Thursday, April 26, 2012

Maternal Transmission of the BSE and Birth Cohorts


with typical c-type BSE, horizontal transmission of this strain is supposedly very low.


with atypical L-type BASE BSE, that's another question, one that has not been answered yet, but one that should be taken very seriously.


then you have the CWD strains in cervids and scrapie strains. once these strains mutate, become more virulent, such as with the atypical L-type BASE BSE, then there should be much more concern for this type transmission.



Vertical Transmission of Bovine Spongiform Encephalopathy Prions Evaluated in a Transgenic Mouse Model



  1. J. M. Torres1,*
+ Author Affiliations
  1. 1Centro de Investigación en Sanidad Animal (CISA-INIA), Ctra. de Valdeolmos a El Casar, Valdeolmos, 28130 Madrid, Spain
  2. 2Departamento de Reproducción Animal y Conservación de Recursos Zoogenéticos (INIA), Avda. Puerta de Hierro s/n, Madrid 28040, Spain

ABSTRACT

In this work we show evidence of mother-to-offspring transmission in a transgenic mouse line expressing bovine PrP (boTg) experimentally infected by intracerebral administration of bovine spongiform encephalopathy (BSE) prions. PrPres was detected in brains of newborns from infected mothers only when mating was allowed near to the clinical stage of disease, when brain PrPres deposition could be detected by Western blot analysis. Attempts to detect infectivity in milk after intracerebral inoculation in boTg mice were unsuccessful, suggesting the involvement of other tissues as carriers of prion dissemination. The results shown here prove the ability of BSE prions to spread centrifugally from the central nervous system to peripheral tissues and to offspring in a mouse model. Also, these results may complement previous epidemiological data supporting the occurrence of vertical BSE transmission in cattle.


FOOTNOTES

    • Received 4 November 2004.
    • Accepted 3 March 2005.
  • ↵*Corresponding author. Mailing address: Centro de Investigación en Sanidad Animal INIA, Valdeolmos, 28130 Madrid, Spain. Phone: 34 91 620 23 00. Fax: 34 91 620 22 47. E-mail: jmtorres@inia.es.




http://jvi.asm.org/content/79/13/8665.abstract









Envt.18: Mother to Offspring Transmission of Chronic Wasting Disease
Candace K. Mathiason,
† Amy Nalls, Kelly Anderson, Jeanette Hayes-Klug, Jenny G. Powers, Nicholas J. Haley and Edward A. Hoover


Colorado State University; Fort Collins, CO USA
†Presenting author; Email: ckm@lamar.colostate.edu


We have developed a new cervid model in small Asian muntjac deer (
Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by four months post infection. Ten fawns were born to these CWD-infected doe— four of the fawns were viable, five were non-viable and one was a first trimester fetus harvested from a CWD-infected doe euthanized at end-stage disease. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn by IHC as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yielded positive results on another fawn at ten days of age. In addition, sPMCA assays have demonstrated amplifiable prions in fetal placental or spleen tissue of three non-viable fawns and mammary tissue of the dams.


Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.



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




PPo3-18: A Possible Case of Maternal Transmission of the BSE Agent within Captive Cheetah Affected with Feline Spongiform Encephalopathy
Anna Bencsik, Sabine Debeer, Thierry Petit and Thierry Baron
Afssa; Unité ATNC; Lyon, France; Zoo de la Palmyre; Les Mathes, France
Key words:
BSE, FSE, vertical transmission

Introduction.
Feline spongiform encephalopathy (FSE) is considered to be related to bovine spongiform encephalopathy (BSE). It has been reported in domestic cats as well as in captive wild cats including cheetahs, first in the United Kingdom (UK) and then in other European countries. In France, several cases were described in cheetahs either imported from UK or born in France. Here we report details of two other FSE cases in captive cheetah. These cases are of particular interest since the 2nd case of FSE in a cheetah born in France, appears most likely due to maternal transmission.1

Results.
Complete PrPd study showed the close likeness between the two cheetah cases. The TgOvPrP4 mouse brains infected with cattle BSE and cheetah FSE revealed similar vacuolar lesion profiles, PrPd brain mapping with occurrence of typical florid plaques.

Materials and Methods.
Using immunohistochemistry (IHC), pathological form of PrP(PrPd) was analyzed in the brains and peripheral organs of these two cheetahs. Transmission studies to the TgOvPrP4 mouse line were also performed, for comparison with the transmission of cattle BSE. Lesion profiles of the infected transgenic mice were analyzed as well as type and brain distribution of PrPd.

Conclusion.
Collectively, these data indicate that both FSE cases harbor the same strain of agent as the cattle BSE agent. Because this is most probably a case of maternal transmission of the disease, this new observation may have some impact on our knowledge of vertical transmission of BSE agent-linked TSEs such as in human variant Creutzfeldt Jakob disease.

References
1. Bencsik et al. PLoS One 2009; 4:6929.
=========================




PPo3-40: Mother to Offspring Transmission of Chronic Wasting Disease
Candace K. Mathiason, Amy V. Nalls, Kelly Anderson, Jeanette Hayes-Klug, Nicholas Haley and Edward A. Hoover
Colorado State University, Department of Microbiology, Immunology and Pathology, Fort Collins, CO USA
Key words: Chronic wasting disease, vertical transmission, muntjac deer

We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by 4 months post infection. Six fawns were born to these CWD-infected doe. Six fawns were born to 6 CWD-infected doe; 4 of the fawns were non-viable. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age. In addition, sPMCA assays have also demonstrated amplifiable prions in maternal placental (caruncule) and mammary tissue of the dam.

Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.
PRION 2011





landesbioscience.com









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





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





clip_image001
Executive Summary

7. The executive summary must not exceed 2 sides in total of A4 and should be understandable to the intelligent non-scientist.
It should cover the main objectives, methods and findings of the research, together with any other significant events and options for new work.







The purpose of this study was to investigate whether sheep, of various PrP genotypes, experimentally infected with BSE could transmit the disease to their offspring. The genotypes of the ewes were chosen as most susceptible (AQ/AQ) through to least susceptible (AR/AR) when challenged orally with BSE. A number of unchallenged ewes were mixed with these sheep to monitor for adventitious lateral transmission of disease.
The sheep were NPU Cheviots which do not always show BSE clinical signs after experimental challenge.Offspring therefore fell into three groups: those from mothers that did develop clinical BSE, those from challenged ewes which remained healthy, and those from control unchallenged ewes.
Over the course of the study the ewes produced eight lamb crops and a total of 144 lambs which were observed for at least 5 years. The lambs were grouped together based on gender while the parturient ewes were mixed together just prior to and after lambing. Ewes were penned separately during the perinatal phase. At weaning the lambs joined the larger groups of lambs.
None of the 144 lambs showed any evidence of contracting BSE from the experimentally dosed sheep, however, two sheep plus one of the unchallenged control ewes did have pathology and PrPSc Western blotting pattern which were indicative of atypical scrapie.
Our results (statistically analysed) suggest that maternal transmission of BSE under the experimental conditions of this study could only occur in NPU Cheviots at a maximum rate less than 28%. However, a further study in sheep (Bellworthy et al 2005) showed that natural transmission of BSE was possible within an experimental flock under certain circumstances although within the 28% margin found in the present study. Studies in goats with BSE (Foster et al 1999) showed a maximum possible transmission rate of 5% while cattle studies (Wilesmith et al 1997) have suggested a rate no higher that 10%.
Taken together these studies provide good evidence that should BSE have infected sheep, it is unlikely to have be maintained within the population by the maternal transmission route.








http://randd.defra.gov.uk/Default.aspx?Menu=Menu&Module=More&Location=None&Completed=0&ProjectID=6168










see USDA et al failed attempt to track down previous herd and birth cohorts of BSE cases...






Thursday, November 17, 2011


International cattle ID and traceability: Competitive implications for the US


Food Policy Volume 37, Issue 1, February 2012, Pages 31-40












SEE MORE HERE ON THE POTENTIAL FOR VERTICAL TRANSMISSION WITH TSE PRION DISEASE ;









http://creutzfeldt-jakob-disease.blogspot.com/2009/12/is-there-evidence-of-vertical.html













spontaneous mutation is a myth. never proven for any natural field case of bse. it's one of three hypothesis put forward by scientist, and the spontaneous mutation theory is at the bottom of the list. sporadic and or spontaneous CJD, which is 85%+ of all CJD, simply means from 'unknown source/origin'. it does NOT mean that 85%+ of all CJD i.e. sporadic/sponaneous just happens from a bad funked out twisted the wrong way protein. atypical L-type BSE or BASE, has been linked to sporadic CJD. it's looking more and more like a link from the L-type atypical BSE to the Transmissible Mink Encephalopathy TME. that would mean L-type BASE BSE would have been in North America for decades. the lies about the feed not being a source for atypical mad cow disease is just that, lies. a day or two before the 4th mad cow, I put out an update on Canada BSE and Canada CJD in two links. see at the bottom...terry





America's Mad Cow crisis by John Stauber



Wednesday, April 25, 2012



America's Mad Cow Crisis by John Stauber













Wednesday, April 25, 2012


4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012







Monday, April 23, 2012


CREUTZFELDT JAKOB DISEASE CJD HUMAN TSE CANADA UPDATE 2012








Monday, April 23, 2012


BOVINE SPONGIFORM ENCEPHALOPATHY BSE CJD TSE PRION DISEASE UPDATE CANADA 2012








Wednesday, April 25, 2012


USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 – 2012








kind regards,

terry
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Wednesday, April 25, 2012

America's Mad Cow Crisis by John Stauber

America's Mad Cow Crisis by John Stauber


Permission granted to reprint this article:


America's Mad Cow Crisis


John Stauber


Americans might remember that when the first mad cow was confirmed in the United States in December, 2003, it was major news. The United States Department of Agriculture (USDA) and the Food and Drug Administration (FDA) had been petitioned for years by lawyers from farm and consumer groups I worked with to stop the cannibal feeding practices that transmit this horrible, always fatal, human and animal dementia. When the first cow was found in Washington state, the government said it would stop such feeding, and the media went away. But once the cameras were off and the reporters were gone nothing substantial changed.


In the United States, dairy calves are still taken from their mothers and fed the blood and fat of dead cattle. This is no doubt a way to infect them with the mad cow disease that has now been incubating here for decades, spread through such animal feeding practices. No one knows how the latest dairy cow was infected, the fourth confirmed in the United States. Maybe it was nursed on cow's blood. Perhaps it was fed feed containing cattle fat with traces of cattle protein. Or perhaps there is a mad cow disease in pigs in the United States, which simply has not been found yet, because pigs are not tested for it at all, even though pigs are fed both pig and cattle byproducts, and then the blood, fat and other waste parts of these pigs are fed to cattle.


All these U.S. cattle feeding methods are long banned and illegal in other countries that suffered through but eventually dealt properly with mad cow disease. Here, rather than stopping the transmission of the disease by stopping the cannibal feeding, mad cow is simply covered up with inadequate testing and very adequate public relations. US cattle are still fed mammalian blood, fat and protein, risking human deaths and threatening the long term safety of human blood products, simply to provide the U.S. livestock industry with a cheap protein source and a cheap way to get rid of dead animal waste.


I began researching this issue around 1989, long before the disease was confirmed to have jumped from cattle to the people eating them, as announced by the British government in 1996. In 1997 I co-authored <http://www.prwatch.org/books/madcow.html> Mad Cow USA, warning that the disease was likely already here and spreading, since the animal cannibalism that caused its outbreak in Britain and spread it to other countries was actually more widespread in the United States than anywhere.


Some years ago responsible U.S. beef companies wanted to test their animals for mad cow disease and label their beef as being disease free, but they were forbidden under penalty of law from doing so. Only the USDA can test for mad cows in America. In 2004 and 2005, after two additional mad cows were discovered in Texas and Alabama, the United Sates government declared that obviously mad cow wasn't much of a problem and gutted it's anemic testing program. Today only about 40,000 cattle a year are tested, out of tens of millions slaughtered. It's amazing that the California cow was even detected given this pathetic testing program that seems well designed to hide rather than find mad cows.


The prevention of mad cow disease is relatively simple. If your country has it, test each animal before it goes to slaughter to keep the diseased animals out of the food chain. Cheap, accurate and easy tests are now available in other countries but illegal here. Testing cattle both identifies the true extent of the disease, and keeps infected animals from being eaten in your sausage or hamburger. In this manner countries like Britain, Germany, France and Japan have controlled their problem through testing and a strict ban on cannibal feed.


Once mad cow disease moves into the human population of a country, all bets are off as to what could happen next. It's a very slow disease, it develops invisibly over decades in someone who has been infected, and it is always fatal. We'll know a lot more in fifty years, but the future looks worrisome. In Britain people are dying from mad cow disease, people who never consumed infected meat. They used medical products containing human blood, and that blood was infected because it was from infected people. There is no test to identify infectious prions, the causal agent, in blood.


Almost none of this information appeared in news stories about the California mad cow. Instead the headlines and the talking heads fed us the line that the United States fixed this problem long ago, and the fact that only 4 mad cows have been detected so far is proof of our success. Oprah Winfrey once tried via her talk show to warn about this, way back in 1996, but Texas cattlemen dragged her and her guest Howard Lyman into court and she had to spend many millions of dollars defending herself from the supposed crime of slandering meat.


Oprah won her case, which was probably unfortunate for the rest of us because had she been convicted the ensuing appeals court trial might have gotten enough attention to wake up Americans to the truth. Instead Oprah learned her lesson - shut up and you won't get sued. Other media learned too that if the government and industry can silence Oprah, they can muzzle anyone. (One of the 4 confirmed U.S. mad cows was later found in Texas, appropriately enough.)


There are a handful of dedicated activists such as Howard Lyman who have been sounding the alarm on this. They include the ecologist Dr. Michael Hansen of Consumers Union and Dr. Michael Greger, a physician. Terry Singeltary Sr., whose mom died of a version of the human form of mad cow disease, has been a relentless, unpaid activist on this issue.


Despite their dedicated work, there is no indication that anything is going to change here in America. The U.S. government refuses to implement the feed ban and the animal testing necessary. It doesn't matter if the President is named Clinton, Bush or Obama because their bureaucrats in the USDA and FDA stay the course and keep the cover up going. Docile, eating what they are fed, trusting the rancher all the way to the slaughterhouse. Is that just the cows, or is it us too?


-- John Stauber: <http://sourcewatch.org/index.php?title=John_Stauber> is an independent author and activist. He founded the Center for Media and Democracy in 1993, retiring in 2009. Way back in 1997 he co-authored Mad Cow USA. <http://www.prwatch.org/books/madcow.html>





 http://www.commondreams.org/view/2012/04/26-1






http://www.electricpolitics.com/2012/04/americas_mad_cow_crisis.html




Tell the USDA to Stop the Spread of Mad Cow Disease!




Terry Singeltary P.O. Box 42 Bacliff, TX 77518-0042




April 25, 2012


Administrator Gregory Parham


12th & Jefferson Drive, SW Whitten Bldg., Room 313-E Washington, DC 20250 Re: Docket No. APHIS-2008-0010


Dear Administrator Parham:


In order to stop the spread of bovine spongiform encephalopathy (BSE or mad cow disease), the US Department of Agriculture should adopt and enforce the same strict standards required by the European Union and Japan:


* Mandatory testing for all cattle brought to slaughter, before they enter the food chain.


* Ban the feeding of blood, manure, and slaughterhouse waste to animals.


In the meantime, the USDA must stop harassing farmers and food processors who are interested in independently testing their own beef for mad cow disease.


Ironically, the news that mad cow is still in our food supply comes at a time that the U.S. Department of Agriculture Animal and Plant Health Inspection Service (APHIS) is proposing to drop significant protections the U.S. has against the importation of cattle infected with mad cow disease.


APHIS proposes to open United States' borders to cattle from countries that have had thousands of cases of BSE, and where new BSE cases continue to be found. The importation of a single infected cow from Canada in 2001 set in motion restrictions on U.S. beef exports that cost the beef industry billions of dollars and that still exist today in several major export markets.


APHIS also proposes to drop important measures that have been used to protect U.S. consumers from these imported cattle and meat products (which have a much higher chance of being infected with BSE than U.S.-raised cattle), and intends to rely almost exclusively on slaughtering techniques, particularly the removal of specified risk materials (SRMs), which we know on occasion is not employed fully or effectively, and which has not been practiced long enough to determine whether it is indeed the panacea APHIS assumes, given the long gestation time of variant Creutzfeldt-Jakob Disease (vCJD) in humans.


I support the view of R-CALF USA CEO Bill Bullard:


"Seventy-six farm and consumer organizations, representing tens of millions of U.S. citizens, recently urged Secretary Vilsack to strengthen, not weaken, our already lax BSE policies by reversing the so-called 'over-thirty-month rule,' which allows Canadian cattle born during the time the BSE agent was known to be circulating in Canada's feed system to be imported into the United States.


"Secretary Vilsack has again ignored our concerns and is putting the self-interests of corporate meatpackers that want access to more meat supplies regardless of risk to humans and livestock, ahead of the health and safety concerns of U.S. citizens.


"The USDA is touting its proposed rule as a trade rule, claiming it will strengthen the United States' negotiating position in trade agreements. This is the same failed argument the Bush Administration used when it first relaxed our U.S. BSE policies in 2004, and the result of that failed argument is that many important export markets imposed long-lasting export restrictions on U.S. beef.


"USDA's proposal amounts to a unilateral disarmament of essential disease protections for U.S. citizens and livestock. It will disadvantage U.S. producers in the global market because other major beef exporters, including Brazil, Australia, and India continue to maintain adequate import standards while the U.S. relaxes its own. This will create unnecessary and avoidable anxieties among other beef consuming nations for U.S. beef.


"Exposing U.S. consumers and U.S. livestock to a heightened risk of BSE introduction is irresponsible and contrary to pledges made by the Obama Administration during his campaign."


This is no time to relax our essential protections against the introduction of mad cow disease.


so, USDA et al accidently find two atypical mad cows in Texas and Alabama during the infamous enhanced BSE cover up back in 2004 and 2005, and then shut the testing down to numbers so low, it's almost impossible to find another mad cow case, unless your country is to a point that mad cow disease can be found in 1 in 40,000, and STILL FIND MAD COW DISEASE, HOUSTON, WE HAVE A PROBLEM. ...


PLEASE UNDERSTAND, the USDA et al are lying about atypical BSE being a spontaneous mutation, NOT caused by feed. spontaneous BSE has NEVER been proven in any natural field case of BSE. feed is the most likely route. ...tss




As previously stated most of the characteristics of atypical BSE have not been defined. In addition to the origin, the risk to other cattle by means of natural transmission, the risk to humans and other animal species suck as chickens and pigs is still unknown as is the distribution of infectivity throughout the body of a bovine. There is little information on clinical manifestation if it occurs at all in certain of the cases. Documented L cases have been diagnosed from samples taken from older ''healthy'' cattle presented for routine slaughter.


While additional surveillance and research is being conducted, it is important for policy make to consider the implications of atypical BSE. They may need to rethink what populations are appropriate targets. It would probably be unwise to prematurely lessen or discontinue the current BSE protection measures.




SNIP...












Atypical BSE: What is it and what is the significance


Linda A. Detwiler, Paul Brown, Lisa M. McShane, and Gianluigi Zanusso




When atypical cases were first reported there was some speculation that these may merely be protein accumulation disorders associated with old age. It has now been shown that both the Land H types of atypical BSE are at least experimentally transmissible. Homogenates from L cases have been transmitted to bovinized transgenic mice, humanized transgenic mice, Cynomolgus monkeys and 1 breed of cattle (Buschmann et al. 2006; Book of abstracts (2006), International Conference on Prion Diseases, Turin, Italy). H cases have been transmitted to bovinized transgenic (Tgbov) and ovinized transgenic mice (Béringue et al. 2006). The incubation times for atypical L cases of BSE were shorter in the Tgbov mice than classical BSE inoculated into Tgbov mice and the H cases had longer incubations.


A variation or mutation of the classical BSE strain 􀂙 A different route of exposure or exposure at an older age 􀂙 A strain of Scrapie transmitted to cattle 􀂙 Sporadic or a spontaneous occurrence of BSE At his point in time, there is no evidence to conclude that any of the theories are or are not a possibility. There is considerable interest in the sporadic theory. If a form of BSE were to ocnaturally, this may suggest that certain control and prevention measure would have to remain in place indefinitely. Proving or disproving the occurrence of a relatively rare sporadic disease poses a significant challenge. It would require between 3 and 4.5 million tests performed on brain samples randomly taken from cattle over 7 years of age in a country with no evidencrisk from orally acquired BSE. It is unlikely that any country would have the will or resources to perform such a study. Lacking this type of evidence, systematic surveillance over a long time period may provide evidence about the nature of atypical BSE.




snip...see full text ;






When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.


This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.








BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!




Tuesday, April 24, 2012


MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA








Wednesday, April 25, 2012


4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012







Wednesday, April 25, 2012


ACTUALITY - USDA Chief Veterinary Officer On Surveillance And Milk Safety and BSE aka MAD COW DISEASE







Wednesday, April 25, 2012


USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 - 2012








layperson




Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net




Sincerely, Terry Singeltary




powered by CQ Roll Call ©2012






Confirmation Your e-mail message was sent to: Administrator Gregory Parham, Administrator, Animal and Plant Health Inspection Service








TSS
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ACTUALITY – USDA Chief Veterinary Officer On Surveillance And Milk Safety and BSE aka MAD COW DISEASE

USDA Chief Veterinary Officer On Surveillance And Milk Safety

A new actuality is available on the USDA FTP site. The actuality can also be seen on USDA's YouTube channel.

Note for broadcasters: B-roll of cows follows Dr. Clifford’s actuality on the file available on the FTP site.

FTP Download instructions:




User name: usdanews


Password: Newscontent1


Filename for TV Actuality: Clifford safeguards


The new file is in QuickTime Movie (H.264)




Please email bob.ellison@usda.gov if you have problems or suggestions.


Also, use this free ftp client if you have problems.





ACTUALITY – USDA Chief Veterinary Officer On Surveillance And Milk Safety





INFO: USDA Chief Veterinary Officer Dr. John Clifford explains the system of strong interlocking safeguards designed to protect human and animal health.


Dr. John Clifford, Chief Veterinary Officer For the United States of America:


Hello, I’m Dr. John Clifford, chief veterinary officer for the United States of America. At USDA, we oversee a system of strong interlocking safeguards that protect human and animal health, as well as food safety in the United States. Those safeguards include targeted surveillance activities. Through that surveillance program, on April 24th we confirmed the nation’s 4th case of bovine spongiform encephalopathy, or BSE, in a dairy cow on the west coast. BSE is a fatal disease affecting the central nervous system of adult cattle. We proactively test for BSE in order to detect the disease at the very low level of less than 1 case per million adult cattle, to assess any change in the BSE status of U.S. cattle, and to identify any rise in BSE prevalence in the country. Our targeted surveillance program has been in place since 1990. We currently test for BSE at levels 10 times greater than World Animal Health Organization standards. We test approximately 40,000 animals per year, taking those samples from cattle where the disease is most likely to be found. This includes animals that have clinical signs consistent with BSE, have other central nervous system abnormalities, die for unknown reasons, or cannot walk or move well. We collect samples from a variety of locations where the targeted groups of animals are found. The samples from the animal in question were taken at a rendering facility in California. Our surveillance works. We found this case of BSE. The carcass of the animal was held at the rendering facility and then will be destroyed. It was never presented for processing for human consumption. At no time did it present a risk to the food supply. Our food supply remains safe. With California being a large dairy state, there have been some concerns raised about milk. Let me assure you, our milk is safe to drink. Scientific research demonstrates that BSE cannot be transmitted in cow’s milk, even if that milk comes from a cow with BSE. The World Health Organization has stated that tests on milk from BSE-infected animals have not shown any BSE infectivity. Milk and milk products, are, therefore considered safe to consume. Let me assure consumers and our trading partners that ongoing BSE surveillance allows the USDA to detect BSE at very low levels in the U.S. cattle population. The safeguarding system is working. For updates on our ongoing investigation and more information about BSE in general, visit our website at www.usda.gov.







these folks should no now to never say never $$$



BOTTOM LINE, milk and atypical L-type BASE BSE, they have no clue yet. they must do transmission studies. with atypical L-type BASE BSE, this type is much more virulent. ...tss



MILK and Transmissible Spongiform Encephalopathy TSE PRION


Terry S. Singeltary Sr.


11/18/2011


TO date, and i imphasize 'to date', there has been no documented evidence of transmission of BSE via milk of BSE infected cow to another cow. however, with the limited testing done to date, on just the c-BSE, you cannot rule this out, especially with the atypical BSE L-type i.e. BASE, being much more virulent. Concern has been increasing due to fluids from TSE species i.e. blood, urine, and milk, and the fact that infectivity has been detected.



Prion infectivity has now been detected in blood, urine and milk.



please see ;




Seven main threats for the future linked to prions


The NeuroPrion network has identified 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


In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.


Third threat


The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.


Fourth threat


Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,


whereas other countries, including the US,


Brazil, and Argentine do not have these constraints.


However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.


Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.


Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.


Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.









Goat BSE: Proposal for Improvement of Goat TSE Discriminative Diagnosis and Susceptibility based Assessment of BSE Infectivity in Goat Milk and Meat



Funded by EU, DEFRA This project is run by a consortium of ten research teams in seven EU countries.



In light of the known ability of the BSE agent to cross the animal/human species barrier, recent evidence establishing the presence of BSE in goat is especially alarming, as it represents a new potential risk of food-born contamination to human consumers of goat milk and meat products. The main objective is to determine the tissue distribution of BSE after oral exposure of goats and to do this while simultaneously generating data on genetic susceptibility in the most common used production breeds. This proposal aims at (i) providing data for the evaluation of human risk associated with goat BSE, (ii) providing pathogenesis data and biological material from first and second passage BSE in goats, (iii) evaluating the possibility of BSE self-maintenance in goat herds through maternal or horizontal transmission, (iv) validating and improving our ability to detect caprine BSE and discriminate it from scrapie in goats. Our approach will establish the influence of PrP gene polymorphisms on scrapie and BSE susceptibility so that genetics could potentially be used for the control of field TSE outbreaks in goats. We will also document European field TSE strain variability in goats by recruiting a large number of TSE goat isolates from affected European countries. Already established or specifically created animal models (strain typing) and biochemical tools (PrPSc typing), will be tested for their ability to efficiently discriminate goat BSE/scrapie. Finally, by measuring infectivity in various tissues collected from goats at different stages of BSE infection, we will provide essential data for quantitative risk assessment.









Vet. Res. (2010) 41:48 Original article




Pathogenesis of natural goat scrapie: modulation by host PRNP genotype and effect of co-existent conditions




Lorenzo González1*, Stuart Martin1, Stephen A.C. Hawkins2, Wilfred Goldmann3, Martin Jeffrey1 and Sílvia Sisó1


1 Veterinary Laboratories Agency (VLA-Lasswade), Pentlands Science Park, Penicuik, Midlothian EH26 0PZ, United Kingdom 2 VLA-Weybridge, Addlestone, Surrey KT15 3NB, United Kingdom 3 The Roslin Institute and R(D)SVS University of Edinburgh, Roslin, Midlothian EH25 9PS, United Kingdom


* Corresponding author: l.gonzalez@vla.defra.gsi.gov.uk


Received: 13 January 2010 Accepted: 7 April 2010


Abstract


After detection of a high prevalence of scrapie in a large dairy goat herd, 72 infected animals were examined by immunohistochemistry with prion protein (PrP) antibody Bar224 to study the pathogenesis of the infection. Tissues examined included the brain and thoracic spinal cord (TSC), a wide selection of lymphoreticular system (LRS) tissues, the distal ileum and its enteric nervous system (ENS), and other organs, including the mammary gland. The whole open reading frame of the PRNP gene was sequenced and antibodies to caprine arthritis-encephalitis virus (CAEV) infection were determined. Unexpectedly, accumulation of disease-associated PrP (PrPd) in the brain was more frequent in methionine carriers at codon 142 (24/32, 75.0%) than amongst isoleucine homozygotes (14/40, 35.0%). The latter, however, showed significantly greater amounts of brain PrPd than the former (average scores of 9.3 and 3.0, respectively). A significant proportion of the 38 goats that were positive in brain were negative in the ENS (44.7%) or in the TSC (39.5%). These results, together with the early and consistent involvement of the circumventricular organs and the hypothalamus, point towards a significant contribution of the haematogenous route in the process of neuroinvasion. Chronic enteritis was observed in 98 of the 200 goats examined, with no association with either scrapie infection or presence of PrPd in the gut. Lymphoproliferative interstitial mastitis was observed in 13/31 CAEV-positive and scrapie-infected goats; PrPd in the mammary gland was detected in five of those 13 goats, suggesting a possible contribution of CAEV infection in scrapie transmission via milk.


Key words: scrapie / goat / prion neuroinvasion / transmissible spongiform encephalopathy / CAEV


© The British Crown, published by INRA/EDP Sciences, 2010








6 January 2010 -


The public “TSEs in goats” website Link:






Since December 2006 a new EU funded project has started that has been essentially developed from NeuroPrion TSEgoat task group members and their progress: “GoatBSE: Proposal for improvement of goat TSE discriminative diagnosis and susceptibility based assessment of BSE infectivity in goat milk and meat.” (European STREP project FOOD-CT-2006-36353, frame work 6, area Thematic priority: Food quality and safety). In this project the focus of study is about consequences of an infection with BSE in goats for disease transmission and product safety.








Sheep with Scrapie and Mastitis Transmit Infectious Prions through the Milk?



Ciriaco Ligios1,†, Maria Giovanna Cancedda1, Antonello Carta2, Cinzia Santucciu1, Caterina Maestrale1, Francesca Demontis1, Mariangela Saba1, Cristiana Patta1, James C. DeMartini3, Adriano Aguzzi4,†,* and Christina J. Sigurdson4,5,6,†,*


+ Author Affiliations


1Istituto Zooprofilattico Sperimentale della Sardegna, Sassari, Italy


2Research Unit of Genetics and Biotechnology, DIRPA, AGRIS Sardinia, Olmedo, Italy


3Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, Colorado


4Institute of Neuropathology, UniversitätsSpital Zürich, Zürich, Switzerland


5 Department of Pathology, School of Medicine, University of California, San Diego, California


6Department of Pathology, Microbiology, and Immunology, University of California, Davis, California


Next Section ABSTRACT


Prions are misfolded proteins that are infectious and naturally transmitted, causing a fatal neurological disease in humans and animals. Prion shedding routes have been shown to be modified by inflammation in excretory organs, such as the kidney. Here, we show that sheep with scrapie and lentiviral mastitis secrete prions into the milk and infect nearly 90% of naïve suckling lambs. Thus, lentiviruses may enhance prion transmission, conceivably sustaining prion infections in flocks for generations. This study also indicates a risk of prion spread to sheep and potentially to other animals through dietary exposure to pooled sheep milk or milk products.











EFSA Journal 2011; 9(1):1945 Suggested citation:


EFSA Panel on Biological Hazards (BIOHAZ);


Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans.



EFSA Journal 2011;9(1):1945. [111 pp.] doi:10.2903/j.efsa.2011.1945. Available online: www.efsa.europa.eu/efsajournal © European Food Safety Authority, 2011 SCIENTIFIC OPINION Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans1 EFSA Panel on Biological Hazards (BIOHAZ)2, 3 European Food Safety Authority (EFSA), Parma, Italy European Centre for Disease Prevention and Control (ECDC)4, 5 Stockholm, Sweden


More recent EFSA opinions focused on the human exposure risk to TSEs through consumption of products deriving from small ruminants (ovine and caprine carcasses below six months, milk and milk products), but only focused on human exposure, without discussing the zoonotic potential of small ruminants TSEs (EFSA, 2008a, 2008c). A recent EFSA opinion (EFSA Panel on Biological Hazards (BIOHAZ), 2010a) provided updated data on the TSE infectivity distribution in small ruminant tissues. It also estimated the relative reduction of BSE infectivity load that can be achieved in the carcass of a small ruminant through the implementation of the current or alternative policies in terms of removal of Specified Risk Material (SRM). The zoonotic potential of TSE agents in small ruminants is, however, not discussed in the opinion.


The TSE agent disseminates to the CNS (brain and spinal cord) apparently via the Enteric Nervous System and its nerves fibers (Andreoletti et al., 2000; Jeffrey et al., 2001; van Keulen et al., 2002), which is considered to accumulate TSE agents until around half of the incubation period. From there the agent could redistribute (centrifugally) to the peripheral nervous system and skeletal muscle (Andreoletti et al., 2004). Additionally, infectivity was also reported to be present in blood (Hunter et al., 2002), and in blood and in milk and colostrum (from the first lactation) from animals during incubation (Konold et al., 2008; Lacroux et al., 2008). In blood, the infectious agent can be detected as early as at 3 months of age and persists throughout the incubation period (Andreoletti et al., 2007).


Finally, protection measures applied all along the food chain against small ruminants TSEs in the EU mainly rely at operational level on specified risk material (SRM) removal, i.e exclusion from food chain of tissues that can contain a high infectious load. However, for practical reasons, the SRM measures do not imply discarding from the food chain of all the infectious tissues and animal products that could contain infectivity (EFSA, 2008c). Moreover, infectivity was recently identified in tissues like skeletal muscles or in products like milk from small ruminants incubating scrapie, tissues that were previously considered to be non infectious.









Commentary


In vitro amplification of prions from milk in the detection of subclinical infections


Volume 3, Issue 4 October/November/December 2009 Pages 236 - 239 http://dx.doi.org/10.4161/pri.3.4.10425


Kevin C. Gough, Claire A. Baker, Maged Taema and Ben C. Maddison


View affiliations


Prions can be amplified by serial protein misfolding cyclic amplification (sPMCA) from the milk of a high proportion of apparently healthy, scrapie exposed sheep with PRNP genotypes not previously associated with high disease penetrance1. These data strongly suggest the widespread presence of subclinical scrapie infections within scrapie-exposed flocks containing sheep with a range of susceptible PRNP genotypes. These data also lead to the hypothesis that similar subclinical disease states may be common for other animal and human prion diseases. Furthermore, the application of sPMCA to milk provides a method to detect such subclinical disease. Here, we describe the high level amplification of bovine spongiform encephalopathy (BSE) prions from both ovine and bovine origin, a methodology that will facilitate the detection of any prions secreted within bovine and ovine milk during subclinical and clinical BSE disease.







Prion Protein in Milk


Nicola Franscini,1 Ahmed El Gedaily,1 Ulrich Matthey,1 Susanne Franitza,1 Man-Sun Sy,2 Alexander Bürkle,3 Martin Groschup,4 Ueli Braun,5 and Ralph Zahn1


Conclusions/Significance


In view of a recent study showing evidence of prion replication occurring in the mammary gland of scrapie infected sheep suffering from mastitis, the appearance of PrPC in milk implies the possibility that milk of TSE-infected animals serves as source for PrPSc.











WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010



snip...



Since the publication in 2006 of Annex 1 (Major Categories of Infectivity) in the ‘‘WHO Guidelines on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies’’, some tissues (ovary, uterus, mammary glands/udder, skin, adipose tissue, and heart/pericardium) and body fluids (saliva, milk, urine, and feces) in which infectivity had not been detected, have since been found to contain infectivity or PrPTSE and therefore have there been moved from the category of ‘‘tissues with no detectable infectivity’’ ’’ to the category of ‘‘lower-infectivity tissues.’’






When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.











Wednesday, March 31, 2010

Atypical BSE in Cattle

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.

In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.


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




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...









PLoS One. 2012; 7(2): e31449.

Published online 2012 February 21. doi: 10.1371/journal.pone.0031449

PMCID: PMC3283643

Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy

The present data offer novel information on the tropism of the BASE agent and highlight relevant public health issues. While the transmission barrier for classical BSE is high in most species, BASE prions are readily transmissible to a variety of mammals including non-human primates [11]–[13], [35]. Accordingly, the possibility of spreading of BASE prions through skeletal muscle to other species should be taken into account and evaluated in risk analysis studies.






PINK SLIME LFTB MSM MRM BSE TSE PRION




Saturday, April 21, 2012



HISD seeks refund on burgers with 'pink slime'














Wednesday, March 14, 2012





PINK SLIME, MRM’s, BSE AKA MAD COW DISEASE, AND THE USDA NSLP














Sunday, August 28, 2011






Rick Perry, Texas, BSE aka mad cow disease, CJD, and 12 years of lies there from

http://sciencebushwhacked.blogspot.com/2011/08/rick-perry-texas-bse-aka-mad-cow.html
BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!
Tuesday, April 24, 2012




MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA







Wednesday, April 25, 2012








4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012






http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/4th-mad-cow-disease-usa-california.html







Wednesday, April 25, 2012




USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 – 2012




http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/usa-mad-cow-disease-and-cjd-there-from.html









America's Mad Cow crisis by John Stauber





http://www.commondreams.org/view/2012/04/26-1








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