jorge Piedrahita2 and
James N. Derr1 Contact Information


(1) Department of Veterinary Pathobiology, College of Veterinary
Medicine, Texas A&M University, College Station, Texas 77843-4467, USA


(2) Department of Molecular Biomedical Sciences, College of Veterinary
Medicine, North Carolina State University, Raliegh, North Carolina
27606, USA

Received: 14 April 2004 Accepted: 8 June 2004

Abstract The recent discovery of significant associations between
bovine spongiform encephalopathy (BSE) susceptibility in German cattle
and the frequency distributions of insertion/deletion (indel)
polymorphisms within the bovine PRNP gene prompted an evaluation of 132
commercial U.S. artificial insemination (AI) sires from 39 breeds.
Forward primer sequences from published primer sets targeting indels
within the putative bovine PRNP promoter, intron 1, and the 3prime UTR
(untranslated region) were synthesized with unique 5prime fluorescent
labels and utilized to develop a rapid multiplexed PCR assay for
identifying BSE-associated indels as well as facilitating polymorphism
analyses and/or marker-assisted selection. Significant differences (p <
0.05 all tests) were detected between the frequencies of bovine PRNP
promoter alleles for 48 healthy German cattle previously described and
132 commercial U.S. cattle sires. The frequency of the 23-bp promoter
allele observed for commercial U.S. cattle sires strongly resembled that
recently described for 43 BSE-affected German cattle. No significant
difference (pthinsp =thinsp 0.051) was detected between the
distributions of promoter genotypes for healthy German cattle and our
panel of commercial U.S. cattle sires. Interestingly, significant
differences (p < 0.01; p < 0.02) were also noted between the frequencies
and distributions of intron 1 alleles and genotypes, respectively, for
BSE-affected German cattle and our panel of U.S. cattle sires. No
significant allelic or genotypic differences were detected for the 14-bp
3prime UTR indel for any given comparison between German cattle and
commercial U.S. cattle sires.

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


Contact Information James N. Derr

Email: jderr@cvm.tamu.edu


http://www.springerlink.com/app/home/contribution.asp?wasp=6n99d5dqql7xuh49vrt0&referrer=parent&backto=issue,8,11;journal,1,108;linkingpublicationresults,1:100364,1


Research

Research >


Title: Identification and Characterization of the First U.S. Bovine
Spongiform Encephalopathy Case Authors

item Richt, Juergen

item Kluge, John - NVSL, APHIS, AMES, IA

item Alt, David

item Kunkle, Robert - bob

item Hamir, Amirali

item Czub, Stefanie - NATL BSE REF LAB, CANADA

item Davis, Arthur - NVSL, APHIS, AMES, IA

item Hall, S Mark - NVSL, APHIS, AMES, IA


Submitted to: Meeting Abstract

Publication Acceptance Date: January 2, 2004

Publication Date: January 4, 2004

Citation: Richt, J.A., Kluge, J.P., Alt, D.P., Kunkle, R.A., Hamir,

A.N., Czub, S., Davis, A.J., Hall, S. 2004. Identification And

Characterization Of The First U.S. Bovine Spongiform Encephalopathy
Case. Poster Created For Use By The USDA At A Meeting With The Office Of
International Epizootics. Technical Abstract: Bovine spongiform
encephalopathy (BSE) is a transmissible spongiform encephalopathy of
cattle, first detected in 1986 in the U.K. and subsequently in other
countries. BSE may have arisen either from the infectious agent scrapie,
which causes a similar disease in sheep and goats, or from a germline
mutation in the protein-coding region of the prion protein (PrP) gene of
affected cattle. Here, we report on the prion protein polypeptide
profile and genotype from the first identified case of BSE in the State
of Washington in the United States. The six-year old Holstein cow was
nonambulatory at slaughter and the formalin-fixed obex area of the
brainstem was found to contain spongiform changes and vacuolated neurons
by histopathology and the abnormal form of the prion protein, PrPBSE, by
immunohistochemistry. Species determination was made on the
formalin-fixed tissue. Extensive PrPBSE deposition in the obex was
confirmed by Western blot analyses and enzyme-linked immunosorbent assay
using brainstem and cerebellum derived from fresh tissue from the
suspect animal. The PrPBSE polypeptide profile from the U.S. BSE case
was characterized by (i) a lower molecular mass of the unglycosylated
PrPBSE polypeptide fragment compared to samples from sheep with scrapie
and deer with chronic wasting disease, (ii) good immunoreactivity with
monoclonal antibody 6H4 directed against the central region of the PrP,
but a lack of staining with monoclonal antibody P4, which recognizes the
protease-resistant N-terminal end of the PrP; and (iii) a glycoform
profile with a high proportion of the diglycosylated PrPBSE isoform.
Comparison of the U.S. BSE isolate to the recent Canadian and European
BSE isolates revealed similar sized PrPBSE polypeptide fragments using
anti-PrP antibody 6H4. The PrP gene from the U.S. BSE case was amplified
from both, fresh and formalin-fixed brain material and found to be of
bovine origin with a normal, rather unremarkable cattle PrP sequence.
This cow had a synonymous polymorphism at codon 192, and both alleles
contained the six-copy octapeptide repeat region. We conclude from these
studies that (i) the PrPBSE profile from the first U.S. BSE case showed
similar molecular properties to the typical PrPBSE pattern described for
the Canadian and European BSE isolates, and (ii) a germline mutation in
the bovine PrP gene is not likely the etiological cause in this case.
This information is consistent with the hypothesis that the U.S. BSE
case - similar to the one in Canada - was most likely exposed to
contaminated feed.


http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=161376


Research

Research >

Title: Experimental Transmission of Sheep Scrapie by Intracerebral and

Oral Routes to Genetically Susceptible Suffolk Sheep in the United

States Authors

item Hamir, Amirali

item Kunkle, Robert - bob

item Richt, Juergen

item Miller, Janice - ARS RETIRED

item Cutlip, Randall - ARS RETIRED

item Jenny, Allen - USDA-VS-APHIS-NVSL


Submitted to: Journal Of Veterinary Diagnostic Investigation
Publication Acceptance Date: June 1, 2004
Publication Date: N/A
Interpretive Summary: Scrapie is a naturally occurring fatal disease of
sheep and goats. It affects nervous system of the animal. Susceptibility
to the disease is dependent upon genetic makeup of the host and
infectious agent. This study documents findings in Suffolk sheep
affected with experimental disease. Four-month-old lambs were utilized
for the study. They were administered (5 in the brain and 19 orally)
scrapie-infected sheep brains. All animals that were administered the
infected material directly into the brain revealed signs of scrapie and
were euthanized between 13'24 months after administration. In sheep
given the material orally, signs of scrapie were seen between 27 and 43
months in 5 of 9 animals. Three of the 4 clinically normal sheep were
found to be positive for scrapie by laboratory tests at 15, 20, and 49
months after administration of infected material. There is lack of
information on experimental transmission of US scrapie agent in
genetically diverse flocks of sheep. This study attempts to partially
fill this void by documenting findings of this disease in Suffolks.
Since similar investigations are also needed for other breeds of sheep
in this country, the present study will serve as a foundation to compare
results of other future studies.


Technical Abstract: Scrapie is a naturally occurring fatal
neurodegenerative disease of sheep and goats. Susceptibility to the
disease is partly dependent upon genetic makeup of the host. This study
documents clinicopathological findings and distribution in tissues of
abnormal prion proteins (PrPres) by immunohistochemical (IHC) and
Western blot (WB) techniques, in tissues of genetically susceptible
sheep inoculated with US sheep scrapie agent. Four-month-old Suffolk
lambs (QQ or HQ at codon 171) were utilized for the study. They were
inoculated (5 intracerebrally and 19 orally) with an inoculum (No. 13-7)
consisting of a pool of scrapie-infected sheep brains. Intracerebrally
inoculated animals were euthanized when advanced clinical signs of
scrapie were observed. Orally inoculated animals were euthanized at
pre-determined time-points (4, 9, 12, 15 and 21 months post inoculation,
PI) and thereafter when the animals had terminal signs of disease. A
detailed postmortem examination was conducted on each carcass and
tissues were examined for microscopic lesions and for the presence of
PrPres by IHC and WB techniques. All intracerebrally inoculated animals
exhibited clinical signs of scrapie and were euthanized between 13 ' 24
months PI. Spongiform lesions in the brains and PrPres deposits in
central nervous system (CNS) and lymphoid tissues were seen in these
sheep. In orally inoculated sheep, clinical signs of scrapie were seen
between 27 and 43 months PI in 5/9 animals. The earliest detectable
PrPres was observed in brainstem and lymphoid tissues of a clinically
normal sheep at 15 months PI. Three of the 4 clinically normal sheep
were found to be positive at 15, 20, and 49 months PI by either
histopathology or the PrPres tests. This study was done to partially
fill a void in information on experimental studies of US scrapie
transmission (by intracerebral and oral routes) in genetically
susceptible sheep.


http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=161349


Research

Research >

Title: Experimental Transmission of Chronic Wasting Disease Agent to

Cattle by Intracerebral Route: Final Outcome of the Study Authors

item Hamir, Amirali

item Kunkle, Robert - bob

item Richt, Juergen

item Cutlip, Randall - ARS RETIRED

item Miller, Janice - ARS RETIRED

item O'Rourke, Katherine

item Williams, Elizabeth - UNIVERSITY OF WYOMING

item Miller, M - COLORADO DIV WILDLIFE

item Stack, Mick - VLA-WEYBRIDGE, UK

item Chaplin, Melanie - VLA-WEYBRIDGE, UK

Submitted to: Meeting Abstract

Publication Acceptance Date: September 29, 2004

Publication Date: N/A
Publisher's URL: http://www.ustse2004.com/
Technical Abstract: Thirteen calves were inoculated intracerebrally with
brain suspension from mule deer naturally affected with CWD. Three other
calves were kept as uninoculated controls. The experiment was terminated
at 6 years post inoculation (PI). During that time, prion protein
(PrPres) was found in the central nervous system (CNS) of 5 cattle. None
of these animals had shown any specific clinical signs that were common
to all. Microscopic lesions suggestive of spongiform encephalopathy in
the brains of these PrPres positive animals were subtle in the first 3
and absent in the latter 2 cases. However, all 5 animals were positive
for PrPres by both immunohistochemistry and Western blot. The 3
uninoculated control cattle and 8 other inoculated animals euthanized
during this time did not have PrPres in their CNS. Degenerative changes
indicative of neuroaxonal dystrophy (NAD) were seen in dorsal medulla
oblongata and appeared to be related to advancing age in both inoculated
and control cattle. Analysis of the gene encoding bovine PRNP revealed
similar findings, i.e., homozygosity for alleles encoding 6 octapeptide
repeats, serine (S) at codon 46 and S at codon 146 in all samples.
Findings of this study show that although PrPres amplification occurred
following direct inoculation into the brain, none of the affected
animals had classical histopathological lesions of spongiform
encephalopathy. Furthermore, only 38% of the inoculated cattle
demonstrated amplification of PrPres. Although intracerebral inoculation
is an unnatural route of exposure, and is the most severe challenge
possible, this experiment shows that CWD transmission in cattle can have
long incubation periods (up to 5 years). This finding suggests that oral
inoculation of cattle with CWD may not result in amplification of PrPres
within CNS tissues during the normal lifespan of cattle. It is possible
that a second bovine passage of material (brain infected with CWDmd)
from this study may result in a larger proportion of affected cattle
with a shortened incubation time, and may produce different clinical and
pathological findings. Such a study is now in progress. Also,
experimental inoculations of cattle with CWD isolates from white-tailed
deer and elk are needed to compare clinicopathological findings with the
present study and these studies will be initiated in the near future.


http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=167759tss


Research

Research >


Title: Experimental Cross-Species Transmission of Chronic Wasting

Disease (Cwd) at the National Animal Disease Center (Nadc), Ames, Iowa:

An Update Author

item Hamir, Amirali

Submitted to: Meeting Abstract
Publication Acceptance Date: September 29, 2004
Publication Date: N/A
Technical Abstract: Experimental cross-species transmission of
transmissible spongiform encephalopathies (TSEs) provides valuable
information for identification of potential host ranges, and generates
much needed prion-infected tissues for research. At NADC, studies
utilizing CWD agent(s) were initiated in 1997. However, since these
studies involve long incubation periods under BL-2 conditions, to date
only one study has been completed. Initially our studies were restricted
to farm livestock (cattle and sheep). However, as a result of increased
demand from our stakeholders, we now also conduct research on wildlife
(herbivores and carnivores). Following are some of the significant
findings of past and on-going experiments at NADC: Completed study:
CATTLE: Intracerebral inoculation of CWD-mule-deer resulted in
amplification of PrPres in a small number of inoculated cattle (5 of 13;
38%). However, none of the animals with PrPres had classic
histopathologic lesions of spongiform encephalopathy. Studies utilizing
CWD-elk and CWD-white-tailed-deer in cattle are in progress. Preliminary
findings of ongoing CWD experiments in other species indicate that: 1.
SHEEP: CWD-mule-deer can be transmitted intracerebrally to sheep (1 of
8; 5 yrs PI). 2. WHITE-TAILED DEER: CWD-elk, CWD-white-tailed-deer, and
CWD-mule-deer are pathogenic for white-tailed deer (60%; 2 yrs PI). 3.
FALLOW DEER: Compared with other cervids studies, appear to be resistant
to intracerebral inoculation of CWD-elk and CWD-white-tailed-deer (0%; 2
yrs PI). White-tailed deer with CWD-mule-deer are pending. 4. RACCOONS:
TME and scrapie can be transmitted within 6 months and 2 years,
respectively, whereas CWD cannot. (Therefore, may be possible to
differentiate these 3 TSE agents in raccoons). Study utilizing BSE in
raccoons is pending.


http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=167763


Prions in skeletal muscle


Patrick J. Bosque*,dagger ,Dagger , Chongsuk Ryou*, Glenn Telling*,§,
David Peretz*,dagger , Giuseppe Legname*,dagger , Stephen J.
DeArmond*,dagger ,¶, and Stanley B. Prusiner*,dagger ,||,**


* Institute for Neurodegenerative Diseases and Departments of dagger
Neurology, ¶ Pathology, and || Biochemistry and Biophysics, University
of California, San Francisco, CA 94143

Contributed by Stanley B. Prusiner, December 28, 2001

Considerable evidence argues that consumption of beef products from
cattle infected with bovine spongiform encephalopathy (BSE) prions
causes new variant Creutzfeldt-Jakob disease. In an effort to prevent
new variant Creutzfeldt-Jakob disease, certain "specified offals,"
including neural and lymphatic tissues, thought to contain high titers
of prions have been excluded from foods destined for human consumption
[Phillips, N. A., Bridgeman, J. & Ferguson-Smith, M. (2000) in The BSE
Inquiry (Stationery Office, London), Vol. 6, pp. 413-451]. Here we
report that mouse skeletal muscle can propagate prions and accumulate
substantial titers of these pathogens. We found both high prion titers
and the disease-causing isoform of the prion protein (PrPSc) in the
skeletal muscle of wild-type mice inoculated with either the Me7 o
Rocky Mountain Laboratory strain of murine prions. Particular muscles
accumulated distinct levels of PrPSc, with the highest levels observed
in muscle from the hind limb. To determine whether prions are produced
or merely accumulate intramuscularly, we established transgenic mice
expressing either mouse or Syrian hamster PrP exclusively in muscle.
Inoculating these mice intramuscularly with prions resulted in the
formation of high titers of nascent prions in muscle. In contrast,
inoculating mice in which PrP expression was targeted to hepatocytes
resulted in low prion titers. Our data demonstrate that factors in
addition to the amount of PrP expressed determine the tropism of prions
for certain tissues. That some muscles are intrinsically capable of
accumulating substantial titers of prions is of particular concern.
Because significant dietary exposure to prions might occur through the
consumption of meat, even if it is largely free of neural and lymphatic
tissue, a comprehensive effort to map the distribution of prions in the
muscle of infected livestock is needed. Furthermore, muscle may provide
a readily biopsied tissue from which to diagnose prion disease in
asymptomatic animals and even humans. Dagger Present address: Department
of Medicine, Denver Health Medical Center, Denver, CO 80204.

§ Present address: Department of Microbiology and Immunology, University
of Kentucky, Lexington, KY 40536-0230.

** To whom reprint requests should be addressed. E-mail: vann@cgl.ucsf.edu.


http://www.pnas.org/

Extraneural Pathologic Prion Protein in Sporadic Creutzfeldt-Jakob Disease

Markus Glatzel, M.D., Eugenio Abela, Manuela Maissen, M.S., and Adriano Aguzzi, M.D., Ph.D.


snip...


Conclusions Using sensitive techniques, we identified extraneural deposition
of PrPSc in spleen and muscle samples from approximately one third of patients
who died with sporadic Creutzfeldt-Jakob disease. Extraneural PrPSc appears
to correlate with a long duration of disease.


http://content.nejm.org/cgi/content/short/349/19/1812?query=TOC


EMBO reports AOP Published online: 11 April 2003

Widespread PrPSc accumulation in muscles of hamsters orally infected with scrapie

Achim Thomzig, Christine Kratzel, Gudrun Lenz, Dominique KrÒ¼ger & Michael
Beekes Robert Koch-Institut, P26, Nordufer 20, D-13353 Berlin, Germany

Received 13 February 2003; Accepted 13 March 2003; Published online 11
April 2003.

Abstract :

Scrapie, bovine spongiform encephalopathy and chronic wasting disease
are orally communicable, transmissible spongiform encephalopathies
(TSEs). As zoonotic transmissions of TSE agents may pose a risk to human
health, the identification of reservoirs for infectivity in animal
tissues and their exclusion from human consumption has become a matter
of great importance for consumer protection. In this study, a variety of
muscles from hamsters that were orally challenged with scrapie was
screened for the presence of a molecular marker for TSE infection, PrPSc
(the pathological isoform of the prion protein PrP). Sensitive western
blotting revealed consistent PrPSc accumulation in skeletal muscles from
forelimb and hindlimb, head, back and shoulder, and in tongue.
Previously, our animal model has provided substantial baseline
information about the peripheral routing of infection in naturally
occurring and orally acquired ruminant TSEs. Therefore, the findings
described here highlight further the necessity to investigate thoroughly
whether muscles of TSE-infected sheep, cattle, elk and deer contain
infectious agents.


http://www.emboreports.org/

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Tuesday, July 29, 2003 1:03 PM
To: fdadockets@oc.fda.gov
Cc: ggraber@cvm.fda.gov; Linda.Grassie@fda.gov; BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

snip...


Greetings FDA,


PLUS, if the USA continues to flagrantly ignore the _documented_ science
to date about the known TSEs in the USA (let alone the undocumented TSEs
in cattle), it is my opinion, every other Country that is dealing with
BSE/TSE should boycott the USA and demand that the SSC reclassify the
USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'.
for the SSC to _flounder_ any longer on this issue, should also be
regarded with great suspicion as well. NOT to leave out the OIE and
it's terribly flawed system of disease surveillance. the OIE should make
a move on CWD in the USA, and make a risk assessment
on this as a threat to human health...

snip...full text;


http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt


EFSA Scientific Report on the Assessment of the Geographical BSE-Risk
(GBR) of the United States of America (USA)
Publication date: 20 August 2004

Adopted July 2004 (Question N° EFSA-Q-2003-083)

* 167 kB Report

* 105 kB Summary


Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working
Group on the Assessment of the Geographical Bovine Spongiform
Encephalopathy (BSE) Risk (GBR) were asked by the European Commission
(EC) to provide an up-to-date scientific report on the GBR in the United
States of America, i.e. the likelihood of the presence of one or more
cattle being infected with BSE, pre-clinically as well as clinically, in
USA. This scientific report addresses the GBR of USA as assessed in 2004
based on data covering the period 1980-2003.

The BSE agent was probably imported into USA and could have reached
domestic cattle in the middle of the eighties. These cattle imported in
the mid eighties could have been rendered in the late eighties and
therefore led to an internal challenge in the early nineties. It is
possible that imported meat and bone meal (MBM) into the USA reached
domestic cattle and leads to an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle
imports from BSE risk countries were slaughtered or died and were
processed (partly) into feed, together with some imports of MBM. This
risk continued to exist, and grew significantly in the mid 90s when
domestic cattle, infected by imported MBM, reached processing. Given the
low stability of the system, the risk increased over the years with
continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is
likely but not confirmed that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent. As long as there are no
significant changes in rendering or feeding, the stability remains
extremely/very unstable. Thus, the probability of cattle to be
(pre-clinically or clinically) infected with the BSE-agent persistently
increases.

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/573_en.html


JAMA,

TO continue to ingore this and the other evidence that is and has been
mounting about sporadic CJD not being as sporadic and or spontaneos as
once thought, to continue this ignorance and blantantly let this
agent continue to spread via the proven routes to date and continue to
infect and kill, should warrant a TSE Inquiry in the USA by a Congressional
Investigation followed by International Council of some kind.
WE are not only infecting US citizens by this ignorance, but also the
International community that visits our Country. With the recent findings
of nv/v CJD transmitting via blood, we must not flounder any longer.

THE time to act has passed...


Summary of SEACs discussion on the second presumed case of blood
transfusion-associated infection with vCJD


>> 7. SEAC agreed that the western blot results and glycotype profile
>> suggested it was unlikely that the infection was preclinical sporadic
>> CJD (sCJD). The committee noted that a single study by Glatzel et al
>> (2003) had reported PrPres in the spleen of sCJD clinical cases.
>> However, the levels of PrPres present in sCJD cases were low and
>> detected in patients with a lengthy clinical illness from sporadic CJD.
>

http://www.seac.gov.uk/statements/state070804.htm

vCJD: Blood Transfusion Incident

http://www.publications.parliament.uk/pa/ld199697/ldhansrd/pdvn/lds03/text/31217-09.htm

THIS following is simply not acceptable;

Dr Pierluigi Gambetti, MD, Director,
National Prion Disease Pathology Surveillance Center

However, the NPDPSC examines about
50% of the approximate 300 cases expected to occur in the US
per year. Again, the number of cases examined by the NPDPSC
must be increased for the surveillance to be effective.

http://www.cjdfoundation.org/pdfs/CJDBrochureFN.pdf

Mad Cow Variant That Hits Humans Is a Puzzle
(Published: 04-Jan-04)

Washington Post | By Rob Stein | January 2, 2004


snip...

"We think we are in the best position to discover if there is an
atypical case," said Pierluigi Gambetti, who directs the Cleveland
center. "We have not seen one case of variant CJD that was a real
American indigenous case."

But Gambetti acknowledged that he gets samples from only perhaps half of
the cases of CJD that would be expected to occur each year in the United
States.

"It's not complete surveillance. It's like you go to the airport, and
half the people go unchecked. You would not be happy to fly in an
airplane where half the people have not been checked at all," Gambetti
said. "If we want to protect Americans, we need to examine many more
cases." ...END


WITH blantant acts of neglect due to corporate interest such as this ;

May 13, 2004

Failure To Test Staggering Cow May Reflect Wider Problems
Rep. Waxman raises concerns that the recent failure of USDA to test an
impaired cow for BSE may not be an isolated incident, citing the failure
of USDA to monitor whether cows condemned for central nervous system
symptoms are actually tested for mad cow disease.

- Letter to USDA

http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf


http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf

FOR IMMEDIATE RELEASE
Statement
May 4, 2004

Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA


Statement on Texas Cow With Central Nervous System Symptoms

http://www.fda.gov/bbs/topics/news/2004/NEW01061.html

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

Issued June 2000

Meat, Poultry, and Egg Products Inspection

1998 Report of the Secretary of Agriculture to the United States Congress

snip...


In March 1998, an FSIS food inspector and a Federal plant in New
York were each sentenced on one felony count of bribery. The
inspector was assessed a criminal fine of $17,000, assessed a $100
special assessment fee, and placed on probation for 5 years. The
inspector was also required to serve 6 months in home detention
and complete 200 hours of community service. The Federal plant was
assessed a criminal fine of $10,000, paid a $100 special
assessment fee, and was placed on probation for 5 years. The
investigation revealed that the inspector accepted money in
exchange for inspecting and passing downer (dying, diseased or
disabled) livestock that were supposed to be inspected by an FSIS
veterinarian and for allowing company employees to slaughter
animals and to use inspection brands when the inspector was not
present.

snip...


Civil Enforcement Actions

The following Civil Enforcement Actions are a representative sample of
actions taken during FY 1998:

* In June 1998, an Illinois Federal plant entered into a settlement
agreement with the USDA and the United States Attorney for
violating the FMIA, PPIA, and False Claims Act (FCA). The firm
agreed to pay the Court-ordered civil penalty of $20,000. The
investigation revealed that the firm prepared various meat and/or
poultry egg rolls without the benefit of Federal inspection, sold
and transported the non-federally inspected products in interstate
commerce, and used the official mark of meat and poultry
inspection without authorization...

snip...

http://www.fsis.usda.gov/OA/pubs/rtc98.htm

FSIS REPORT TO CONGRESS 1996

HELL, why not sell those 'DOWNERS' for our GIs to eat,
maybe that is why some got CJD;

In June 1996, a U.S. District Court for the Northern District of
California in
Oakland, California, sentenced the former vice president of a closed meat
processing establishment and the establishment for violations of the
Federal
Meat Inspection Act. The official paid $250,000 as part of a
restitution/fine
payment, received 5 years' probation, and was required to perform 1,000
hours
of community service. The firm was ordered to pay $500,000 in
restitution to
the Defense Logistics Agency of the U.S. Department of Defense. In
addition,
three co-defendants were sentenced for selling adulterated meat to the now
defunct establishment. The co-defendants were convicted of illegally
slaughtering cattle and transporting and selling the adulterated meat to
the now defunct firm, knowing the meat would be processed for resale and
human consumption. The former vice president admitted buying dead, dying,
diseased, or disabled cattle from the co-defendants and using the
adulterated
meat to prepare meat products for commercial sales and for Government
military contracts. The investigation was conducted in 1993 by the USDA
Office of Inspector General, officials from the Defense Criminal
Investigation
Service, and FSIS compliance officers. Restitution to the military was
initiated under the Affirmative Civil Enforcement program...

snip...

http://www.fsis.usda.gov/OA/pubs/rtc96.pdf

February 2003


Meat, Poultry, and Egg Products Inspection
2000 Report of the Secretary of Agriculture to the U.S. Congress

snip...

MORE BRIBERY FOR PASSING DOWNERS FOR HUMAN/ANIMAL
CONSUMPTION...TSS

* June 2000. A USDA Judicial Officer (JO) issued a Decision
upholding indefinite withdrawal of inspection services from a meat
and poultry company located in Greenville, New York. The JOâ¬"s
Decision upheld an Administrative Law Judgeâ¬"s (ALJ) Decision. The
decisions were the result of an administrative hearing before the
ALJ wherein USDA presented evidence to show that the company was
â¬Sunfit⬝ for inspection service. The proceeding to withdraw
inspection was based on the companyâ¬"s felony conviction of bribing
a public official. An investigation revealed that the company
provided money to an inspector in exchange for inspecting and
passing dying, diseased, or disabled livestock requiring
additional inspection by a Veterinary Medical Officer. The
inspector and company were convicted in separate trials. The
company has appealed to a U.S. District Court...

snip...


http://www.fsis.usda.gov/OA/pubs/rtc2000/rtc2000chap3.htm#4

March 2001


Meat, Poultry, and Egg Products Inspection
1999 Report of the Secretary of Agriculture to the U.S. Congress


Preface

snip...

January 1999. The owner of an export inspection station was sentenced on
two felony counts for using simulated export certificates with intent to
defraud. The defendant was sentenced to 3 years' probation and fined
$10,000. The investigation revealed that the defendant fraudulently
exported approximately 3 million pounds of meat and poultry products to
Mexico.

snip...

http://www.fsis.usda.gov/OA/pubs/rtc99/rtc99chap3.htm

WITH MAMMALIAN FEED BAN VIOLATIONS STILL HAPPENING IN THE USA 2004;

PRODUCT
Product is custom made deer feed packaged in 100 lb. poly bags. The
product has no labeling. Recall # V-003-5.
CODE
The product has no lot code. All custom made feed purchased between June
24, 2004 and September 8, 2004.
RECALLING FIRM/MANUFACTURER
Farmers Elevator Co, Houston, OH, by telephone and letter dated
September 27, 2004. Firm initiated recall is ongoing.
REASON
Feed may contain protein derived from mammalian tissues which is
prohibited in ruminant feed.
VOLUME OF PRODUCT IN COMMERCE
Approximately 6 tons.
DISTRIBUTION
OH.

END OF ENFORCEMENT REPORT FOR October 20, 2004

PRODUCT
Product is custom made steer/cattle feed packaged in 100 lb. poly bags.
The product has no labeling. Recall # V-001-5.
CODE
The product has no lot code. All custom made feed purchased between June
24, 2004 and September 8, 2004.
RECALLING FIRM/MANUFACTURER
Farmers Elevator Co, Houston, OH, by telephone and letter dated
September 27, 2004. Firm initiated recall is ongoing.
REASON
Feed may contain protein derived from mammalian tissues which is
prohibited in ruminant feed.
VOLUME OF PRODUCT IN COMMERCE
Approximately 80 1û2 tons of steer/cattle feed.
DISTRIBUTION
OH.

_______________________________

PRODUCT
Product is custom made sheep/goat feed packaged in 100 lb. poly bags.
The product has no labeling. Recall # V-002-5.
CODE
The product has no lot code. All custom made feed purchased between June
24, 2004 and September 8, 2004.
RECALLING FIRM/MANUFACTURER
Farmers Elevator Co, Houston, OH, by telephone and letter dated
September 27, 2004. Firm initiated recall is ongoing.
REASON
Feed may contain protein derived from mammalian tissues which is
prohibited in ruminant feed.
VOLUME OF PRODUCT IN COMMERCE
Approximately 8 tons.
DISTRIBUTION
OH.

_______________________________

END OF ENFORCEMENT REPORT FOR October 20, 2004

http://www.fda.gov/

PRODUCT
a) Product is 9 Mile Steer Feed, packaged in white poly weaved
bags, each containing 100 lbs. A white label tied to the
inlet of each bag with twine identifies the product. Recall
# V-187-4;
b) Product is 9 Mile Pig and Sow Feed, packaged in white poly
weaved bags, each bag containing 100 lbs. A white label tied
to the inlet of each bag with twine identifies the product.
Recall # V-188-4.
CODE
The products contain no code date.
RECALLING FIRM/MANUFACTURER
Farmers Elevator, Co., Houston, OH, by telephone and letters dated
September 8, 2004. Firm initiated recall is ongoing.
REASON
Products may contain protein derived from mammalian tissues which is
prohibited in ruminant (steer) feed. FDA regulation, if the feed is
intended for non-ruminants (pigs), the bag labels must bear the
statement ìDo not feed to cattle or other ruminantsî.
VOLUME OF PRODUCT IN COMMERCE
700 lbs. Steer feed and 1,500 lb. Pig and sow fed.
DISTRIBUTION
OH.

http://www.fda.gov/bbs/topics/enforce/2004/ENF00869.html

PRODUCT
a) Premier Catfish Food, packaged in 50 pound bags (white paper
with an orange label). Recall #V-190-4;
b) Happy Fisherman Fish Food, pellet form, 50 pound bags.
Recall # V-191-4.
CODE
a) T1 Best By 08/27/05;
b) T21 Best By 11 DEC 05 and T11 Best By 02 OCT 05.
RECALLING FIRM/MANUFACTURER
Sunshine Mills, Inc., Tupelo, MS, by telephone beginning on April 14,
2004. Firm initiated recall is complete.
REASON
The catfish food contains prohibited material (meat & bone meal) but
does not contain the cautionary statement, "Do not feed to cattle or
other ruminants" on the label.
VOLUME OF PRODUCT IN COMMERCE
1,092  50 pound bags.
DISTRIBUTION
TX and MO.

http://www.fda.gov/bbs/topics/enforce/2004/ENF00869.html


Public Health Service
Food and Drug Administration

San Francisco District
1431 Harbor Bay Parkway
Alameda, CA 94502-7070
Telephone: 510/337-6700


VIA HAND DELIVERY

Our Reference No. 1000123954

June 23, 2004

Ronald M. Foster, Manager
Randall C. Boyce, Manager
Trevor O. Foster, Manager
George P. Foster, Manager
Fresno Farming LLC
P.O. Box 457
1000 Davis Street
Livingston, California

WARNING LETTER

Dear Mssrs. Foster, Boyce, Foster, and Foster:

The U.S. Food and Drug Administration (FDA) conducted an inspection of
your medicated animal feed mill operation, Fresco Farming LLC, located
in Traver, California from April 14, 2004 through May 6, 2004, and found
significant deviations from the requirements set forth in Title 21, Code
of Federal Regulations, Section 589.2000 (21 C.F.R. 589.2000) - Animal
Proteins Prohibited in Ruminant Feed. The regulation is intended to
prevent the establishment and amplification of Bovine Spongiform
Encephalopathy (BSE). Because you failed to follow this rule, products
you manufactured and distributed are adulterated within the meaning of
Section 402(a)(4) of the Federal Food, Drug, and Cosmetic Act (the Act)
because they were prepared, packed, or held under insanitary conditions
whereby they may have been rendered injurious to health.

Our inspection found the following violations of 21 C.F.R. 589.2000:

1. Failure to provide for measures to avoid commingling or
cross-contamination of products that contain or may contain protein
derived from mammalian tissues into animal protein or feeds that may be
used for ruminants to comply with 21 C.F.R. 589.2000(e)(1)(iii).

* Your firm uses a vacuum system to clean up spilled product in the
tunnel area. This tunnel area houses the two receiving conveyor
systems and the elevators for the two conveyor systems. When
product, including ruminant meat and bone meal, is spilled onto
the floor of this area, the spilled product is vacuumed up by the
vacuum system and, via a discharge hose, was placed into a
conveyor system that your firm had designated as free of ruminant
meat and bone meal. Your firm admitted that it was unaware of the
vacuum system discharging into the conveyor systems designated as
free of ruminant meat and bone meal and that this had been in
place since April 2003. Your firm remedied this problem during
FDAs April/May 2004 inspection by removing the discharge hose
connection to the conveyer system that your firm had designated as
free of ruminant meat and bone meal .
* Your firm uses a dust collection system that pulls dust from
systems that receive both ruminant meat and bone meal and feed
ingredients intended for ruminants. This dust system then
discharged collected product back into the two conveyor systems
via a cross connection, thereby making it likely that ruminant
meat and bone meal became commingled with ruminant feed
ingredients. Your firm admitted that it was unaware of the cross
connection and that it had been in place since April 2003. Your
firm removed the cross connection during FDAs April/May 2004
inspection.

2. Failure to maintain written procedures specifying the clean-out
procedure or other means, and specifying the procedures for separating
products that contain or may contain protein derived from mammalian
tissue from all other protein products from the time of receipt until
the time of shipment, to comply with 21 C.F.R. 589.2000(e)(1)(iv). This
observation was also noted during FDAs July/August 2003 inspection of
your firm.

* There are no written procedures for separating products that
contain prohibited material from ingredients used in ruminant
feeds from the time of receipt until the time of shipment.
* The written procedure for cleaning out or flushing equipment after
mixing feeds containing prohibited material was not adequate to
prevent contamination of ruminant feed with prohibited material.

3. Failure to maintain records sufficient to track materials that
contain protein derived from mammalian tissues throughout their receipt,
processing, and distribution to comply with 21 C.F.R. 589.2000(e)(1)(i).
This observation was also noted during FDAs July/August 2003 inspection
of your firm.

* Specifically, your firm has failed to develop and implement
complete written procedures to separate ruminant meat and bone
meal from feed ingredients intended for ruminants from the time of
receipt until the time of distribution. The written procedures
that do exist fail to address the use of equipment common to
ruminant meat and bone meal and ruminant feed ingredients.

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

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

Please send your reply to the U.S. Food and Drug Administration,
Attention: Ms. Harumi Kishida, Compliance Officer, 1431 Harbor Bay
Parkway, Alameda, California 94502-7070. If you have questions regarding
this letter, please contact Ms. Kishida at (510) 337-6824.

Sincerely,

/s/

CD Moss, Acting DD for
Barbara J. Cassens
District Director
San Francisco District

cc:
VIA CERTIFIED MAIL
RETURN RECEIPT REQUESTED
C. Michael Blasco, Feed Mill Manager
Fresno Farming LLC
P.O. Box 430
Traver, California 93673

http://www.fda.gov/foi/warning_letters/g4849d.htm


Public Health Service
Food and Drug Administration

Chicago District
550 West Jackson Blvd., 15th Floor
Chicago, Illinois 60661
Telephone: 312-353-5863


July 12, 2004

WARNING LETTER
CHI-16-04

CERTIFIED MAIL
RETURN RECEIPT REQUESTED

Mr. Donald E. Hamilton, President/Owner
Illini Feeds, Inc.
P.O. Box 86, 1145 State Hwy. 94
Aledo, Illinois 61231

Dear Mr. Hamilton:

On February 19 and 20, 2004, the Food and Drug Administration (FDA)
conducted an inspection of your animal feed handling facility located at
1145 State Highway 94, Aledo, Illinois. The inspection found significant
deviations from the requirements set forth in Title 21, Code of Federal
Regulations, Part 589.2000 (21 CFR 589.2000) - Animal Proteins
Prohibited in Ruminant Feed. This regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy
(BSE). The deviations cause the swine feed manufactured by your facility
to be misbranded within the meaning of Section 403(a)(1) of the Federal
Food, Drug, and Cosmetic Act (the Act).

Our investigation found that salvaged pet food containing prohibited
material was added as an ingredient to the swine products manufactured
at your facility. During the inspection, our investigator found that you
failed to label your non-ruminant products with the required caution
statement - Do not feed to cattle or other ruminants. [21 CFR
589.2000(d)(1)]

The above is not intended to be an all-inclusive list of violations. As
a manufacturer of materials intended for use in animal feed, you are
responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law.

You should take prompt action to correct this violation, and you should
establish a system whereby such violations do not recur. Failure to
promptly correct this violation may result in regulatory action without
further notice, such as seizure and/or injunction.

During the inspection, you told the investigator that you would put the
required cautionary statement on your products that contain prohibited
material, and maintain tracking documents for all incoming ingredients,
including animal proteins prohibited in ruminant feed. Please notify
this office in writing within 15 working days of receiving this letter
of any further steps you have taken to assure that your firm is in
compliance with the law. Your response should also include an
explanation of each step taken to correct the violations, and prevent
their recurrence. Please include copies of any available documentation
such as written procedures, corrected labeling, etc., demonstrating that
corrections have been made. If corrections cannot be completed within 15
working days, state the reason for the delay and the date by which the
corrections will be completed.

Your reply should be directed to Paul A. Boehmer, Compliance Officer, at
the above address.

Sincerely,

/s/

Scott J. MacIntire
District Director

http://www.fda.gov/foi/warning_letters/g4840d.htm


Public Health Service
Food and Drug Administration

Chicago District
550 West Jackson Blvd., 15th Floor
Chicago, Illinois 60661
Telephone: 312-353-5863


June 15, 2004

WARNING LETTER

CERTIFIED MAIL
RETURN RECEIPT REQUESTED

Mr. David W. Bernauer
CEO and Chairman of the Board
Walgreen co.
200 Wilmot Rd.
Deerfield, IL 60015

Dear Mr. Bernauer:

Inspection of your firms warehouse at 5100 Lake Terrace N.E., Mt.
Vernon, Illinois, by the Illinois Department of Public Health and the
U.S. Food and Drug Administration (FDA) on February 25, 26, and 27, and
March 2, 2004, documented numerous insanitary conditions which caused
the food and drug products stored there to become adulterated.

Our inspection showed that the food and drug products stored and held at
your facility violated the Federal Food, Drug, and Cosmetic Act (the
Act), rendering them adulterated. These adulterated fwd and drug
products: a) consisted in whole or in part of filthy substances,
including rodent fecal pellets, rodent hair, and insects, in violation
of Section 402(a)(3) of the Act [21 U.S.C. 342(a)(3)]; and/or b) had
been held under insanitary conditions whereby they have become
contaminated with rodent filth, in violation of Sections 402(a)(4) and
501(a)(2)(a) of the Act [21 U.S.C. 342(a)(4), 351(a)(2)(a)].

Evidence of rodent activity documented throughout the old and new
warehouse included dead mice in traps, excreta pellets, and gnawed paper
material observed in, on, and near food and drugs stored in the
warehouse. Rodents gnaw holes were observed into several packaged food
products with rodent hairs at gnaw holes into products. Many more fecal
pellets were on food and drug packages and still more were found near
the stored foods, drugs, and cosmetics in the warehouse.

Other conditions observed during the inspection that could be
contributing factors to rodent infestation include damaged and/or poorly
fitting rail and truck dock doors, gaps around a conduit entry into the
building, and the structural condition of the concrete and expansion
gaps at floor/wall/support beam junctions in various areas of the
warehouse allowing the entry or harborage of pests. Additionally, the
investigators observed cobwebs, dead insects, dust, debris, product
spillage, and papers in the warehouse, indicating a general lack of good
sanitation practices.

Also, products that contain or may contain animal protein prohibited
ruminant feed (BSE material) failed to bear the caution statement, Do
not feed to cattle or other ruminants. Specifically, pet food products
were salvaged, repackaged, and donated to [redacted] and other similar
organizations in the area, without the proper labeling and agreement
that they would not be used for ruminants. Please refer to Title 21,
Code of Federal Regulations, Section 589.2000, concerning these
requirements.

Our laboratory confirmed the findings of rodent excreta, rodent hairs on
product gnaw holes, and rodent gnawed fibers (packaging material)
sampled from the warehouse during the inspection.

The above listed violations are not intended to be all-inclusive. It is
your responsibility to assure adherence with each requirement of the Act
and its implementing regulations. The investigators reported that you
destroyed food products that showed evidence of contamination and began
to take some steps to correct the insanitary conditions in your
facility. We request that you take prompt action to correct all violations.

Please provide this office, within 15 working days of receipt of this
letter, a detailed response stating the actions you plan to take and
have taken to correct and prevent the recurrence of these objectionable
conditions. Provide the time within which corrections will be completed,
reasons why any corrective action cannot be completed, and documentation
to show that corrections have been made. Failure to take prompt action
to correct all violations may result in regulatory action without
further notice. Such action includes seizure and/or injunction.

Your reply should be directed to Paul A. Boehmer, Compliance Officer, at
the Chicago District Office.

Sincerely,

/s/

Scott J. MacIntire
District Director

cc:
Stephen J. Lawrence,
Distribution Center Manager
Walgreen Co.
5100 Lake Terrace NE
Mount Vernon, IL 62864-9665

http://www.fda.gov/foi/warning_letters/g4853d.htm

RECALLS AND FIELD CORRECTIONS: VETERINARY - CLASS II

_______________________________

PRODUCT

a) Bulk whole corn. Recall # V-150-4;
b) Bulk rolled corn. Recall # V-151-4;
c) Bulk rolled corn with added fat. Recall # V-152-4.

CODE

No coding information is used.

RECALLING FIRM/MANUFACTURER

Fresno Farming LlC, Traver, CA, by letters on June 30, 2004. Firm
initiated recall is ongoing.

REASON
Corn for feed may be contaminated with RUMINANT MEAT AND BONE MEAL.

VOLUME OF PRODUCT IN COMMERCE
Unknown.

DISTRIBUTION
Unknown.
____________________________

http://www.fda.gov/bbs/topics/enforce/2004/ENF00857.html


PLUS THESE TSE BLOOD VIOLATIONS ;

PRODUCT
Source Plasma. Recall # B-0004-5.
CODE
Units BY0081013, BY0081234, BY0081539, BY0081749, BY0082116, BY0082324,
BY0082909, BY0082977.
RECALLING FIRM/MANUFACTURER
DCI Biologicals Bryan, LLC, Bryan, TX, by facsimile dated November 6,
2002. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who lived in western Europe, were
distributed.
VOLUME OF PRODUCT IN COMMERCE
8 units.
DISTRIBUTION
NY.

___________________________________

PRODUCT
Source Plasma. Recall # B-0038-5.
CODE
Units CS0179785, CS0195693.
RECALLING FIRM/MANUFACTURER
Westgate Biologicals, LLC, College Station, TX, by letter dated January
2, 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
2 units.
DISTRIBUTION
NY.

_______________________________

PRODUCT
Red Blood Cells Leukocytes Reduced. Recall # B-0041-5.
CODE
Unit 2372493 (split unit).
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
March 7, 20, and 27, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who was at risk for
Creutzfeldt-Jakob Disease (CJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units.
DISTRIBUTION
TX.

_______________________________

PRODUCT
a) Red Blood Cells Leukocytes Reduced. Recall # 0044-5;
b) Fresh Frozen Plasma. Recall # B-0045-5.
CODE
a) and b) Unit 2374447.
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
January 22, and February 21, 2003. Firm initiated recall is complete.
REASON
Blood product, which was collected from a donor who was at risk for
Creutzfeldt-Jakob Disease (CJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units.
DISTRIBUTION
TX.

_______________________________

PRODUCT
a) Red Blood Cells, Leukocytes Reduced. Recall # B-0049-5;
b) Recovered Plasma. Recall # B-0050-5.
CODE
a) and b) Unit 2368943.
RECALLING FIRM/MANUFACTURER
South Texas Blood & Tissue Center, San Antonio, TX, by facsimile dated
February 13, 2003, and April 10, 2003. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who lived in western Europe, were
distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units.
DISTRIBUTION
Vienna, Austria, and TX.
_______________________________

PRODUCT
a) Red Blood Cells, Leukocytes Reduced. Recall # B-0056-5;
b) Cryoprecipitated AHF. Recall # B-0057-5;
c) Recovered Plasma. Recall # B-0058-5.
CODE
a), b), and c) Unit number 2372945.
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
February 25, 2003. Firm initiated recall is complete.
REASON
Blood products collected from an unsuitable donor due to a history of
residing in an area considered at increased risk of exposure to variant
Creutzfeldt-Jakob Disease (vCJD).
VOLUME OF PRODUCT IN COMMERCE
3 units.
DISTRIBUTION
TX, and Switzerland.

_______________________________

PRODUCT
Red Blood Cells, Leukocytes Reduced. Recall # B-0059-5;
Recovered Plasma. Recall # B-0060-5.
CODE
a) and b) Unit number 2348391.
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
February 12, and 19, 2003. Firm initiated recall is complete.
REASON
Blood products collected from an unsuitable donor due to a history of
residing in an area considered at increased risk of exposure to variant
Creutzfeldt-Jakob Disease (vCJD).
VOLUME OF PRODUCT IN COMMERCE
2 units.
DISTRIBUTION
TX and Austria.

_______________________________

PRODUCT
a) Red Blood Cells, Leukocytes Reduced. Recall # B-0080-5;
b) Fresh Frozen Plasma. Recall # B-0081-5.
CODE
a) and b) Unit 2356608.
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
March 20, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who was at risk for
Creuztfeldt Jakob Disease (CJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units.
DISTRIBUTION
TX.

_______________________________

END OF ENFORCEMENT REPORT FOR October 20, 2004

http://www.fda.gov/

PRODUCT
Red Blood Cells, Leukocytes Reduced. Recall B-0008-5.
CODE
Unit number 6684748 (distributed as two split units).
RECALLING FIRM/MANUFACTURER
Suncoast Communities Blood Bank, Sarasota, FL, by telephone on October
28, 2003. Firm initiated recall is complete.
REASON
Blood product, collected from an unsuitable donor due to a history of
residing in an area considered at increased risk of exposure to new
variant Creutzfeldt-Jakob Disease (nvCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units.
DISTRIBUTION
FL.

_______________________________

PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-0025-5;
b) Cryoprecipitated AHF, Recall # B-0026-5;
c) Plasma Cryoprecipitate Reduced, Recall # B-0027-5.
CODE
a), b), and c) Unit 20GM75704.
RECALLING FIRM/MANUFACTURER
American Red Cross Blood Services, Boise, ID, by telephone on April 4,
2003 and by letter dated August 6, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who was at risk for
Creuztfeldt Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
3 units.
DISTRIBUTION
MT.
_______________________________

PRODUCT
a) Red Blood Cells, Leukocytes Reduced. Recall # B-0036-5;
b) Fresh Frozen Plasma. Recall # B-0037-5.
CODE
a) and b) Unit number 2383755.
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
February 4, 2003, and August 13, 2003. Firm initiated recall is complete.
REASON
Blood products collected from an unsuitable donor due to a history of
residing in an area considered at increased risk of exposure to variant
Creutzfeldt-Jakob Disease (vCJD).
VOLUME OF PRODUCT IN COMMERCE
2 units.
DISTRIBUTION
TX.


RECALLS AND FIELD CORRECTIONS: BIOLOGICS  CLASS III

_______________________________

PRODUCT
Recovered Plasma. Recall # B-0012-5.
CODE
Unit numbers D03-02509 and D04-00404.
RECALLING FIRM/MANUFACTURER
Metrowest Medical Center, Farmingham, MA, by letter on August 10, 2004.
Firm initiated recall is complete.
REASON
Blood products, collected from an unsuitable donor due to a history of
residing in an area considered at increased risk of exposure to variant
Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units.
DISTRIBUTION
PA.
_______________________________

http://www.fda.gov/bbs/topics/enforce/2004/ENF00869.html


WITH ALL THIS, THE only solution in making sure there is an effective
human TSE surveillance in the USA and the entire
Globe;

CJD (all human TSEs) should be made reportable Nationally and
Internationally immediately, with a follow up investigation and
questionnaire of each victim (family) asking questions pertaining to
route and source of agent. ALL ages must be included in this. Anything
less will only allow the agent to continue to spread and kill...

Thank You,

with kindest regards,

I am sincerely,

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA
CJD WATCH





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