Friday, January 7, 2011

MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION

Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066


MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION


Christopher J. Johnson1, Debbie McKenzie2, Joel A. Pedersen3, Judd M. Aiken4

1Prion Research Laboratory, USGS National Wildlife Health Center, Madison, Wisconsin, USA 2Centre for Prions and Protein Folding Diseases, Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada 3Department of Soil Science and Molecular and Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin, USA 4Centre for Prions and Protein Folding Diseases, Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, Alberta, Canada

Ingestion of prion-contaminated materials is postulated to be a primary route of prion disease transmission. Binding of prions to soil (micro)particles dramatically enhances peroral disease transmission relative to unbound prions, and it was hypothesized that micrometer– sized particles present in other consumed materials may affect prion disease transmission via the oral route of exposure. Small, insoluble particles are present in many substances, including soil, human foods, pharmaceuticals, and animal feeds. It is known that meat and bone meal (MBM), a feed additive believed responsible for the spread of bovine spongiform encephalopathy (BSE), contains particles smaller than 20 ìm and that the pathogenic prion protein binds to MBM. The potentiation of disease transmission via the oral route by exposure to MBM or three micrometer-sized mineral feed additives was determined. Data showed that when the disease agent was bound to any of the tested materials, the penetrance of disease was increased compared to unbound prions. Our data suggest that in feed or other prion– contaminated substances consumed by animals or, potentially, humans, the addition of MBM or the presence of microparticles could heighten risks of prion disease acquisition.

SNIP...

CONCLUSIONS

Should prions be present in animal feed, their association with MBM or insoluble particles such as those tested (viz. Mte, Kte, and SiO2) could substantially increase the risk of disease acquisition compared to consumption of prions alone. While care needs to be exercised when extrapolating results from laboratory rodent models to ruminants, these data may explain how MBM produced BSE transmission despite the presumably low titers of infectious agent present in cattle feed (Taylor et al., 1995). In addition, inorganic particles in commercial feeds or mineral licks may pose a previously unrecognized risk of enhancing TSE transmission to domestic and wildlife species from agents contaminating these materials or infectivity shed onto feed or licks.

Following consumption, (sub)micrometersized particles can be absorbed by the gut. Goblet cells (Doyle-McCullough et al., 2007), M cells in Peyer’s patches (Florence, 1997), and persorptive mechanisms at the tips of broken intestinal villi (Hillyer & Albrecht, 2001; Volkheimer, 2001) all contribute to intestinal particle uptake. Increased uptake of particlebound prions might explain enhanced oral transmissibility. Alternatively, aluminosilicates may increase residence time of agent in the digestive system (Bringe & Schultz, 1969; Collings et al., 1980; Quisenberry, 1968) and elevate exposure time at sites of conversion. Further investigation into these mechanisms, the effect of digestive processes on bound prions, and alterations of agent physicochemical properties upon binding is warranted.

It is noteworthy that microparticles find widespread use as human food and pharmaceutical additives in Western diets (Lomer et al., 2000, 2004). The average daily consumption dietary microparticles from food, pharmaceuticals, and dentifrices is approximately 40 mg (approximately 1012 particles) per person (Powell et al., 2007). The extent to which microparticles in the human diet influence prion disease acquisition is currently unknown, but these data suggest that microparticle consumption needs to be investigated as a potential risk factor in human TSE acquisition.

SEE FULL TEXT ;

http://www.informaworld.com/smpp/content~content=a931920802~db=all~jumptype=rss


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

http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm


BANNED MAD COW FEED IN COMMERCE IN ALABAMA (where h-g-BSEalabama mad cow was documented)

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

______________________________

http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html


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

###

http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html


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

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


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

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html


Tuesday, March 2, 2010

Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA

http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html


Monday, March 1, 2010

ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010

http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html



Terry S. Singeltary Sr. (Submitted question): Monday, April 5, 2010

Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010

http://madcowfeed.blogspot.com/2010/04/update-on-feed-enforcement-activities.html



Friday, April 23, 2010

Upcoming BSE Webinar on Thursday, April 22, 2010 a review

http://bseusa.blogspot.com/2010/04/upcoming-bse-webinar-on-thursday-april.html



Friday, October 8, 2010

Scientific reasons for a feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food

http://madcowfeed.blogspot.com/2010/10/scientific-reasons-for-feed-ban-of-meat.html



O.4.3

Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission

Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany

Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).

Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.

Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.

Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.

Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.

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 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.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf



P03.137

Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC

Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan

Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.


P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf



Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf



WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

snip...

BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa


It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf



it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf



Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

http://madcowfeed.blogspot.com/2008/07/docket-no-04-047-l-regulatory.html


BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8



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

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



Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html


PART 2

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html


Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Docket Type Rulemaking Document APHIS-2007-0033-0001 Document Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Public Submission APHIS-2007-0033-0002.1 Public Submission Title Attachment to Singeltary comment

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002;

[TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]

http://www.aphis.usda.gov/vs/ceah/cei/bse_greece0701.htm

Greetings list members,

i just cannot accept this;

23 kg of meat in a suitcase (suitcase bomb...TSS)

The data do not provide a species of origin code for these

products, therefore they may not contain any ruminant product.

what kind of statement is this? how stupid do they think we are? it could also very well mean that _all_ of it was ruminant based products !

Terry S. Singeltary Sr., Bacliff, Texas USA

What is the level of passenger traffic arriving in the United States from Slovenia?

There were no direct flights from Slovenia to the US in fiscal year 2000.

APHIS-PPQ’s agriculture quarantine inspection monitoring sampled 27 air passengers from Slovenia for items of agricultural interest in fiscal year 2000.

One of these 27 passengers was carrying two kilograms of a meat item that could potentially harbor pathogens that cause BSE. This passenger arrived to Elizabeth, New York, in June 2000 and declared no intention to visit a farm or ranch in the US.

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

http://www.aphis.usda.gov/vs/ceah/cei/bse_slovenia1101.htm

What is the level of passenger traffic arriving in the United States from the affected country?

A total of 45,438 passengers arrived in the US on direct flights from the Czech Republic in fiscal year 2000. It is likely that additional passengers originating in the Czech Republic traveled to the US on non-direct flights.

As part of APHIS-PPQ’s Agriculture Quarantine Inspection Monitoring, 238 air passengers from the Czech Republic were inspected for items of agricultural interest in fiscal year 2000. Of these, 10, or 4.2%, were found to be carrying a total of 17 kg of items that could potentially present a risk for BSE. None of the passengers with items reported plans to visit or work on a farm or ranch while in the US.

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

http://www.aphis.usda.gov/vs/ceah/cei/bse_cz0601.htm

What are the US imports of affected animals or animal products from Austria?

Between 1998 and June 2001, US imports from Austria included goat meat, animal feeds, and sausage. The sausage and animals feeds were from unspecified species. Source: World Trade Atlas

snip...

What is the level of passenger traffic arriving in the United States from Austria?

A total of 168,598 passengers on direct flights from Austria arrived at US airports in fiscal year 2000.

An undetermined number of passengers from Austria arrived in the US via indirect flights. Under APHIS-PPQ’s agricultural quarantine inspection monitoring, 565 air passengers from Austria were sampled for items of agricultural interest in fiscal year 2000. Ten (10) of these passengers, or 1.7 percent, carried a total of 23 kg meat (non-pork) items that could potentially harbor the pathogen(s) that cause BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the US.

Source: US Dept. of Transportation; APHIS-PPQ

http://www.aphis.usda.gov/vs/ceah/cei/bse_austria1201.htm

Greetings FDA and public,

if you go to the below site, and search all BSE known countries and check out their air traffic illegal meat they have confiscated, and check out the low number checked, compared to actual passenger traffic, would not take too much for some nut to bring in FMD/TSEs into the USA as a 'suitcase bomb'.

[[Under APHIS-PPQ's agricultural quarantine inspection monitoring, 284 air passengers from Israel were sampled for items of agricultural interest in fiscal year 2001. Seven of these passengers, or 2 percent, carried a total of 11 kg of meat items that could potentially harbor the pathogen that causes BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the U.S.]]

if they were to have questioned the terrorist that bombed the Twin Towers with jets, if they were to have questioned them at flight school in the USA, i am sure that they would have said they did not intend to visit the Twin Towers as a flying bomb either. what am i thinking, they probably did ask this? stupid me.

http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm


http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=090000648027c28e


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.

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf


***

P.9.21

Molecular characterization of BSE in Canada

Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.

Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *** It also suggests a similar cause or source for atypical BSE in these countries.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf


Tuesday, December 14, 2010 TAFS1ripmomdod12-14-97hvcjd

Position Paper on Relaxation of the Feed Ban in the EU SUMMARY © TAFS, Berne, 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/tafs1-position-paper-on-relaxation-of.html


Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129


2010 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.

http://www.neuroprion.org/en/np-neuroprion.html


TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY UPDATE NORTH AMERICA JANUARY 2011

Wednesday, December 29, 2010

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PRION END OF YEAR REPORT DECEMBER 29, 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/transmissible-spongiform-encephalopathy.html


Saturday, December 18, 2010

OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011

snip...

Greetings,

Thank for your support to the OIE objectives for a safe world.

NOT !

I see again that the OIE has done little to help eradicate all animal TSE from the globe, and in fact in my opinion, have help enhance the spread of BSE and other animal TSE globally by their industry friendly regulations. I tried to warn the OIE in 2002 about CWD and the potential, but very real threat of CWD to humans. I was told that they were seriously considering this. what happened ? NOW, the OIE and the USDA collaborate to make legal the trading of all strains of atypical BSE legal, and in fact have done so with the atypical scrapie, when science has made perfectly clear the risk factors to humans and other species. I have said it once (see below), and i will say again ;

"THE OIE has now shown they are nothing more than a National Trading Brokerage for all strains of animal TSE. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization."

NOW, some history on the failed OIE BSE/TSE policy, and why the OIE allowed BSE and other TSE to spread around the globe $$$

snip...

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html


Tuesday, November 02, 2010

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html


Saturday, December 11, 2010

Species-barrier-independent prion replication in apparently resistant species

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/species-barrier-independent-prion.html


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.

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf


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.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2


Rural and Regional Affairs and Transport References Committee The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010

2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49

2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50

http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf


Wednesday, March 31, 2010

Atypical BSE in Cattle

http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html


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.

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156


http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF



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)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html



Saturday, June 12, 2010

PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse

http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html



Wednesday, July 28, 2010

re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010

http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html



Wednesday, December 29, 2010

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PRION END OF YEAR REPORT DECEMBER 29, 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/transmissible-spongiform-encephalopathy.html




Thursday, September 10, 2009

Experimental oral transmission of CWD to red deer (Cervus elaphus elaphus): early detection and late stage distribution of protease-resistant protein

http://chronic-wasting-disease.blogspot.com/2009/09/experimental-oral-transmission-of.html


Research Project: Transmissible Spongiform Encephalopathies: the Role of Genetics, Strain Variation, and Environmental Contamination in Disease Control Location: Animal Diseases Research

Title: Experimental oral transmission of chronic wasting disease to red deer (Cervus elaphus elaphus): Early detection and late stage distribution of protease-resistant prion protein

Authors

Balachandran, A - CANADIAN FOOD INSPCTN AG Harrington, Noel - CANADIAN FOOD INSPCTN AG Algire, James - CANADIAN FOOD INSPCTN AG Souyrine, Andre - CANADIAN FOOD INSPCTN AG Spraker, Terry - COLORADO ST UNIV Jeffrey, Martin - Gonzalez, Lorenzo - Orourke, Katherine

Submitted to: Canadian Veterinary Journal Publication Type: Peer Reviewed Journal Publication Acceptance Date: December 1, 2008 Publication Date: March 11, 2010 Reprint URL: http://ddr.nal.usda.gov/dspace/bitstream/10113/40677/1/IND44334511.pdf Citation: Balachandran, A., Harrington, N., Algire, J., Souyrine, A., Spraker, T., Jeffrey, M., Gonzalez, L., Orourke, K.I. 2010. Experimental oral transmission of chronic wasting disease to red deer (Cervus elaphus elaphus): Early detection and late stage distribution of protease-resistant prion protein. Canadian Veterinary Journal. Canadian Veterinary Journal. 51:169-178.

Interpretive Summary: Farmed cervids may be exposed to the prion disorder chronic wasting disease through contact with free ranging or farmed infected Rocky Mountain elk, white tailed deer, mule deer, or moose. This is the first report of experimental transmission of chronic wasting disease to red deer, an economically important agricultural commodity in parts of North America. Brain tissue from infected Rocky Mountain elk was administered by the oral route of red deer. Deer were examined at 18 months after infection for evidence of abnormal prion protein, the marker for the disease. The abnormal protein was found throughout the brain, spinal cord and lymphoid tissues, with variable distribution in other organ systems. This finding confirms the potential susceptibility of this species to disease under natural conditions and the reliability of the current testing format for identifying the abnormal protein in the tissues routinely collected in surveillance programs. The widespread distribution of the abnormal protein in red deer indicates the potential for shedding of the agent into the environment. Technical Abstract: Chronic wasting disease CWD is the transmissible spongiform encephalopathy or prion disease of wild and farmed cervid ruminants, including Rocky Mountain elk (Cervus elaphus nelsoni), white tailed deer (Odocoileus virginianus), mule deer (Odocoileus hemionus), or moose (Alces alces). Reliable data on the susceptibility of other farmed cervid species, the distribution of the abnormal prion protein marker in brain and lymphoid tissues collected in surveillance programs, and the role of prion genotype are necessary for design of control programs for CWD in farmed cervids. In this study, red deer (Cervus elaphus elaphus) were exposed to the prion agent by oral administration of brain homogenates from infected Rocky Mountain elk. Antemortem testing was performed at 7 months post infection and the deer were euthanized when clinical disease was observed at approximately 18 months after infection. The abnormal prion protein was assayed by immunohistochemistry, enzyme linked immunosorbent assay and western blot. Abnormal prion protein was found in the spinal cord, brainstem, cerebellum, midbrain, thalamus, and cerebrum in all 4 infected red deer. Most of the lymph nodes throughout the body were positive for abnormal prion proteins. Abnromal prion protein was observed in some additional peripheral tissues in some but not all of the deer. In particular, most areas of the gastrointestinal tract were positive for abnormal prions, although the salivary glands were rarely positive. This study demonstrates the potential for oral transmission of chronic wasting disease to red deer and confirms the usefulness of the current testing methods for post mortem diagnosis of the disease in this species.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=228787


http://www.ncbi.nlm.nih.gov/pubmed/20436863


Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.html


CWD, GAME FARMS, BAITING, AND POLITICS

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html


http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html


Monday, February 22, 2010

Aerosol and Nasal Transmission of Chronic Wasting Disease in Cervidized Mice

http://chronic-wasting-disease.blogspot.com/2010/02/aerosol-and-nasal-transmission-of.html


AS THE CROW FLIES, SO DOES CWD

Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html


Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/07/deer-carcass-decomposition-and.html


SO, as i said, once established, it is very difficult to extinguish completely. the trading of cervids from state to state (legal and illegal), is another problem. deer urine scents is another problem, you have hunters that pour this stuff on themselves, and it's just plain stupid, from what science is telling us.

Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer

http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html


THEN YOU have water that has been contaminated from a CWD-endemic area ;

Wednesday, October 14, 2009

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html


ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD ;

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html


http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf



-------- Original Message --------

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

Date: Fri, 16 May 2003 11:47:37 -0500

From: "Terry S. Singeltary Sr."

To: fdadockets@oc.fda.gov

Greetings FDA,

i would kindly like to comment on; Docket 03D-0186FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;

1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the_total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test toassure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthyones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in theUSA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread theseTSE mad cow agents in the USA.

I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in theUSA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make the same mistakes...

references

snip...

Oral transmission and early lymphoid tropism of chronic wasting diseasePrPres in mule deer fawns (Odocoileus hemionus )

Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1Department of Pathology, College of Veterinary Medicine and BiomedicalSciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1Department of Veterinary Sciences, University of Wyoming, 1174 SnowyRange Road, University of Wyoming, Laramie, WY 82070, USA 2Colorado Division of Wildlife, Wildlife Research Center, 317 WestProspect Road, Fort Collins, CO 80526-2097, USA3Colorado State University Veterinary Diagnostic Laboratory, 300 WestDrake Road, Fort Collins, CO 80523-1671, USA4Animal Disease Research Unit, Agricultural Research Service, USDepartment of Agriculture, 337 Bustad Hall, Washington State University,Pullman, WA 99164-7030, USA5Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mailehoover@lamar.colostate.eduMule

deer fawns (Odocoileus hemionus) were inoculated orally with abrain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associatedl ymphoid tissues (one or more of the following: retropharyngeal lymphnode, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonalantibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.

snip...

These results indicate that mule deer fawns develop detectable PrPres after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoidtissues draining the oral and intestinal mucosa (i.e. there tropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileumand spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node.He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings supportoral exposure as a natural route of CWD infection in deer and supportoral inoculation as a reasonable exposure route for experimental studies of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757


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

now, just what is in that deer feed? _ANIMAL PROTEIN_

Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES

Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-LTo: BSE-L

8420-20.5% Antler DeveloperFor Deer and Game in the wildGuaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400A RATION FOR DEERNET WEIGHT 50 POUNDS22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

IngredientsGrain Products, Plant Protein Products, Processed Grain By-Products,Forage Products, Roughage Products 15%, Molasses Products,

__Animal Protein Products__,

Monocalcium Phosphate, Dicalcium Pyosphate, Salt,Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, CholineChloride, Folic Acid, Menadione Soduim Bisulfite Complex, PyridoxineHydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, ZincOxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, DriedSacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,Artificial Flavors added.http://www.bodefeed.com/prod6.htm

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MORE ANIMAL PROTEIN PRODUCTS FOR DEER

Bode's #1 Game PelletsA RATION FOR DEERF3153GUARANTEED ANALYSISCrude Protein (Min) 16%Crude Fat (Min) 2.0%Crude Fiber (Max) 19%Calcium (Ca) (Min) 1.25%Calcium (Ca) (Max) 1.75%Phosphorus (P) (Min) 1.0%Salt (Min) .30%Salt (Max) .70%IngredientsGrain Products, Plant Protein Products, Processed Grain By-Products,Forage Products, Roughage Products, 15% Molasses Products,

__Animal Protein Products__,

Monocalcium Phosphate, Dicalcium Phosphate, Salt,Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, CholineChloride, Folic Acid, Menadione Sodium Bisulfite Complex, PyridoxineHydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, ZincOxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, DriedSaccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,Artificial Flavors added.FEEDING DIRECTIONSFeed as Creep Feed with Normal Diet

http://www.bodefeed.com/prod8.htm

INGREDIENTS

Grain Products, Roughage Products (not more than 35%), Processed GrainBy-Products, Plant Protein Products, Forage Products,

__Animal Protein Products__,

L-Lysine, Calcium Carbonate, Salt, Monocalcium/DicalciumPhosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, BasicCopper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin ASupplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, CalciumLignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium BisulfiteComplex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate

DIRECTIONS FOR USE

Deer Builder Pellets is designed to be fed to deer under rangeconditions or deer that require higher levels of protein. Feed to deerduring gestation, fawning, lactation, antler growth and pre-rut, allphases which require a higher level of nutrition. Provide adequateamounts of good quality roughage and fresh water at all times.

http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html

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DEPARTMENT OF HEALTH & HUMAN SERVICESPUBLIC HEALTH SERVICEFOOD AND DRUG ADMINISTRATIONApril 9, 2001 WARNING LETTER01-PHI-12CERTIFIED MAILRETURN RECEIPT REQUESTED

Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145

PHILADELPHIA DISTRICT

Tel: 215-597-4390

Dear Mr. Raymond:Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23,2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattleor other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal.Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.The above is not intended to be an all-inclusive list of deviations fromthe regulations. As a manufacturer of materials intended for animalfeed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance withthe law. We have enclosed a copy of FDA's Small Entity Compliance Guideto assist you with complying with the regulation... blah, blah, blah...

http://www.fda.gov/foi/warning_letters/g1115d.pdf

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snip...end...full text ;

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 1 Terry S. Singeltary Sr. Vol #: 1

http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm


2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 7 Terry S. Singeltary Sr. Vol #: 1

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 7 Terry S. Singeltary Sr. Vol #: 1

http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm


01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm


above urls dead, go here ;

http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html


Zoo Prion Disease: Review of Scientific Literature

http://www.mad-cow.org/zoo_cites_annotated.html


PPo3-30:

Immunohistochemical and Biochemical Characteristics of BSE and CWD in Experimentally Infected European Red Deer (Cervus Elaphus)

Stuart Martin,1 Martin Jeffrey,1 Lorenzo González,1 Sílvia Sisó,1 Hugh Reid,2 Philip Steele,2 Mark Dagleish,2 Michael Stack,1 Melanie Chaplin,1 John Spiropoulos,1 Marion Simmons,1 Wilfred Goldmann3 and Aru Balachandran4 1Veterinary Laboratories Agency; Addlestone, Surrey UK; 2Moredun Research Institute, Penicuik, Midlothian, Scotland UK; 3Neuropathology Unit; Roslin, Scotland UK; 4Canadian Food Inspection Agency

Key words: red deer, BSE, CWD, IHC, WB, polymorphism, bioassay

Thirty-two deer were orally or intra-cerebrally dosed with homogenate from a pool of five BSE-positive bovine brains and negative control animals underwent identical procedures with sterile saline buffer. An extensive range of samples was tested by immunohistochemistry (IHC), western blot (WB, brainstem only) and mouse bioassay (2 positive deer). In the absence of clinical signs, none of the 12 orally-dosed deer culled after 6 or 12 months, nor 5 of 6 culled at the termination of the experiment (72 months), showed any evidence of abnormal PrP accumulation by IHC or WB. In contrast, all the 6 intra-cerebrally challenged and 1 of 6 orally dosed deer developed clinical disease at various times after infection. These deer showed widespread accumulation of disease specific PrP in the CNS, PNS and ENS but none in the LRS. Both IHC and WB features were similar to those of BSE in sheep, goats and cattle but unlike those seen in CWD in elk or scrapie in sheep. Analysis of the PrP ORF of all deer in the experiment identified a Q to E polymorphism at codon 226. Interestingly, the single deer that succumbed to oral BSE infection was the only QQ deer of the 6 allowed to develop clinical disease, suggesting that such polymorphism may influence the susceptibility of deer to oral BSE. Brain homogenates from positive deer were inoculated into panels of 20 Tg(cerPrP) 1536+/- mice, which developed neurological signs with an incubation period of 202–298 days post inoculation and attack rates of 90–95%.

http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099


see ;

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010 PRION 2010

International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


Wednesday, December 29, 2010

CWD Update 99 December 13, 2010

http://chronic-wasting-disease.blogspot.com/2010/12/cwd-update-99-december-13-2010.html


Sunday, October 31, 2010

Scientific Opinion on the results of the EU survey for Chronic Wasting Disease (CWD) in cervids EFSA Panel on Biological Hazards (BIOHAZ) (October) 20

http://chronic-wasting-disease.blogspot.com/2010/10/scientific-opinion-on-results-of-eu.html


PLEASE SEE the dramatic increase in sporadic CJD cases in documented BSE countries, then think, BSE can propagate as nvCJD and sporadic CJD in the lab ;

TOTAL CASES OF SPORADIC CJD (DEATHS) DEFINITE AND PROBABLE CASES

Australia Austria Canada France Germany Italy Netherlands Slovakia Spain Switzerland UK

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


USA

5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

2010

PLEASE NOTE REFERENCE LINES 5. AND 6.

Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1996 & earlier 51 33 28 5 0 0

1997 114 68 59 9 0 0

1998 88 52 44 7 1 0

1999 120 72 64 8 0 0

2000 146 103 89 14 0 0

2001 209 119 109 10 0 0

2002 248 149 125 22 2 0

2003 274 176 137 39 0 0

2004 325 186 164 21 0 1(3)

2005 344 194 157 36 1 0

2006 383 197 166 29 0 2(4)

2007 377 214 187 27 0 0

2008 394 231 204 25 0 0

2009 425 259 216 43 0 0

2010 204 124 85 20 0 0

TOTAL 3702(5) 2177(6) 1834 315 4 3

1 Listed based on the year of death or, if not available, on year of referral;

2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;

3 Disease acquired in the United Kingdom;

4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;

5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

http://www.cjdsurveillance.com/pdf/case-table.pdf


Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)

(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)

http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html


Monday, August 9, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?

http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html


Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011

Prions

David W. Colby1,* and Stanley B. Prusiner1,2

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

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