Wednesday, March 18, 2015

Changes in Retinal Function and Morphology Are Early Clinical Signs of Disease in Cattle with Bovine Spongiform Encephalopathy

Research Article

 

Changes in Retinal Function and Morphology Are Early Clinical Signs of Disease in Cattle with Bovine Spongiform Encephalopathy

 

M. Heather West Greenlee ,

 

Jodi D. Smith,

 

Ekundayo M. Platt,

 

 Jessica R. Juarez,

 

 Leo L. Timms,

 

 Justin J. Greenlee

 

PLOS

 

Published: March 10, 2015 •DOI: 10.1371/journal.pone.0119431

 

Abstract

 

Bovine spongiform encephalopathy (BSE) belongs to a group of fatal, transmissible protein misfolding diseases known as transmissible spongiform encephalopathies (TSEs). All TSEs are caused by accumulation of misfolded prion protein (PrPSc) throughout the central nervous system (CNS), which results in neuronal loss and ultimately death. Like other protein misfolding diseases including Parkinson’s disease and Alzheimer’s disease, TSEs are generally not diagnosed until the onset of disease after the appearance of unequivocal clinical signs. As such, identification of the earliest clinical signs of disease may facilitate diagnosis. The retina is the most accessible part of the central nervous system, and retinal pathology in TSE affected animals has been previously reported. Here we describe antemortem changes in retinal function and morphology that are detectable in BSE inoculated animals several months (up to 11 months) prior to the appearance of any other signs of clinical disease. We also demonstrate that differences in the severity of these clinical signs reflect the amount of PrPSc accumulation in the retina and the resulting inflammatory response of the tissue. These results are the earliest reported clinical signs associated with TSE infection and provide a basis for understanding the pathology and evaluating therapeutic interventions.

 

snip...

 

Discussion

 

snip...

 

Though there were only subtle histopathologic differences between retinas from cattle inoculated with classical BSE and BSE-H, immunohistochemical analysis did demonstrate differences in accumulation of PrPSc and activation of Müller glia and microglia, with BSE-H having markedly more PrPSc accumulation, Müller glia and microglia activation. Interestingly, these pathologic features correlate with the more robust phenotype of the electroretinograms in clinically ill BSE-H cattle. That is, when comparing clinical values from BSE-H to classical BSE inoculated animals, b-wave implicit times are longer and their amplitudes are markedly smaller. The b-wave amplitude can be used as an indirect measure of photoreceptor function, as death of photoreceptors results in a decrease in the b-wave amplitude. Though cattle inoculated with BSE-H did have a decreased b-wave amplitude and animals inoculated with classical BSE did not, we did not observe any major differences in the photoreceptor layer between these two groups. This may be due to changes in photoreceptor number in BSE-H cattle below our level of detection, or instead impairment of synaptic communication between photoreceptors and their post-synaptic cells (the bipolar cells). The b-wave implicit time (time for peak to reach maximum amplitude) is generated by retinal bipolar cells and Müller glia [39]. Of these two cell types, we observed changes in only the Müller glia. Both the decrease in b-wave amplitude and the increase in b-wave implicit time can be explained by synaptic dysfunction in the outer plexiform layer, the synaptic interface between photoreceptors and bipolar cells. This would be consistent with accumulation of PrPSc causing synaptic dysfunction (reviewed in [46]), and correlates with the differences in PrPSc accumulation between classical BSE and BSE-H.

 

The more robust retinal histologic changes in BSE-H inoculated cattle also correlates with a shorter incubation time in these animals. It has been shown previously that PrPSc from BSE-H has a higher stability when compared to classical BSE [47]. Our observation that the higher stability BSE-H has a shorter incubation time, and accumulates in the soma of retinal ganglion cells is consistent with similar observations by Ayers et al, who reported shorter incubation times and intraneuronal accumulation of PrPSc in higher stability prion strains [48]. In addition, we observed more a robust activation of retinal Müller glia and microglia in retinas from animals inoculated with BSE-H. Experiments to study the relationship between PrPSc stability, incubation time and glial activation are ongoing.

 

As an extension of the central nervous system, the retina may have diagnostic potential for several protein misfolding neurodegenerative disorders. Recent studies demonstrate that both retinal function and morphology in patients with Parkinson’s disease are significant predictors of disease severity and quality of life [49–53]. Changes in the retinal nerve fiber layer measured by OCT have been reported in patients with Alzheimer’s Disease [54], and measurements of the choroid (the vascular rich layer of the eye deep to the retina) have shown significant choroidal thinning in AD patients as well [55].

 

Here we demonstrate that the retina is an important tool to study the pathogenesis of prion disease. The retina is an isolated structure, and thus accumulation of PrPSc can be precisely quantified, as compared to the rest of the brain where quantification of regional accumulation is affected by dissection. Further, different functional assessment approaches can test different cell populations. The assessments used in this work test photoreceptors, bipolar cells and Müller glia, and our results demonstrate that our functional assessment was sensitive enough to differentiate between classical BSE and BSE-H, which at terminal stages have differences in PrPSc accumulation, Müller glia and microglia activation However, the results presented here are from animals inoculated with BSE intracranially. Ongoing studies will determine if similar changes can be detected in animals inoculated by the oronasal route.

 

The suitability of retinal assessment for diagnosis of prion disease in animals or humans remains an open question. Unequivocal diagnosis of prion disease depends upon the detection of misfolded prion protein (PrPSc). Several promising diagnostics for Creutzfeldt-Jakob Disease (CJD; the most common human prion disease) include amplification of PrPSc from nasal brushings [16], blood [15] and urine [14]. Detection of PrPSc associated with nasal brushings appears to be highly sensitive and specific and can detect both sporadic CJD as well has genetic CJD [16]. Experimentally, PrPSc can be detected prior to clinical illness in blood from macaques infected with BSE (the agent of variant CJD), and in blood samples from a small number of human CJD patients. PrPSc was detectable in patients with variant CJD and not sporadic CJD [15], raising the possibility that PrPSc in blood may be specific to vCJD. In a separate study of human vCJD patients, PrPSc was detected in the urine from 13/14 individuals [14,15]. The latter two studies demonstrate the utility of bodily fluids for detection of vCJD in clinical and potentially pre-clinical individuals. Though the retinal changes that we describe precede the clinical phase of illness in cattle, it is not yet known how this may relate clinical disease in humans. However, our results, taken with retinal imaging studies of individuals with Parkinson’s and Alzheimer’s disease, suggest that retinal imaging of CJD patients may prove useful.

 

The preponderance of evidence demonstrates that the retina is affected by protein misfolding disorders long thought to be confined to the brain. Thus, the retina holds tremendous potential for the study of disease pathogenesis, and evaluation of potential therapeutic interventions for multiple protein misfolding disorders. Transmissible spongiform encephalopathies are an infectious and highly predictable model of protein misfolding neurodegenerative disease. Predictable incubation times and PrPSc accumulation paired with detectable preclinical morphologic and functional deficits make the retina an excellent model for future studies to understand the detailed relationship between accumulation of misfolded protein and specific changes in neural function.

 

Supporting Information

 

snip...please see full text ;

 


 

again, many thanks to PLoS et al, and all Scientist for the OPEN ACCESS for scientific research. ...terry

 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

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

 


 

BANNED MAD COW FEED IN COMMERCE IN ALABAMA

 

______________________________

 

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

 

a) Dairy feed, custom, Recall # V-134-6;

 

b) Custom Dairy Feed with Monensin, Recall # V-135-6.

 

CODE

 

None. Bulk product

 

RECALLING FIRM/MANUFACTURER

 

Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006.

 

Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete.

 

REASON

 

Possible contamination of dairy feeds with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

1,484 tons

 

DISTRIBUTION

 

TN and WV

 

END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006

 

###

 


 

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-115-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing.

 

REASON

 

Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

Approximately 2,223 tons

 

DISTRIBUTION

 

KY

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-116-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing.

 

REASON

 

Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

1,220 tons

 

DISTRIBUTION

 

KY

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-117-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed.

 

REASON

 

Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

40 tons

 

DISTRIBUTION

 

LA and MS

 

______________________________

 

PRODUCT

 

Bulk Dairy Feed, Recall V-118-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete.

 

REASON

 

Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

7,150 tons

 

DISTRIBUTION

 

MS

 

______________________________

 

PRODUCT

 

Bulk custom dairy pre-mixes, Recall # V-119-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Walthall County Co-op, Tylertown, MS, by telephone on June 26, 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

 

87 tons

 

DISTRIBUTION

 

MS

 

______________________________

 

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

 

###

 


 

what about that ALABAMA MAD COW, AND MAD COW FEED THERE FROM IN THAT STATE ???

 

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

 

______________________________

 


 

 

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

 


 

2013

 

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

 


 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

Tuesday, February 17, 2015

 

Could we spot the next BSE?, asks BVA President

 


 


 

PLOS Singeltary Comment ;

 

*** ruminant feed ban for cervids in the United States ? ***

 

31 Jan 2015 at 20:14 GMT

 


 

Saturday, January 24, 2015

 

Bovine Spongiform Encephalopathy: Atypical Pros and Cons

 


 

Saturday, January 31, 2015

 

RAPID ADVICE 17-2014 : Evaluation of the risk for public health of casings in countries with a “negligible risk status for BSE” and on the risk of modification of the list of specified risk materials (SRM) with regard to BSE

 


 

Conclusion/Significance: Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.

 


 


 


 


 

SPONTANEOUS TSE

 

Perspectives BIOMEDICINE: A Fresh Look at BSE Bruce Chesebro*

 

Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle form of a family of progressive brain diseases. These diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease (CWD) in deer and elk. They are also known as either "prion diseases" because of the association of a misfolded cellular prion protein in pathogenesis or "transmissible spongiform encephalopathies" (TSEs) because of the spongelike nature of the damaged brain tissue (1).

 

The recent discovery of two BSE-infected cows, one in Canada and one in the United States, has dramatically increased concern in North America among meat producers and consumers alike over the extent to which BSE poses a threat to humans as well as to domestic and wild animals. The European BSE epidemic of the late-1980s seems to have been initiated a decade earlier in the United Kingdom by changes in the production of meat and bone meal (MBM) from rendered livestock, which led to contamination of MBM with the BSE infectious agent. Furthermore, the fact that UK farmers fed this rendered MBM to younger animals and that this MBM was distributed to many countries may have contributed to the ensuing BSE epidemic in the United Kingdom and internationally (2).

 

Despite extensive knowledge about the spread of BSE through contaminated MBM, the source of BSE in Europe remains an unsolved mystery (2). It has been proposed that BSE could be derived from a cross-species infection, perhaps through contamination of MBM by scrapie-infected sheep tissues (see the figure). Alternatively, BSE may have been an endemic disease in cattle that went unnoticed because of its low level of horizontal transmission. Lastly, BSE might have originated by "spontaneous" misfolding of the normal cellular prion protein into the disease-associated abnormal isoform (3), which is postulated to be the infectious agent or "prion."

 

Five possible sources of BSE in North American cattle. Sheep, deer, and elk could spread prion diseases (TSEs) to cattle through direct animal contact or contamination of pastures. Endemic BSE has not been proven to exist anywhere in the world, but it is difficult to exclude this possibility because of the inefficient spread of BSE infectivity between individual animals (2). BSE caused by spontaneous misfolding of the prion protein has not been proven. CREDIT: KATHARINE SUTLIFF/SCIENCE

 

snip...

 

Nevertheless, the idea that BSE might originate due to the spontaneous misfolding of prion proteins has received renewed interest in the wake of reports suggesting the occurrence of atypical BSE (9-11). These results imply that new strains of cattle BSE might have originated separately from the main UK outbreak. Where and how might such strains have originated? Although such rare events cannot be studied directly, any number of sources of the original BSE strain could also explain the discovery of additional BSE strains in cattle (see the figure). However, it would be worrisome if spontaneous BSE were really a valid etiology because such a mechanism would be impossible to prevent--unlike other possible scenarios that could be controlled by large-scale eradication of TSE-positive animals.

 

Another way to look at this problem is to examine evidence for possible spontaneous TSE disease in other animals besides cattle. Spontaneous BSE would be extremely difficult to detect in cattle, where horizontal spread is minimal. However, in the case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at birth as well as between adults, spontaneous disease should be detectable as new foci of clinical infection. In the early 1950s scrapie was eradicated in both Australia and New Zealand, and the mainland of both these countries has remained scrapie-free ever since. This scrapie-free status is not the result of selection of sheep resistant to scrapie because sheep from New Zealand are as susceptible as their UK counterparts to experimental scrapie infection (12). These experiments of man and nature appear to indicate that spontaneous clinical scrapie does not occur in sheep. Similarly, because CWD is known to spread horizontally, the lack of CWD in the deer or elk of eastern North America but its presence in western regions would also argue against a spontaneous disease mechanism. This is particularly noteworthy in New Zealand, where there are large numbers of deer and elk farms and yet no evidence of spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer, this would suggest that spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are unlikely to be found in cattle or humans. The main caveat to this notion is that spontaneous disease may arise in some animal species but not others. In humans, sCJD--which is considered by some researchers to begin by spontaneous misfolding of the prion protein--usually takes more than 50 years to appear. Thus, in animals with a shorter life-span, such as sheep, deer, and cattle, an analogous disease mechanism might not have time to develop.

 

What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? "Sporadic" pertains to the rarity of disease occurrence. "Spontaneous" pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE of unknown etiology--might be a better term to describe the origin of this malady. ...

 

snip...full text ;

 


 

 

DR. DEHAVEN: “All right. I think we've got three different questions in there, and I'll try to touch on each one of them.

 

“First of all, let me correct just a technical issue, and that is you mentioned 1 in 10,000. And actually our surveillance system currently is designed, the one that we have in place now is designed to detect 1 positive in 1 million cattle, and I gave some numbers between 200,000 and 268,000 that would allow us to detect 1 in 10 million as opposed to 1 in 10,000.

 

“So we would, if we were able to collect in the ballpark of those numbers of samples then we with increasing numbers of samples have an increasingly statistically valid sample from which to determine, one, whether or not the disease exists and, if so, at what prevalence level.

 

“So our real emphasis is to test as many of those animals as we can, ensure that we get an appropriate geographical distribution, but not setting a specific number as far as a target. Again, consistent with the recommendation from the International Review Team, their recommendation was to test all of them.

 

“So that's consistent with where we're going is to test as many as we possibly can.

 

*** “As far as spontaneous cases, that is a very difficult issue. There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative. We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million. We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.

 

“Again, it's a very difficult situation to prove a negative.

 

“So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.

 

snip...

 


 


 

1. The BSE epidemic

 

1.1. The origin of the BSE epidemic will probably never be determined with certainty.

 

1.2. We do not know whether or not some of the BARB cases represent truly sporadic classical BSE. If there are spontaneous cases then BSE will never be eradicated although reducing surveillance could make it appear that BSE has been eradicated.

 

snip...

 

5.3. It was stated that the number of sporadic CJD cases was rising. Participants were invited to discuss the reason for this. It was suggested that this was likely to be due to improved surveillance with more cases of sporadic CJD being detected (i.e. through MRI scans). There had been a similar increase in sporadic CJD in countries which did not have a BSE epidemic but improved their surveillance. This supported this theory and suggested that the increase in sporadic CJD was not related to the BSE outbreak.

 


 

Atypical BSE: Transmissibility

 

Linda Detwiller, 5/10/2011

 

 BASE (L) transmitted to:  cattle (IC) - inc < 20 mos and oral?)

 

 Cynomolgus macaques (IC)

 

 Mouse lemurs (IC and oral)

 

 wild-type mice (IC)

 

 bovinized transgenic mice (IC and IP)

 

 humanized transgenic mice (IC)

 

 H cases transmitted to:

 

 cattle – IC incubations < 20 months

 

 bovinized transgenic mice (IC)

 

 ovinized transgenic mice (IC)

 

 C57BL mice (IC)

 

 One study did not transmit to humanized PrP Met 129 mice

 

Evaluation of Possibility of Atypical

 

BSE Transmitting to Humans

 

 Possble interpretation:

 

 L type seems to transmit to nonhuman primates with greater ease than classical BSE

 

 L type also transmitted to humanized transgenic mice with higher attack rate and shorter incubation period than classical?

 

 H type did not transmit to Tg Hu transgenic mice

 

Linda Detwiller, 5/10/2011

 


 

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 ;

 

.....snip

 

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

 

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.

 


 


 

P.4.23 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 argely 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.

 


 


 


 

14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)

 

18.173 page 189

 

Experimental Challenge of Cattle with H-type and L-type Atypical BSE

 

A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada

 

Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.

 

Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions. At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.

 

Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathoge esis and agent distribution for these novel BSE types.

 

Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.

 


 

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.

 


 

snip... see more breaches in the BSE aka mad cow Triple Firewall, that never was here ;

 

Friday, January 23, 2015

 

*** Replacement of soybean meal in compound feed by European protein sources and relaxing the mad cow ban $

 


 

Comment from Terry Singeltary Sr. This is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products

 

For related information, Open Docket Folder Docket folder icon

 

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Comment View document:Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission ;

 

I believe that there is more risk to the world from Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from the United States and all of North America, than there is risk coming to the USA and North America, from other Countries. I am NOT saying I dont think there is any risk for the BSE type TSE prion coming from other Countries, I am just saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present mad cow risk factors in North America like they are not here?

 

North America has more strains of TSE prion disease, in more species (excluding zoo animals in the early BSE days, and excluding the Feline TSE and or Canine TSE, because they dont look, and yes, there has been documented evidence and scientific studies, and DEFRA Hound study, that shows the canine spongiform encephalopathy is very possible, if it has not already happened, just not documented), then any other Country in the world. Mink TME, Deer Elk cervid CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type BSE cattle, atyical HG type BSE cow (the only cow documented in the world to date with this strain), typical sheep goat Scrapie (multiple strains), and the atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical Scrapie has spread from coast to coast. sporadic CJD on the rise, with different strains mounting, victims becoming younger, with the latest nvCJD human mad cow case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL CDC.

 

typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al), and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. its all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$

 

the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing but ink on paper.

 

for this very reason I believe the BSE MRR policy is a total failure, and that this policy should be immediately withdrawn, and set back in place the BSE GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all TSE PRION disease in all species of animals, and that the BSE GBR risk assessments be made stronger than before.

 

lets start with the recent notice that beef from Ireland will be coming to America.

 

Ireland confirmed around 1655 cases of mad cow disease. with the highest year confirming about 333 cases in 2002, with numbers of BSE confirmed cases dropping from that point on, to a documentation of 1 confirmed case in 2013, to date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad cow feed ban, and the enforcement of that ban, has drastically reduced the number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in 2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow disease in the USA, we still have no clue as to the true number of cases of BSE mad cow disease in the USA or North America as a whole. ...just saying.

 

Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide* (excluding the United Kingdom)

 

Country/Year

 

snip...please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS No documents available. AttachmentsView All (1) Empty Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission View Attachment:

 


 

Sunday, January 11, 2015

 

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

 


 


 

Friday, January 23, 2015

 

*** Replacement of soybean meal in compound feed by European protein sources and relaxing the mad cow ban $

 


 

Saturday, January 24, 2015

 

*** Bovine Spongiform Encephalopathy: Atypical Pros and Cons

 


 

Monday, December 1, 2014

 

Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review December 1, 2014

 


 

Thursday, January 29, 2015

 

Identification of H-type BSE in Portugal

 


 

Thursday, January 29, 2015

 

OIE REPORT Bovine spongiform encephalopathy Prion (atypical BSE type H), Norway Information received on 29/01/2015

 


 

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

 


 

Sunday, December 28, 2014

 

Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014

 


 

 
Monday, February 23, 2015
 
20th BSE Case Raises New Concerns about Canada's Feeding Practices and Voluntary Testing Program; Highlights Importance of COOL
 

 

 

Saturday, February 28, 2015

 

BSE CANADA UPDATE Transcript - Technical Briefing to Provide an Update on Investigation of Bovine Spongiform Encephalopathy in Alberta February 27, 2015 4:00 p.m.

 


 

 

Friday, January 30, 2015

 

*** Scrapie: a particularly persistent pathogen ***

 


 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

Saturday, August 30, 2014

 

Maine Firm Recalls Ribeye and Carcass Products That May Contain Specified Risk Materials SRM TSE PRION aka mad cow type disease

 


 

Friday, December 19, 2014

 

Rancho Alleged Cancerous Eyeball Case Going To Trial

 


 

Thursday, November 28, 2013

 

Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows

 


 

seems USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ???

 

Saturday, September 21, 2013

 

Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT

 


 

DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ??? this recall was not for the welfare of the animals. ...tss you can check and see here ; (link now dead, does not work...tss)

 


 

try this link ;

 


 

Sunday, November 13, 2011

 

*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock

 


 

Monday, October 10, 2011

 

EFSA Journal 2011 The European Response to BSE: A Success Story

 

snip...

 

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far

 

*** 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...

 


 


 

Thursday, August 12, 2010

 

Seven main threats for the future linked to prions

 

First threat

 

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

 

*** 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...

 


 

 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...

 


 

 

 nvCJD CONFIRMED TEXAS USA 2014

 

‘’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.’’

 

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.

 


 

Sunday, November 23, 2014

 

Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European

 


 

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).

 


 

Thursday, January 15, 2015

 

41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report

 


 

Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type disease

 

what is CJD ? just ask USDA inc., and the OIE, they are still feeding the public and the media industry fed junk science that is 30 years old.

 

why doesn’t some of you try reading the facts, instead of rubber stamping everything the USDA inc says.

 

sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and there is much concern now for CWD and risk factor for humans.

 

My sincere condolences to the family and friends of the House Speaker Becky Lockhart. I am deeply saddened hear this.

 

with that said, with great respect, I must ask each and every one of you Politicians that are so deeply saddened to hear of this needless death of the Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am seriously going to ask you all this...I have been diplomatic for about 17 years and it has got no where. people are still dying. so, are you all stupid or what??? how many more need to die ??? how much is global trade of beef and other meat products that are not tested for the TSE prion disease, how much and how many bodies is this market worth?

 

Saturday, January 17, 2015

 

*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease

 


 

*** 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 ***

 


 

Tuesday, November 04, 2014

 

Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease

 


 

Thursday, January 22, 2015

 

Transmission properties of atypical Creutzfeldt-Jakob disease: a clue to disease etiology?

 


 


 

Sunday, July 06, 2014

 

Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory Case-Control Study

 

Conclusions—The a priori hypotheses were supported.

 

*Consumption of various meat products may be one method of transmission of the infectious agent for sCJD.

 


 

PLEASE REMEMBER ;

 

The Akron, Ohio-based CJD Foundation said the Center for Disease Control revised that number in October of 2004 to about one in 9,000 CJD cases per year in the population group age 55 and older.

 

HAVE YOU GOT YOUR CJD QUESTIONNAIRE ASKING REAL QUESTIONS PERTAINING TO ROUTE AND SOURCE OF THE TSE AGENT THAT KILLED YOUR LOVED ONE ???

 

if not, why not...

 

Friday, November 30, 2007

 

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION

 


 


 

Friday, January 10, 2014

 

vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???

 


 


 

Sunday, February 08, 2015

 

FDA SCIENCE BOARD TO THE FOOD AND DRUG ADMINISTRATION BOVINE HEPARIN BSE CJD TSE PRION Wednesday, June 4, 2014

 


 

Tuesday, March 5, 2013

 

Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)

 

FDA believes current regulation protects the public from BSE but reopens comment period due to new studies

 


 

Monday, March 02, 2015

Rapid and Sensitive RT-QuIC Detection of Human Creutzfeldt-Jakob Disease Using Cerebrospinal Fluid
http://creutzfeldt-jakob-disease.blogspot.com/2015/03/rapid-and-sensitive-rt-quic-detection.html

 

TSS

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