'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:
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
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.
Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=1891
Date of submission:
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
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 ...
TSS