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Molecular Barriers to Zoonotic Transmission of Prions (CWD, not good for hunters)

flounder9

flounder9

Member
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.



http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm


http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html


kind regards,
terry
 
CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ???

P07 Behavioral Neurology: Aging and Dementia MRI More Useful Than PET for Diagnosis of Heidenhain Variant Creutzfeldt-Jacob Disease (P07.163)

Jonathan Beary1 and Edward Manno2 1 General Neurology, Neurological Institute Cleveland Clinic Cleveland OH 2 Cerebrovascular Neurology, Neurological Institute Cleveland Clinic Cleveland OH

OBJECTIVE: To demonstrate that MRI detection of subtle focal cortical abnormalities can prove more useful than positron emission tomography (PET) in the diagnosis of Heidenhain variant Creutzfeldt-Jakob Disease (hvCJD).

BACKGROUND: hvCJD is a rare neurodegenerative, spongiform encephalopathy with an aggressive clinical course. PET brain imaging has been reported to detect focal cortical abnormalities in hvCJD with greater sensitivity than MRI. However, because PET is both more costly and less accessable than MRI, early diagnosis of this disease and subsequent prognostication may be unnecessarily delayed. The reliability of MRI over PET in detecting isolated occipital cortical changes suggestive of hvCJD has not been well studied.

DESIGN/METHODS: This is a case report with relevent neuroimaging review.

RESULTS: A 70 year-old right-handed male experienced visual hallucinations and visuospatial disorientation with worsening ataxia followed by progressive anterograde amnesia and cortical blindness. Six weeks later he was comatose with startle myoclonus. A sharply-contoured periodic pattern was evident posteriorly on continuous EEG monitoring with brain MRI revealing subtle bilateral occipital cortical diffusion restriction. PET brain imaging showed diffuse non-focal cortical hypometabolism. Both cerebrospinal fluid (CSF) 14-3-3 and tau protein studies were positive. EEG progressed to refractory status epilepticus and the patient died four days later. ***The presence of abnormal brain protease-resistant prion protein and MM1 genotype at autopsy supported the diagnosis of hvCJD.

CONCLUSIONS: hvCJD should be considered in patients with rapid-onset idiopathic visual disturbance and dementia. When combined with EEG and CSF analysis, isolated MRI visual cortex diffusion restriction is suggestive of this ultra-aggressive prion variant. MRI is able to efficiently facilitate valuable prognostication early in hvCJD and can be more useful than costly PET imaging.

Disclosure: Dr. Beary has nothing to disclose. Dr. Manno has nothing to disclose.


http://www.neurology.org/cgi/content/meeting_abstract/80/1_MeetingAbstracts/P07.163


> The presence of abnormal brain protease-resistant prion protein and MM1 genotype at autopsy supported the diagnosis of hvCJD.


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.

http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm

http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html


Subtype 1: (sCJDMM1 and sCJDMV1)

This subtype is observed in patients who are MM homozygous or MV heterozygous at codon 129 of the PrP gene (PRNP) and carry PrPSc Type 1. Clinical duration is short, 3‑4 months.32 The most common presentation in sCJDMM1 patients is cognitive impairment leading to frank dementia, gait or limb ataxia, myoclonic jerks and visual signs leading to cortical blindness (Heidenhain’s syndrome)...

https://www.landesbioscience.com/pdf/06Ahmad_Liberski.pdf


Animals injected with iatrogenic Creutzfeldt–Jakob disease MM1 and genetic Creutzfeldt–Jakob disease MM1 linked to the E200K mutation showed the same phenotypic features as those infected with sporadic Creutzfeldt–Jakob disease MM1 prions...

http://brain.oxfordjournals.org/content/early/2010/09/07/brain.awq234.full.pdf


*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***


http://www.jbc.org/cgi/content/abstract/M704597200v1?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Cross-sequence+transmission+of+sporadic+Creutzfeldt-Jakob+disease+creates+a+new+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT


snip...see full text ;


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html


Wednesday, June 16, 2010

Defining sporadic Creutzfeldt-Jakob disease strains and their transmission properties

The epidemiological findings in sCJD demonstrate that approximately 80% of patients are diagnosed with “classic CJD” types MM1 and MV1, which might intriguingly suggest an infectious rather than genetic origin for the majority of sCJD cases.

snip...

Therefore if sCJD(MV2) and sCJD(VV2) were to become iatrogenic sources of human infection, the host response may be indistinguishable from sCJD(MM1) and more transmissible with respect to further infection.

END...TSS

http://creutzfeldt-jakob-disease.blogspot.com/2010/06/defining-sporadic-creutzfeldt-jakob.html


Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'

DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough Bldg. Galveston, Texas 77555-0785

FAX COVER SHEET

DATE: 4-23-98

TO: Mr. Terry Singeltary @ -------

FROM: Gerald Campbell

FAX: (409) 772-5315 PHONE: (409) 772-2881

Number of Pages (including cover sheet):

Message:

*CONFIDENTIALITY NOTICE*

This document accompanying this transmission contains confidential information belonging to the sender that is legally privileged. This information is intended only for the use of the individual or entry names above. If you are not the intended recipient, you are hereby notified that any disclosure, copying distribution, or the taking of any action in reliances on the contents of this telefaxed information is strictly prohibited. If you received this telefax in error, please notify us by telephone immediately to arrange for return of the original documents.

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

Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Admitting Race: C

Attending Dr.: Date / Time Admitted : 12/14/97 1228 Copies to:

UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report

FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858

Autopsy NO.: AU-97-00435

AUTOPSY INFORMATION: Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00 Pathologist/Resident: Pencil/Fernandez Service: Private Restriction: Brain only

FINAL AUTOPSY DIAGNOSIS

I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

snip...see full text ;

http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html


Wednesday, January 01, 2014

APHIS-2006-0118-0100 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

http://chronic-wasting-disease.blogspot.com/2014/01/aphis-2006-0118-0100-chronic-wasting.html


Monday, December 02, 2013

*** A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD – the human form of ‘mad cow’ disease – may be being spread by medical procedures

http://creutzfeldt-jakob-disease.blogspot.com/2013/12/a-parliamentary-inquiry-has-been.html


Wednesday, December 11, 2013

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

http://creutzfeldt-jakob-disease.blogspot.com/2013/12/detection-of-infectivity-in-blood-of.html


http://www.plosone.org/annotation/listThread.action;jsessionid=43759816BCF4952B7D9504B8FD9D5CA7?root=363


Friday, November 22, 2013

Chronic Wasting disease CWD is threat to the entire UK deer population Singeltary submission to the Scottish Parliament

http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html



Terry S. Singeltary Sr., MOM DOD 12/14/97 confirmed Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD...just made a promise to her, never forget, and never let them forget. ...



Thursday, January 2, 2014

CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ???

http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/cwd-tse-prion-in-cervids-to-htgmice.html
 
Flounder, do you have a point here or do you just like posting PhD level research that most on here can't understand and all on here don't want to have to dig through even if they could understand it?

I have a feeling you are trying to make a valid point that there is some concern here. Help us out!!!
 
2-bucks said:
Flounder, do you have a point here or do you just like posting PhD level research that most on here can't understand and all on here don't want to have to dig through even if they could understand it?

I have a feeling you are trying to make a valid point that there is some concern here. Help us out!!!
Click to expand...



AS with BSE aka mad cow disease in cattle, they have now linked CWD in the lab, they have now linked CWD to the MM1 type sporadic CJD i.e. hvCJD (type my mother died from), and the other science I submitted there was the iatrogenic potential for CWD as in friendly fire, second hand transmission, pass it forward mode of transmission, you consume CWD, you never go clinical, maybe die from something else before CWD has time to go clinical in you, and maybe you never get it, BUT, you go on to have a medical/surgical/blood procedure, and then taint the surgical arena with CWD/TSE, and from there, even though you never go clinical, and are oblivious of this fact that you are exposed, you have exposed every other person that used those same surgical instruments, used your tissue, blood, etc. _iatrogenic_, and they become exposed, some go clinical and die from what you ate, long after you ate it, thus the case goes down as sporadic CJD, from unknown route and source of the TSE agent. and the TSE prion agent continues to spread. ...


1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract





New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.


http://www.pnas.org/content/97/7/3418.full


Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/


Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
T

he data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.

http://www.landesbioscience.com/journals/prion/NicholsPRION3-3.pdf


A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE

In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.

http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract


Wednesday, July 10, 2013

Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals

BMC Veterinary Research 2013, 9:134 doi:10.1186/1746-6148-9-134

http://transmissiblespongiformencep...07/rapid-assessment-of-bovine-spongiform.html


PPo4-4:


Survival and Limited Spread of TSE Infectivity after Burial


Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK


Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.

The authors gratefully acknowledge funding from DEFRA.


http://www.prion2010.org/bilder/pri...39&PHPSESSID=a30a38202cfec579000b77af81be3099




*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.



http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf



kind regards, terry
 
Last edited:
flounder9 said:
AS with BSE aka mad cow disease in cattle, they have now linked CWD in the lab, they have now linked CWD to the MM1 type sporadic CJD i.e. hvCJD (type my mother died from), and the other science I submitted there was the iatrogenic potential for CWD as in friendly fire, second hand transmission, pass it forward mode of transmission, you consume CWD, you never go clinical, maybe die from something else before CWD has time to go clinical in you, and maybe you never get it, BUT, you go on to have a medical/surgical/blood procedure, and then taint the surgical arena with CWD/TSE, and from there, even though you never go clinical, and are oblivious of this fact that you are exposed, you have exposed every other person that used those same surgical instruments, used your tissue, blood, etc. _iatrogenic_, and they become exposed, some go clinical and die from what you ate, long after you ate it, thus the case goes down as sporadic CJD, from unknown route and source of the TSE agent. and the TSE prion agent continues to spread. ...


And there you have it.....damn, one more thing....
Click to expand...
 
Rather than go back to school after 40 years to decipher this, I think in laymen terms it means if humans eat venison infected with CWD there's a good chance of having our brains eaten away slowly! Scary to think that we can't hunt and consume deer if it ever becomes a pandemic, life would not be the same for me :(
 
i think what it comes down to is if a human eats a deer with CWD then the zombie apocalypse will soon follow...WALKING DEAD!!!
 
Lucky13 said:
i think what it comes down to is if a human eats a deer with CWD then the zombie apocalypse will soon follow...WALKING DEAD!!!
Click to expand...

That is just great! I remember the good old days when the stuff that killed you was big and scarey, not prions, mosquitos, ticks and midges.
 
flounder, instead of just posting copy and paste info, why not let everybody know why you started this crusade of yours over a decade ago?
 
Flounder.....I hope you dont think the encyclopedia you attached to my question answered it.

As Shovelbuck states please enlighten us on this topic if this is something you have been passionate about for over a decade. If you respond with more cut and paste from medical journals I promise to stop asking as it will be clear you either don't have the will or maybe don't have the ability to have a logical down to earth conversation on something that may be important.
 
flounder9 said:
AS with BSE aka mad cow disease in cattle, they have now linked CWD in the lab, they have now linked CWD to the MM1 type sporadic CJD i.e. hvCJD (type my mother died from), and the other science I submitted there was the iatrogenic potential for CWD as in friendly fire, second hand transmission, pass it forward mode of transmission, you consume CWD, you never go clinical, maybe die from something else before CWD has time to go clinical in you, and maybe you never get it, BUT, you go on to have a medical/surgical/blood procedure, and then taint the surgical arena with CWD/TSE, and from there, even though you never go clinical, and are oblivious of this fact that you are exposed, you have exposed every other person that used those same surgical instruments, used your tissue, blood, etc. _iatrogenic_, and they become exposed, some go clinical and die from what you ate, long after you ate it, thus the case goes down as sporadic CJD, from unknown route and source of the TSE agent. and the TSE prion agent continues to spread. ...
Click to expand...

He said taint.:D
 
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