ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report
History nvCJD USA ;
FLORIDA
Variant Creutzfeldt-Jakob Disease Death, United States: 1st Case Report
The only variant Creutzfeldt-Jakob disease (vCJD) patient identified in the
United States died in 2004, and the diagnosis was confirmed by analysis of
autopsy tissue. The patient likely acquired the disease while growing up in
Great Britain before immigrating to the United States in 1992. Additional vCJD
patients continue to be identified outside the United Kingdom, including 2 more
patients in Ireland, and 1 patient each in Japan, Portugal, Saudi Arabia, Spain
and the Netherlands. The reports of bloodborne transmission of vCJD in 2
patients, 1 of whom was heterozygous for methionine and valine at polymorphic
codon 129, add to the uncertainty about the future of the vCJD outbreak.
snip...
see case history on 1st nvCJD case in USA here ;
A 22-year-old Florida resident became the first person in the USA to be
diagnosed with probable variant Creutzfeldt-Jakob disease (vCJD), according to
the US Centers for Disease Control and Prevention (CDC). Because the young woman
was raised in the UK when the BSE outbreak was at its peak, officials believe
that she contracted the disease there. The case report, which is published in
Morbidity and Mortality Weekly Report (2002; 51: 927—29;
Probable Variant Creutzfeldt-Jakob Disease in a US Resident—Florida,
2002
JAMA. 2002;288:2965-2967.
MMWR. 2002;51:927-929
On April 18, 2002, the Florida Department of Health and CDC announced the
occurrence of a likely case of variant Creutzfeldt-Jakob disease (vCJD) in a
Florida resident aged 22 years. This report documents the investigation of this
case and underscores the importance of physicians increasing their suspicion for
vCJD in patients presenting with clinical features described in this report who
have spent time in areas in which bovine spongiform encephalopathy (BSE) is
endemic.
In early November 2001, the patient sought medical care for depression and
memory loss that adversely affected the patient's work performance. The
primary-care physician referred the patient to a psychologist. In early December
2001, the patient received a traffic ticket for failing to yield the right of
way. In mid-December 2001, the patient had involuntary muscular movements, gait
changes, difficulty dressing, and incontinence. In January 2002, the patient was
evaluated in a local emergency department for these symptoms. A computerized
tomography scan of the head revealed no abnormalities; a panic attack was
diagnosed, and the patient was treated with an anti-anxiety medication.
In late January 2002, the patient's mother, a resident of the United
Kingdom, took the patient to England, where medical evaluations were conducted
during the next 3 months. During this period, the patient's memory loss and
other neurologic symptoms worsened. The patient experienced falls with minor
injuries, had difficulty taking a shower and dressing, and was unable to
remember a home telephone number or to make accurate mathematical calculations.
The patient subsequently became confused, hallucinated, and had speech
abnormalities with lack of content, bradykinesia, and spasticity. The patient
was referred to a neurologist, who suspected vCJD and subsequently referred the
patient to the National Prion Clinic in the United Kingdom.
Medical evaluations at the National Prion Clinic included an
electroencephalogram (EEG), which revealed a normal alpharhythm, and magnetic
resonance imaging (MRI) studies, which revealed signal abnormalities in the
pulvinar and metathalamus region that were suggestive of vCJD. The patient had a
tonsil biopsy, and a Western blot analysis of the biopsy tissue demonstrated the
presence of protease-resistant prion protein (PrP-res) with the characteristic
pattern of vCJD; an immunohistochemical test for PrP-res also supported a
diagnosis of vCJD. Analysis of the prion protein gene detected no mutation and
showed methionine homozygosity at codon 129, consistent with all 105 vCJD
patients tested in the United Kingdom (R. Will, Western General Hospital,
Edinburgh, Scotland, personal communication, 2002).
The patient received experimental treatment with quinacrine for 3 months.
As of late September 2002, the patient had become bedridden, experienced
considerable weight loss requiring surgical insertion of a feeding tube, and was
no longer communicating with family members. On the basis of a case definition
developed in the United Kingdom, the patient's illness met criteria for a
probable case of vCJD.1
The patient was born in the United Kingdom in 1979 and moved to Florida in
1992. The patient never had donated or received blood, plasma, or organs and
never had received human growth hormone. There was no family history of CJD. In
October 2001, before the onset of the illness, the patient's wisdom teeth were
extracted, but there was no history of major surgery.
Reported by:
S Wiersma, MD, State Epidemiologist, Florida Dept of Health. S Cooper,
MRCP, R Knight, FRCP, National Creutzfeldt-Jakob Disease Surveillance Unit,
Western General Hospital, Edinburgh, Scotland; AM Kennedy, MD, National Prion
Clinic, Dept of Neurology, St. Mary's Hospital, London; S Joiner, MSc, Medical
Research Council Prion Unit, Dept of Neurodegenerative Disease, Institute of
Neurology, London, United Kingdom. E Belay, MD, LB Schonberger, MD, Div of Viral
and Rickettsial Diseases, National Center for Infectious Diseases, CDC.
CDC Editorial Note:
snip...full text ;
TEXAS
Variant Creutzfeldt-Jakob Disease Death, United States: 2nd Case Report
vCJD (Variant Creutzfeldt-Jakob Disease)
Update: Variant Creutzfeldt-Jakob Disease in a U.K. Citizen Who Had
Temporarily Resided in Texas, 2001-2005
In November 2005, the U.K. National Creutzfeldt-Jakob Disease (CJD)
Surveillance Unit in Edinburgh, Scotland notified the Centers for Disease
Control and Prevention (CDC) about a probable variant CJD diagnosis in a
30-year-old man who resided in Texas during 2001-2005. The patient had onset of
symptoms in early 2005 while in Texas. He then returned to the United Kingdom,
where his illness progressed, and a diagnosis of variant CJD was made. This
diagnosis was confirmed neuropathologically after the patient's death.
The variant CJD diagnosis was initially based on typical clinical
manifestations of the disease and demonstration of the characteristic “pulvinar
sign” on magnetic resonance imaging of the brain. No biopsy tissues are
available for pathologic confirmation of the diagnosis. While living in the
United States, the patient had no history of hospitalization, of having invasive
medical procedures, or of donation or receipt of blood and blood products.
The patient almost certainly acquired the disease in the United Kingdom. He
was born in the United Kingdom and lived there throughout the defined period of
risk (1980-1996) for human exposure to the agent of bovine spongiform
encephalopathy (BSE, commonly known as “mad cow” disease). His stay in the
United States was too brief relative to what is known about the incubation
period for variant CJD. For additional information about the incubation period
for variant CJD, see Belay ED, Sejvar JJ, Shieh WJ, et al. “Variant
Creutzfeldt-Jakob Disease Death, United States,” Emerg Infect Dis 2005;
available at
By convention, variant CJD cases are ascribed to the country of initial
symptom onset, regardless of where the exposure occurred. Since variant CJD was
first reported in 1996, a total of 195 patients with this disease from 11
countries have been identified. As of August 11, 2006, variant CJD cases have
been reported from the following countries: 162 from the United Kingdom, 20 from
France, 4 from Ireland, 2 from the United States (including the current case),
and one each from Canada, Italy, Japan, Netherlands, Portugal, Saudi Arabia, and
Spain. Similar to the two U.S. cases, two of the four cases from Ireland and the
single cases from Canada and Japan were likely exposed to the BSE agent while
residing in the United Kingdom. One of the 20 French cases may also have been
infected in the United Kingdom. Strong scientific evidence indicates that
variant CJD results from the transmission to humans of the agent that causes BSE
in cattle. The BSE outbreak in cattle that was first detected in the 1980s in
the United Kingdom has spread to many other European countries, and cases in
cattle have been identified outside of Europe, in Canada, Israel, Japan, and the
United States.
Date: August 14, 2006 Content source: National Center for Infectious
Diseases
VIRGINIA
Variant Creutzfeldt-Jakob Disease Death, United States: 3rd Case
Report
vCJD (Variant Creutzfeldt-Jakob Disease)
Confirmed Case of Variant Creutzfeldt Jakob Disease (vCJD) in the United
States in a Patient from the Middle East
The Virginia Department of Health and the Centers for Disease Control and
Prevention announce the recent confirmation of a vCJD case in a U.S. resident.
This is the third vCJD case identified in a U.S. resident. This latest U.S. case
occurred in a young adult who was born and raised in Saudi Arabia and has lived
in the United States since late 2005. The patient occasionally stayed in the
United States for up to 3 months at a time since 2001 and there was a shorter
visit in 1989. In late November 2006, the Clinical Prion Research Team at the
University of California San Francisco Memory and Aging Center confirmed the
vCJD clinical diagnosis by pathologic study of adenoid and brain biopsy tissues.
The two previously reported vCJD case-patients in U.S. residents were each born
and raised in the United Kingdom (U.K.), where they were believed to have been
infected by the agent responsible for their disease. There is strong scientific
evidence that the agent causing vCJD is the same agent that causes bovine
spongiform encephalopathy (BSE, commonly known as mad cow disease).
Variant CJD is a rare, degenerative, fatal brain disorder that emerged in
the United Kingdom in the mid-1990s. Although experience with this new disease
is limited, evidence to date indicates that there has never been a case
transmitted from person-to-person except through blood transfusion. Instead, the
disease is thought to result primarily from consumption of cattle products
contaminated with the BSE agent. Although no cases of BSE in cattle have been
reported in Saudi Arabia, potentially contaminated cattle products from the
United Kingdom may have been exported to Saudi Arabia for many years during the
large U.K. BSE outbreak.
The current case-patient has no history of receipt of blood, a past
neurosurgical procedure, or residing in or visiting countries of Europe. Based
on the patient's history, the occurrence of a previously reported Saudi case of
vCJD attributed to likely consumption of BSE-contaminated cattle products in
Saudi Arabia, and the expected greater than 7 year incubation period for
food-related vCJD, this U.S. case-patient was most likely infected from
contaminated cattle products consumed as a child when living in Saudi Arabia
(1). The current patient has no history of donating blood and the public health
investigation has identified no risk of transmission to U.S. residents from this
patient.
As of November 2006, 200 vCJD patients were reported world-wide, including
164 patients identified in the United Kingdom, 21 in France, 4 in the Republic
of Ireland, 3 in the United States (including the present case-patient), 2 in
the Netherlands and 1 each in Canada, Italy, Japan, Portugal, Saudi Arabia and
Spain. Of the 200 reported vCJD patients, all except 10 of them (including the
present case-patient) had resided either in the United Kingdom (170 cases) for
over 6 months during the 1980-1996 period of the large UK BSE outbreak or
alternatively in France (20 cases).
As reported in 2005 (1), the U.S. National Prion Disease Pathology
Surveillance Center at Case Western Reserve University confirmed the diagnosis
in the one previously identified case of vCJD in a Saudi resident. He was
hospitalized in Saudi Arabia and his brain biopsy specimen was shipped to the
United States for analysis. This earlier vCJD case-patient was believed to have
contracted his fatal disease in Saudi Arabia (1).
1) Belay ED, Sejvar JJ, Shieh W-J, Wiersma ST, Zou W-Q, Gambetti P, Hunter
S, Maddox RA, Crockett L, Zaki SR, Schonberger LB. Variant Creutzfeldt-Jakob
disease death, United States. Emerg Infect Dis 2005, 11 (9):1351-1354.
Date: November 29, 2006
The third US resident with vCJD was born and raised in Saudi Arabia and
beginning in 2001 he occasionally stayed in the United States for periods of up
to 3 months duration [30], [31]. The patient relocated to the United States in
2005 where onset of vCJD symptoms was experienced in the spring of 2006. The
diagnosis of vCJD was confirmed based on pathological study of adenoid and brain
biopsy tissues in November 2006. The patient died later in 2006. The patient had
no past history of neurosurgical procedures or visits to European countries. A
previous case of vCJD attributed to consumption of BSE-contaminated cattle
products had been reported in a Saudi Arabian resident [13].
Eurosurveillance, Volume 11, Issue 49, 07 December 2006 Articles Editorial
team1
--------------------------------------------------------------------------------
Citation style for this article: Editorial team. Third case of vCJD
reported in the United States. Euro Surveill. 2006;11(49):pii=3091. Available
online:
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3091
Date of submission:
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
Third case of vCJD reported in the United States
Editorial Team (eurosurveillance.weekly@hpa.org.uk), Eurosurveillance
editorial office
A clinical diagnosis of variant Creutzfeldt Jakob Disease (vCJD) was
confirmed after brain biopsy investigations in a United States (US) resident and
reported in November [1]. The patient is a young man who grew up in Saudi Arabia
and lived in the US since late 2005. Before that he visited the US once in 1989
and several times after 2001. He has never visited any country in Europe or
received a blood transfusion nor has he undergone any neurosurgical procedure.
This vCJD case is the third in a US resident. The previous two patients both
grew up in the United Kingdom (UK), and this is where they were believed to have
been infected [2].
In Saudi Arabia, the first and only previous case of vCJD was reported in
2005. This was suspected to be related to consumption of meat contaminated with
the prion agent which causes bovine spongiform encephalitis in cattle (BSE). The
European Food Safety Authority (
http://www.efsa.org)/ has not published a
geographical BSE risk assessment for Saudi Arabia [3] and there have been no
cases of BSE in cattle reported by Saudi Arabia to the World Organisation for
Animal Health (
http://www.oie.int)/. Although
the UK is not the only potential beef exporter to have had a BSE epidemic, it
remains plausible, subject to Saudi Arabia's import policy, that contaminated
beef was inadvertently imported from the UK to Saudi Arabia in the period before
1996 (when the EU banned the export of UK beef and cattle).
Based on this patient's history, the occurrence of a previously reported
case of vCJD in Saudi Arabia, and the expected length of the incubation period
for food-related vCJD, the most likely source of infection is thought to be
contaminated meat products the patient consumed as a child when living in Saudi
Arabia. The patient has no known history of donating blood, and investigations
have identified no risk of onwards transmission within the US.
Variant Creutzfeldt-Jakob disease was first identified in the United
Kingdom in the mid-1990s. As of November 2006, worldwide there have been 200
vCJD cases: 164 patients in the United Kingdom, 21 in France, four in Ireland,
three in the US (including the present case), two in the Netherlands and one
each in Canada, Italy, Japan, Portugal, Saudi Arabia and Spain [4]. All
patients, except 10 (including the present case) had lived either in the United
Kingdom (170 cases) or in France (20 cases). Evidence so far indicates that the
most probable source of infection in most cases was consumption of meat products
contaminated with the prion agent causing BSE.
References: Centers for Disease Control and Prevention. Confirmed Case of
Variant Creutzfeldt Jakob Disease (vCJD) in the United States in a Patient from
the Middle East. (
http://www.cdc.gov/ncidod/dvrd/vcjd/other/vCJD_112906.htm)
Belay ED, Sejvar JJ, Shieh W-J, Wiersma ST, Zou W-Q, Gambetti P, Hunter S,
Maddox RA, Crockett L, Zaki SR, Schonberger LB. Variant Creutzfeldt-Jakob
disease death, United States. Emerg Infect Dis 2005, 11 (9):1351-1354. European
Food Safety Authority . Geographical BSE Risk (GBR) assessments covering
2000-2006. List of countries and their GBR level of risk as assessed by the
Scientific Steering Committee and the (EFSA). 1 August 2006. (
http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/summary_list_countries.Par.0001.File.dat/GBR_assessments_table_Overview_assessed_countries_2002-2006.pdf)
Variant Creuzfeldt-Jakob disease. Current
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3091
TEXAS
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in
June 2014 *No* link to EU or Saudi
>>>the patient had resided in Kuwait, Russia and Lebanon.
>>>The completed investigation did not support the patient's
having had extended travel to European countries, including the United Kingdom,
or travel to Saudi Arabia.
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in
Texas
Updated: October 7, 2014
CDC and the Texas Department of State Health Services (DSHS) have completed
the investigation of the recently reported fourth vCJD case in the United
States. It confirmed that the case was in a US citizen born outside the Americas
and indicated that the patient's exposure to the BSE/vCJD agent most likely
occurred before he moved to the United States; the patient had resided in
Kuwait, Russia and Lebanon. The completed investigation did not support the
patient's having had extended travel to European countries, including the United
Kingdom, or travel to Saudi Arabia. The specific overseas country where this
patient’s infection occurred is less clear largely because the investigation did
not definitely link him to a country where other known vCJD cases likely had
been infected.
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
Confirmed Variant CJD Case in Texas Lab tests have confirmed a diagnosis of
variant Creutzfeldt-Jakob Disease (CJD) in a patient who recently died in Texas.
Variant CJD is a rare, fatal brain disorder, first described in 1996 in the
United Kingdom and associated with beef consumption overseas. This is the fourth
case ever reported in the United States. In each of the three previous cases,
infection likely occurred outside the United States, including the United
Kingdom and Saudi Arabia. The history of this fourth patient includes extensive
travel to Europe and the Middle East, and infection likely occurred outside the
United States. The CDC and DSHS continue to investigate the case. There are no
Texas public health concerns or threats associated with this case. CDC
Confirmation Information:
http://www.cdc.gov/ncidod/dvrd/vcjd/other/confirmed-case-in-texas.htm
CDC Fact Sheet:
http://www.cdc.gov/ncidod/dvrd/vcjd/factsheet_nvcjd.htm
Texas CJD Information:
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/
http://www.dshs.state.tx.us/
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
Posted: June 2, 2014 Laboratory tests have confirmed a diagnosis of variant
CJD (a fatal brain disorder) in a patient who recently died in Texas. The
confirmation was made when laboratory results from an autopsy of the patient’s
brain tested positive for variant CJD.
First described in 1996 in the United Kingdom, variant CJD is a rare,
degenerative, fatal brain disorder in humans. It is believed to be caused by
consumption of products from cows with the disease bovine spongiform
encephalopathy (BSE, or "mad cow" disease).
Worldwide, more than 220 variant CJD patients have been reported, with a
majority of them in the United Kingdom (177 cases) and France (27 cases). This
case is the fourth to be reported in the United States. In each of the three
previous cases, infection likely occurred outside the United States, including
the United Kingdom (2 cases) and Saudi Arabia (1 case). The history of this
fourth patient, including extensive travel to Europe and the Middle East,
supports the likelihood that infection occurred outside the United States.
CDC assisted the Texas Department of State Health Services (DSHS)'s
investigation of this case and will continue to help confirm further details of
the patient's history, including the potential source of infection.
A classic form of CJD, which is not caused by the BSE agent, occurs
worldwide, including in the United States. Annually, for every 1 million people
in the United States, 1 to 2 develops classic CJD. More information about
variant CJD, including how it differs from classic CJD, is available in the
Variant Creutzfeldt-Jakob Disease Fact Sheet. Date: June 2, 2014 Content source:
Centers for Disease Control and Prevention National Center for Emerging and
Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and
Pathology (DHCPP
a review of my correspondence about my concerns with the lack of
information in this case of nvCJD in Texas ;
From: Williams,Carrie C (DSHS) Sent: Wednesday, June 04, 2014 11:52 AM To:
Terry S. Singeltary Sr. Subject: RE: nvCJD Texas ???
Adult male from Texas with extensive travel history. That’s the extent of
the information I can provide at this time.
......................................................
Carrie Williams
Director of Media Relations
512-776-7119
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Wednesday, June 04, 2014 11:51 AM
To: Williams,Carrie C (DSHS)
Subject: Re: nvCJD Texas ???
Thank you for your kind reply. can you please tell me anything else? age?
sex? length of stay here in USA, diet, surgeries, blood, etc., anything???
kind regards, terry
From: Williams,Carrie C (DSHS)
Sent: Tuesday, June 03, 2014 9:08 AM
To: Terry S. Singeltary Sr.
Subject: Re: nvCJD Texas ???
Yes, we have some info and links on our home page -
www.dshs.state.tx.us
Sent from my iPhone
On Jun 2, 2014, at 8:12 PM, "Terry S. Singeltary Sr."
wrote:
Greetings Carrie,
I am wondering if there is any validity to this news report, and if so, is
there a statement from DSHS or anyone else in Texas ?
Published On: Mon, Jun 2nd, 2014
Outbreak News / US News | By Robert Herriman
Texas: Variant Creutzfeldt-Jakob Disease death confirmed, infection likely
occurred overseas
kind regards,
terry
==================
From: Fischer,Michael (DSHS)
Sent: Wednesday, June 04, 2014 3:50 PM
To: flounder9@verizon.net
Cc: Cantu,Rita M (DSHS) ; Bastis,David (DSHS) ; DSHS IDCU, Feedback
Subject: RE: nvCJD case confirmed Texas question please
Thank you for your interest.
As this is an ongoing investigation, the information stated on our website
is all that we can provide at this time.
Sincerely,
Michael P. Fischer, MD, MPH & TM
Emerging and Acute Infectious Disease Branch
Infectious Disease Control Unit
Telephone: 512-776-6338 ~ Fax: 512-776-7616
E-mail: michael.fischer@dshs.state.tx.us
Mailing Address:
MC 1960
P.O. Box 149347
Austin, Texas 78714-9347
From: Cantu,Rita M (DSHS) On Behalf Of DSHS IDCU, Feedback
Sent: Wednesday, June 04, 2014 3:26 PM
To: Fischer,Michael (DSHS)
Subject: FW: nvCJD case confirmed Texas question please
Please forward to correct person or respond with a cc to DSHS IDCU,
Feedback, thanks!
Rita Cantu
Infectious Disease Control Unit
Texas Department of State Health Services P.O. Box 149347 Austin, Texas
78714-9347
Phone (512) 776-6281
rita.cantu@dshs.state.tx.us
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Wednesday, June 04, 2014 11:59 AM
To: DSHS IDCU, Feedback
Subject: nvCJD case confirmed Texas question please
Greetings Texas IDCU et al,
I have followed closely the cjd bse saga since December 14, 1997, when I
lost my mom to the hvCJD.
can you please at least tell us the age of this vCJD or nvCJD victim
???
kind regards, terry
======================
From: Hammett, Teresa (CDC/OID/NCEZID)
Sent: Thursday, June 05, 2014 1:49 PM
To: Terry S. Singeltary Sr.
Subject: RE: re-human bse nvcjd TEXAS USA
Dear Mr Singeltary,
You will have to make this inquiry to the Texas Department of Health. The
contact person there is:
Michael Fischer, MD
Emerging and Acute Infectious Disease Branch
Infectious Disease Control Unit
Telephone: 512-776-6338
E-mail: michael.fischer@dshs.state.tx.us
--------------------------------------------------------------------------------
From: Terry S. Singeltary Sr.
Sent: Tuesday, June 03, 2014 9:40:19 PM (UTC-05:00) Eastern Time (US &
Canada) To: PRION (CDC)
Subject: re-human bse nvcjd TEXAS USA
NO AGE ??? any help here ???
kind regards, terry
====================
From: Terry S. Singeltary Sr.
Sent: Sunday, September 28, 2014 5:14 PM
To: Eric.Fonken@dshs.state.tx.us
Cc: michael.fischer@dshs.state.tx.us ; marilyn.felkner@dshs.state.tx.us ;
rita.cantu@dshs.state.tx.us
Subject: USA 4TH CASE VCJD (aka nvCJD) HUMAN MAD COW,
THE SILENCE IS DEAFENING BSE, CWD, AND SCRAPIE TSE PRION DISEASE
USA 4TH CASE VCJD (aka nvCJD) HUMAN MAD COW,
THE SILENCE IS DEAFENING BSE, CWD, AND SCRAPIE TSE PRION DISEASE
Greetings DSHS, Dr. Fishcer, et al,
I know that most in the USA could care less about the CJD TSE prion disease
aka mad cow type disease. but there are some of us here that will never forget.
you can cover up what ever you want. we all know. I have seen it happen too
many times here in Texas with BSE TSE prion, either the typical or the atypical
strains, or with the feed, or, with cwd, or scrapie as that goes, but we are
still here, and we will never forget...
kind regards, terry
===================
From: Fischer,Michael (DSHS)
Sent: Monday, November 10, 2014 2:26 PM
To: Terry S. Singeltary Sr.
Subject: RE: Current Prion Disease Statics in Texas
Terry,
You are welcome.
Sincerely,
Michael P. Fischer, MD, MPH & TM
Emerging and Acute Infectious Disease Branch
Infectious Disease Control Unit
Telephone: 512-776-6338 ~ Fax: 512-776-7616
E-mail: michael.fischer@dshs.state.tx.us
Mailing Address:
MC 1960
P.O. Box 149347
Austin, Texas 78714-9347
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Monday, November 10, 2014 2:20 PM
To: Fischer,Michael (DSHS) Cc: DSHS IDCU, Feedback
Subject: Re: Current Prion Disease Statics in Texas
Thank you kindly there Dr. Fischer. ...terry
From: Fischer,Michael (DSHS)
Sent: Monday, November 10, 2014 12:49 PM
To: flounder9@verizon.net
Cc: DSHS IDCU, Feedback
Subject: Re: Current Prion Disease Statics in Texas
Dear Mr. Singeltary Sr.,
Thank you for your inquiry into the Texas prion disease surveillance
program statistics. We periodically update the Texas Department of State Health
Service’s website, the prion disease statistics are updated annually. The
current year’s data (2014 data and statistics) will not be posted until all case
counts and investigations are reported to DSHS and verified, the prion disease
update typically occurs sometime after the middle of the following year
(2015).
You are welcome to visit our prion disease web pages on the DSHS website
for data and statistics which includes 2013 data.
If I can be of further assistance, please let me know.
Sincerely,
Michael P. Fischer, MD, MPH & TM
Emerging and Acute Infectious Disease Branch
Infectious Disease Control Unit
Telephone: 512-776-6338 ~ Fax: 512-776-7616
E-mail: michael.fischer@dshs.state.tx.us
Mailing Address:
MC 1960
P.O. Box 149347
Austin, Texas 78714-9347
====================
***In addition, non-human primates are specifically susceptible for
atypical BSE as demonstrated by an approximately 50% shortened incubation time
for L-type BSE as compared to C-type. Considering the current scientific
information available, it cannot be assumed that these different BSE types pose
the same human health risks as C-type BSE or that these risks are mitigated by
the same protective measures.
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent.
*** Lending support to this hypothesis, pathological and biochemical
similarities have been observed between L-BSE and an sCJD subtype (MV genotype
at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and
another sCJD subtype (MM genotype) [15].
snip...
Thursday, August 12, 2010
Seven main threats for the future linked to prions
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
***These atypical BSE cases constitute an unforeseen first threat that
could sharply modify the European approach to prion diseases.
Second threat
snip...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
***Moreover, transmission experiments to non-human primates suggest that
some TSE agents in addition to Classical BSE prions in cattle (namely L-type
Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME)
and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion
strains in transgenic mice expressing human prion protein
*** 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 BSEderived 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.
snip...
These studies further strengthen the evidence that vCJD is caused by a
BSE-like prion strain.
Also, remarkably, the key neuropathological hallmark of vCJD, the presence
of abundant florid PrP plaques, can be recapitulated on BSE or vCJD transmission
to these mice.
***However, the most surprising aspect of the studies was the finding that
an alternate pattern of disease can be induced in 129MM Tg35 mice from primary
transmission of BSE, with a molecular phenotype indistinguishable from that of a
subtype of sporadic CJD. This finding has important potential implications as it
raises the possibility that some humans infected with BSE prions may develop a
clinical disease indistinguishable from classical CJD associated with type 2
PrPSc. This is, in our experience, the commonest molecular sub-type of sporadic
CJD. In this regard, it is of interest that the reported incidence of sporadic
CJD has risen in the UK since the 1970s (Cousens et al., 1997)...
To date the OIE/WAHO assumes that the human and animal health standards set
out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE
which include the H-type and L-type atypical forms. This assumption is
scientifically not completely justified and accumulating evidence suggests that
this may in fact not be the case. Molecular characterization and the spatial
distribution pattern of histopathologic lesions and immunohistochemistry (IHC)
signals are used to identify and characterize atypical BSE. Both the L-type and
H-type atypical cases display significant differences in the conformation and
spatial accumulation of the disease associated prion protein (PrPSc) in brains
of afflicted cattle. Transmission studies in bovine transgenic and wild type
mouse models support that the atypical BSE types might be unique strains because
they have different incubation times and lesion profiles when compared to C-type
BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE.
***In addition, non-human primates are specifically susceptible for
atypical BSE as demonstrated by an approximately 50% shortened incubation time
for L-type BSE as compared to C-type. Considering the current scientific
information available, it cannot be assumed that these different BSE types pose
the same human health risks as C-type BSE or that these risks are mitigated by
the same protective measures.
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a
Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have
attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you
will find in the paper, we have managed to associate the alternate phenotype to
type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim
any further sub-classification in respect of Heidenhain variant CJD or Vicky
Rimmer's version. It will take further studies, which are on-going, to establish
if there are sub-types to our initial finding which we are now reporting. The
main point of the paper is that, as well as leading to the expected new variant
CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an
alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can
be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial
College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44
(0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until
9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
____________________________________ END
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis *video*
Jeff Schwan, sporadic cjd, clustering, and BSE aka mad cow type disease, is
there a link ? *video*
1997-11-10: Panorama - The british disease *video*
Sunday, September 6, 2009
MAD COW USA 1997 *video*
Monday, November 3, 2014
USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014
National Prion Disease Pathology Surveillance Center Cases Examined1
(October 7, 2014)
***6 Includes 11 cases in which the diagnosis is pending, and 19
inconclusive cases;
***7 Includes 12 (11 from 2014) cases with type determination pending in
which the diagnosis of vCJD has been excluded.
***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob
disease (sCJD),
***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)
***and 21 cases of sporadic Fatal Insomnia (sFI).
Monday, November 3, 2014
The prion protein protease sensitivity, stability and seeding activity in
variably protease sensitive prionopathy brain tissue suggests molecular overlaps
with sporadic Creutzfeldt-Jakob disease
Sunday, November 23, 2014
Transmission Characteristics of Variably Protease-Sensitive Prionopathy
* We concluded that VPSPr is transmissible; thus, it is an authentic prion
disease.
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
sporadic FFI or nvCJD Texas style ???
Sunday, July 11, 2010
CJD or prion disease 2 CASES McLennan County Texas population 230,213 both
cases in their 40s
2 mysterious cases of disease in McLennan County a rarity, but no cause for
alarm
By Cindy V. Culp Tribune-Herald staff writer
Friday July 9, 2010
Two likely cases of a mysterious, fatal brain disorder have been reported
in McLennan County — a statistical anomaly considering that only one in 1
million people worldwide is affected by the condition in any given year.
Adding to the peculiarity is that the noncontagious disorder belongs to the
same family as Creutzfeldt-Jakob disease.
One of its forms is believed to be triggered by people eating meat from
cattle infected with mad cow disease.
As frightening as that might sound, officials said residents shouldn’t be
alarmed.
One of the local cases definitely is not the type associated with mad cow
disease, and there is no evidence the other one is, either. More importantly,
the disorder cannot be transmitted from person to person, officials said.
“To have potentially two cases this close together is statistically
unusual,” said Dr. Farley Verner, an infectious disease specialist who advises
the Waco-McLennan County Public Health District. “But because of the type of
disorder it is, and because of what we know about how it develops, it’s not a
worrisome coincidence. It’s just a coincidence.”
Because of privacy laws, health officials can release only limited details
about the local cases. Both were reported in May.
The first case involved a 49-year-old man from McGregor, Hammad Akram, the
health district’s epidemiologist, said. The man has since died.
Initial results from an autopsy show he had some type of human prion
disease, a family of diseases involving an abnormal protein.
Creutzfeldt-Jakob disease, or CJD, is the most common type of human prion
disease. The autopsy ruled out CJD, however, Akram said.
The second case involves a Waco woman in her late 40s, Akram said. Her
symptoms point to CJD, but since the only way to confirm the disease is to study
brain tissue after death, that diagnosis is not confirmed, he said.
No apparent link
There is no apparent link between the two local victims, Akram said.
Prion disease usually occurs in people older than age 60.
Doctors give patients a “working diagnosis” of human prion disease based on
certain symptoms, combined with results from a blood test, Farley said.
The symptoms are similar to those of other neurological conditions:
confusion, difficulty remembering recent events, loss of feeling in certain body
parts, balance problems, difficulty walking and muscle jerks and spasms.
If a physician rules out other causes for such symptoms, a blood test can
be done that indicates whether the person has a genetic mutation associated with
human prion disease. The test cannot confirm it, but positive results make the
diagnosis more likely, Verner said.
The name of the disease category comes from a protein called a prion.
People have normal prions, which are concentrated in the brain. But in some
instances, there is abnormal prion protein, which causes normal prions to be
converted to abnormal form.
That destroys brain tissue and is eventually fatal. The process can take
years, but most people die within three months to a year of having symptoms.
There are three main categories of human prion disease — sporadic, familial
and acquired.
Sporadic cases start spontaneously, without a clearly identifiable cause.
They account for about 85 percent of all human prion disease, according to the
National Prion Disease Pathology Surveillance Center.
Familial cases are inherited and are caused by a defect in the prion
protein gene, the center said.
Acquired cases are transmitted by infection, which can occur if a person
receives a transplant infected with prion disease or undergoes surgery where
contaminated instruments are used, according to the center.
Another avenue of infection is when someone eats contaminated beef, the
center said. That’s where the connection to mad cow disease comes in.
Only three cases linked to contaminated beef have been found in the United
States, according to health officials. In all three cases, the victims are
thought to have been infected while living overseas.
In Texas, about 120 people died from human prion disease between 2000-08,
according to state data.
Last year, there were 19 probable or confirmed cases of sporadic CJD and
two familial CJD cases statewide.
McLennan County has not had any human prion disease cases in the past
decade, according to state records. Verner said he can only recall two or three
cases in the 25 years he has been here.
cculp@wacotrib.com
757-5744
> "It’s just a coincidence.”
r i g h t. $$$
cjd = one-in-a-million ???
McLennan County, Texas population 2008 230,213
sporadic FFI or nvCJD Texas style ???
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN
AND SPINAL CORD MATTER
>>> Up until about 6 years ago, the pt worked at Tyson foods where
she worked on the assembly line, slaughtering cattle and preparing them for
packaging. She was exposed to brain and spinal cord matter when she would
euthanize the cattle. <<<
>>> Up until about 6 years ago, the pt worked at Tyson foods where
she worked on the assembly line, slaughtering cattle and preparing them for
packaging. She was exposed to brain and spinal cord matter when she would
euthanize the cattle. <<<
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN
AND SPINAL CORD MATTER
PPS POLITICAL PRION SCIENCE $$$
Creutzfeldt-Jakob Disease Surveillance in Texas
Sunday, July 11, 2010
CJD or prion disease 2 CASES McLennan County Texas population 230,213 both
cases in their 40s
see the continuing rise of sporadic CJD in Texas here ;
*** Bovine Spongiform Encephalopathy BSE aka Mad Cow disease TEXAS, a
review of history
TSS REPORT ON 2ND TEJAS MAD COW
Mon, 22 Nov 2004 17:12:15 –0600
(the one that did NOT get away, thanks to the Honorable Phyllis Fong)
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to
unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food
chain?
and i see the TEXAS department of animal health is ramping up forsomething,
but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you
confirm???terry
==============================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 –0600
From: Carla Everett To: "Terry S. Singeltary Sr."
References: <[log in to unmask]>
The USDA has made a statement, and we are referring all callers to the USDA
web site. We have no information about the animal being in Texas.
Carla
At 09:44 AM 11/19/2004, you wrote:
>Greetings Carla,
>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow
is from
>TEXAS. can you comment on this either way please?
>>thank you,
>Terry S. Singeltary Sr.>>
===================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 –0600
From: Carla Everett
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
<[log in to unmask] us> <[log in to unmask]> <[log in to unmask]
us> <[log in to unmask]>
our computer department was working on a place holder we could post USDA's
announcement of any results. There are no results to be announced tonight by
NVSL, so we are back in a waiting mode and will post the USDA announcement when
we hear something.
At 06:05 PM 11/22/2004, you wrote:
>why was the announcement on your TAHC site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
>>>no confirmation on the U.S.' inconclusive test...
>>no confirmation on location of
animal.>>>>>>
==========================
THEN, 7+ MONTHS OF COVER-UP BY JOHANN ET AL! no doubt about it now
$$$
NO, it's not pretty, hell, im not pretty, but these are the facts, take em
or leave em, however, you cannot change them.
with kindest regards,
I am still sincerely disgusted and tired in sunny Bacliff, Texas USA
77518
Terry S. Singeltary Sr.
FULL 130 LASHINGS TO USDA BY OIG again
FDA STATEMENT FOR IMMEDIATE RELEASE
May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries:
888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30th, the Food and Drug Administration learned that a cow
with central nervous system symptoms had been killed and shipped to a processor
for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the animal
came from, and the processor that initially received the cow from the
slaughterhouse.
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That material is
being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as "mad
cow disease," can exhibit such symptoms. In this case, there is no way now to
test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit
the feeding of its rendered protein to other ruminant animals (e.g., cows,
goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing
the firm that FDA will not object to use of this material in swine feed only. If
it is not used in swine feed, this material will be destroyed. Pigs have been
shown not to be susceptible to BSE. If the firm agrees to use the material for
swine feed only, FDA will track the material all the way through the supply
chain from the processor to the farm to ensure that the feed is properly
monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the U.K.
showed that the disease spreads by feeding infected ruminant protein to
cattle.
Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action specifying
that the material go only into swine feed means also that it will not be fed to
poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely
with the U.S. Department of Agriculture on all BSE issues. The animal feed rule
provides crucial protection against the spread of BSE, but it is only one of
several such firewalls. FDA will soon be improving the animal feed rule, to make
this strong system even stronger.
#
ONE HUNDRED EIGHTH CONGRESS
COMMITTEE ON GOVERNMENT REFORM
May 13,2004
The Honorable Ann M. Veneman Secretary of Agriculture Department of
Agriculture1400 Independence Avenue, SW Washington, DC 20250
Dear Madam Secretary:
I am writing to express concern that the recent failure of the U.S.
Department of Agriculture (USDA) to test a Texas cow with neurological syrnptoms
for bovine spongifonnencephalopathy (BSE) may reflect wider problems in the
surveillance program. USDA apparently does not keep track of how many cows
condemned for central nervous system symptoms are tested for BSE nor does it
require that suspect carcasses be held pending testing...
FULL TEXT ;
News Release Texas Animal Health Commission Box l2966 * Austin, Texas 78711
* (800) 550-8242 * FAX (512) 719-0719 Bob Hillman, DVM * Executive Director For
info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710,
or ceverett@tahc.state.tx.us
For immediate release---
State-Federal Team Responds to Texas BSE Case
The US Department of Agriculture announced June 29 that genetic testing has
verified that an aged cow that tested positive for Bovine Spongiform
Encephalopathy or BSE originated from a Texas beef cattle herd. Tissues for
laboratory testing were initially collected from the animal in November 2004,
and the carcass was incinerated and did not enter the human food, animal feed or
fertilizer supply system. While tests in November indicated the animal did not
have BSE, retesting in England in June confirmed the animal had the disease. The
Texas Animal Health Commission (TAHC), the state’s livestock and poultry health
regulatory agency, and USDA have jointly assigned a state-federal team to
conduct the epidemiological investigation and response.
“The TAHC and US Department of Agriculture’s Veterinary Services are
working with a complement of experts from federal and state animal health, food
safety, public health and feed regulatory agencies to ensure the continued
safety and wholesomeness of our meat supply,” said Dr. Bob Hillman, Texas state
veterinarian and executive director of the TAHC, the state’s livestock and
poultry health regulatory agency. “Epidemiological investigations are thorough
and focus on verifying the herd of origin, and when, where and how the animal
and potentially, any herd mates, were exposed to the abnormal prion, or disease
agent, that causes BSE. Additionally, epidemiology investigations trace the
infected animal’s movement and herd mates. Animals potentially exposed to the
disease will be depopulated, with proper disposal. The animals will not be
introduced into the human or animal food chain.”
The USDA’s BSE testing protocol requires testing of emaciated or injured
cattle, cattle that exhibit central nervous system disorder, cattle unable to
rise or to walk normally, and cattle that die of unknown causes. Since June 1,
2004, brain tissue samples from more than 394,000 cattle have been tested in the
U.S. and were negative for BSE. Of those, 38,320 were tested in Texas, Dr.
Hillman noted. BSE surveillance has been conducted in the U.S. since l990.
The U.S. has taken preventive measures against the introduction of BSE
since l989, when prohibitions were placed on cattle and other ruminants from
BSE-affected countries, noted Dr. Hillman. In 1997, the importation ban was
extended to all of Europe.
Dr. Hillman said the U.S. Food and Drug Administration (FDA) in 1997 banned
the use of ruminant-derived protein (from animals such as cattle and sheep) in
feed for cattle and other ruminants. There is no evidence that BSE spreads from
live animal to animal in the herd, but cattle can be exposed by eating feed that
contains rendered protein from infected animals. “These measures taken by the
USDA and the FDA are safeguards that work to protect livestock, and ultimately,
our meat supply,” he said.
--30--
Report on Food & Drug Administration Dallas District Investigation of
Bovine Spongiform Encephalopathy Event in Texas 2005 - August 30, 2005 Executive
Summary:
On June 24, 2005, USDA informed FDA that a cow in Texas tested positive for
Bovine Spongiform Encephalopathy (BSE). Information provided by APHIS was that
the BSE positive cow was born and raised in a herd in Texas and was
approximately 12 years old. The animal was sampled for BSE at a pet food plant
in Texas on November 15, 2004, as part of USDA’s enhanced surveillance program.
The animal was disposed of by incineration and did not enter the human food or
animal feed chains. Although the positive animal posed no risk to the animal
feed supply, FDA, APHIS, the Texas Animal Health Commission (TAHC), and the
Texas Feed and Fertilizer Control Service (TFFCS) conducted a feed investigation
with two main objectives. The first objective was to identify all protein
sources in the animal’s feed history that could potentially have been the source
of the BSE agent. The second objective was to verify that cattle leaving the
herd after 1997 that were identified by USDA/APHIS as animals of concern (e.g.
progeny and feed cohorts), were rendered at facilities in compliance with the
regulation (21 CFR 589.2000) that prohibits most mammalian protein in feed for
ruminants that became effective August 4, 1997 (herein called BSE/Ruminant Feed
rule).
The feed history investigation identified 21 feed products that had been
used on the farm since 1990. These feed products were purchased from three
retail feed stores and had been manufactured at nine different feed mills. The
investigators visited these establishments to collect information on
formulations, shipping invoices, and use of ruminant meat and bone meal (MBM) on
the premises both pre-1997 feed ban and post-1997 feed ban. This investigation
found no feed products used on the farm since 1997 that had been formulated to
contain prohibited mammalian protein.
The investigation identified one feed which contained an animal protein
source that could not be identified. The investigation also found one feed mill
that supplied feed to the farm that had used ruminant MBM in feed formulations
for non-ruminant species after the BSE/Ruminant Feed rule went into effect,
which is permitted under the rule, and that several feed mills had used ruminant
MBM in feeds prior to the feed ban. Although the investigation did not identify
a specific feed source as the likely cause of this animal’s infection, it is
probable that the most likely route of exposure for this animal was consumption
of an animal feed containing mammalian protein prior to the implementation of
the BSE/Ruminant Feed rule in 1997.
The investigation into the disposition of herd mates from this farm
involved visits to nine slaughter plants and eight rendering plants. The
investigation found that all rendering plants were operating in compliance with
the BSE/ruminant feed ban regulation. A review of the inspection history of each
of these rendering firms found no violations.
Background of Investigation:
When notified on June 24, 2005, FDA Headquarters and Dallas District
management officials immediately began making contacts with their Federal, State
and Local counterparts to plan for and initiate follow-up investigational
activities to determine the feed history in this herd and to assure the safety
of the animal feed supply by evaluating current and historic compliance with the
BSE/ruminant feed ban rule.
APHIS established a joint Incident Command Post and FDA Dallas District
staffed this post full time with a Supervisory Investigator charged with
coordinating activities between FDA, APHIS, TAHC and TFFCS. Coordination
conference calls were set up with all Federal and State agencies involved in the
investigation to keep everyone apprised of investigational developments.
Animal Tracing Activities and Renderer Follow-up Inspections:
One of APHIS’ primary objectives was to identify and trace the animals of
interest (animals of interest would include any animals which could have been
potential birth cohorts or feed cohorts of the index animal, or potential
offspring of the index animal within the two years prior to the positive
diagnosis) from the index herd. This objective included the identification of
points of sale and ultimately the actual slaughter facilities for animals of
interest that left the farm. As the trace information was developed, APHIS
shared this information with FDA. Further information on animal of interest
identification and tracing can be found in the USDA Texas BSE Final Epidemiology
report.
APHIS identified nine slaughter establishments receiving these animals of
interest. Eight of the slaughter establishments were located in the State of
Texas and one was located in the State of Georgia. Dallas District Investigators
notified USDA/FSIS of our plans to visit each slaughter establishment to
identify rendering facilities receiving materials from these slaughter
establishments during the timeframe they received animals of interest. Dallas
District also issued an assignment to Atlanta District to visit and inspect the
one slaughter/renderer establishment located in the State of Georgia.
Eight renderers and one protein source broker were identified as receiving
materials from these slaughter establishments. Each rendering facility
identified was inspected for current compliance with the mammalian protein feed
ban rule. Each firm’s operations during the period of time of receipt of these
animals post 1997 were evaluated from a historical viewpoint and no evidence of
noncompliance was detected.
In all, FDA visited nine slaughter facilities, eight rendering facilities
and one broker of these materials. All facilities inspected were found to be in
compliance with the BSE/ruminant feed ban rule
Feed Investigation:
As information was learned about the index herd, FDA Investigators working
with TAHC officials conducted multiple interviews with the producer of the
animal regarding possible feeds, feed sources, animal husbandry practices, and
other events which may have changed normal feeding practices over the course of
the index animal’s life in the herd and any other information which may have
been helpful in identifying the possible sources of feed for this animal and
herd. FDA corroborated this information through interviews at the retail feed
supply stores where the producer purchased feeds.
Follow-up at these retail feed supply stores identified 21 possible feed
products the producer may have used during the history of the herd. Fifteen
purchased feed products were identified, along with hay, native grass, rice
straw, soybean meal, milk replacer/colostrum and bagged corn. These products
were identified as originating from nine different manufacturers. Each of these
manufacturers was inspected by FDA Dallas District and TFFCS
Investigators.
Feed manufacturers were located throughout the State of Texas. An
assignment was also issued to another FDA District to visit a Corporate
Headquarters facility in an effort to review archived feed formulations and
labels. During each of these inspections, the firm’s current compliance with the
BSE/ruminant feed ban rule was evaluated and attempts were made to determine the
protein sources used in feeds on the index farm. Many of the feeds investigated
were manufactured and used prior to the implementation of the BSE/ruminant feed
ban rule in 1997. Feed products of particular interest included any which may
have contained a protein source and the primary focus was on identifying any
possible mammalian protein source material in those feed products. We found that
ruminant feeds that had contained mammalian meat and bone meal (MBM) prior to
the BSE/ruminant feed ban rule had been discontinued or reformulated upon the
implementation of these rules. There is no regulatory requirement for a feed
mill to archive formulations for that length of time, so in those instances
where an actual formulation could not be obtained, experienced employees of the
firms were interviewed and their recollections recorded.
Of all the feeds in use by the producer since 1997, none were discovered to
have contained prohibited material (mammalian protein). Since the age of the
index animal was determined to be approximately 12 years, investigating and
reconstructing a feed history over such a long period of time is challenging.
This ranch is a beef cow-calf operation and minimal feed records were
maintained. Due to the nature of this investigation, it is difficult to
determine what feeds were in use at specific times and what the formulation of
those feeds were at the time they were fed. A feed history was developed through
interviews with the producer and other farm personnel since they did not
maintain any feed history documentation. Interviews with personnel at retail
establishments disclosed incomplete records and cash sales that did not always
identify the purchaser. Dallas District investigated any and all feed
ingredients that were identified as being fed or potentially fed over the course
of the last 15 years of this herd’s operation. Feeds discovered during this
investigation with potential mammalian protein sources are as below:
One feed, used prior to 1996, before the implementation of the feed ban,
was suspected to contain mammalian meat and bone meal, but this could not be
confirmed as no formulation records were available. The producer recalled using
a particular feed sporadically during the 1980’s and 1990’s, however, he could
not remember the name or manufacturer of the feed and had no records identifying
the product. It is not known whether this feed contained an animal protein
source. Attempts to identify this feed through interviews with retail sources
were unsuccessful. The producer identified one feed product that has been used
since the year 2000 which contains fish meal as a protein source. Further
investigation revealed that this product had contained mammalian meat and bone
meal prior to 1997, but that it had been reformulated at that time using fish
meal to replace the MBM. A tabular representation of the feed inspection
follow-up activities is presented below:
Feed Dates of Use Protein Source Current BSE Inspection BSE Compliance
History Feed #1 - Range Meal 1980’s - 2000 Unknown - Unable to determine actual
manufacturer, no records available from producer N/A N/A Feed #2 - High Protein
Starter Feed 2001 to present Feather meal BSE Compliant BSE Compliant Feed #3 -
High Protein Starter Feed ~1995 - 2001 Feather meal BSE Compliant BSE Compliant
Feed #4 - Cottonseed cake Prior to 1990 Cottonseed meal BSE Compliant BSE
Compliant Feed #5 - Cottonseed cake Early 1980’s - 1990’s Cottonseed meal BSE
Compliant BSE Compliant Feed #6 - Limiter 2001 to present Feather meal BSE
Compliant BSE Compliant Feed #7 - Creep pellets Prior to 1970 Likely feather
meal - no formulation could be obtained N/A N/A Feed #8 - Lick tub Since 2000
MBM prior to 1997 Fish Meal since 1997 BSE Compliant BSE Compliant Feed #9 -
Cottonseed meal Continuously Cottonseed meal BSE Compliant BSE Compliant Feed
#10 - Range Cubes Continuously since 1990 Feather meal BSE Compliant BSE
Compliant[1] Feed #11 - Sulfur Salt Block Continuously Minerals; calcium - all
non-animal derived BSE Compliant BSE Compliant Feed #12 - Lick tub Continuously
since 1995 Feather meal BSE Compliant BSE Compliant Feed #13 - Beef Supplement
Prior to 1996 Prior to 1997, suspect MBM - Not able to confirm, no formulation
available BSE Compliant Same manufacturer as Feed #10[1] Feed #14 - Mineralized
Salt Continuously since 1998 Minerals; calcium - all non-animal derived BSE
Compliant BSE Compliant Feed #15 - Soybean meal Since 2000, sparingly Soybean
meal N/A N/A Feed #16 - Corn Continuously Corn N/A N/A Feed #17 - Rice straw
1996, during dry year Rice straw N/A N/A Feed #18 - Hay Continuously Hay N/A N/A
Feed #19 - Milk Replacer Since 2000, Infrequent use Dehydrated colostrums, whey
N/A N/A Feed #20 - Grass Continuously Native grass N/A N/A Feed #21 - Soybean
meal Since 2000, sparingly Soybean meal N/A N/A
[1] Dallas District previously documented one incident of the accidental
addition of mammalian protein to a feed that was to be used for cattle at this
facility. This incident was isolated to the manufacture of one lot of a custom
cattle feed. A cross contamination error resulted in mammalian meat and bone
meal being accidentally included in a feed. The error was detected soon after
production. The firm acted swiftly in recalling the product and purchasing the
animals that had consumed the feed. No products entered the human food or
ruminant feed chain.
Dallas District Compliance History with BSE Feed Ban Rules:
Prior to 1997, feed manufacturers were not required to differentiate
between protein sources used in ruminant and non-ruminant feeds. For a period of
time following the implementation of the BSE/ruminant feed ban rule, some feed
manufacturers continued to use both prohibited material and non-prohibited
material within the same facility, employing separation and cleanout procedures
to minimize cross-contamination. Although the regulations allow this practice,
the potential for cross-contamination of ruminant feeds is greater. Most feed
mills have found this practice to be difficult and have abandoned this
practice.
Since the implementation of the BSE/ruminant feed ban rule in 1997, Dallas
District and its State partners have inspected every known or registered feed
manufacturer located in the states of Texas, Oklahoma and Arkansas. Further,
every rendering operation and feed manufacturer actually processing with
prohibited materials has been inspected annually. The compliance rate of the
industry has been excellent.
Results:
In total FDA, along with TFFCS, conducted 33 inspections, investigations
and interviews of the producer, retail feed establishments, feed manufacturers,
corporate headquarters, slaughter facilities, renderers and a protein source
broker. The FDA Dallas District follow-up to this incident resulted in the
coordination of efforts of multiple Federal and State agencies. This report is
the physical output of many hours of research, planning and coordination. All of
the inspections conducted confirmed the feed manufacturers and rendering
operations to be in compliance with the current BSE/ruminant feed ban
rule.
Dallas District conducts annual inspections of all feed mills and rendering
facilities who handle, use or produce PM for feed use. Inspections performed
since the initiation of the BSE/ruminant feed ban rules in 1997 have confirmed a
high degree of industry wide compliance with these important safeguards. The
district also routinely coordinates and shares information regarding feed
inspections with the TFFCS who are also responsible for the evaluating feed ban
compliance in the state of Texas.
Food and Drug Administration August 30, 2005 Minor edit September 8,
2005
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media : 301-827-6242
Consumer Inquiries: 888-INFO-FDA Note: On Dec. 23, 2003, the U.S. Department of
Agriculture reported that a cow in Washington state had tested positive for
bovine spongiform encephalopathy (BSE, or mad cow disease). As a result,
information on this Web page stating that no BSE cases had been found in the
United States is now incorrect. However, because other information on this page
continues to have value, the page will remain available for viewing.
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken
on feed used at a Texas feedlot that was suspected of containing meat and bone
meal from other domestic cattle -- a violation of FDA's 1997 prohibition on
using ruminant material in feed for other ruminants. Results indicate that a
very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams - approximately a quarter ounce -- of prohibited
material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin
(therefore not likely to contain infected material because there is no evidence
of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy
Commissioner, "The challenge to regulators and industry is to keep this disease
out of the United States. One important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined with
other steps, like U.S. Department of Agriculture's (USDA) ban on the importation
of live ruminant animals from affected countries, these steps represent a series
of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing
that it is voluntarily purchasing all 1,222 of the animals held in Texas and
mistakenly fed the animal feed containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA believes any
cattle that did not consume feed containing the prohibited material are
unaffected by this incident, and should be handled in the beef supply clearance
process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting
the human error that resulted in the misformulation of the animal feed
supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food supply and that continued vigilance
needs to be taken, by all concerned, to ensure these rules are followed
routinely.
FDA will continue working with USDA as well as State and local officials to
ensure that companies and individuals comply with all laws and regulations
designed to protect the U.S. food supply.
Office of Public Affairs 2001-JAN-30
''FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams - approximately a quarter ounce -- of prohibited
material. These animals weigh approximately 600 pounds.'' ???
January 29, 2001 Email: sma@tca.net Volume 5, Issue 6 Home Page Address:
http://www.southwestmeat.org Edited by
Phyllis Zimmerman S O U T H W E S T M E A T A S S O C I A T I O N 4103 SOUTH
TEXAS AVENUE, SUITE 101 BRYAN, TX 77802 (979) 846-9011 FAX (979) 846-8198
Texas Cattle Quarantined in Feed Ban Violation
More than 1,200 head of Texas cattle were under quarantine last Friday
after possibly consuming feed containing meat and bone meal. Purina Mills, Inc.,
the largest livestock feed producer in the United States, confirmed it prepared
a feed supplement containing ruminant byproducts at a Gonzales, Texas plant last
week, and then shipped the feed to the feedlot in error. The company said the
mix up involved 22 tons of feed mixed the evening of January 16. The mill
immediately notified the Food and Drug Administration (FDA) and the feedlot of
the mix up, and set in motion the precautionary measures being taken. Samples of
the feed are being tested by the FDA and cattle that may have ingested the feed
are being held pending further testing. However, the news sent feeder cattle
futures falling in Friday morning trading on the Chicago Mercantile Exchange.
The FDA has forbidden U.S. feed manufacturers from mixing animal products into
ruminant feed as a preemptive measure to safeguard against the spread of bovine
spongiform encephalopathy (BSE) or mad cow disease. Although no cases of BSE
have ever been reported in the U.S., every precaution is being taken to protect
the food chain. Dr. Murray Lumpkin, senior medical adviser at the FDA, said, “We
do know that the feed was American in origin, so there is no evidence at this
point in time that the feed that the cows might have gotten might have been
infected with BSE. Chances of that are very, very small. The bottom line is if
we feel there was any exposure to a human safety issue, we will not allow them
into the food chain.” Animal byproducts are added to feed as a protein
supplement, and are considered safe for use in swine and poultry feed. Burt
Rutherford, a spokesman for the Texas Cattle Feeders Association, praised the
mill for their quick notification of the FDA and the feedlot. The company said
the error was discovered through its “quality assurance program” of internal
controls. A Purina Mills spokesman said the company has begun phasing out the
use of meat and bone meal from cows in any of its livestock feed. “It’s a
voluntary move on our behalf and takes us down to a zero risk factor for a
misformulation in the future,” said Max Fisher. Tests on the feed samples should
be complete early this week.
Audit Report
Animal and Plant Health Inspection Service
Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II and
Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat
Recovery Products - Phase III
snip...
We attribute the failure to identify the BSE positive sample to rigid
protocols, as well as the lack of adequate quality assurance controls over its
testing program. Details of our concerns are discussed in Findings 3 and
4.
snip...
Section 2. Testing Protocols and Quality Assurance Controls
In November 2004, USDA announced that its rapid screening test, Bio-Rad
Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test
result as part of its enhanced BSE surveillance program. The ELISA rapid
screening test performed at a BSE contract laboratory produced three high
positive reactive results.40 As required,41 the contract laboratory forwarded
the inconclusive sample to the APHIS National Veterinary Services Laboratories
(NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again
produced three high positive reactive results.42 In accordance with its
established protocol, NVSL ran its confirmatory test, an immunohistochemistry
(IHC) test, which was interpreted as negative for BSE. In addition, NVSL
performed a histological43 examination of the tissue and did not detect
lesions44 consistent with BSE.
Faced with conflicting results, NVSL scientists recommended additional
testing to resolve the discrepancy but APHIS headquarters officials concluded no
further testing was necessary because testing protocols were followed. In our
discussions with APHIS officials, they justified their decision not to do
additional testing because the IHC is internationally recognized as the “gold
standard.” Also, they believed that conducting additional tests would undermine
confidence in USDA’s established testing protocols. However, OIG obtained
evidence that indicated additional testing was prudent to ensure that USDA’s
testing protocols were effective in detecting BSE and that confidence in USDA’s
testing procedures was maintained. OIG came to this conclusion because the rapid
tests produced six high positive reactive results, confirmatory testing
conflicted with the rapid test results, and various standard operating
procedures were not followed. Also, our review of scientific literature, other
country protocols, as well as discussions with internationally recognized
experts led us to conclude that confirmatory testing should not be limited when
conflicting test results are obtained. To maintain objectivity and independence
in our assessment, we requested the USDA Agricultural Research Service (ARS)
perform the Office International des Epizooties (OIE) Scrapie-Associated Fibrils
(SAF)
40 ELISA test procedures require two additional (duplicate) tests if the
initial test is reactive, before final interpretation. If either of the
duplicate tests is reactive, the test is deemed inconclusive. 41 Protocol for
BSE Contract Laboratories to Receive and Test Bovine Brain Samples and Report
Results for BSE Surveillance Standard Operating Procedure (SOP), dated October
26, 2004. 42 The NVSL conducted an ELISA test on the original material tested at
the contract laboratory and on two new cuts from the sample tissue. 43 A visual
examination of brain tissue by a microscope. 44 A localized pathological change
in a bodily organ or tissue.
USDA/OIG-A/50601-10-KC Page 31
immunoblot.45 ARS performed the test at the National Animal Disease Center
because NVSL did not have the necessary equipment46 (ultracentrifuge) to do the
test. APHIS scientists observed and participated, as appropriate, in this
effort.
The additional tests conducted by ARS produced positive results. To confirm
this finding, the Secretary requested the internationally recognized BSE
reference laboratory in Weybridge, England, (Weybridge) to perform additional
confirmatory testing. Weybridge conducted various tests, including their own IHC
methods, as well as three Western blot methods. The tests confirmed that the
suspect cow was infected with BSE. Also, Weybridge confirmed this case as an
unequivocal positive case of BSE on the basis of IHC. As a result of this
finding, the Secretary immediately directed USDA scientists to work with
international experts to develop a new protocol that includes performing dual
confirmatory tests in the event of another inconclusive BSE screening
test.
snip...
Release No. 0336.05 Contact: USDA Jim Rogers 202-690-4755 FDA Rae Jones
301-827- 6242
Printable version Email this page
U.S. Department of Agriculture (USDA) Food and Drug Administration
(FDA)
Investigation Results of Texas Cow That Tested Positive for Bovine
Spongiform Encephalopathy (BSE) Aug. 30, 2005
The U.S. Department of Agriculture's Animal and Plant Health Inspection
Service (APHIS) and the U.S. Department of Health and Human Services' Food and
Drug Administration (FDA) have completed their investigations regarding a cow
that tested positive for bovine spongiform encephalopathy (BSE) in June 2005.
The agencies conducted these investigations in collaboration with the Texas
Animal Health Commission and the Texas Feed and Fertilizer Control
Service.
Our results indicate that the positive animal, called the index animal, was
born and raised on a ranch (termed the "index farm") in Texas. It was a cream
colored Brahma cross approximately 12 years old at the time of its death. It was
born prior to the implementation of the 1997 feed ban instituted by FDA to help
minimize the risk that a cow might consume feed contaminated with the agent
thought to cause BSE. The animal was sold through a livestock sale in November
of 2004 and transported to a packing plant. The animal was dead upon arrival at
the packing plant and was then shipped to a pet food plant where it was sampled
for BSE. The plant did not use the animal in its product, and the carcass was
destroyed in November 2004.
APHIS attempted to trace all adult animals that left the index farm after
1990, as well as all progeny born within 2 years of the index animal's death.
Together, these animals are called animals of interest.
During the course of the investigation, USDA removed and tested a total of
67 animals of interest from the farm where the index animal's herd originated.
All of these animals tested negative for BSE. 200 adult animals of interest were
determined to have left the index farm. Of these 200, APHIS officials determined
that 143 had gone to slaughter, two were found alive (one was determined not to
be of interest because of its age and the other tested negative), 34 are
presumed dead, one is known dead and 20 have been classified as untraceable. In
addition to the adult animals, APHIS was looking for two calves born to the
index animal. Due to record keeping and identification issues, APHIS had to
trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter
channels, four are presumed to have entered feeding and slaughter channels and
one calf was untraceable.
To determine whether contaminated feed could have played a role in the
index animal's infection, FDA and the Texas Feed and Fertilizer Control Service
conducted a feed investigation with two main objectives: 1) to identify all
protein sources in the animal=s feed history that could potentially have been
the source of the BSE agent, and 2) to verify that cattle leaving the herd after
1997 were identified by USDA as animals of interest and were rendered in
compliance with the 1997 BSE/ruminant feed rule.
The feed history investigation identified 21 feeds or feed supplements that
were used on the farm since 1990. These feed ingredients were purchased from
three retail feed stores and were manufactured at nine feed mills. This
investigation found that no feed or feed supplements used on the farm since 1997
were formulated to contain prohibited mammalian protein. Due to this finding,
FDA has concluded that the animal was most likely infected prior to the 1997
BSE/ruminant feed rule.
The investigation into the disposition of herd mates from this farm
involved visits to nine slaughter plants and eight rendering plants. The
investigation found that all of the rendering plants were operating in
compliance with the BSE/ruminant feed rule. A review of the inspection history
of each of these rendering firms found no violations of the FDA feed ban
rule.
APHIS and FDA are very pleased with the results of their investigations,
which show the animals of interest did not present a threat to livestock and
that the ruminant feed rule is being followed. The U.S. maintains an
interlocking system of safeguards designed to prevent BSE from entering the
human and animal food chain. USDA also remains vigilant in its attempt to find
BSE in the United States. To date, there have been more than 450,000 animals
tested in the last 14 months and only two BSE positive animals found in this
country.
For more information on FDA's feed investigation, please visit the FDA's
website at
Last Modified: 08/31/2005
U.S. Completes Investigation of BSE-Infected Cow in Texas FDA Veterinarian
Newsletter July/August 2005 Volume XX, No IV
After investigating the report of a cow in Texas found in June to be
infected with bovine spongiform encephalopathy (BSE), Federal officials reported
that appropriate safeguards were in place and working, which prevented the
further spread of the disease.
The infected animal was destroyed and did not get into the food, feed, or
pet food supply, officials said. This was the first native born cow in the
United States found to be infected with BSE.
The U.S. Department of Agriculture (USDA), which is in charge of tracking
and preventing animal disease, reported the infected animal to the Food and Drug
Administration (FDA) on June 24, 2005. To determine if any other animals or
offspring of animals from the herd of the infected animal were infected with
BSE, USDA tracked down as many as it could of the 200 adult and 213 calves
associated with the infected animals. No additional BSE was found.
Meanwhile, FDA officials, along with the Texas Animal Health Commission and
the Texas Feed and Fertilizer Control Service, investigated the sources of feed
given the infected animal to see if they could discover the source of the
infectious material. In addition, the Federal and State authorities tracked the
disposition of all animals associated with the infected cow to be sure the
provisions of FDA’s 1997 BSE rule were followed.
The investigation concluded that the 1997 feed rule, which prohibits the
feeding of most mammalian protein to cattle and other ruminants, was being
followed. At an August 30 press teleconference, Dr. Stephen Sundlof, director of
FDA’s Center for Veterinary Medicine, said that the investigation revealed that
all companies involved were complying with the 1997 BSE feed rule.
FDA’s investigation identified 21 feed products used on the farm. FDA and
State investigators went to three retail feed stores that had supplied the feed,
and to nine feed mills that made the feed. According to Dr. Sundlof, “This
investigation found no feed products used on the farm since 1997 had been
formulated to contain prohibited mammalian protein.”
According to Dr. Sundlof, the infected cow, which was approximately 12
years old, had “very likely consumed contaminated feed well before 1997….”
The animals associated with the infected cow were properly handled during
slaughter and disposition under the feed rule, Dr. Sundlof said: “The
investigation into the disposition of herd-mates from this farm involved visits
to nine slaughter plants and eight rendering plants. The investigation found
that all rendering plants were operating in compliance with the BSE ruminant
feed rule. A review of the inspection history of each of these rendering firms
found no violation.”
On October 6, FDA announced proposed rules to further reduce the risk of
BSE in the United States. The proposal would ban certain high risk cattle
material from use in all feeds and pet foods. (See related story on page 1, “FDA
Proposes Tighter Feed Ban to Prevent BSE.”)
Office of Inspector General Semiannual Report to Congress FY 2007 – 2nd
Half
Two Texas Companies Sentenced and Fined for Misbranding Meat Products In
April 2007, two closely held and related Texas companies pled guilty in Federal
court and were sentenced to 12 months of probation and ordered to pay $10,250 in
fines for misbranding meat products. One of the companies sold adulterated meat
products to a retail store in New Mexico. Additionally, portions of the invoices
failed to properly and consistently identify the meat products as being from
cattle more than 30 months old at time of slaughter. This information is
required to be disclosed because of bovine spongiform encephalopathy (BSE, or
“mad cow disease”) concerns. No adulterated meat reached consumers.
Scientific Report of the European Food Safety Authority on the Assessment
of the Geographical BSE-Risk (GBR) of United States of America (USA)
Question N° EFSA-Q-2003-083
Adopted July 2004
Summary of 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 90’s 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.
Key words: BSE, geographical risk assessment, GBR, USA, third
countries
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the
Geographical BSE Risk of USA - 1 - European Food Safety Authority Scientific
Expert Working Group on GBR Working Group Report on the Assessment of the
Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the
Geographical BSE Risk of USA - 7 - 2.3
Overall assessment of the external challenge
The level of the external challenge that has to be met by the BSE/cattle
system is estimated according to the guidance given by the SSC in its final
opinion on the GBR of July 2000 (as updated in January 2002). Live cattle
imports: In total the country imported 2038 (other sources) or 1128 (CD) live
cattle from BSE risk countries other than Canada, of which 327 (other sources)
or 323 (CD) came from the UK. From Canada the imports were >500,000 animals
per year. The numbers shown in table 1 are the raw import figures and are not
reflecting the adjusted imports for the assessment of the external challenge.
Broken down to 5 year periods the resulting external challenge is as given in
table 3. This assessment takes into account the different aspects discussed
above that allow to assume that certain imported cattle did not enter the
domestic BSE-cattle system, i.e. were not rendered into feed. In the case of the
USA, all the animals for which tracing information showed that they were not
rendered were excluded from the external challenge.
MBM imports:
In total the country imported 689 tons MBM (CD) or 2,230 tons MBM (other
sources) from BSE risk countries other than Canada, of which 5 tons (CD) or 101
tons (other sources) were exported from the UK (UK export data). From Canada,
the imports were about 30 000 tons per year. The numbers shown in table 2 are
the raw import figures and are not reflecting the adjusted imports for the
assessment of the external challenge. Broken down to 5 year periods the
resulting external challenge is as given in table 3. This assessment takes into
account the different aspects discussed above that allow to assume that certain
imported MBM did not enter the domestic BSE/cattle system or did not represent
an external challenge for other reasons. As it was illegal to export mammalian
MBM from UK since 27/03/1996, exports indicated after that date should only have
included non-mammalian MBM. In the case of the USA imported MBM from UK in 1989
and between 1997 and 1999 was not taken into account.
Feeding Use of MBM in cattle feed
• Until 1997 ruminant MBM (RMBM) could legally be included in cattle feed
and was indeed commonly fed to cattle of different age and type. Prior to the
feed ban the US authorities estimated that 10% of all MBM would deliberately
have been fed to cattle. Feed bans
• A ban to feed (several types of) MMBM to ruminants was put in place in
August 1997. Derogation from the ban was granted for pure porcine and equine
protein (MBM) coming from designated (single species) rendering plants. This
MMBM might still be fed to cattle. Therefore this feed ban is a ruminant to
ruminant ban.
• It is planned to prohibit the use of all mammalian and poultry protein in
ruminant feed and prohibiting materials from non-ambulatory disabled cattle and
dead stock from use in all animal feed.
Conclusion on the ability to avoid recycling
• Before 1997, US system would not have been able to avoid recycling of the
BSEagent to any measurable extent. If the BSE-agent was introduced into the feed
chain, it could have reached cattle.
• After the introduction of the 1997 ban in August 1997, the ability to
avoid recycling of BSE-infectivity was somewhat improved. However, the rendering
of ruminant material (including SRM and fallen stock) is inadequate (non
pressurized), and cross-contamination potentials of cattle feed with other feeds
remain.
• Therefore, the system is still unable to avoid recycling of
BSE-infectivity if already present in the system or incoming.
Feeding
Until August 1997, RMBM was legally fed to cattle. Feeding was therefore
"not OK". In August 1997 an RMBM-ban was introduced but feeding of non-ruminant
MBM to cattle remained legal as well as feeding of RMBM to non-ruminant animals
(farm animals and pets). An RMBM ban is difficult to maintain, as only labels
can distinguish the various MMBMs. This makes control of the feed ban very
difficult because analytical differentiation between ruminant and non-ruminant
MBM is difficult if not impossible.
Due to the highly specialised production system in the USA, various
mammalian MBM streams can be separated. Such a feed ban would therefore be
assessed as "reasonably OK", for all regions where this highly specialised
system exists. However, several areas in the USA do have mixed farming and mixed
feed mills, and in such regions an RMBM ban would not suffice. Additionally,
official controls for cattle feeds to control for compliance with the ban
started in 2002. Thus, for the whole country, the assessment of the feeding
after 1997 remains "not OK", but improving.
Rendering
The rendering industry is operating with processes that are not known to
reduce
infectivity. It is therefore concluded that rendering was and is "not
OK".
SRM-removal
SRM were and are still rendered for feed, as are (parts of) the fallen
stock. SRMremoval
is therefore regarded as "not OK".
BSE-surveillance
Before 1989, the ability of the system to identify (and eliminate)
BSE-cases was
limited. Since 1990 this ability is improved, thanks to a specific
(passive) BSE
surveillance. The initiated introduction of active surveillance in risk
populations
should improve the system significantly.
On the basis of the available information, it has to be concluded that the
country's
BSE/cattle system was extremely unstable until today, i.e., it would have
recycled and
amplified BSE-infectivity very fast, should it have entered the system. The
stability of
the BSE/cattle system in the USA overtime is as given in table 4.
The present assessment modifies the stability assessment of the previous
GBR report
in 2000 mainly due to a different perception of the impact of BSE
surveillance on
stability and of the efficiency of the RMBM feed ban.
Interaction of stability and external challenge in the USA
Period Stability External Challenge Internal challenge
1980 to
1985
1986 to
1990
Moderate Possibly present
1991 to 1995
Very high
1996 to
2000
2001 to
2003
Extremely unstable Extremely high Likely to be present and growing
5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK
5.1 The current GBR as function of the past stability and challenge
• The current geographical BSE risk (GBR) level is III, i.e. it is likely
but not
confirmed that domestic cattle are (clinically or pre-clinically) infected
with the
BSE-agent.
Note1: It is also worth noting that the current GBR conclusions are not
dependent on
the large exchange of imports between USA and Canada. External challenge
due to
exports to the USA from European countries varied from moderate to high.
These
challenges indicate that it was likely that BSE infectivity was introduced
into the
North American continent.
snip...please see full text ;
EFSA publishes Geographical BSE-Risk (GBR) assessments for Australia,
Canada, Mexico, Norway, South Africa, Sweden and the United States of
America
Communiqué de presse 20 août 2004
The European Food Safety Authority (EFSA) has issued today seven up-to-date
scientific reports on the Geographical Bovine Spongiform Encephalopathy (BSE)
Risk (GBR) assessments for Australia, Canada, Mexico, Norway, South Africa
Sweden and the United States of America. While Australia’s GBR level I (i.e.
presence of BSE in domestic cattle is highly unlikely) is maintained, that of
Norway has been raised to level II (presence of BSE unlikely but not excluded),
Sweden remains at GBR level II and those of Canada and the United States have
been raised to level III (presence of BSE likely but not confirmed, or confirmed
at a lower level) following a new assessment taking into account the most recent
evidence. EFSA’s Scientific Expert Working Group on geographic BSE risk
assessment also evaluated the status of Mexico and South Africa which were
classified as level III.
UK EXPORTS OF LIVE CATTLE BY VALUE 1986-96
U.K. EXPORTS OF MEAL OF MEAT AND MEAT OFFAL; GREAVES ;
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.???
From: S.J.Pearsall@esg.maff.gsi.gov.uk
Date: Tue, 8 Feb 2000 14:03:16 +0000
To: flounder@wt.net (Receipt Notification Requested) (Non Receipt
Notification Requested)
Terry Meat and bonemeal is not specifically classified for overseas trade
purposes. The nearest equivalent is listed as flours and meals of meat or offals
(including tankage), unfit for human consumption; greaves.
UK exports of this to the US are listed below:
Country Tonnes
1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990
Data for exports between 1975 and 1979 are not readily available. These can
be obtained (at a charge) from data retailers appointed by HM Customs and
Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222).
Best wishes Simon Pearsall
Overseas trade statistics Stats (C&F)C
====================================== END...TSS
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and
BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals
may have been contaminated with prohibited material Recall # V-258-2009
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited
materials Bulk Whole Barley, Recall # V-256-2009
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS:
VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash
Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and
01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by
conversation on February 5, 2007. Firm initiated recall is ongoing.
REASON Blood meal used to make cattle feed was recalled because it was
cross- contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION WI
___________________________________
PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL
Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal,
TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY
Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST
POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY
Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC
MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR,
V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML
W/SMARTA, Recall # V-025-2007 CODE The firm does not utilize a code - only
shipping documentation with commodity and weights identified. RECALLING
FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete.
REASON Products manufactured from bulk feed containing blood meal that was
cross contaminated with prohibited meat and bone meal and the labeling did not
bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
NEW URL
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH
ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS
ANYMORE $$$
Tuesday, November 04, 2014
The pathological and molecular but not clinical phenotypes are maintained
after second passage of experimental atypical bovine spongiform encephalopathy
in cattle
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Thursday, October 02, 2014
[Docket No. APHIS-2013-0064] Concurrence With OIE Risk Designations for
Bovine Spongiform Encephalopathy
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
BANNED SUSPECT MAD COW FEED IN COMMERCE 2006-2007, SOME 10 YEARS AFTER THE
INFAMOUS PARTIAL AND VOLUNTARY MAD COW FEED BAN or August 4, 1997, that was
nothing more than ink on paper, so really, there was no BSE triple fire wall at
all, and this was improving ???
*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
THIS is just ONE month report, of TWO recalls of prohibited banned MBM,
which is illegal, mixed with 85% blood meal, which is still legal, but yet we
know the TSE/BSE agent will transmit blood. we have this l-BSE in North America
that is much more virulent and there is much concern with blood issue and l-BSE
as there is with nvCJD in humans. some are even starting to be concerned with
sporadic CJD and blood, and there are studies showing transmission there as
well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD
COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that
reaches commerce is ever returned via recall, very, very little. this was 2007,
TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN
THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow
feed that was in ALABAMA in one of the links too, this is where the infamous
g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the
USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5,
2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
see Alabama banned suspect mad cow feed in commerce ;
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R
Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter
dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based
protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc.,
Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.
REASON Possible contamination of dairy animal feeds with ruminant derived meat
and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb.
bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags,
Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall #
V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50
lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall #
V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall #
V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall #
V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING
FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by
telephone and visit on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall
is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with
ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall #
V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50
lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%,
Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to
20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall #
V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall #
108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall #
V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL,
by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is
complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant
based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE
Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),
Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED,
Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL,
by telephone on June 15, 2006 and by press release on June 16, 2006. Firm
initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the
EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a
non-profit Swiss Foundation
Tuesday, November 04, 2014
The pathological and molecular but not clinical phenotypes are maintained
after second passage of experimental atypical bovine spongiform encephalopathy
in cattle
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Singeltary Response to USDA, and USDA RESPONSE TO SINGELTARY ON HARVARD BSE
RISK ASSESSMENT
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE) Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
Sunday, December 15, 2013
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE ***
SUMMARY REPORT CALIFORNIA ATYPICAL L-TYPE BOVINE SPONGIFORM ENCEPHALOPATHY
CASE INVESTIGATION JULY 2012 CALIFORNIA
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
LET'S take a closer look at this new prionpathy or prionopathy, and then
let's look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the
genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_
mad cow in the world to date like this, ......wait, it get's better. this new
prionpathy is killing young and old humans, with LONG DURATION from onset of
symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and
the plaques are very similar in some cases too, bbbut, it's not related to the
g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that
they claim is a genetic TSE, has no relation to any gene mutation in that
family. daaa, ya think it could be related to that mad cow with the same genetic
make-up ??? there were literally tons and tons of banned mad cow protein in
Alabama in commerce, and none of it transmitted to cows, and the cows to humans
there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we
identified a novel mutation in the bovine prion protein gene (Prnp), called
E211K, of a confirmed BSE positive cow from Alabama, United States of America.
This mutation is identical to the E200K pathogenic mutation found in humans with
a genetic form of CJD. This finding represents the first report of a confirmed
case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We
hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in
"the approximately 10-year-old cow" carrying the E221K mutation.
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)
her healthy calf also carried the mutation
(J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic
in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the
UK epidemic had most likely originated from such a mutation and argued against
the scrapierelated assumption. Such rare potential pathogenic PRNP mutations
could occur in countries at present considered to be free of BSE, such as
Australia and New Zealand. So it is important to maintain strict surveillance
for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many
countries still feed ruminant proteins to pigs). Removal of specified risk
material, such as brain and spinal cord, from cattle at slaughter prevents
infected material from entering the human food chain. Routine genetic screening
of cattle for PRNP mutations, which is now available, could provide additional
data on the risk to the public. Because the point mutation identified in the
Alabama animals is identical to that responsible for the commonest type of
familial (genetic) CJD in humans, it is possible that the resulting infective
prion protein might cross the bovine-human species barrier more easily. Patients
with vCJD continue to be identified. The fact that this is happening less often
should not lead to relaxation of the controls necessary to prevent future
outbreaks.
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary
Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen
A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier
Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
Thursday, July 24, 2014
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05
Study of Atypical Bse
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Wednesday, August 27, 2014
Highly sensitive detection of small ruminant BSE within TSE mixes by serial
Protein Misfolding Cyclic Amplification
Thursday, December 05, 2013
National Scrapie Eradication Program October 2013 Monthly Report Fiscal
Year 2014 TSE PRION REPORT
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
CHRONIC WASTING DISEASE CWD
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting
Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time.
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans
Pecos
Thursday, October 03, 2013
*** TAHC ADOPTS CWD RULE THAT the amendments __REMOVE__ the requirement for
a specific fence height for captives ***
Texas Animal Health Commission (TAHC)
October 3, 2013
Sunday, August 24, 2014
USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program
Goals TSE PRION October 17 – 23, 2013
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION
CONGRESS SEPTEMBER 8-11 2010
Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation 2012
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
Thursday, November 21, 2013
*** Assessing the susceptibility of transgenic mice over-expressing deer
prion protein to bovine spongiform encephalopathy
The present study was designed to assess the susceptibility of the
prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy
(BSE) prions, which have the ability to overcome species barriers.
Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a
90-100% attack rates, BSE from cattle failed to transmit, indicating agent
adaptation in the deer.
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
NOW, what is the latest on human risk factors to CWD strains ???
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
***However, they also show that there is no absolute barrier to conversion of
human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
there is in fact evidence that the potential for cwd transmission to humans
can NOT be ruled out.
I thought your readers and hunters and those that consume the venison,
should have all the scientific facts, personally, I don’t care what you eat, but
if it effects me and my family down the road, it should then concern everyone,
and the potential of iatrogenic transmission of the TSE prion is real i.e.
‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there
from...like deer antler velvet and TSE prions and nutritional supplements there
from, all a potential risk factor that should not be ignored or silenced. ...
the prion gods at the cdc state that there is ;
''no strong evidence''
but let's see exactly what the authors of this cwd to human at the cdc
state ;
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD
transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article
and call me if you have questions or need more clarification (phone:
404-639-3091). Also, we do not claim that "no-one has ever been infected with
prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip...
full text ;
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
*** We hypothesize that both BSE prions and CWD prions passaged through
felines will seed human recPrP more efficiently than BSE or CWD from the
original hosts, evidence that the new host will dampen the species barrier
between humans and BSE or CWD. The new host effect is particularly relevant as
we investigate potential means of trans-species transmission of prion disease.
Monday, August 8, 2011
*** Susceptibility of Domestic Cats to CWD Infection ***
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program
Standards
>>>The CWD herd certification program is a voluntary, cooperative
program that establishes minimum requirements for the interstate movement of
farmed or captive cervids, provisions for participating States to administer
Approved State CWD Herd Certification Programs, and provisions for participating
herds to become certified as having a low risk of being infected with
CWD<<<
Greetings USDA/APHIS et al,
I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting
Disease Herd Certification Program and Interstate Movement of Farmed or Captive
Deer, Elk, and Moose; Program Standards.
I believe, and in my opinion, and this has been proven by scientific facts,
that without a validated and certified test for chronic wasting disease cwd,
that is 100% sensitive, and in use, any voluntary effort will be futile. the
voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow
surveillance program has failed terribly, as well as the testing for bse tse
prion in cattle, this too has failed terrible. all this has been proven time and
time again via OIG reports and GOA reports.
I believe that until this happens, 100% cwd testing with validated test,
ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO
INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.
In my opinion, and the opinions of many scientists and DNR officials, that
these so called game farms are the cause of the spreading of chronic wasting
disease cwd through much negligence. the game farms in my opinion are not the
only cause, but a big factor. I kindly wish to submit the following to show what
these factors are, and why interstate movement of cervids must be banned.
...
snip...see full text and PDF ATTACHMENT HERE ;
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper
(Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE PRION
disease in cervids
***SINGELTARY SUBMISSION
The Scottish Parliament’s Rural Affairs, Climate Change and Environment
Committee has been looking into deer management, as you can see from the
following press release,
***and your email has been forwarded to the committee for information:
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
Sunday, July 21, 2013
Welsh Government and Food Standards Agency Wales Joint Public Consultation
on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations
2013
*** Singeltary Submission WG18417
Sunday, November 10, 2013
*** LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER
ANTLER VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated
venison in an Upstate New York community: risk behaviours and health outcomes
2005–2011
*** our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions. ***
snip...see full text ;
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
Thursday, January 2, 2014
CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob
Disease MM1 genotype, and iatrogenic CJD ???
Sunday, November 17, 2013
L-BSE in Genetically Susceptible and Resistant Sheep: Changes in Prion
Strain or Phenotypic Plasticity of the Disease-Associated Prion Protein?
2002ish DeepThroat
The most frightening thing I have read all day is the report of Gambetti's
finding of a new strain of sporadic cjd in young people.........Dear God, what
in the name of all that is holy is that!!! If the US has different strains of
scrapie.....why???? than the UK...then would the same mechanisms that make
different strains of scrapie here make different strains of BSE...if the
patterns are different in sheep and mice for scrapie.....could not the BSE be
different in the cattle, in the mink, in the humans.......I really think the
slides or tissues and everything from these young people with the new strain of
sporadic cjd should be put up to be analyzed by many, many experts in
cjd........bse.....scrapie Scrape the damn slide and put it into
mice.....wait.....chop up the mouse brain and and spinal cord........put into
some more mice.....dammit amplify the thing and start the damned
research.....This is NOT rocket science...we need to use what we know and get
off our butts and move....the whining about how long everything takes.....well
it takes a whole lot longer if you whine for a year and then start the
research!!! Not sure where I read this but it was a recent press release or
something like that: I thought I would fall out of my chair when I read about
how there was no worry about infectivity from a histopath slide or tissues
because they are preserved in formic acid, or formalin or formaldehyde.....for
God's sake........ Ask any pathologist in the UK what the brain tissues in the
formalin looks like after a year.......it is a big fat sponge...the agent
continues to eat the brain ......you can't make slides anymore because the agent
has never stopped........and the old slides that are stained with Hemolysin and
Eosin......they get holier and holier and degenerate and continue...what you
looked at 6 months ago is not there........Gambetti better be photographing
every damned thing he is looking at.....
Okay, you need to know. You don't need to pass it on as nothing will come
of it and there is not a damned thing anyone can do about it. Don't even hint at
it as it will be denied and laughed at.......... USDA is gonna do as little as
possible until there is actually a human case in the USA of the nvcjd........if
you want to move this thing along and shake the earth....then we gotta get the
victims families to make sure whoever is doing the autopsy is credible,
trustworthy, and a saint with the courage of Joan of Arc........I am not
kidding!!!! so, unless we get a human death from EXACTLY the same form with
EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any
action........it is ALL gonna be sporadic!!!
And, if there is a case.......there is gonna be every effort to link it to
international travel, international food, etc. etc. etc. etc. etc. They will go
so far as to find out if a sex partner had ever traveled to the UK/europe, etc.
etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth.
They have all the cards, all the money, and are willing to threaten and carry
out those threats....and this may be their biggest downfall...
Thanks as always for your help.
(Recently had a very startling revelation from a rather senior person in
government here..........knocked me out of my chair........you must keep
pushing. If I was a power person....I would be demanding that there be a least a
million bovine tested as soon as possible and agressively seeking this disease.
The big players are coming out of the woodwork as there is money to be made!!!
In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the
burden to bare if there is any coverup!"
again it was said years ago and it should be taken seriously....BSE will
NEVER be found in the US! As for the BSE conference call...I think you did a
great service to freedom of information and making some people feign
integrity...I find it scary to see that most of the "experts" are employed by
the federal government or are supported on the "teat" of federal funds. A scary
picture! I hope there is a confidential panel organized by the new government to
really investigate this thing.
You need to watch your back........but keep picking at them.......like a
buzzard to the bone...you just may get to the truth!!! (You probably have more
support than you know. Too many people are afraid to show you or let anyone else
know. I have heard a few things myself... you ask the questions that everyone
else is too afraid to ask.)
==============end...TSS=============
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001 Date: Tue, 9 Jan
2001 16:49:00 –0800 From: "Terry S. Singeltary Sr." flounder@wt.net Reply-To:
Bovine Spongiform Encephalopathy BSE-L@uni-karlsruhe.de To:
BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy
#########
Greetings List Members,
I was lucky enough to sit in on this BSE conference call today and even
managed to ask a question. that is when the trouble started.
I submitted a version of my notes to Sandra Blakeslee of the New York
Times, whom seemed very upset, and rightly so.
"They tell me it is a closed meeting and they will release whatever
information they deem fit. Rather infuriating."
and i would have been doing just fine, until i asked my question. i was
surprised my time to ask a question so quick.
(understand, these are taken from my notes for now. the spelling of names
and such could be off.)
[host Richard Barns] and now a question from Terry S. Singeltary of CJD
Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for
serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have
him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue
donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
from this point, i was still connected, got to listen and tape the whole
conference. at one point someone came on, a woman, and ask again;
[unknown woman] what group are you with?
[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD
and other human TSE's world wide. i was invited to sit in on this from someone
inside the USDA/APHIS and that is why i am here. do you intend on banning me
from this conference now?
at this point the conference was turned back up, and i got to finish
listening. They never answered or even addressed my one question, or even
addressed the issue. BUT, i will try and give you a run-down for now, of the
conference.
IF i were another Country, I would take heed to my notes, BUT PLEASE do not
depend on them. ask for transcript from;
RBARNS@ORA.FDA.GOV 301-827-6906
he would be glad to give you one ;-)
Rockville Maryland, Richard Barns Host
BSE issues in the U.S., How they were labelling ruminant feed? Revising
issues.
The conference opened up with the explaining of the U.K. BSE epidemic
winding down with about 30 cases a week.
although new cases in other countries were now appearing.
Look at Germany whom said NO BSE and now have BSE.
BSE increasing across Europe.
Because of Temporary Ban on certain rendered product, heightened interest
in U.S.
A recent statement in Washington Post, said the New Administration (old GW)
has a list of issues. BSE is one of the issues.
BSE Risk is still low, minimal in U.S. with a greater interest in MBM not
to enter U.S.
HOWEVER, if BSE were to enter the U.S. it would be economically disastrous
to the render, feed, cattle, industries, and for human health.
(human health-they just threw that in cause i was listening. I will now jot
down some figures in which they told you, 'no need to write them down'. just
hope i have them correct. hmmm, maybe i hope i don't ???)
80% inspection of rendering
*Problem-Complete coverage of rendering HAS NOT occurred.
sizeable number of 1st time FAILED INITIAL INSPECTION, have not been
reinspected (70% to 80%).
Compliance critical, Compliance poor in U.K. and other European Firms.
Gloria Dunason Major Assignment 1998 goal TOTAL compliance. This _did not_
occur. Mixed level of compliance, depending on firm.
Rendering FDA license and NON FDA license
system in place for home rendering & feed 76% in compliance 79% cross
contamination 21% DID NOT have system 92% record keeping less than 60% total
compliance
279 inspectors 185 handling prohibited materials
Renderer at top of pyramid, significant part of compliance. 84% compliance
failed to have caution statement render 72% compliance & cross
contamination caution statement on feed, 'DO NOT FEED TO CATTLE'
56 FIRMS NEVER INSPECTED
1240 FDA license feed mills 846 inspected
"close to 400 feed mills have not been inspected"
80% compliance for feed.
10% don't have system.
NON-FDA licensed mills There is NO inventory on non licensed mills.
approximately 6000 to 8000 Firms ??? 4,344 ever inspected. "FDA does not have a
lot of experience with"
40% do NOT have caution statement 'DO NOT FEED'.
74% Commingling compliance
"This industry needs a lot of work and only half gotten to"
"700 Firms that were falitive, and need to be re-inspected, in addition to
the 8,000 Firms."
Quote to do BSE inspection in 19 states by end of January or 30 days, and
other states 60 days. to change feed status??? Contract check and ask questions
and pass info.
At this time, we will take questions.
[I was about the third or fourth to ask question. then all B.S.eee broke
loose, and i lost my train of thought for a few minutes. picked back up here]
someone asking about nutritional supplements and sourcing, did not get
name. something about inspectors not knowing of BSE risk??? the conference
person assuring that Steve Follum? and the TSE advisory Committee were handling
that.
Some other Dr. Vet, whom were asking questions that did not know what to
do???
[Dennis Wilson] California Food Agr. Imports, are they looking at imports?
[Conference person] they are looking at imports, FDA issued imports
Bulletin.
[Linda Singeltary ??? this was a another phone in question, not related i
don't think] Why do we have non-licensed facilities?
(conference person) other feed mills do not handle as potent drugs???
Dennis Blank, Ken Jackson licensed 400 non FDA 4400 inspected of a total of
6000 to 8000,
(they really don't know how many non licensed Firms in U.S. they guess 6000
to 8000??? TSS)
Linda Detwiler asking everyone (me) not to use emergency BSE number, unless
last resort. (i thought of calling them today, and reporting the whole damn U.S.
cattle herd ;-) 'not'
Warren-Maryland Dept. Agr. Prudent to re-inspect after 3 years. concerned
of Firms that have changed owners.
THE END
TSS
FROM New York TIMES
Subject: Re: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA
Posting of cut version... Date: Thu, 11 Jan 2001 22:02:47 –0700 From: "Sandy
Blakeslee" sblakeslee@mindspring.com To: "Terry S. Singeltary Sr."
References: 1
Hi terry -- thanks for all your help. I know it made a difference with the
FDA getting out that release.
----- Original Message ----- From: "Terry S. Singeltary Sr."
flounder@wt.net To: sblakeslee@mindspring.com Sent: Thursday, January 11, 2001
2:06 PM Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA
Posting of cut version...
> > hi sandy,
>From the New York Times NYTimes.com, January 11, 2001
Many Makers of Feed Fail to Heed Rules on Mad Cow Disease By SANDRA
BLAKESLEE
Large numbers of companies involved in manufacturing animal feed are not
complying with regulations meant to prevent the emergence and spread of mad cow
disease in the United States, the Food and Drug Administration said yesterday.
The widespread failure of companies to follow the regulations, adopted in
August 1997, does not mean that the American food supply is unsafe, Dr. Stephen
Sundlof, director of the Center for Veterinary Medicine at the F.D.A., said in
an interview.
But much more needs to be done to ensure that mad cow disease does not
arise in this country, Dr. Sundlof said.
The regulations state that feed manufacturers and companies that render
slaughtered animals into useful products generally may not feed mammals to
cud-chewing animals, or ruminants, which can carry mad cow disease.
All products that contain rendered cattle or sheep must have a label that
says, "Do not feed to ruminants," Dr. Sundlof said. Manufacturers must also have
a system to prevent ruminant products from being commingled with other rendered
material like that from chicken, fish or pork. Finally, all companies must keep
records of where their products originated and where they were sold.
Under the regulations, F.D.A. district offices and state veterinary offices
were required to inspect all rendering plants and feed mills to make sure
companies complied. But results issued yesterday demonstrate that more than
three years later, different segments of the feed industry show varying levels
of compliance.
Among 180 large companies that render cattle and another ruminant, sheep,
nearly a quarter were not properly labeling their products and did not have a
system to prevent commingling, the F.D.A. said. And among 347 F.D.A.-licensed
feed mills that handle ruminant materials - these tend to be large operators
that mix drugs into their products - 20 percent were not using labels with the
required caution statement, and 25 percent did not have a system to prevent
commingling.
Then there are some 6,000 to 8,000 feed mills so small they do not require
F.D.A. licenses. They are nonetheless subject to the regulations, and of 1,593
small feed producers that handle ruminant material and have been inspected, 40
percent were not using approved labels and 25 percent had no system in place to
prevent commingling.
On the other hand, fewer than 10 percent of companies, big and small, were
failing to comply with the record-keeping regulations.
The American Feed Industry Association in Arlington, Va., did not return
phone calls seeking comment.
Subject: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan.
9, 2001 Date: Wed, 10 Jan 2001 14:04:21 -0500 From: "Gomez, Thomas M."
tmg1@CDC.GOV Reply-To: Bovine Spongiform Encephalopathy BSE-L@uni-karlsruhe.de
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy
#########
USDA/APHIS would like to provide clarification on the following point from
Mr. Singeltary's 9 Jan posting regarding the 50 state conference call.
[Linda Detwiler asking everyone (me) not to use emergency BSE number,
unless last resort. (i thought of calling them today, and reporting the whole
damn U.S. cattle herd ;-) 'not']
Dr. Detwiler was responding to an announcement made during the call to use
the FDA emergency number if anyone wanted to report a cow with signs suspect for
BSE. Mr. Singeltary is correct that Dr. Detwiler asked participants to use the
FDA emergency number as a last resort to report cattle suspect for BSE. What Mr.
Singeltary failed to do was provide the List with Dr. Detwiler's entire
statement. Surveillance for BSE in the United States is a cooperative effort
between states, producers, private veterinarians, veterinary hospitals and the
USDA. The system has been in place for over 10 years. Each state has a system in
place wherein cases are reported to either the State Veterinarian, the federal
Veterinarian in Charge or through the veterinary diagnostic laboratory system.
The states also have provisions with emergency numbers. Dr. Detwiler asked
participants to use the systems currently in place to avoid the possibility of a
BSE-suspect report falling through the cracks. Use of the FDA emergency number
has not been established as a means to report diseased cattle of any nature.
Subject: Re: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL
Jan.9, 2001 Date: Wed, 10 Jan 2001 13:44:49 -0800 From: "Terry S. Singeltary
Sr." flounder@wt.net Reply-To: Bovine Spongiform Encephalopathy
BSE-L@uni-karlsruhe.de To: BSE-L@uni-karlsruhe.de References: 1
######### Bovine Spongiform Encephalopathy
#########
Hello Mr. Thomas,
> What Mr. Singeltary failed to do was provide > the List with Dr.
Detwiler's entire statement.
would you and the USDA/APHIS be so kind as to supply this list with a full
text version of the conference call and or post on your web-site? if so when,
and thank you. if not, why not?
> The system has been in place for over 10 years.
that seems to be a very long time for a system to be in place, and only
test 10,700 cattle from some 1.5 BILLION head (including calf crop). Especially
since French are testing some 20,000 weekly and the E.U. as a whole, are testing
many many more than the U.S., with less cattle, same risk of BSE/TSEs.
Why does the U.S. insist on not doing massive testing with the tests which
the E.U. are using? Why is this, please explain?
Please tell me why my question was not answered?
> U.S. cattle, what kind of guarantee can you > give for serum or
tissue donor herds?
It was a very simple question, a very important question, one that
pertained to the topic of BSE/feed, and asked in a very diplomatic way. why was
it not answered?
If all these years, we have been hearing that pharmaceutical grade bovines
were raised for pharmaceuticals vaccines etc. But yet the USA cannot comply with
feed regulations of the ruminant feed ban, PLUS cannot even comply with the
proper labelling of the feed, cross contamination etc. Then how in the world can
you Guarantee the feed fed to pharmaceutical grade bovine, were actually non
ruminant feed?
Before i was ask to be 'disconnected', i did hear someone in the background
say 'we can't'-- have him ask the question again.
could you please be so kind, as to answer these questions?
thank you, Terry S. Singeltary Sr. Bacliff, Texas USA
P.S. if you will also notice, i did not post that emergency phone number
and do not intend on passing it on to anyone. I was joking when i said i should
call and report the whole damn U.S. Herd. So please pass that on to Dr.
Detwiler, so she can rest easily.
BUT, they should be reported, some are infected with TSE. The U.S. is just
acting as stupid as Germany and other Countries that insist they are free of
BSE.
TSS
Subject: Report on the assessment of the Georgraphical BSE-risk of the USA
July 2000 (not good) Date: Wed, 17 Jan 2001 21:23:51 -0800 From: "Terry S.
Singeltary Sr." flounder@wt.net Reply-To: Bovine Spongiform Encephalopathy
BSE-L@uni-karlsruhe.de To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy
#########
Greetings List Members and ALL EU Countries,
Because of this report, and the recent findings of the 50-state BSE
Conference call, I respectfully seriously suggest that these Countries and the
SSC re-evaluate the U.S.A. G.B.R. to a risk factor of #3.
I attempted to post this to list in full text, but would not accept...
thank you, kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
Report on the assessment of the Geographical BSE-risk of the USA July 2000
PART II
REPORT ON THE ASSESSMENT OF THE GEOGRAPHICAL BSE RISK OF THE UNITED STATES
OF AMERICA
- 29 -
Report on the assessment of the Geographical BSE-risk of the USA July 2000
EXECUTIVE SUMMARY
OVERALL ASSESSMENT
The current geographical BSE-risk (GBR) level is II, i.e. it is unlikely
but cannot be excluded that domestic cattle are (clinically or pre-clinically)
infected with the BSE-agent.
Stability: Before 1990 the system was extremely unstable because feeding of
MBM to cattle happened, rendering was inappropriate with regard to deactivation
of the BSE-agent and SRM and fallen stock were rendered for feed. From 1990 to
1997 it improved to very unstable, thanks to efforts undertaken to trace
imported animals and exclude them from the feed chain and intensive
surveillance. In 1998 the system became neutrally stable after the RMBM-ban of
1997.
External challenges: A moderate external challenge occurred in the period
before 1990 because of importation of live animals from BSE-affected countries,
in particular from the UK and Ireland. It cannot be excluded that some
BSE-infected animals have been imported by this route and did enter the US
rendering and feed production system. The efforts undertaken since 1990 to trace
back UK-imported cattle and to exclude them from the feed chain reduced the
impact of the external challenge significantly.
Interaction of external challenges and stability: While extremely unstable,
the US system was exposed to a moderate external challenge, mainly resulting
from cattle imports from the UK. It can not be excluded that BSE-infectivity
entered the country by this route and has been recycled to domestic cattle. The
resulting domestic cases would have been processed while the system was still
very unstable or unstable and would hence have initiated a number of second or
third generation cases. However, the level of the possible domestic prevalence
must be below the low detection level of the surveillance in place.
As long as there are no changes in stability or challenge the probability
of cattle to be (pre-clinically or clinically) infected with the BSE-agent will
remain at the current level.
JUSTIFICATION
1. DATA
The available information was suitable to carry out the GBR risk
assessment.
- 30 -
Report on the assessment of the Geographical BSE-risk of the USA July 2000
2. STABILITY
2.1 Overall appreciation of the ability to identify BSE-cases and to
eliminate animals at risk of being infected before they are processed
· Before 1989, the ability of the system to identify (and eliminate) BSE
cases was limited. · Since 1990 this ability is significantly improved, thanks
to a good BSE-surveillance and culling system (contingency plan). · Today the
surveillance should be able to detect clinical BSE-cases within the limits set
by an essential passive surveillance system, i.e. some cases might remain
undetected.
2.2 Overall appreciation of the ability to avoid recycling BSE-infectivity,
should it enter processing
· Before 1997 the US rendering and feed producing system would not have
been able to avoid recycling of the BSE agent to any measurable extent. If the
BSE-agent was introduced the feed chain, it could probably have reached cattle.
· After the introduction of the RMBM-to-ruminants-ban in August 1997 the ability
of the system to avoid recycling of BSE-infectivity was somewhat increased. It
is still rather low due to the rendering system of ruminant material (including
SRM and fallen stock) and the persisting potential for cross-contamination of
cattle feed with other feeds and hence RMBM.
2.3 Overall assessment of the Stability
· Until 1990 the US BSE/cattle system was extremely unstable as RMBM was
commonly fed to cattle, the rendering system was not able to reduce
BSE-infectivity and SRM were rendered. This means that incoming BSE infectivity
would have been most probably recycled to cattle and amplified and the disease
propagated. · Between 1990 and 1995 improvements in the BSE surveillance and the
efforts to trace back and remove imported cattle gradually improved the
stability but the system remained very unstable. In 1998 the system became
unstable because of an RMBM-ban introduced in 1997. After 1998 the ban was fully
implemented and the system is regarded to be neutrally stable since 1998. The US
system is therefore seen to neither be able to amplify nor to reduce circulating
or incoming BSE-infectivity.
3. CHALLENGES
A moderate external challenge occurred in the period 1980-1989 because of
importation of live animals from the UK. imports from other countries are
regarded to have been negligible challenges. · As a consequence of this external
challenge, infectivity could have entered the feed cycle and domestic animals
could have been exposed to the agent. These domestic BSE-incubating animals
might have again entered processing, leading to an internal challenge since
1991. · This internal challenge could have produced domestic cases of BSE, yet
prevalence levels could have been below the detection limits of the surveillance
system until now. (According to US calculations, the current surveillance
-31 -
Report on the assessment of the Geographical BSE-risk of the USA July 2000
system could detect clinical incidence of 1-3 cases per year per million
adult cattle, i.e. in absolute numbers 43-129 cases per year). Between 1990 und
1995, with the exclusion of the imported animals from Europe from the feed
chain, the effect of the external challenges decreased.
4. CONCLUSION ON THE RESULTING RISKS
4.1 Interaction of stability and challenqe
· In the late 80s, early 90s a moderate external challenges met an
extremely unstable system. This would have amplified the incoming
BSE-infectivity and propagated the disease. · With the exclusion of the imported
animals from Europe from the feed chain between 1990 and 1995 the effect of the
external challenge decreased. · Before 1998 an internal challenge, if it
developed, would have met a still unstable system (inappropriate rendering, no
SRM ban, RMBM ban only after 1997) and the BSE-infectivity could have been
recycled and amplified. · After 1998 the neutrally stable system could still
recycle the BSE-agent but due to the RMBM-ban of 1997 the BSE-infectivity
circulating in the system would probably not be amplified.
4.2 Risk that BSE-infectivity enters processing
· A very low processing risk developed in the late 80s when the UK-imports
were slaughtered or died. It increased until 1990 because of the higher risk to
be infected with BSE of cattle imported from the UK in 1988/89, as these animals
could have been processed prior to the back-tracing of the UK-imports in 1990. ·
From 1990 to 1995 a combination of surviving non-traced UK imports and some
domestic (pre-)clinical cases could have arrived at processing resulting in an
assumed constant low but non-negligible processing risk. · After 1995 any
processing risk relates to assumed domestic cases arriving at processing. · The
fact that no domestic cases have been shown-up in the BSE-surveillance is
reassuring - it indicates that BSE is in fact not present in the country at
levels above the detection limits of the country's surveillance system. This
detection level has been calculated according to US-experts to be between 1
& 3 clinical cases per million adult cattle per year.
Note: The high turnover in parts of the dairy cattle population with a
young age at slaughter makes it unlikely that fully developed clinical cases
would occur (and could be detected) or enter processing. However, the
theoretical infective load of the pre-clinical BSE-cases that under this
scenario could be processed, can be assumed to remain relatively low.
4.3 Risk that BSE-infectivity is recycled and propagated
· During the period covered by this assessment (1980-1999) the US-system
was not able to prevent propagation of BSE should it have entered, even if this
ability was significantly improved with the MBM-ban of 1997. · However, since
the likelihood that BSE-infectivity entered the system is regarded to be small
but non-negligible, the risk that propagation of the disease took place is also
small but not negligible.
- 32 -
Report on the assessment of the Geographical BSE-risk of the USA July 2000
5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK
5.1 The current GBR
The current geographical BSE-risk (GBR) level is II, i.e. it is unlikely
but cannot be excluded that domestic cattle are (clinically or pre-clinically)
infected with the BSE-agent.
5.2 The expected development of the GBR
As long as there are no changes in stability or challenge the probability
of cattle to be (pre-clinically or clinically) infected with the BSE-agent
remains at the current level.
5.3 Recommendations for influencin.q the future GBR
· As long as the stability of the US system is not significantly enbanced
above neutral levels it remains critically important to avoid any new external
challenges. · All measures that would improve the stability of the system, in
particular with regard to its ability to avoid recycling of the BSE-agent should
it be present in the cattle population, would reduce, over time, the probability
that cattle could be infected with the BSE-agent. Possible actions include:
removal of SRMs and/or fallen stock from rendering, better rendering processes,
improved compliance with the MBM-ban including control and reduction of
cross-contamination. · Results from an improved intensive surveillance
programme, targeting at risk sub-populations such as adult cattle in fallen
stock or in emergency slaughter, could verify the current assessment.
snip...
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
HUMAN TSE PRION DISEASE
FACT is, BSE cases in Europe of the past years have dropped dramatically
due to feed ban that was enforced, and extensive BSE testing, in large numbers.
just the opposite has happened in the USA. it’s all been documented. there is
ample evidence that there is as much of a chance (if not more), that this victim
contracted human mad cow disease from sources right here in the USA. this PR
push to alienate a USA source factor for human BSE in the USA is a PR stunt by
the USDA inc., and not justified now, in my opinion. compare BSE testing figures
in the EU compared to the USA, compare mad cow feed ban breaches, and you will
see. hell, the 2004 enhanced BSE surveillance program was flawed so bad, the top
Prion God at the NIH TSE prion expert Paul Brown, says he does not trust
anything from the USDA since Texas covered up a mad cow for 7 months, on a 48
hour confirmation turn around. it’s all documented below in link. USDA inc shut
down the mad cow testing after so many atypical BSE cases started showing up.
...
Singeltary submission to PLOS ;
RE: re-Human Prion Diseases in the United States part 2 flounder replied to
flounder on 02 Jan 2010 at 21:26 GMT
No competing interests declared.
No competing interests declared.
see full text ;
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, 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, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL
TEXT
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember,
the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been
documented in North America, along with the typical scrapie's, and atypical
Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these
TSE in different species have been rendered and fed to food producing animals
for humans and animals in North America (TSE in cats and dogs ?), and that the
trading of these TSEs via animals and products via the USA and Canada has been
immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances
and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD
only theory in 2009. With all the science to date refuting it, to continue to
validate this old myth, will only spread this TSE agent through a multitude of
potential routes and sources i.e. consumption, medical i.e., surgical, blood,
dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and
the urgent need to make all human TSE in the USA a reportable disease, in every
state, of every age group, and to make this mandatory immediately without
further delay. The ramifications of not doing so will only allow this agent to
spread further in the medical, dental, surgical arena's. Restricting the
reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO
age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al
and many more, that the world of TSE Transmissible Spongiform Encephalopathy is
far from an exact science, but there is enough proven science to date that this
myth should be put to rest once and for all, and that we move forward with a new
classification for human and animal TSE that would properly identify the
infected species, the source species, and then the route.
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
Singeltary comment ;
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been
discovered in a wide verity of species across North America. typical C-BSE,
atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine,
typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98
Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD
in cervid is slowly spreading without any stopping it in Canada and the USA and
now has mutated into many different strains. Transmissible Mink Encephalopathy
TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease
have been silently mutating and spreading in different species in North America
for decades.
The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion
Firewall, of which we now know without a doubt, that it was nothing but ink on
paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of
banned mad cow feed has been put out into commerce, never to return, as late as
December of 2013, serious, serious breaches in the FDA mad cow feed ban have
been documented. The 2004 enhanced BSE surveillance program was so flawed, that
one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown,
who is preparing a scientific paper based on the latest two mad cow cases to
estimate the maximum number of infected cows that occurred in the United States,
said he has "absolutely no confidence in USDA tests before one year ago" because
of the agency's reluctance to retest the Texas cow that initially tested
positive.
see ;
The BSE surveillance and testing have also been proven to be flawed, and
the GAO and OIG have both raised serious question as to just how flawed it has
been (see GAO and OIG reports). North America has more documented TSE prion
disease, in different documented species (excluding the Zoo BSE animals in the
EU), then any other place on the Globe. This does not include the very
likelihood that TSE prion disease in the domestic feline and canine have been
exposed to high doses of the TSE prion disease vid pet food. To date, it’s still
legal to include deer from cwd zone into pet food or deer food. Specified Risk
Material i.e. SRM bans still being breach, as recently as just last month.
nvCJD or what they now call vCJD, another case documented in Texas last
month, with very little information being released to the public on about this
case? with still the same line of thought from federal officials, ‘it can’t
happen here’, so another vCJD blamed on travel of a foreign animal disease from
another country, while ignoring all the BSE TSE Prion risk factors we have here
in the USA and Canada, and the time that this victim and others, do spend in the
USA, and exposed to these risk factors, apparently do not count in any way with
regard to risk factor. a flawed process of risk assessment.
sporadic CJD, along with new TSE prion disease in humans, of which the
young are dying, of which long duration of illness from onset of symptoms to
death have been documented, only to have a new name added to the pot of prion
disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a
familial type disease could be sporadic with no genetic link to any family
member? when the USA is the only documented Country in the world to have
documented two different cases of atypical H-type BSE, with one case being
called atypical H-G BSE with the G meaning Genetic, with new science now showing
that indeed atypical H-type BSE is very possible transmitted to cattle via oral
transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada,
USA, and the UK, with the same old excuse, better surveillance. You can only use
that excuse for so many years, for so many decades, until one must conclude that
CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a
blip or a reason of better surveillance, it is a mathematical rise in numbers.
More and more we are seeing more humans exposed in various circumstance in the
Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same
time in North America, more and more humans are becoming exposed to the TSE
prion disease via consumption of the TSE prion via deer and elk, cattle, sheep
and goats, and for those that are exposed via or consumption, go on to further
expose many others via the iatrogenic modes of transmission of the TSE prion
disease i.e. friendly fire. I pondered this mode of transmission via the victims
of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone
sub-clinical with sFFI or sGSS ? what if?
Two decades have passed since Dr. Ironside first confirmed his first ten
nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first
ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is
transmissible. yet all these TSE prion disease and victims in the USA and Canada
are being pawned off as a spontaneous event, yet science has shown, the
spontaneous theory has never been proven in any natural case of TSE prion
disease, and scientist have warned, that they have now linked some sporadic CJD
cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about
this in the public domain. We must make all human and animal TSE prion disease
reportable in every age group, in ever state and internationally, we must have a
serious re-evaluation and testing of the USA cattle herds, and we must ban
interstate movement of all cervids. Any voluntary effort to do any of this will
fail. Folks, we have let the industry run science far too long with regards to
the TSE prion disease. While the industry and their lobbyist continues to funnel
junk science to our decision policy makers, Rome burns. ...end
REFERENCES
Sunday, June 29, 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
CJD QUESTIONNAIRE USA
CJD VOICE
PRIONOPATHY OR PRIONOBALONEY $$$
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Sunday, May 18, 2008
BSE Inquiry DRAFT FACTUAL ACCOUNT DFA
BSE Inquiry DRAFT FACTUAL ACCOUNTS DFA's
Sunday, May 18, 2008
***BSE, CJD, and Baby foods (the great debate 1999 to 2005)
Sunday, May 18, 2008
***MAD COW DISEASE BSE CJD CHILDREN VACCINES
layperson
just made a promise, never forget, never let them forget...
MOM DOD 12/14/97 confirmed hvCJD Heidenhain Variant Creutzfeldt Jakob
Disease Case Report
snip...
Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'
DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114
McCullough Bldg. Galveston, Texas 77555-0785 FAX COVER SHEET DATE: 4-23-98 TO:
Mr. Terry Singeltary @ ------- FROM: Gerald Campbell FAX: (409) 772-5315 PHONE:
(409) 772-2881 Number of Pages (including cover sheet): Message:
*CONFIDENTIALITY NOTICE* This document accompanying this transmission contains
confidential information belonging to the sender that is legally privileged.
This information is intended only for the use of the individual or entry names
above. If you are not the intended recipient, you are hereby notified that any
disclosure, copying distribution, or the taking of any action in reliances on
the contents of this telefaxed information is strictly prohibited. If you
received this telefax in error, please notify us by telephone immediately to
arrange for return of the original documents.
--------------------------
Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q
Patient Name: POULTER, BARBARA
Age: 63
YRS DOB: 10/17/34
Sex: F
Admitting Race: C
Attending Dr.: Date / Time Admitted : 12/14/97 1228
Copies to: UTMB University of Texas Medical Branch Galveston, Texas
77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS
Autopsy' Office (409)772-2858 Autopsy NO.: AU-97-00435 AUTOPSY INFORMATION:
Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time
of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00
Pathologist/Resident: Pencil/Fernandez Service: Private Restriction:
Brain only FINAL AUTOPSY DIAGNOSIS I. Brain: Creutzfeldt-Jakob disease,
Heidenhain variant.
snip...see full text ;
Sunday, December 7, 2014
Scientific update on the potential for transmissibility of non-prion
protein misfolding diseases PRIONOIDS
Saturday, December 13, 2014
Terry S. Singeltary Sr. Publications TSE prion disease
for my files...tss
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
snip...
well, it’s been 17 years to the day.
just made a promise to Mom, DOD December 14, 1997 confirmed hvCJD, never
forget, and never let them forget...
Terry S. Singeltary Sr.
