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Germany Identifies First ‘Mad Cow’ Case Since 2009

German officials have identified one beef cow with a case of bovine spongiform encephalitis (BSE), the fatal neurological disorder also known as “Mad Cow Disease.”

This is Germany’s first reported case since 2009. The cow was killed and its body destroyed, with none of the meat entering the human food chain.

Health officials said that the animal showed no symptoms of BSE when it was initially slaughtered for consumption, but, because it was 10 years old, it underwent a BSE test. That’s when it tested positive for an atypical type of BSE, L-type, which develops spontaneously in older cattle.

Epidemiological tracebacks identified seven offspring of the cow, five of which were already slaughtered. The other two were still on the cow’s farm of origin, where they were tested and subsequently killed, according to protocol for handling BSE cases.

The diseased cow’s herd is under quarantine until clearing further testing, although BSE is not considered contagious.

The incident is not expected to alter Germany’s beef consumption or rules regarding BSE. Germany’s BSE screening protocols require any beef cattle older than eight years to automatically be tested for BSE.

Germany’s first cases of BSE were discovered in 2000. The country has seen a total of 312 cases, compared to the United Kingdom’s 183,000 and the United States’ four.

The first known case of BSE occurred in the U.K. in 1986. Since then, more than 150 people in the U.K. have fallen ill and died from the human counterpart to BSE, variant Creutzfeldt-Jakob Disease (vCJD).

The disease originated with the practice of feeding cattle meat and bone meal to cattle herds as a substitute for soy beans, which can be difficult to grow in Europe.

Humans can contract vCJD from eating meat contaminated with brain or spinal tissue from cattle infected with BSE, which is not destroyed when cooked.

The U.S. Department of Agriculture recently announced plans to ease regulations on beef imports in regard to BSE. The U.S. has banned beef imports from Europe since 1998 due to mad cow scares.

The latest USDA move would align the U.S. with international policies on BSE, while potentially opening up U.S. beef exports to new markets. The U.S. was recently adjusted to the safest classification for BSE risk, according to international standards set by the World Organization for Animal Health.

The most recent case of BSE in the U.S. occurred in 2012 in a California dairy cow which had developed the L-type BSE as in the latest German case. The other three U.S. cases occurred in 2003, 2004 and 2006.

Another 19 BSE cases have occurred in Canada, the first being a 1993 case in a cow imported from the U.K.

In the U.S. and other countries regulating BSE, cattle feed can no longer contain the meat of other ruminant animals. USDA runs a surveillance program for BSE, and slaughterhouses are required to remove the brains and spinal cords from all carcasses.

© Food Safety News
  • Oginikwe

    More questions than answers in this article. First, the case from Brazil needs to be cited:

    Brazil Kept Mad Cow Secret for Two Years (Food Safety News) 12/10/2012: http://www.foodsafetynews.com/2012/12/boys-from-brazil-kept-mad-cow-secret-for-two-years/

    Then: “. . .it tested positive for an atypical type of BSE, L-type, which develops spontaneously in older cattle.” Since when was this discovered/decided? Just like they tell us that it’s “normal” for older people to develop cancer when cancer used to be a rare disease? This smacks of more of making the abnormal “normal.”

    “The U.S. Department of Agriculture recently announced plans to ease regulations on beef imports . . .” Why are we importing beef at all? We can meet all of our domestic needs and don’t need to import beef.

    “In the U.S. and other countries regulating BSE, cattle feed can no longer contain the meat of other ruminant animals.” While that is true, we feed chickens ruminants and then turn around and feed chicken by-products to the cows giving consumers a false sense of security:
    We Feed Cows Chicken Poop: http://www.motherjones.com/environment/2013/12/we-feed-cows-chicken-poop

    • john mark carter

      BSE and the other transmissible spongiform encephalopathy diseases are indeed enigmatic.
      Yes, the L-type of BSE seems to occur spontaneously, no matter what the cattle eat. It is similar to “sporadic” Creutzfeld-Jacob disease in humans, which has always affected about 1 in 1,000,000 persons. We figured out “spontaneous” BSE at the end of the epidemic, once we figured out how to tell the different kinds of BSE apart.
      No, the US doesn’t NEED to import beef. We do it because Americans are willing to pay for little freedoms and choices, like where their beef was raised.
      We may all feel secure that the BSE epidemic is over. The “feed ban” solved the problem. We can guess about cycling between chickens and cattle, but it’s not happening, or we would see BSE among those cattle who eat poultry litter.

      • Oginikwe

        Thank you for your response.
        But might we see BSE in cattle who eat poultry litter if they lived longer? It maybe that slaughter at two years or so doesn’t allow for symptoms to develop even though they have it. The ones that we have seen with BSE have been older animals. Feeding bovine by products to chickens and then feeding poultry byproducts to cattle seems to be a dangerous, closed-loop system.

    • there is NO scientific data to back up any claim for a spontaneous disease in atypical L-type BASE BSE TSE prion disease. atypical BSE is transmissible. please see ;

      ***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.


      full text ;

      atypical L-type BASE BSE

      Saturday, January 18, 2014

      Bovine spongiform encephalopathy ,Germany Information received on 17/01/2014

      O.I.E. REPORT


      Saturday, January 18, 2014

      However, a BSE expert said that consumption of infected material is the only known way that cattle get the disease under natural conditons.

      *** “In view of what we know about BSE after almost 20 years experience, contaminated feed has been the source of the epidemic,” said Paul Brown, a scientist retired from the National Institute of Neurological Diseases and Stroke. BSE is not caused by a microbe. It is caused by the misfolding of the so-called “prion protein” that is a normal constituent of brain and other tissues. If a diseased version of the protein enters the brain somehow, it can slowly cause all the normal versions to become misfolded. It is possible the disease could arise spontaneously, though such an event has never been recorded, Brown said.


      *** 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.”


      2012 ATYPICAL L-TYPE BSE BASE CALIFORNIA ‘confirmed’ Saturday, August 4, 2012

      *** Final Feed Investigation Summary – California BSE Case – July 2012


      Saturday, August 14, 2010

      BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

      (see mad cow feed in COMMERCE IN ALABAMA…TSS)


      Friday, January 17, 2014

      *** Annual report of the Scientific Network on BSE-TSE EFSA, Question No EFSA-Q-2013-01004, approved on 11 December 2013

      kind regards,

    • Friday, December 07, 2012



      Wednesday, December 19, 2012

      Scientific Report of the European Food Safety Authority on the Assessment
      of the Geographical BSE Risk (GBR) of Brazil


      Friday, January 17, 2014

      *** Annual report of the Scientific Network on BSE-CWD-TSE EFSA, Question No
      EFSA-Q-2013-01004, approved on 11 December 2013



      kind regards,

      • Oginikwe

        Thank you for your responses and links Mr. Singeltary.

      • Oginikwe

        I have a question, Mr. Singeltary.
        If the average age of the patients was/is almost 59 years old, does this mean that CJD takes a long, long time to show up or were these men just unlucky enough to have eaten infected beef within a certain time frame in Brazil?

        • > Oginikwe Terry S. Singeltary Sr.

          > • 5 days ago

          > I have a question, Mr. Singeltary.

          > If the average age of the patients was/is almost 59 years old, does this mean that CJD takes a long, long time to show up or were these men just unlucky enough to have eaten infected beef within a certain time frame in Brazil?

          Greetings Oginikwe, my apologize for my late reply. I did not see the question until today.

          in terms of sporadic cjd, it is noted that the one in a million is a red herring, actually, in 55 years and older, the number 1 in 9,000, the figures via the CJD Foundation.

          in reality, and with all the many strains now being discovered, and sub-types there from, it’s now difficult to determine and differentiate, with current science and diagnostic criteria, especially with a link to some sub-types of sporadic CJD, to atypical BSE and typical c-BSE. you have sub-types and different strains of the sporadic CJD that have the same symptoms, and duration of the disease from onset of symptoms to death, such as individuals with nvCJD or what they now call vCJD. for instance, with my mother, she died from hvCJD the Heidenhain Variant of Creutzfeldt Jakob Disease a sub-type of the sporadic CJD’s. from onset of symptoms to death was very very fast, about 10 weeks, with blindness and severe myoclonic jerks. very extreme. she did everything linda blair did in the movie the exorcist, except spin her head 360 degrees. she jerked so bad she levitated in bed. it took 3 big adults to hold her down, while she screamed, God, what’s wrong with me. that was Christmas 1997, and I still hear her screams today.

          you must remember, with typical scrapie, last I counted, there were over 20+ strains of the typical scrapie, then you have the atypical Nor-98 Scrapie, add on top of that BSE from cattle in sheep and goats, and we have a terrible mess here.

          a few examples of difficulty, with sCJDvv2 type, Creutzfeldt Jakob disease, the average disease duration is 21 months. this mimics nvCJD in terms of the long duration from onset of symptoms to death.

          Bio.144: Analyses of PrPSc Aggregation State and Protease-Resistance in Human Prions

          Daniela Saverioni,1,† Silvio Notari,2 Sabina Capellari1 and Piero Parchi1

          1Department of Neurological Sciences, University of Bologna; Bologna, Italy; 2Department of Pathology, National Prion Disease Pathology Surveillance Center, Case Western Reserve University; Cleveland, OH USA†Presenting author; Email: daniela.saverioni@studio.unibo.it

          Background. Given the complexity and costs of transmission studies, the analyses of PrPSc properties is increasingly used as surrogate marker for strain typing. Early studies showed that PrPSc extracted from distinct disease phenotypes, in both animals and humans, often differ in physicochemical properties, such as fragment size after protease treatment or glycoform ratio. More recently, studies mainly conducted with scrapie strains isolated in mice or hamster have also reported strain-specific PrPSc differences in the degree of protease resistance, aggregation state, or conformational stability.

          Objectives. To establish across the phenotypic spectrum of human prion disease: (1) whether and to what extent distinct PrPSc isoforms differ in protease-resistance; (2) whether and to what extent this PrPSc property is related to the aggregation state of the protein and (3) the relative amount of PK-sensitive PrPSc.

          Materials and Methods. Frontal cortex PrPSc from the whole spectrum of sCJD subtypes, vCJD and VPsPr (MM and MV codon 129 genotypes) was purified through sample dilution in Sarkosyl and sequential ultracentrifugation in sucrose cushion and pellet resuspensions by sonication. PrPSc aggregates of different size were isolated after ultracentrifugation in sucrose gradient and fraction (12) collection. Whole purified samples and selected fractions of the sucrose gradient preparation were digested using a wide range of PK activities. A curve or “profile” of PrPSc digestion and the corresponding ED50 (PK activity required to decrease PrPSc by 50%) were obtained for each human strain analyzed.

          Results. Protease resistance varied significantly among the TSE groups analysed, being highest in vCJD and sCJDVV2 and lowest in sCJDVV1. Fractions 1–4 always contained a fully PK-sensitive form of PrPSc (PrP-sen). However, PrP-sen only accounted for less than 10% of total purified PrPSc in all subtypes analyzed. Overall, the more “sensitive” subtypes contained a larger proportion of “small” PrPSc aggregates 82 Prion Volume 5 Supplement

          (fractions 1–6) with respect to the more “resistant” ones. Nevertheless, PK-resistant aggregates of equal size (fractions 6, 9 and 12) extracted from sCJDMM1 and VV2 maintained, at least in part, the different degree of resistance.

          Discussion. Our results indicate that: (1) only a limited portion of PrPSc associated to the majority of human prion strains is fully protease sensitive; (2) the analyses of PrP-sen does not differentiate among human prion strains; (3) the PrPSc forms associated to distinct human prion strains show a significant heterogeneity in the degree of protease resistance, which is at least partially explained by their differing aggregation state.

          also, the GSS and FFi, both familial type TSE prion disease, tied to a genetic make-up. well now, we have …(I hate this terminology, it just means they don’t know, NOT spontaneous event)…’’SPORADIC’’. YES, we now have sporadic GSS and sporadic FFI. not tied to ANY genetic link. ??? so, what does this mean ??? could it be an iatrogenic event, from a victim with GSS or FFI or vpspr ??? it would explain the no genetic link, to a genetic disease. I am just hypothesizing here out loud. Confucius is confused again, and I put all this in a link ‘’vpspr, what it ???’’ don’t matter though, no PhDs, nobody listens. only a layperson here.

          I must get long winded to try and explain the best I can. please see below.

          few things, shall we ;


          The cases are further characterised by having remarkably low ages at onset for CJD and other atypical features

          kuru-type plaques

          including a generally protracted and unusual clinical course and absence of EEG changes typical of CJD.

          Psychiatric symptoms are prominent

          These findings raise the possibility that the cases represent a new clinicopathological variant of CJD.


          mean age onset 37 years (range 19-55)…(that will pretty much cover them all here in the USA, want it $$$)

          average disease duration is 21 months, (ranging from 19-55)

          EEG shows NO PSW complexes.

          14-3-3 is positive 100%

          MRI shows signal increase in the cerebral cortex in 100% and The sporadic cases include 2500 cases of sporadic Creutzfeldt-Jakob disease (sCJD), ***48 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and *** 19 cases of sporadic Fatal Insomnia (sFI).


          Sunday, January 19, 2014

          *** National Prion Disease Pathology Surveillance Center Cases Examined1 as of January 8, 2014


          Friday, January 10, 2014

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


          Monday, January 13, 2014

          Prions in Variably Protease-Sensitive Prionopathy: An Update Pathogens 2013

          Pathogens 2013, 2, 457-471; doi:10.3390/pathogens2030457


          Monday, September 26, 2011

          Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011


          *** vpspr – None of the subjects had mutations in the PrP gene coding region.


          *** sporadic FFI – Genetic tests identified no prion protein (PrP) gene mutation


          sporadic GSS –

          We report here an unusual sporadic case of Creutzfeldt-Jakob disease (CJD) characterized by an abundance of prion protein (PrP)-immunopositive kuru and multicentric but not florid plaques. Molecular genetic analysis of the PRNP open reading frame region spanning codons 8-221 was performed. Neither deletion nor insertion mutations were detected in the repeat area of the PRNP. No pathogenic mutation was found in the sequenced region between codon 108-221. Restriction analysis of the amplified fragment using restriction endonucleases DdeI, PvuII and AluI did not show any of the previously described pathogenic mutations at codon 102, 105, and 117 associated with Gerstmann-Sträussler-Scheinker (GSS). The patient was heterozygous for the methionine/valine coding triplet at polymorphic codon 129 of the PRNP gene by sequence, restriction endonuclease analysis and hybridization with allele-specific nucleotides. Furthermore, hybridization with 32P-labeled allele-specific oligonucleotides confirmed the absence of pathogenic mutations at codons 102, 200 and 178. Such a case may present a missing “link” between sporadic CJD and familial GSS.


          Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy



          Tuesday, August 03, 2010

          Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein


          Tuesday, October 29, 2013



          Wednesday, October 09, 2013

          *** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT’S FALLACY, £41,078,281 in compensation REVISED


          greetings TSE PRION WORLD,

          i am reminded of a few things deep throat told me years ago;

          *** The most frightening thing I have read all day is the report of Gambetti’s finding of a new strain of sporadic cjd in young people………

          Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie….. why???? than the UK… then would the same mechanisms that make different strains of scrapie here make different strains of BSE… if the patterns are different in sheep and mice for scrapie….. could not the BSE be different in the cattle, in the mink, in the humans……. I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd…….. bse….. scrapie

          Scrape the damn slide and put it into mice….. wait….. chop up the mouse brain and and spinal cord…….. put into some more mice….. dammit amplify the thing and start the damned research….. This is NOT rocket science… we need to use what we know and get off our butts and move…. the whining about how long everything takes….. well it takes a whole lot longer if you whine for a year and then start the research!!!

          Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde….. for God’s sake…….. Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year……. it is a big fat sponge… the agent continues to eat the brain …… you can’t make slides anymore because the agent has never stopped…….. and the old slides that are stained with Hemolysin and Eosin…… they get holier and holier and degenerate and continue… what you looked at 6 months ago is not there…….. Gambetti better be photographing every damned thing he is looking at…..

          ***Okay, you need to know. You don’t need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don’t even hint at it as it will be denied and laughed at………. USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd…….. if you want to move this thing along and shake the earth…. then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc…….. I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd…….. forget any action…….. it is ALL gonna be sporadic!!! And, if there is a case……. there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. …. It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats…. and this may be their biggest downfall…***

          Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here………. knocked me out of my chair…….. you must keep pushing. If I was a power person…. I would be demanding that there be at least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the wood work as there is money to be made!!!

          In short: “FIRE AT WILL”!!! for the very dumb…. who’s “will”! “Will be the burden to bare if there is any coverup!”

          again it was said years ago and it should be taken seriously…. BSE will NEVER be found in the US!

          As for the BSE conference call… I think you did agreat service to freedom of information and making some people feign integrity… I find it scary to see that most of the “experts” are employed by the federal government or are supported on the “teat” of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

          You need to watch your back…….. but keep picking at them……. like a buzzard to the bone… you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself… you ask the questions that everyone else is too afraid to ask.)


          greetings again,

          then i remind everyone to read this;

          ‘As implied in the Inset 25 we must not assume that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.’


          Wednesday, December 11, 2013

          *** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease



          Monday, January 13, 2014

          *** Prions in Variably Protease-Sensitive Prionopathy: An Update Pathogens 2013 Pathogens 2013, 2, 457-471; doi:10.3390/pathogens2030457


          Friday, January 10, 2014

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


          *** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

          Wednesday, January 01, 2014

          Molecular Barriers to Zoonotic Transmission of Prions

          *** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

          *** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.



          Saturday, November 16, 2013

          Management of neurosurgical instruments and patients exposed to creutzfeldt-jakob disease 2013 December

          Infect Control Hosp Epidemiol.


          Thursday, November 14, 2013

          Prion diseases in humans: Oral and dental implications


          Saturday, November 2, 2013

          Recommendation of the Swiss Expert Committee for Biosafety on the classification of activities using prion genes and prion protein January 2013


          Thursday, January 23, 2014

          *** Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) [Docket No. FDA–2013–D–1574]


          I hope this helped out,

          kind regards,



          Terry S. Singeltary Sr.

  • KatMT

    What about the dog food…I have heard of dogs getting mad cow. Are they using “downer cow” or BSE cows for dog food ? I am only hearing about the “human food chain” …..!

  • BB

    I’m just trying to comment before Terry S. Singeltary Sr.:)

  • flame4justice

    If the USA tested more then there might be more BSE cases. Even if they found BSE from more testing you couldn’t rely on being told the truth by anyone.

  • Nathália Kneipp Sena

    The veterinarians who say atypical BSE is not transmissible should volunteer to participate in researches that will present a conclusion about this matter. Many CJD cases in Parana, Curitiba (Brasil, same place as the cow with BSE) are not going to be counted. The day people with transmissible spongiform encephalopaties start to be counted (and be in the news) just like the BSE cows, than things will start to change. A CJD planetary Occurrrence Map is a MUST, it will show the clusters…different routes of transmission.

    • Oginikwe

      How is it that the cases in Brasil aren’t being counted? That doesn’t make any sense . . .

      • Nathália Kneipp Sena

        First of all, if atypical BSE is something “spontaneous” in old cattle (lets say a result of inflamation process), I find it hard to believe that among 200 million heads of cattle in the all history of this country we have found just one animal with BSE. As for TSEs in humans, the ones I say that the cases are not being counted, the plot is the following: Notificiation for TSEs is mandatory in Brazil, the forms were basically copied from the Canadian version, which is good (Canadians do a good job), but incomplete. As the V..I.P. (very important problem) CJD is only vCJD or nvCJD (sCJD, even being iatrogenic doesn´t seem to matter to anyone except the victim and the family) and this is revealed only by hystopathology, the discovery of their incident depends on tonsil, olfatory or brain biopsies or autopsy. Pathologists in Brazil refuse to do autopsies (what happened to my mother, for example) saying they might be contaminated with prions in the process. The people that should work in order to make autopsies possible, are working against a definite diagnosis, therefore many individuals with the diagnosis of hypothetical CJD will not have a final word stating that they had indeed this disease. Therefore, they will not be counted as CJD cases, they will be in the statics that indicate the cause of death as pneumonia… etc. Does it make sense to you now?

        • Oginikwe

          Thank you for explaining that. Yes, it makes perfect sense when someone wants to manipulate the data.