REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
On May 8, 2009, the Alberta Provincial Laboratory informed the CFIA Edmonton District office of a BSE Surveillance sample (collected through the Canada Alberta BSE Surveillance Program) with a reaction on the BIO-RAD rapid test that did not rule-out BSE.
Brain samples were forwarded to the National BSE Reference Laboratory in Lethbridge, Alberta. The sample was confirmed as BSE positive using the Scrapie Associated Fibril Immunoblot and mAB 6H4 on May 14, 2009.
Additional testing included the Prionics-Check Priostrip performed on May 12, 2009, Prionics-Check Western, Hybrid Western Blot and BioRad TeSeE ELISA performed on May 13, 2009. All tests were positive. Western blot results indicate the case was c-type (classical) BSE.
The carcass was secured at the sampling site (on farm) and transferred to CFIA’s Lethbridge laboratory for incineration. No part of the carcass entered the human food supply or animal feed chain.
The CFIA immediately initiated an epidemiological investigation based on the recommended BSE guidelines (Terrestrial Animal Health Code 2008) of the World Organisation for Animal Health, referred to as the OIE. Specifically, the CFIA followed the recommended BSE guidelines for a country with controlled risk status and investigated:
• the feed cohort, comprising all cattle which, during their first year of life, were reared with the BSE case during its first year of life, and which investigation showed consumed the same potentially contaminated feed during that period, or
• the birth cohort, comprising all cattle born in the same herd as, and within 12 months of the birth of the BSE case, if the above cannot be identified and
• feed to which the animal may have been exposed early in its life.
The positive animal was a registered Holstein cow born on August 26, 2002. She was 80 months of age at the time of death. The animal was born, raised and had spent her entire life on the same farm. The producer reported the duration of illness as approximately two weeks. Retrospectively, the owner acknowledged a change in behaviour starting at the end of February, 2009 with the animal exhibiting erratic behaviour, trying to jump the gutters in the barn and falling down a few times.
The case animal became progressively more nervous around the other cows and her status in the herd changed from a dominant position to one of the lowest in the herd. She became stiff gaited in all four legs and during the last week of life she became hypersensitive to touch and reacted abnormally to visual stimuli.
Weight loss and decreased milk production were also reported. At the time of examination by the private veterinarian, she appeared weak with subtle to mild ataxia of the hind legs. The producer elected to have the animal humanely destroyed. Since the inclusion criteria of Canada’s National BSE Surveillance Program were met, arrangements were made to forward appropriate samples for laboratory evaluation.
The birth farm was a dairy operation located in Northern Alberta. The feed/ birth cohort was determined to comprise 213 animals which, along with the case animal, were raised on the farm. This cohort consisted of male and female Holsteins. The trace-out investigation located 19 live animals on five premises including the case farm. These animals were quarantined and eight of the 19 live cohorts have been humanely destroyed and their carcasses disposed of by incineration in accordance with the OIE recommendations. The same approach will be followed for the remaining live cohorts.
The following is the disposition of the other animals in the birth/feed cohort:
• 77 animals were traced and confirmed to have died or been slaughtered;
• 67 animals were traced and presumed to have died or been slaughtered;
• three animals were traced and confirmed to have been exported for slaughter and the importing country has been notified
• 47 animals were determined to be untraceable because of records limitations
The feed investigation focussed on feeds to which the case animal may have had access during its first year of life and the manufacturing practices used to produce each of these feeds.
Investigation at the farm revealed dairy cattle to be the only commercially farmed species. Other animals present included a dog and several cats.
There was no pasture use on the farm and all forages were farm-grown and harvested using farm-owned equipment. Non-forage feed products included grain (barley) which was farm-grown or purchased, milk replacer, three different commercially prepared complete feeds and mineral and salt products in block or loose form. All products, with the exception of a commercially prepared complete lactation feed delivered in bulk, were supplied in packages (bagged or blocks) of 20 or 25 kg.
Heifer calves were initially fed colostrum, followed by milk replacer and calf starter beginning within three days of age and with no clearly defined weaning age. Feeding of the calf starter continued to approximately six months with forages and mineral and salt blocks introduced at approximately three months of age. From approximately six months of age onwards, heifers were fed forages, barley, and mineral products only. Bull calves were occasionally kept beyond two weeks of age and, if so, were fed the same way as described for the heifers.
Commercially prepared lactation feed was delivered directly into a bulk storage bin associated with the milking barn for use in preparing a total mixed ration for the lactating herd only. The storage, location, and intended use of this feed, in combination with the separate housing for heifers and lactating cows, as well as a lack of shared mixing or handling equipment, eliminated this feed from further investigation.
Feeds included in the investigation due to direct feeding were: milk replacer, calf starter, barley, mineral blocks and salt blocks. Feeds included in the investigation because exposure could not be eliminated were a small amount of loose mineral and breeder ration.
While much of the barley used was grown on farm, there were purchases for which specific source information was not available. There was also reported use of a third party mobile mix and roller mill employed to roll barley for the farm. Records of other products and how they were used in this roller mill were not available but it was reportedly used to mix grains with commercial supplements for nonruminants at other locations. Its use can not be eliminated as a source of potential contamination for rolled barley fed on the farm. Investigations of sources of milk replacer and salt products identified that these products were produced in specialized facilities dedicated to non-prohibited material products only, thereby ruling them out as possible sources of contamination.
Investigation at the manufacturer supplying the mineral block products identified these were produced in a facility that also produced feeds containing prohibited material. Cross-utilized equipment at the facility included equipment used to receive bulk ingredients and batch mixing equipment. Review of records associated with these points of production indicated procedures to prevent cross contamination with prohibited material were in place and documented.
The calf starter used during the period of interest was identified as manufactured at two different facilities. One facility provided 125 kg of product within the case animal’s first month of life. The other facility provided 4550 kg of product within the case animal’s first six months of life.
Production records for the facility manufacturing the 125 kg of calf starter were not available. One of the mixed pelleted ingredients used in this feed was manufactured in another facility which handled prohibited material but specific production records were not available.
The facility manufacturing the majority of the calf starter also manufactured two other products distributed to the farm (a loose mineral and breeder ration) which the case animal could have been exposed to. This facility also manufactured feeds containing prohibited material with shared equipment throughout all major points of manufacturing. Procedures to prevent cross contamination with prohibited material were in place and documented. Documentation failures at point of bulk ingredient receiving were noted on two occasions.
Findings of the investigation suggest the most likely exposure to infectious material to be through crosscontamination of ingredients used in the manufacture of calf starter fed during the first six months of life (either manufacturer). Additional sources, particularly barley potentially contaminated by cross utilized rolling equipment, can not be ruled out.
The detection of this case does not change any of Canada's BSE risk parameters. The location and age of the animal are consistent with previous cases. Surveillance results to date, including this case, reflect an extremely low level of BSE in Canada.
Since the confirmation of BSE in a native-born animal in May 2003, Canada has significantly increased its targeted testing of cattle in high-risk categories advocated by the OIE. This effort is directed at determining the level of BSE in Canada while monitoring the effectiveness of the risk-mitigating measures in place. Canada's National BSE Surveillance Program continues to demonstrate an extremely low level of BSE in Canada, with 16 positive animals detected.
With respect to BSE, the safety of beef produced in Canada is assured by public health measures further enhanced in 2003. The removal of specific risk material (SRM) - the tissues that have been demonstrated to have the potential to harbour BSE infectivity - from all animals slaughtered for human consumption is the most effective single measure to protect consumers in Canada and importing countries from exposure to BSE infectivity in meat products.
As demonstrated by the surveillance system, the feed ban implemented in 1997 is effectively preventing the amplification of BSE in Canada. Additional regulations to enhance Canada's feed ban were enacted in 2007. The most important change is the removal of SRM from all animal feeds, pet food and fertilizer. The enhancement will accelerate progress toward eradicating BSE from the national cattle herd by preventing more than 99 percent of potential BSE infectivity from entering the Canadian feed system. These measures are effectively minimizing the risk of BSE transmission.
Canada is officially categorized under the OIE's science-based system as a controlled BSE risk country. This status clearly recognizes the effectiveness of Canada's surveillance, mitigation and eradication measures, and acknowledges the work done by all levels of government, the cattle industry, veterinarians and ranchers to effectively manage and eventually eradicate BSE in Canada.
=====================END REPORT TSS======================
LET'S LOOK AT THE USA COVER-UP OF MAD COW DISEASE, AND HUMAN CJD CASES THERE FROM
National Prion Disease Pathology Surveillance Center Cases Examined1 (July 31, 2010)
(TURN IT UP AND PLEASE WATCH THE VIDEO AT BOTTOM OF URL BELOW)
HOW can you have a new prionpathy in young in the USA, and call it a genetic disease, but that is not a genetic disease, but really is sporadic, due to no related gene mutation, however, this same genetic TSE, that is not genetic, but sporadic for humans, matches the Alabama mad cow exactly, and it not be related ???
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein
>>> Because 8 out of 10 patients had a positive family history of dementia in the original study, a genetic cause was suspected. Although all cases were homozygous for valine at codon 129 of the PrP gene, NO mutations were detected. <<<
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.
see page 114 ;
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong,
PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA END...TSS
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.
Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice.
Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
Wednesday, March 31, 2010
Atypical BSE in Cattle 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. This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
SEE FULL TEXT ;
Monday, August 9, 2010
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease. snip...
In Confidence Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells 3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
Sunday, September 6, 2009 MAD COW USA 1997 [SECRET VIDEO]
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? [SEE VIDEO at bottom]
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN [SEE VIDEO]
Sunday, April 12, 2009
r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada
Saturday, April 11, 2009
CJD FOUNDATION SIDES WITH R-CALFERS NO BSE OR HUMAN TSE THERE OF IN USA 'don't be fooled'
Thursday, June 24, 2010
Accumulation of L-type Bovine Prions in Peripheral Nerve Tissues
Volume 16, Number 7–July 2010
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
Archive Number 20100405.1091 Published Date 05-APR-2010 Subject PRO/AH/EDR> Prion disease update 1010 (04)
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
> 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
Monday, April 5, 2010
UPDATE - CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
Tuesday, June 1, 2010
USA cases of dpCJD rising with 24 cases so far in 2010
Sunday, July 11, 2010
CJD or prion disease 2 CASES McLennan County Texas population 230,213 both cases in their 40s
Friday, February 05, 2010
New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review
Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary
Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
my comments to PLosone here ;
HOW many of you recieved a written CJD Questionnaire asking real questions pertaining to route and source (and there are many here in North America) ?
IS every case getting a cjd questionnaire asking real questions ???
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION USA PRION UNIT
BSE MAD COW FIREWALL IN THE USA, THE MAD COW FEED BAN, WHAT BAN ?
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
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
Cattle feed delivered between 01/12/2007 and 01/26/2007
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
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
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
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
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
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
WHAT ABOUT THAT g-c-BSE-alabama mad cow, what about that mad cow feed 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.
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
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
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 09:22 184.108.40.206
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
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
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.
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
END OF ENFORCEMENT REPORT FOR July 12, 2006
JOURNAL OF NEUROLOGY
MARCH 26, 2003
Send Post-Publication Peer Review to journal:
Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
Newsdesk The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
"My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem." 49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)-the relative of mad cow disease seen among deer and elk in the USA. Although his feverish.
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.
THE PATHOLOGICAL PROTEIN
BY Philip Yam
Yam Philip Yam News Editor Scientific American www.sciam.com
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
Are prion diseases more prevalent than we thought?
Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongiform encephalopathy was a zoonosis-an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?
Revisiting Sporadic CJD
It's not hard to get Terry Singeltary going. "I have my conspiracy theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.
Singeltary has similar inclinations. ...
DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehördensind lax.Link auf diesen Artikel im Archiv: http://service.spiegel.de/digas/find?DID=18578755
"Löcher wie in einem Schweizer Käse" hat auch Terry Singeltary im Regelwerk der FDA ausgemacht. Der Texaner kam auf einem tragischen Umweg zu dem Thema: Nachdem seine Mutter 1997 binnen weniger Wochen an der Creutzfeldt-Jakob-Krankheit gestorben war, versuchte er, die Ursachen der Infektion aufzuspüren. Er klagte auf die Herausgabe von Regierungsdokumenten und arbeitete sich durch Fachliteratur; heute ist er überzeugt, dass seine Mutter durch die stetige Einnahme von angeblich kräftigenden Mitteln erkrankte, in denen - völlig legal - Anteile aus Rinderprodukten enthalten sind.
Von der Fachwelt wurde Singeltary lange als versponnener Außenseiter belächelt. Doch mittlerweile sorgen sich auch Experten, dass ausgerechnet diese verschreibungsfreien Wundercocktails zur Stärkung von Intelligenz, Immunsystem oder Libido von den Importbeschränkungen ausgenommen sind. Dabei enthalten die Pillen und Ampullen, die in Supermärkten verkauft werden, exotische Mixturen aus Rinderaugen; dazu Extrakte von Hypophyse oder Kälberföten, Prostata, Lymphknoten und gefriergetrocknetem Schweinemagen. In die USA hereingelassen werden auch Blut, Fett, Gelatine und Samen. Diese Stoffe tauchen noch immer in US-Produkten auf, inklusive Medizin und Kosmetika. Selbst in Impfstoffen waren möglicherweise gefährliche Rinderprodukte enthalten. Zwar fordert die FDA schon seit acht Jahren die US-Pharmaindustrie auf, keine Stoffe aus Ländern zu benutzen, in denen die Gefahr einer BSE-Infizierung besteht. Aber erst kürzlich verpflichteten sich fünf Unternehmen, darunter Branchenführer wie GlaxoSmithKline, Aventis und American Home Products, ihre Seren nur noch aus unverdächtigem Material herzustellen.
"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
28 Mar 01
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518