Saturday, December 15, 2012

Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012

Short Report



Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update



Timm Konold, Mark E Arnold, Anthony R Austin, Saira Cawthraw, Steve AC Hawkins, Michael J Stack, Marion M Simmons, A Robin Sayers, Michael Dawson, John W Wilesmith and Gerald AH Wells




BMC Research Notes 2012, 5:674 doi:10.1186/1756-0500-5-674



Published: 5 December 2012




Abstract (provisional) Background To provide information on dose--response and aid in modelling the exposure dynamics of the BSE epidemic in the United Kingdom groups of cattle were exposed orally to a range of different doses of brainstem homogenate of known infectious titre from clinical cases of classical bovine spongiform encephalopathy (BSE). Interim data from this study was published in 2007. This communication documents additional BSE cases, which occurred subsequently, examines possible influence of the bovine prion protein gene (PRNP) on disease incidence and revises estimates of effective oral exposure.



Findings



Following interim published results, two further cattle, one dosed with 100 mg and culled at 127 months post exposure and the other dosed with 10 mg and culled at 110 months post exposure, developed BSE. Both had a similar pathological phenotype to previous cases. Based on attack rate and incubation period distribution according to dose, the dose estimate at which 50% of confirmed cases would be clinically affected was revised to 0.15 g of the brain homogenate used in the experiment, with a 95% confidence interval of 0.03--0.79 g. Neither the full open reading frame nor the promoter region of the prion protein gene of dosed cattle appeared to influence susceptibility to BSE, but this may be due to the sample size.



Conclusions Oral exposure of cattle to a large range of doses of a BSE brainstem homogenate produced disease in all dose groups. The pathological presentation resembled natural disease. The attack rate and incubation period were dependent on the dose.








Results and discussion




Previously published results of the first phase of the study established BSE in all ten cattle dosed with 3×100 g (IP range: 33–45 mpe) and 100 g (IP range: 31–60 mpe), in seven of nine cattle dosed with 10 g (IP range 41–72 mpe, the tenth died of an intercurrent disease at 14 mpe), and in seven of ten cattle dosed with 1 g (IP range: 45–72 mpe) [1]. In the second phase interim published results reported BSE in three of four cattle dosed with 1 g (IP range: 58–73 mpe), in seven of fifteen dosed with 100 mg (IP range: 53–98 mpe) and in single cattle from groups of fifteen dosed with 10 mg (IP: 56 mpe) or 1 mg (IP: 68 mpe).




After publication of the interim findings, two further cases of BSE were diagnosed in cattle in the second phase, one dosed with 100 mg and the other with 10 mg. For completeness of the data from the second phase the times from exposure to onset of the different clinical stages and cull for all BSE-positive cases are given in Table 1 and for all other cattle where BSE was excluded by postmortem tests in Table 2. Neuropathological examination confirmed a vacuolar profile in the brain of the case dosed with 10 mg consistent with that reported previously in the study and with that of naturally affected cattle [1]. The animal dosed with 100 mg and culled with spastic syndrome, did not present with vacuolar changes in the brain but in both cases the diagnosis of BSE was confirmed by detection of PrPd immunohistochemically and PrPres on WB.




snip...




Preliminary findings from the original study contributed to quantitative risk assessment of the exposure of humans to consumption of infected bovine products [9]. An estimate of human ID50 assumed the worst case of a cattle to human species barrier of a factor of one, giving the range of human oral ID50s in 1 g of brain from a clinically affected cow as approximately 0.52 to 5. Data from the previously published interim results revised this estimate to 1.0 to 20 and additional results in the present study indicate that this range should now be revised to 1.3 to 33.3, although, as previously, it could be greater with higher titres of BSE affected brain than used in the present study. These estimates have been used to assess the impact of BSE control measures on potential consumption of BSE infectivity (BSE control model [10]). Although the reduced ID50 based on the present results would increase estimates of the exposure of humans in terms of bovine oral ID50s, the effect would be comparatively small relative to the uncertainty in such risk assessments. Nevertheless, with decline of the BSE epidemic and the potential for relaxation of certain controls, the revised estimate of human oral ID50 is available to revisit risk assessments.




The present data do not affect the previous approximation that single doses in the range from 100 mg to 1 g of the brainstem homogenate used correspond to the range of mean IPs of cattle through the BSE epidemic [1]. The observation that a relatively small, single exposure (less than 1 g of high titre brain) can result in infection reinforces the importance of preventing cross-contamination during feed ingredient storage and feed production. This proved to be problematical in feed mills producing ruminant and non-ruminant feedstuffs as is evident from the incomplete effect of the initial statutory control on the feeding of meat and bone meal to ruminants introduced in the UK in 1988. The low dose phenomenon, together with the persistent viability of the BSE agent, has required the removal of specific high risk tissues from cattle at slaughter and the total ban on the use of mammalian meat and bone meal for use in farmed livestock [11].




Conclusions




The present results concur with the interim findings of this study, that the oral exposure of cattle to BSE brain homogenate produced dose dependent effects on IP and attack rate such that in general the higher the dose the shorter the IPs and the greater the attack rate. In all cases the induced disease closely resembled the pathology of the natural disease. This is in keeping with the analysis of the pathology in orally dosed cattle from another study [12] and reinforces the validity of the oral exposure model for the study of classical BSE in the natural host. The estimate of a cattle oral ID50 is revised to 0.15 g brain material used for the studies. Decline of the BSE epidemic indicates that the use of a revised estimate of human oral ID50 in risk assessments is, in future, likely to contribute mainly to reassessments in relation to possible relaxation of controls.









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.









PRION 2009 CONGRESS BOOK OF ABSTRACTS


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.









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 v CJD as fast as intracerebrally inoculated animals.


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







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






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








Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........






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






6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.






2012



***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...






MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...


***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model






***Infectivity in skeletal muscle of BASE-infected cattle






***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.






***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.






The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.


In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.






2012 CALIFORNIA ATYPICAL L-TYPE BASE BSE MAD COW, SPONTANEOUS AND FEED $$$



Saturday, May 26, 2012



Are USDA assurances on mad cow case 'gross oversimplification'?



SNIP...



What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”



The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”



“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.



In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said



The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.



SNIP...








in the url that follows, I have posted




SRM breaches first, as late as 2011.



then



MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007, when they ceased posting them.



then,



MAD COW SURVEILLANCE BREACHES.




Friday, May 18, 2012


Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012






Wednesday, May 30, 2012


PO-028: Oral transmission of L-type bovine spongiform encephalopathy (L-BSE) in primate model Microcebus murinus






1997 USDA/FDA MAD COW BSE PARTIAL AND VOLUNTARY MAD COW FEED BAN...10 YEARS LATER ;




2007




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









2006




Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV


Date: September 6, 2006 at 7:58 am PST


PRODUCT


a) EVSRC Custom dairy feed, Recall # V-130-6;


b) Performance Chick Starter, Recall # V-131-6;


c) Performance Quail Grower, Recall # V-132-6;


d) Performance Pheasant Finisher, Recall # V-133-6.


CODE


None


RECALLING FIRM/MANUFACTURER


Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.


REASON


Dairy and poultry feeds were possibly contaminated with ruminant based protein.


VOLUME OF PRODUCT IN COMMERCE


477.72 tons


DISTRIBUTION


AL


______________________________


PRODUCT


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






Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS


Date: August 16, 2006 at 9:19 am PST


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 MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs


Date: August 6, 2006 at 6:14 pm PST


PRODUCT


Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6


CODE


All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.


RECALLING FIRM/MANUFACTURER


Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.


REASON


The feed was manufactured from materials that may have been contaminated with mammalian protein.


VOLUME OF PRODUCT IN COMMERCE


27,694,240 lbs


DISTRIBUTION


MI


END OF ENFORCEMENT REPORT FOR AUGUST 2, 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


###






Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ?????


Date: August 6, 2006 at 6:19 pm PST


PRODUCT


Bulk custom made dairy feed, Recall # V-114-6


CODE


None


RECALLING FIRM/MANUFACTURER


Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm 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


?????


DISTRIBUTION


KY


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


###






2005




SNIP...




SEE MORE MAD COW FEED BAN WARNINGS AND LETTERS HERE ;




Saturday, August 4, 2012


Final Feed Investigation Summary - California BSE Case - July 2012







Tuesday, July 17, 2012


O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012








Wednesday, May 25, 2011


O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011


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


From: Terry S. Singeltary Sr.


To: BSE-L@LISTS.AEGEE.ORG


Cc: trade@oie.int ; oie@oie.int ; f.diaz@oie.int ; scientific.dept@oie.int ; cjdvoice@yahoogroups.com ; BLOODCJD@YAHOOGROUPS.COM


Sent: Tuesday, May 24, 2011 2:24 PM


Subject: O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011







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







Monday, November 23, 2009


BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E. COMMISSION DECISION of 11 November 2009 amending the Annex to Decision 2007/453/EC as regards the BSE status of Chile, Colombia and Japan (notified under document C(2009) 8590)







IT'S as obvious as day and night, either Larry, Curley, and Mo have been at the helm of the USDA/APHIS/FSIS/FDA/CDC/NIH et al for many many years, or the incompetence of these agencies are so inept, either through ignorance and or just too overweight with industry reps., they then should be all done away with and a single agency brought forth, and if not, how will you correct this ongoing problem ?









Wednesday, March 28, 2012


VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up again $







Tuesday, November 6, 2012


Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and Sporadic CJD, November-December 2012 update







Friday, November 23, 2012


sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA







Sunday, December 2, 2012


CANADA 19 cases of mad cow disease SCENARIO 4: ‘WE HAD OUR CHANCE AND WE BLEW IT’








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...









Are some commoner types of neurodegenerative disease (including Alzheimer's disease and Parkinson's disease) also transmissible? Some recent scientific research has suggested this possibility





Friday, September 3, 2010



Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE









Wednesday, September 21, 2011


PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)










Wednesday, January 5, 2011


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


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












Wednesday, May 16, 2012


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Proposal ID: 29403










layperson




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




MOM DOD 12/14/97 CONFIRMED hvCJD...

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