Monday, September 07, 2015

ITALY REPORTING INCREASE IN CASES OF MAD COW TYPE TSE PRION DISEASE IN HUMANS CJD

'Mad cow' fears after man dies in Turin

 

The Local · 7 Sep 2015, 10:21

 

Published: 07 Sep 2015 10:21 GMT+02:00

 

An investigation has been opened after a man died from suspected 'mad cow' disease in Turin last week.

 

Francesco Catapano, a 53 year old from Ottaviano near Naples, was hospitalized in Turin in June and was later diagnosed with Creutzfeldt-Jakob Disease, otherwise known as 'mad cow”disease.

 

He died on September 1st at Turin's Molinette hospital.

 

The illness causes the brain tissue to deteriorate rapidly, resulting in death, usually within months.

 

It became notorious in the 1990s after an outbreak was attributed to eating infected meat and dubbed 'mad cow' disease by the media.

 

Only one form of the disease, variant CJD, is due to eating contaminated food, but officials believe this could be the cause of Catapano's death.

 

“Genetic predisposition was not revealed during early exams and some of the results from the diagnostic procedure suggest that the case may be down to contaminated food,” Antonio Scarmozzino, health director at Molinette hospital, told La Stampa.

 

Cases of variant CJD can only be determined via an autopsy carried out on cerebral tissue post-mortem.

 

However, the testing process is slow as it requires that tissue samples are kept under a formalin solution before testing.

 

Ahead of the autopsy results in October, magistrate Raffaele Guariniello has asked Italy's health police, Nas, to analyze Catapano's medical records.

 

Even if the case is shown to be down to eating contaminated food, it will be impossible to determine the source as the disease can have incubation periods of up to 20 years.

 

Italy has only ever seen two deaths from variant CJD and has one of the lowest incidences of the disease in the EU. But the alarm was raised in August when two people died of CJD in Puglia in the same week.

 

The last recorded case of the disease in an Italian cow was in 2011.

 


 

Two dead from 'mad cow' disease in Lecce Patrick Browne · 6 Aug 2015, 10:36

 

Published: 06 Aug 2015 10:36 GMT+02:00

 

A 67-year-old man died of 'mad cow' disease earlier this week at his home in Lecce - the second death caused by the disease in the Puglia province this week.

 

The man was diagnosed on July 10th, after he fainted.

 

His death comes after the illness claimed the life of a 49-year old woman in the nearby town of Casarano on Saturday, and is the fourth case of the disease to hit the province of Lecce, part of the Salento area, this year.

 

Known officially as Creutzfeldt-Jakob Disease (CJD), the disease became notorious in the 1990s after an outbreak was attributed to eating infected meat. It was dubbed 'mad cow' disease by the media.

 

The illness causes the brain tissue to deteriorate rapidly, resulting in death, usually within months.

 

But it can have many causes and is not only due to eating meat contaminated with the disease.

 

Giovanni Gorgoni, the general manager of the local health authority, moved quickly to quell fears that infected meat had caused the outbreak.

 

“Until today, no cases of the disease caused by eating infected meat have been recorded in Salento,” he told Leccepirma.it.

 

“The strict protocols for tracing and checking meat that were brought in following the epidemic in Britain reassure us that this will continue to be the case.”

 

Samples of the deceased patients' cerebral tissue have been sent for analysis in Bologna to establish which form of CJD they were infected with.

 

Only one form of the disease, variant CJD, is caused by eating contaminated food and 10 to 15 percent of all cases are genetic.

 

For more news from Italy, join us on Facebook and Twitter.

 

Patrick Browne (patrick.browne@thelocal.com)

 


 

Thursday, January 06, 2011

 

Italy: 'Mad cow disease' claims second Italian victim

 


 

1ST CASE NVCJD ITALY 2002

 

Eurosurveillance, Volume 6, Issue 6, 07 February 2002 Articles S Salmaso1

 

--------------------------------------------------------------------------------

 

Citation style for this article: Salmaso S.

 

First case of vCJD reported in Italy.

 

Euro Surveill. 2002;6(6):pii=2022.

 

Available online:

 


 

Date of submission:

 

--------------------------------------------------------------------------------

 

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First case of vCJD reported in Italy

 

The first case of variant Creutzfeld-Jakob Disease (vCJD) has been reported in Italy (1). The case from Sicily was diagnosed in Italy and Great Britain on the basis of clinical and instrumental tests and tonsillar biopsy. The Istituto Superiore di Sanità (ISS) has classified the case as probable, but since the patient is still alive, the ISS has not released any additional information. The surveillance and reporting of CJD has been mandatory in Italy since the beginning of 2002. A ban on feeding mammalian protein to ruminants was approved on 28 July 1984, and enforced from 15 September that year. The prevalence of indigenous cases of bovine spongiform encephalopathy per 10 000 tests was 1.03 for the year 2001 (2).

 

References :

 

1.Ministero della Salute. Segnalato caso variante malattia Creutzfeldt-Jakob. Press release 05/02/2002 N° 40, 5 February 2002.

 


 

2.Centro per lo Studio e le Ricerche sulle Encefalopatie Animali e Neuropatologie Comparate. Focolai BSE in Italia: 2001/2002.

 


 

Reported by Stefania Salmaso

 

(salmaso@iss.it), Istituto Superiore di Sanità, Italy.

 


 

 Eurosurveillance, Volume 6, Issue 40, 03 October 2002

 

Articles

 

A M Molesworth1

 

--------------------------------------------------------------------------------

 

Citation style for this article: Molesworth AM.

 

First case of variant Creutzfeldt-Jakob disease reported in Italy - update. Euro Surveill. 2002;6(40):pii=1891.

 


 

--------------------------------------------------------------------------------

 

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First case of variant Creutzfeldt-Jakob disease reported in Italy - update

 

A paper published in the Lancet this week describes the first case of variant Creutzfeldt-Jakob disease (vCJD) in Italy (1). The patient, a 25 year old Sicilian woman, developed clinical symptoms in 2001 and was first reported in February this year (2). Although definitive diagnosis of vCJD requires neuropathological confirmation, the woman’s illness fulfils the diagnostic criteria for probable vCJD (3), a brain scan was characteristic of vCJD and the abnormal protein associated with vCJD has been detected in a tonsil biopsy.

 

The patient had never undergone neurosurgery, or received a blood transfusion or any other treatment that might be associated with transmission of a prion disease. Scientific evidence suggests that vCJD is, however, caused by transmission of the bovine spongiform encephalopathy agent (BSE) to humans. The woman is likely to have acquired her infection within Italy, having never travelled to the United Kingdom (UK) or any other country with reported BSE. Cases of indigenous BSE were first reported in Italy following the implementation, in 2001, of mandatory testing of cattle older than 30 months destined for slaughter (4). By the end of September 2002 70 indigenous cases and two British imported cases had been identified (5).

 

To date, in addition to the Italian case, single cases of definite or probable vCJD have been diagnosed with onset in each of the Republic of Ireland, Canada and the United States, a further six in France and 127 in the UK (see EUROCJD, http://www.eurocjd.ed.ac.uk/). The occurrence of cases both within and outside the UK remains a concern, supporting the need for continuous surveillance programmes of transmissible spongiform encephalopathies in humans and animals in the UK and other countries.

 

References :

 

La Bella V, Collinge J, Pocchiari M, Piccoli F. Variant Creutzfeldt-Jakob disease in an Italian woman. Lancet 2002; 360: 997-8. (http://pdf.thelancet.com/pdfdownload?uid=llan.360.9338.original_research.22571.1&x=x.pdf).

 

 Salmaso S. First case of vCJD reported in Italy. Eurosurveillance Weekly 2002; 6: 020207. (http://www.eurosurveillance.org/ew/2002/020207.asp).

 

 Will RG, Zeidler M, Stewart GE, Macleod MA, Ironside JW, Cousens SN, et al. Diagnosis of new variant Creutzfeldt-Jakob disease. Ann Neurol 2000;47: 575-82.

 

 European Commission. Regulation (EC) No 999/2001 of the European Parliament and of the Council of 22 May 2001 (http://europa.eu.int/comm/food/fs/bse/bse36_en.pdf)

 

 Centro per lo Studio e le Ricerche sulle Encefalopatie Animali e Neuropatologie Comparate. Focolai BSE in Italia [BSE Outbreaks in Italy]: 2001/2002 (http://www.to.izs.it)

 

 Reported by Anna Molesworth (amolesworth@phls.org.uk) and Peter Horby, Public Health Laboratory Service Communicable Disease Surveillance Centre, London, England.

 


 

In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported.

 

The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.

 


 

Image] Research letters Volume 352, Number 9134 [Image] 3 October1998[Previous] [Next] [Image][Image]

 

Simultaneous occurrence of spongiform encephalopathy in a manand his cat in Italy

 

[Image] Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, SergioFerrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, SalvatoreMonaco

 

Transmissible spongiform encephalopathies (TSE) encompass inherited,acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four types of PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 inthe UK.5

 

We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.

 

snip...

 

Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2

 

snip...end

 


 


 

Subject: ITALY: Two More Cases BSE Confirmed after some 54,500 tests since Jan. 1, 2001 (U.S.A. only 12,000 tests in 12 YEARS ???) Date: Tue, 27 Mar 2001 10:13:48 -0800 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de

 

 ######### Bovine Spongiform Encephalopathy #########

 

Italy: Two More Cases BSE Confirmed

 

ROME (AP) - Italy confirmed two more cases of mad cow disease Tuesday, bringing the total number of infected animals to nine.

 

Another suspected case in central Italy awaits final results.

 

The infected cows were found in two separate farms in the northern Lombardy region, said the Health Ministry.

 

Final analyses of the brain tissue were conducted in a Turin-based zoological institute.

 

Italy has tested more than 54,500 animals since the beginning of the year, when the European Union began requiring tests on cattle older than 30 months destined for slaughter. About 1,000 tests await final results, the Health Ministry said.

 

Many experts believe that bovine spongiform encephalopathy, the formal name for mad cow disease, can be transmitted to people who eat meat from infected animals.

 

So far, Italy has had no human cases.

 

Article Copyright 2001 Associated Press.

 


 

amazing, a Country the size Italy testing this many animals, but yet the U.S. still standing with finger in ?????????? ear....

 

i would be curious to know the total cattle population of Italy compared to U.S. ???

 

kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA

 

New cases in Italy (+2), Belgium (+2), France (+1), Great Britain (+23)

 

BSE in EUROPE INCIDENCE OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE-statistics http://ourworld.cs.com/_ht_a/j1braakman/BSE.htm or http://go.to/mad-cow

 

TSS

 

 

SEE FRANCE INCREASE OF SPORADIC CJD ;

 


 

nvCJD worldwide statistics that have been documented

 


 

see increased sporadic cjd cases in different BSE countries here ;

 


 


 


 


 


 

 

ITALY BSE

 

Italye   BSE
1994-2b
2001-48
2002-38
2003-29
2004-7
2005-8
2006-7
2007-2
2008-1
2009-2

 

e
Italy:
Year 2002 - Includes 2 imported cases.

 

 


 


 


 


 

 

***UPDATE TSE PRION AKA MAD COW TYPE DISEASE 2015***

 

 BSE, SCRAPIE, AND CWD HAVE NOW BEEN LINKED TO SPORADIC CJD. just saying, ignore these facts if you must, don’t report it to the public, but it does not change the science. ...tss

 

 PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 

THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.

 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. ***We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. ***Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

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

 

***thus questioning the origin of human sporadic cases...

 

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

 


 

 ***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

 

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

 

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

 

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

 


 


 

 

***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.

 

***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

 

IBNC Tauopathy or TSE Prion disease, it appears, no one is sure

 

Posted by flounder on 03 Jul 2015 at 16:53 GMT

 


 

 

10 years post mad cow feed ban August 1997

 

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

 


 

16 years post mad cow feed ban August 1997

 

2013

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

17 years post mad cow feed ban August 1997

 

Tuesday, December 23, 2014

 

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

 


 

Australia

 

COMMONWEALTH OF AUSTRALIA Official Committee Hansard SENATE RURAL AND REGIONAL AFFAIRS AND TRANSPORT REFERENCES COMMITTEE Reference: Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 CANBERRA BY AUTHORITY OF THE SENATE

 

RRA&T 2 Senate Friday, 5 February 2010 RURAL AND REGIONAL AFFAIRS AND TRANSPORT

 

[9.03 am]

 

BELLINGER, Mr Brad, Chairman, Australian Beef Association

 

CARTER, Mr John Edward, Director, Australian Beef Association

 

CHAIR—Welcome. Would you like to make an opening statement?

 

Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14

 

December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:

 

snip...end

 

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

 


 

We have shown that cattle-adapted TME is the third cattle prion strain (joining classical and L-type BSE) to be transmissible both to non-human primates and transgenic mice overexpressing human PrP. However, the successful transmission of raccoon TME to primate, inducing a disease with similar features as cattle TME, extends this notion to TME-related strains independent of host origin. Pathological, biochemical and bioassay investigations converged to demonstrate the similarity between cattle-adapted TME and L-BSE.

 


 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

31 Jan 2015 at 20:14 GMT

 

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

 

Singeltary et al

 

31 Jan 2015 at 20:14 GMT

 


 

 

PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

 

*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

 

O18

 

Zoonotic Potential of CWD Prions

 

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

 

*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.

 

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

 

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

 

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

 

P.105: RT-QuIC models trans-species prion transmission

 

Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

 

Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.

 

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

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

 

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

 


 

From: Terry S. Singeltary Sr.

 

Sent: Saturday, November 15, 2014 9:29 PM

 

To: Terry S. Singeltary Sr.

 

Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984

 

THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE

 

R. G. WILL

 

1984

 

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

 

snip...

 


 

 PLEASE REMEMBER, all iatrogenic CJD is, is sporadic CJD, until the route, source, time of the iatrogenic event is discovered, documented, and then put into the academic and then the public domain, which very seldom happens do to it’s long incubation period, and the lack of trace back efforts. ...terry

 

Sunday, July 06, 2014

 

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

 

Conclusions—The a priori hypotheses were supported.

 

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

 


 

Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease

 

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

 


 

*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent

 

*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,

 

*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.

 

PPo2-27:

 

Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

 

*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

 

PPo2-7:

 

Biochemical and Biophysical Characterization of Different CWD Isolates

 

*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.

 


 

Envt.07:

 

Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease

 

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

 


 

>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<

 

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

 

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 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.

 


 


 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

HD.13: CWD infection in the spleen of humanized transgenic mice

 

***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.

 

Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.

 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

 


 

Friday, November 09, 2012

 

*** Chronic Wasting Disease CWD in cervidae and transmission to other species

 


 

the raw, uncut, and uncensored version...of the truth. I am getting old, tired, and my patience is running thin, from the sheer ignorance of it all $$$

 

Sunday, August 23, 2015

 

*** TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas ***

 


 

human cwd will NOT look like nvCJD. in fact, see ;

 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

 


 

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

 

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

 

snip...

 

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

 


 

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

 

3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...

 


 

Thursday, July 30, 2015

 

*** Professor Lacey believes sporadic CJD itself originates from a cattle infection number of cattle farmers falling victim to Creutzfeld-Jakob Disease is much too high to be mere chance ***

 


 

BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein

 

*** Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2.

 

These data suggest that more than one BSEderived prion strain might infect humans;

 

***it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.

 

snip...

 

These studies further strengthen the evidence that vCJD is caused by a BSE-like prion strain.

 

Also, remarkably, the key neuropathological hallmark of vCJD, the presence of abundant florid PrP plaques, can be recapitulated on BSE or vCJD transmission to these mice.

 

***However, the most surprising aspect of the studies was the finding that an alternate pattern of disease can be induced in 129MM Tg35 mice from primary transmission of BSE, with a molecular phenotype indistinguishable from that of a subtype of sporadic CJD. This finding has important potential implications as it raises the possibility that some humans infected with BSE prions may develop a clinical disease indistinguishable from classical CJD associated with type 2 PrPSc. This is, in our experience, the commonest molecular sub-type of sporadic CJD. In this regard, it is of interest that the reported incidence of sporadic CJD has risen in the UK since the 1970s (Cousens et al., 1997)...

 


 

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

 

Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD

 

Date: Thu, 28 Nov 2002 10:23:43 -0000

 

From: "Asante, Emmanuel A" e.asante@ic.ac.uk

 

To: "'flounder@wt.net'" flounder@wt.net

 

Dear Terry,

 

I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.

 

Thank you for your interest in the paper.

 

In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.

 

I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.

 

Emmanuel Asante

 

<>

 

____________________________________

 

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)

 

____________________________________

 

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...

 


 

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...

 


 


 

Medical Sciences

 

Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease

 

Cristina Casalone *{dagger} , Gianluigi Zanusso {dagger} {ddagger} , Pierluigi Acutis *, Sergio Ferrari {ddagger} , Lorenzo Capucci § , Fabrizio Tagliavini ¶, Salvatore Monaco {ddagger} ||, and Maria Caramelli *

 

*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; {ddagger} Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; § Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy

 

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)

 

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.

 

------------------------------------------------------------------------

 

{dagger} C.C. and G.Z. contributed equally to this work.

 

||To whom correspondence should be addressed.

 

E-ma;. www.pnas.org/cgi/doi/10.1073/pnas.0305777101

 


 

Tuesday, August 4, 2015

 

FDA U.S. Measures to Protect Against BSE

 


 

 

NOW THINK EXPOSURE THERE FROM ALL THE ABOVE, AT A HOSPITAL NEAR YOU, what if ???

 

 

Tuesday, May 26, 2015

 

*** Minimise transmission risk of CJD and vCJD in healthcare settings ***

 

Last updated 15 May 2015

 


 

Thursday, August 13, 2015

 

Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years

 


 

Monday, August 17, 2015

 

FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS

 

I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al...

 

see ;

 


 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

 

Terry S. Singeltary, Sr Bacliff, Tex

 

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.

 


 

Singeltary publishing’s ...

 

 
 
 
 
 
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