Sunday, December 14, 2014

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

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

 

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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.

 

The hyperlink to prion disease data page is http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/data/

 

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 USDA's epidemiological investigation and a copy of the report, please visit the APHIS website at http://www.aphis.usda.gov/lpa/issues/bse/bse.html or

 


 

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 $$$

 


 


 


 


 


 


 


 


 


 


 


 

BSE INQUIRY DFAs

 


 

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.

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